• TABLE OF CONTENTS
HIDE
 Front Cover
 Title Page
 Table of Contents
 Foreword
 Introduction
 Sources of minerals for grazing...
 Factors affecting mineral content...
 Mineral requirements
 Incidence of mineral deficiencies...
 Calcium and phosphorus
 Magnesium
 Potassium
 Sodium and chlorine
 Sulfur
 Cobalt
 Copper and molybdenum
 Iodine
 Iron and manganese
 Selenium
 Zinc
 Newer trace elements
 Toxic elements
 Fluorine
 Diagnosis of mineral deficiencies...
 A mapping technique for determining...
 Production response from mineral...
 Mineral supplementation for grazing...
 Mineral feeders for ruminants
 Summary
 Literature cited
 Acknowledgement
 Back Cover






Group Title: Bulletin - Department of Animal Science, Center for Tropical Agriculture, University of Florida
Title: Minerals for grazing ruminants in tropical regions
CITATION PAGE IMAGE ZOOMABLE PAGE TEXT
Full Citation
STANDARD VIEW MARC VIEW
Permanent Link: http://ufdc.ufl.edu/UF00054813/00001
 Material Information
Title: Minerals for grazing ruminants in tropical regions
Series Title: Bulletin Department of Animal Science, Center for Tropical Agriculture, University of Florida
Physical Description: 86 p. : ill. (some col.) ; 28 cm.
Language: English
Creator: McDowell, L. R., 1941-
University of Florida -- Dept. of Animal Science
United States -- Agency for International Development
Publisher: Dept. of Animal Science, Center for Tropical Agriculture, University of Florida, Gainesville
U.S. Agency for International Development
Place of Publication: Gainesville Fla.
Washington D.C.
Publication Date: [1983]
 Subjects
Subject: Minerals in animal nutrition -- Tropics   ( lcsh )
Livestock -- Tropics   ( lcsh )
Ruminants -- Feeding and feeds -- Tropics   ( lcsh )
Deficiency diseases in domestic animals -- Tropics   ( lcsh )
Grazing -- Tropics   ( lcsh )
Mineral metabolism   ( lcsh )
Veterinary toxicology -- Tropics   ( lcsh )
Genre: government publication (state, provincial, terriorial, dependent)   ( marcgt )
bibliography   ( marcgt )
non-fiction   ( marcgt )
 Notes
Bibliography: Bibliography: p. 78-82.
Statement of Responsibility: L.R. McDowell ... et al..
Funding: Electronic resources created as part of a prototype UF Institutional Repository and Faculty Papers project by the University of Florida.
 Record Information
Bibliographic ID: UF00054813
Volume ID: VID00001
Source Institution: University of Florida
Holding Location: University of Florida
Rights Management: All rights reserved, Board of Trustees of the University of Florida
Resource Identifier: aleph - 002876531
oclc - 12793511
notis - APA7772
lccn - 84070238

Table of Contents
    Front Cover
        Front Cover 1
        Front Cover 2
    Title Page
        Title Page
    Table of Contents
        Page 1
        Page 2
        Page 3
    Foreword
        Page 4
    Introduction
        Page 5
    Sources of minerals for grazing livestock
        Page 5
        Page 6
    Factors affecting mineral content of plants
        Page 7
        Page 8
    Mineral requirements
        Page 9
        Page 10
    Incidence of mineral deficiencies and toxicities
        Page 11
    Calcium and phosphorus
        Page 11
        Page 12
        Requirement
            Page 13
        Deficiency
            Page 13
            Page 14
            Page 15
            Page 16
    Magnesium
        Page 17
        Metabolism
            Page 17
        Requirement
            Page 18
        Deficiency
            Page 18
            Page 19
    Potassium
        Page 20
        Page 21
        Metabolism
            Page 20
        Requirement
            Page 20
        Deficiency
            Page 22
        Prevention and control
            Page 22
        Toxicity
            Page 22
    Sodium and chlorine
        Page 22
        Metabolism
            Page 22
        Requirement
            Page 22
        Deficiency
            Page 23
        Prevention and control
            Page 23
        Toxicity
            Page 23
            Page 24
    Sulfur
        Page 25
        Metabolism
            Page 25
        Requirement
            Page 25
        Deficiency
            Page 25
        Prevention and control
            Page 25
            Page 26
        Toxicity and interrelationships
            Page 27
    Cobalt
        Page 27
        Metabolism
            Page 27
        Requirement
            Page 27
        Deficiency
            Page 28
        Pervention and control
            Page 28
            Page 29
        Toxicity
            Page 30
    Copper and molybdenum
        Page 30
        Metabolism
            Page 30
        Requirement
            Page 30
        Deficiency
            Page 30
            Page 31
            Page 32
    Iodine
        Page 33
        Pervention and control
            Page 33
        Toxicity
            Page 33
            Page 34
        Deficiency
            Page 35
        Metabolism
            Page 35
        Requirement
            Page 35
            Page 36
            Page 37
            Page 38
    Iron and manganese
        Page 39
        Metabolism
            Page 39
        Requirement
            Page 39
        Deficiency
            Page 39
        Prevention and control
            Page 39
        Toxicity
            Page 40
    Selenium
        Page 40
        Metabolism
            Page 40
        Requirement
            Page 40
        Deficiency
            Page 40
        Prevention and control
            Page 41
            Page 42
            Page 43
    Zinc
        Page 44
        Metabolism
            Page 44
        Requirements
            Page 44
        Deficiency
            Page 44
            Page 45
        Prevention and control
            Page 46
        Toxicity
            Page 46
    Newer trace elements
        Page 46
    Toxic elements
        Page 46
    Fluorine
        Page 47
        Essentiality
            Page 47
        Toxicity
            Page 47
        Chemical forms
            Page 48
        Pervention and control
            Page 48
    Diagnosis of mineral deficiencies and imbalances
        Page 48
        Page 49
        Page 50
        Page 51
        Page 52
    A mapping technique for determining mineral deficiencies and toxicities
        Page 53
    Production response from mineral supplementation
        Page 53
        Page 54
        Page 55
        Page 56
        Page 57
    Mineral supplementation for grazing livestock
        Page 58
        Page 59
        Page 60
        Requirements
            Page 61
        Biological availability
            Page 61
        Intake of mineral mixture and dry matter
            Page 61
            Page 62
        Concentration of elements in mineral mixture
            Page 63
            Page 64
            Page 65
            Page 66
        Tag
            Page 67
            Page 68
    Mineral feeders for ruminants
        Page 69
        Page 70
        Page 71
        Page 72
        Page 73
        Page 74
        Page 75
        Page 76
    Summary
        Page 77
    Literature cited
        Page 78
        Page 79
        Page 80
        Page 81
        Page 82
    Acknowledgement
        Page 83
        Page 84
        Page 85
        Page 86
        Page 87
    Back Cover
        Back Cover
Full Text
Lc010 a I


Minerals for Grazing Ruminants

in Tropical Regions


L. R. McDowell, J. H. Conrad, G. L. Ellis and J. K. Loosli
Department of Animal Science
Center for Tropical Agriculture
University of Florida, Gainesville
and
The U. S. Agency for International Development


Vi'4-
ert
T L7



























Figure 7. A cow in Argentina suffers from Figure 15. Hair color changes as a result of copper
botulism as a result of eating bones. deficiency. The dark color is normal
The animal is weak and has difficulty when animals receive adequate copper.
rising. (Courtesy Bernardo Jorge (Courtesy Bernardo Jorge Carrillo,
Carrillo, C.I.C., INTA, Castelar, Argen- C.I.C., INTA, Castelar, Argentina).
tina).


Figure 14. Cobalt deficient cattle in northern
Mato Grosso, Brazil. (Courtesy Jiirgen
Dbbereiner and Carlos H. Tokarnia,
EMBRAPA, Rio de Janeiro, Brazil).


Zinc deficiency lesions in grazing cattle
observed in Bethlehem, Orange Free
State, South Africa. The major clinical
sign is widespread alopecia. The most
severe lesions were between the rear
and front legs, which cannot be seen.
Bleeding of the cracked skin in this area
was sometimes observed. (Courtesy
B. D. H. Van Niekerk, Voermol
Products Ltd., Natal, South Africa).


Cover: Mineral feeder at Pichilingue Experiment Station in Ecuador (top). Empty mineral feeder in the
Colombian llanos (bottom) (L. R. McDowell, University of Florida).





BULLETIN


Minerals for Grazing Ruminants
in Tropical Regions
1983

L. R. McDowell, J. H. Conrad, G. L. Ellis and J. K. Loosli

Department of Animal Science
Center for Tropical Agriculture
University of Florida, Gainesville
and
The U. S. Agency for International Development


Library of Congress Catalog Card Number 84-70238









CONTENTS

PAGE NUMBER
FOREW ORD ....................................................... 4

INTRODUCTION ................................................... 5

SOURCES OF MINERALS FOR GRAZING LIVESTOCK. .................... 5

Forages.......................................................... 5
W ater and Soil...................................................... 7

FACTORS AFFECTING MINERAL CONTENT OF PLANTS .................. 7

MINERAL REQUIREMENTS ........................................... 9

INCIDENCE OF MINERAL DEFICIENCIES AND TOXICITIES. .............. .11

CALCIUM AND PHOSPHORUS ........................................ 11

M etabolism ................................... .................. 11
Requirement ......................................................13
Deficiency............................................ ............. 13
Prevention and Control ............................................. 17

M AGNESIUM ..................................................... 17

M etabolism ..................................................... 17
Requirement ..................................................... 18
D efficiency ....................................................... 18
Prevention and Control.............................................. 18

POTASSIUM ....................................................... 20

M etabolism ..................................................... 20
Requirement ..................................................... 20
D efficiency ...................................................... 22
Prevention and Control............................................ 22
Toxicity ............................. ............... ... ......... 22

SODIUM AND CHLORINE ........................................... 22

M etabolism ....................................................... 22
Requirement........................ ........... ....... ............ 22
D eficiency....................... .............................. .23
Prevention and Control.............................................. 23
Toxicity ............................................. .......... .......... 23

SULFUR.......................... ..... ... ......................... 25

M etabolism .................... ......... ............... ......... 25
Requirem ent................................... ................. 25
D eficiency.................................... .................. 25
Prevention and Control ............................................. 25
Toxicity and Interrelationships........................................ 27



1









PAGE NUMBER

COBALT........................................................... 27

Metabolism ......................................................27
R equirem ent ...................................... .. ............ 27
Deficiency................. ; ...................................... 28
Prevention and Control............................................. 28
T oxicity ........................................................ 30

COPPER AND MOLYBDENUM..................................... ....30

Metabolism ..................................... ................. 30
Requirement ..................................................... 30
Deficiency ....................................................... 30
Prevention and Control ............................................ 33
T oxicity ........................................................ 33

IODINE ...........................................................33

M etabolism ..................................................... 33
Requirement ..................................................... 33
Deficiency ....................................................... 35
Prevention and Control...............................................35
T oxicity ........................................................ 35

IRON AND MANGANESE..............................................39

M etabolism ..................................................... 39
Require ent ................................................... 39
D efficiency ....................................................... 39
Prevention and Control............................................. 39
T oxicity ........................................................ 40

SELENIUM ...................................................... .40

M etabolism ....................................................... 40
Require ent ......................................................40
Deficiency ........................................................ 40
Prevention and Control.............................................. 41
T oxicity ........................................................ 44

ZINC............................................................. 44

M etabolism ..................................................... 44
Requirement ..................................................... 44
Deficiency ....................................................... 44
Prevention and Control...............................................46
T oxicity ......................................................... 46

NEWER TRACE ELEMENTS............................................46

TOXIC ELEMENTS ............... .................................. 46









PAGE NUMBER

FLUORINE........................................................ .47

Essentiality .......................................................47
T oxicity ........................................................ 47
Chem ical Form s ................................................. 48
Prevention and Control...............................................48

DIAGNOSIS OF MINERAL DEFICIENCIES AND IMBALANCES .............. 48

A MAPPING TECHNIQUE FOR DETERMINING
MINERAL DEFICIENCIES AND TOXICITIES .............................53

PRODUCTION RESPONSES FROM MINERAL SUPPLEMENTATION .......... 53

MINERAL SUPPLEMENTATION FOR GRAZING LIVESTOCK ............... 58

Require ents ................................................... 61
Biological Availability ...............................................61
Intake of Mineral Mixtures and Dry Matter. .............................. 61
Concentration of Elements in Mineral Mixtures ........................... .63
Tag ............................................................ 67

MINERAL FEEDERS FOR RUMINANTS ................................ 69

SUMMARY....................................................... .77

LITERATURE CITED ............................................... 78

ACKNOWLEDGMENTS .............................................. 83









FOREWORD

This publication focuses on the most nutritionally important
minerals for grazing ruminants in the tropics. It was prepared by the
Department of Animal Science, Center for Tropical Agriculture, Institute
of Food and Agricultural Sciences, University of Florida with funds from
the Office of Agriculture, Bureau for Science and Technology, United
States Agency for International Development (USAID), Washington, D.C.
The University of Florida has had a contract with USAID for the past
nine years to support the study of mineral deficiencies and toxicities
in grazing ruminants in the tropics. The project title is "Development
of Efficient Mineral Supplementation Regimes for Grazing Ruminants in
the Tropics", contract number AID/ta-c-1153. Collaborative mineral
research between the University of Florida and cooperating research
groups is or has been in progress in Bolivia, Brazil, Colombia, Costa
Rica, Dominican Republic, Ecuador, El Salvador, Guatemala, Haiti,
Indonesia, Kenya, Malawi, Malaysia, Mexico, Panama, Paraguay, Peru,
Philippines, Sudan, Swaziland, Trinidad, Thailand, Uruguay, Venezuela
and Zaire. For information concerning these programs, contact the
Department of Animal Science, Animal Science Building, University of
Florida, Gainesville, Florida, 32611.

Sections of the present publication have been modified from those
in the Florida Extension Bulletin 683 (Revised) titled "Minerals for
Beef Cattle in Florida" prepared by C.B. Ammerman, R.L. Shirley, H.L.
Chapman, Jr., J.F. Hentges, Jr., F.M. Pate, L.R. McDowell and J.H.
Conrad.









INTRODUCTION

Undernutrition is commonly accepted as one of the most important
limitations to grazing livestock production in tropical countries. The
lack of sufficient energy and protein is often responsible for sub-
optimum livestock production. However, numerous investigators have
observed that cattle sometimes deteriorate in spite of an abundant feed
supply. Mineral imbalances (deficiencies or excesses) in soils and
forages have long been held responsible for low production and repro-
ductive problems among grazing ruminants in the tropics. Wasting
diseases, loss of hair, depigmented hair, skin disorders, non-infectious
abortion, diarrhea, anemia, loss of appetite, bone abnormalities,
tetany, low fertility and pica are clinical signs often suggestive of
mineral deficiencies throughout the world.

Mineral elements are dietary essentials for all animals and influ-
ence the efficiency of livestock production. In fact, approximately five
percent of the body weight of an animal consists of minerals. At least
15 mineral elements have been identified as nutritionally essential for
ruminants. There are seven major or macrominerals calcium (Ca),
phosphorus (P), potassium (K), sodium (Na), chlorine (Cl), magnesium (Mg)
and sulfur (S) and eight trace or microminerals cobalt (Co), copper
(Cu), iodine (I), iron (Fe), manganese (Mn), molybdenum (Mo), selenium
(Se) and zinc (Zn). In specific regions, toxic concentrations of Cu,
Fluorine, Mn, Mo or Se may limit grazing livestock production. Addi-
tional toxic elements aluminum (Al), arsenic (As), cadmium (Cd), lead
(Pb) and mercury (Hg) for ruminants as well as the possible signifi-
cance of newly discovered essential elements As, chromium (Cr), F,
nickel (Ni), silicon (Si) tin (Sn) and vanadium (V) have been reviewed.
Practical significance of the "newer" trace elements for ruminants has
not been found, with evidence for essentiality based almost exclusively
on growth effects in animals receiving highly purified diets in
controlled environments.

Forages grown on tropical soils have been shown to be highly defi-
cient in a number of the macro- and micromineral elements needed by the
animal. Thus, it is necessary to provide these elements as dietary
supplemental minerals to promote efficient and profitable livestock
production in warm climate regions. It is the purpose of this publi-
cation to summarize the information currently available on mineral
nutrition of livestock and to make recommendations on how these minerals
should be provided to grazing ruminants.

SOURCES OF MINERALS FOR GRAZING LIVESTOCK

Forages
Grazing livestock from tropical countries often do not receive
mineral supplementation except for common salt and must depend almost
exclusively upon forages for their requirements. Only rarely, however,
can tropical forages completely satisfy all mineral requirements. Table
1 summarizes the mineral concentrations of 2615 Latin American forages.
Borderline to deficient levels of certain elements were noted for many
entries: Co, 43%; Cu, 47%; Mg, 35%; P, 73%; Na, 60%; and Zn, 75%.









INTRODUCTION

Undernutrition is commonly accepted as one of the most important
limitations to grazing livestock production in tropical countries. The
lack of sufficient energy and protein is often responsible for sub-
optimum livestock production. However, numerous investigators have
observed that cattle sometimes deteriorate in spite of an abundant feed
supply. Mineral imbalances (deficiencies or excesses) in soils and
forages have long been held responsible for low production and repro-
ductive problems among grazing ruminants in the tropics. Wasting
diseases, loss of hair, depigmented hair, skin disorders, non-infectious
abortion, diarrhea, anemia, loss of appetite, bone abnormalities,
tetany, low fertility and pica are clinical signs often suggestive of
mineral deficiencies throughout the world.

Mineral elements are dietary essentials for all animals and influ-
ence the efficiency of livestock production. In fact, approximately five
percent of the body weight of an animal consists of minerals. At least
15 mineral elements have been identified as nutritionally essential for
ruminants. There are seven major or macrominerals calcium (Ca),
phosphorus (P), potassium (K), sodium (Na), chlorine (Cl), magnesium (Mg)
and sulfur (S) and eight trace or microminerals cobalt (Co), copper
(Cu), iodine (I), iron (Fe), manganese (Mn), molybdenum (Mo), selenium
(Se) and zinc (Zn). In specific regions, toxic concentrations of Cu,
Fluorine, Mn, Mo or Se may limit grazing livestock production. Addi-
tional toxic elements aluminum (Al), arsenic (As), cadmium (Cd), lead
(Pb) and mercury (Hg) for ruminants as well as the possible signifi-
cance of newly discovered essential elements As, chromium (Cr), F,
nickel (Ni), silicon (Si) tin (Sn) and vanadium (V) have been reviewed.
Practical significance of the "newer" trace elements for ruminants has
not been found, with evidence for essentiality based almost exclusively
on growth effects in animals receiving highly purified diets in
controlled environments.

Forages grown on tropical soils have been shown to be highly defi-
cient in a number of the macro- and micromineral elements needed by the
animal. Thus, it is necessary to provide these elements as dietary
supplemental minerals to promote efficient and profitable livestock
production in warm climate regions. It is the purpose of this publi-
cation to summarize the information currently available on mineral
nutrition of livestock and to make recommendations on how these minerals
should be provided to grazing ruminants.

SOURCES OF MINERALS FOR GRAZING LIVESTOCK

Forages
Grazing livestock from tropical countries often do not receive
mineral supplementation except for common salt and must depend almost
exclusively upon forages for their requirements. Only rarely, however,
can tropical forages completely satisfy all mineral requirements. Table
1 summarizes the mineral concentrations of 2615 Latin American forages.
Borderline to deficient levels of certain elements were noted for many
entries: Co, 43%; Cu, 47%; Mg, 35%; P, 73%; Na, 60%; and Zn, 75%.













Table 1. MINERAL BREAKDOWN AND CONCENTRATIONS OF 2615 LATIN AMERICAN FORAGES (DRY BASIS)a


Percentage of
forage with
entries

42.9

5.4

9.0

9.8

11.1

11.2

5.1

43.2

7.6

5.6

6.9


No. of
entries

1123

140

236

256

290

293

133

1129

198

146

177


Requirements

0.18-0.60%

0.05-0.10 ppm

4.00-10.0 ppm

10.0 -100. ppm

0.04-0.18 ppm

20.0 -40.0 ppm

0.01 ppm or less

0.18-0.43%

0.60-0.80%

0.10%

10.0 -50.0 ppm


Concentrations, %
% of total
Concentrations, ppm
% of total
Concentrations, ppm
% of total
Concentrations, ppm
% of total
Concentrations, %
% of total
Concentrations, ppm
% of total
Concentrations, ppm
% of total
Concentrations, %
% of total
Concentrations, %
% of total
Concentrations, %
% of total
Concentrations, ppm
% of total


aLatin American Tables of Feed Composition McDowell et al. (1974); McDowell et al. (1977)

bLess than 1% of the other minerals were included.

cSummarzed by McDowell et al. (1977).


Element

Calcium

Cobalt

Copper

Iron

Magnesium

Manganese

Molybdenum

Phosphorus

Potassium

Sodium

Zinc


0- 0.30
31.1
0- 0.10
43.1
0-10.0
46.6
0-100
24.1
0- 0.20
35.2
0-40.0
21.0
0- 3.0
86.4
0- 0.30
72.8
0- 0.80
15.1
0- 0.10
59.5
0-50.0
74.6


over 0.30
68.9
over 0.10
56.9
over 10.0
53.4
over 100
75.9
over 0.20
64.8
over 40.0
79.0
over 3.0
13.6
over 0.30
27.2
over 0.80
84.9
over 0.10
40.5
over 50.0
22.4









Water and Soil
Water is not normally a major source of minerals. Nevertheless,
although highly variable, all essential mineral elements occur to some
extent in water. Animals sometimes consume appreciable amounts of soil
but this is also highly variable. High soil ingestion is favored by
soils with a weak structure and poor drainage, high stocking rates, high
earthworm populations and during months when pasture growth is poor.
From New Zealand, annual ingestion of soil reached 75 kg for sheep and
600 kg for dairy animals (Healy, 1974). Soil ingestion, direct or due to
pasture contamination, can result in higher intakes of Co and I since
soils contain appreciably higher concentrations than plants, but the
animal may also consume toxic elements or substances. Rosa (1980)
reported that inclusion of 10% Costa Rican soil in the diet of sheep
decreased apparent and true P absorption. Direct consumption of large
quantities of soil (Figure 1) or bones (Figure 2) is often an indication
of a mineral deficiency.

FACTORS AFFECTING MINERAL CONTENT OF PLANTS

Concentrations of mineral elements in forage are dependent upon the
interaction of a number of factors, including soil, plant species, stage
of maturity, yield, pasture management and climate. The influence of
soil chemistry and soil characteristics on the occurrence of mineral
problems for grazing ruminants has been reviewed (Reid and Horvath,
1980). Most naturally occurring mineral deficiencies in herbivores are
associated with specific regions and are directly related to soil charac-
teristics. Young and alkaline geological formations are more abundant in
most trace elements than the older, more acid, coarse, sandy formations.
There is a marked leaching and weathering of soils in tropical regions
under conditions of heavy rainfall and high temperature, making them
deficient in plant minerals. Poor drainage conditions often increase
extractable trace elements (i.e., Mn and Co), thereby resulting in a
corresponding increase in plant uptake. As the soil pH increases, the
availability and uptake of forage Fe, Mn, Zn, Cu and Co decrease, whereas
Mo and Se concentrations increase.

Large variations in mineral content of different plant species grown
on the same soil have been reported. From Kenya, 58 grasses grown on the
same soil had the following range of concentrations on a dry basis:
total ash, 4.0 12.2%; Ca, 0.09 0.55%; and P, 0.05 0.37% (Dougall
and Bogdan, 1958). It is a generally accepted view that herbs and
legumes are richer in a number of mineral elements than are grasses. For
most minerals, "accumulator" plants exist which contain extremely high
levels of a specific mineral. As plants mature, mineral content declines
due to a natural dilution process and translocation of nutrients to the
root system. In most circumstances, P, K, Mg, Na, Cl, Cu, Co, Fe, Se, Zn
and Mo decline as the plant matures.

Climate, forage management and yield influence plant mineral compo-
sition. Grazing pressures will influence the species of forage predomi-
nating and also change the leaf/stem ratio radically, thereby having a
direct bearing on the mineral content of the sward. Increasing crop
yields remove minerals from the soil at a faster rate so deficiencies are
frequently found on the most progressive farms. Overuse of nitrogen and





















v-' Ci~k
r-- i
ic't~
`~?;-
~r;.` ,
: C11*it~
'-


Figure 1. Cattle consuming soil at "Hato El Frio" in the Llanos state of Apure, Venezuela.
Note holes in soil from previous consumption. Excessive soil consumption is associ-
ated with pronounced mineral deficiencies. (Courtesy Eliecer Alberto Velasco,
Hato El Frio, Apure State, Venezuela).


Figure 2. A cow chewing bone in the Llanos region of Santa Maria de Ipire, state of Guarico,
Venezuela. Bone chewing is often associated with a phosphorus deficiency. (Cour-
tesy David Morillo, Centro de Investigaciones Agronomicas, Maracay, Venezuela).









K fertilizers increases the incidence of grass tetany, with K also drama-
tically reducing forage Na content. Overliming can accentuate a Se or Mo
toxicity in livestock by increasing plant concentrations of these ele-
ments and at the same time favor Co and Mn deficiencies due to lowered
plant uptake.

MINERAL REQUIREMENTS

Approximate mineral requirements and toxic levels for various
ruminant livestock are presented in Table 2. Many factors affect mineral
requirements, including nature and level of production, age, level and
chemical form of elements in the feed ingredients, interrelationships
with other nutrients, supplemental mineral intake, breed and animal adap-
tation. Mineral requirements are highly dependent on the level of produ-
ctivity. The criterion of adequacy is important as illustrated by the
fact that minimum Zn requirements for spermatogenesis and testicular
development in male sheep are higher than for growth, and Mn requirements
are similarly lower for growth than for fertility in sheep (Underwood,
1981).

Improved management practices that lead to improved milk production
and growth rates for ruminants will necessitate more attention to mineral
nutrition. Marginal mineral deficiencies, under low levels of produc-
tion, become more severe with increased levels of production, and previ-
ously unsuspected nutritional deficiency signs usually occur as
production levels increase.

Specific mineral requirements are difficult to define since exact
needs depend on chemical form and numerous mineral interrelationships.
The chemical form of mineral elements varies greatly in amount of dietary
minerals supplied and in biological availability. As an example,
elemental Se is largely unavailable for chicks but is quite effective in
protecting against Se deficiency in sheep and cattle (Underwood, 1981).

Important differences in mineral metabolism can be attributed to
breed and adaptation. The effect of breed differences on mineral
requirements has often been observed in ruminants. Marked ruminant
animal variation within breeds in the efficiency of mineral absorption
from the diet has been reported to be 5-35% for Mg, 40-80% for P and
2-10% for Cu. It is not unusual for cattle introduced into an area to
show deficiency signs while the indigenous breeds that are slow-growing
and late-maturing do not exhibit the deficiencies to the same degree.
Unacclimatized cattle of temperate types which sweat profusely and lose
saliva and mucus from the mouth may lose significant quantities of
minerals, particularly in the arid tropics.

Adequate intake of forages by grazing ruminants is essential in
meeting mineral requirements. Factors which greatly reduce forage
intake, such as low protein (<7.0%) content and increased degree of
lignification, likewise reduce the total minerals consumed.

Since tropical forages contain less minerals during the dry season,
it is logical to assume that grazing livestock would most likely suffer
mineral inadequacies during this time. On the contrary, numerous











Table 2. SUGGESTED MINERAL REQUIREMENTS AND TOXICITIES FOR RUMINANTS (Dry Basis)


Beef Cattlea Lactating Dairy Cowsb Sheepc Goatsd,f
Suggested Suggested Suggested Suggested
Required Elements Value Range Value Range Value Range Value Range

Macroelements
Calcium, % (Table 4) -----------.--- (Table 5) 0.43-0.60 -------------.-- 0.21-0.52 --- --- ---------
Phosphorus, % (Table 4) ...------------- (Table 5) 0.31-0.40 ----------------- 0.16-0.37 ---------- ------
Magnesium, % 0.10 .05-.25 0.20 ..------------- ------------.. 0.04-0.08 --- --- --------
Potassium, % 0.65 .5-.7 0.80 0.80-1.20 0.50 ---------.--- ---------------. 0.5-0.8
Sodium, % 0.08 .06-.10 0.18 ------------. ------------- 0.04-0.1 ---------- -- --.........
Sulfur, % 0.10 .08-.15 0.2 ------------- --------------- 0.14-0.26 ---------------- 0.16-0.32
Microelements
Cobalt, ppm 0.10 .07-.11 0.1 ----------.-- 0.1 ------------- 0.1 ------
Copper, ppm 8.0 4 -10 10.0 ------------- 5.0 ------- ---.-------- -----------
Iodine, ppm 0.50 .2-2.0 0.5 -----------. -.----------- 0.1-0.8 -------------- -------
Iron, ppm 20.0 10-50 50 ------------- -. ----------- 30-50 -------------- --------
Manganese, ppm 20.0 10-40 40 -------.---- ------------- 20-40 >5.5 --------
Molybdenum, ppm 0.01 ...-- --.. -----... ............... >0.5 ..---------- ------------------ ----------
Selenium, ppm 0.10 .05-.30 0.1 ------------- 0.1 ------------- ------------------ ----------
Zinc, ppm 30.0 20-40 40 ..------------ ------------- 35-50 >10.0 --
Toxic Elementse
Copper, ppm 115 80 8-25 ?
Fluorine, ppm 30-100 30 60-200 ?
Molybdenum, ppm 6 6 5-20 ?
Selenium, ppm 5 5 >2.0 ?'
Zinc, ppm 500 500 1000 1000


The listing of a range recognizes that requirements for most minerals are affected by a variety of dietary and animal factors.

aNRC (1983), bNRC (1978), CNRC (1975), dNRC (1981), eNRC (1980).

fMineral requirements for goats have not been studied in detail. Lactating dairy goats have requirements similar to lactating dairy cattle. Other goats have mineral
requirements similar to sheep (Haenlin, 1980).









reports, including those from Kenya, Brazil and South Africa, have noted
that specific mineral deficiencies are more prevalent during the wet
season. Grazing cattle are more prone to develop Co or P deficiencies,
and the clinical signs are most severe after the rains when pastures are
green and plentiful. Increased incidence of mineral deficiencies during
the wet season is less related to forage mineral concentrations than to
the greatly increased requirements for these elements by the grazing
animal. During the wet season, livestock gain weight rapidly since
energy and protein supplies are adequate and thus the mineral require-
ments are high. During the dry season, inadequate protein and energy
result in animals losing weight which lowers mineral requirements.

There are notable exceptions as to season of the year when mineral
supplementation is most critical. In the wet llanos of Venezuela,
Colombia and Bolivia, as water recedes in the dry season, cattle enter
the lowlands to graze a great variety of plant species. Under these
conditions, incidence of mineral deficiencies would not be expected to be
more prevalent during the wet season.

INCIDENCE OF MINERAL DEFICIENCIES AND TOXICITIES

Mineral deficiencies and imbalances for herbivores are reported from
almost all tropical regions of the world. Table 3 lists reports of
mineral deficiencies or toxicities in tropical countries of Africa, Latin
America and Asia. These reports include both confirmed and highly
suspected geographical areas of mineral deficiencies and toxicities in
cattle. Listing countries constitutes a very generalized approach, with
important geographical omissions inevitable, but it does indicate the
scope of the problem. The extent of affected areas is not generally
appreciated and it is logical that reports of mineral inadequacies will
greatly increase as more tropical countries undertake mineral research
and thereby improve their methods of detection.

The mineral elements most likely to be lacking under tropical
conditions are Ca, P, Na, Co, Cu, I, Se and Zn. In some regions, under
specific conditions, Mg, K, Fe, and Mn may be deficient and excesses of
F, Mo and Se are extremely detrimental.

CALCIUM AND PHOSPHORUS

Metabolism
Calcium and P have a vital function in almost all tissues in the
body and must be available to livestock in the proper quantities and
ratio. These elements make up over 70% of the total mineral elements in
the body. Ninety-nine percent of the Ca and 80% of the P in the entire
body are found in bones and teeth.

Approximately 1% of the body Ca is not in the skeleton and is widely
distributed in soft tissues, with the largest concentration in blood
plasma. Calcium is essential for skeletal formation, normal blood
clotting, rhythmic heart action, neuromuscular excitability, enzyme acti-
vation, and permeability of membranes. Approximately 20% of body P is
not in the skeleton and is distributed throughout the soft tissues, being
especially concentrated in red blood cells, muscle and nerve tissues. In









reports, including those from Kenya, Brazil and South Africa, have noted
that specific mineral deficiencies are more prevalent during the wet
season. Grazing cattle are more prone to develop Co or P deficiencies,
and the clinical signs are most severe after the rains when pastures are
green and plentiful. Increased incidence of mineral deficiencies during
the wet season is less related to forage mineral concentrations than to
the greatly increased requirements for these elements by the grazing
animal. During the wet season, livestock gain weight rapidly since
energy and protein supplies are adequate and thus the mineral require-
ments are high. During the dry season, inadequate protein and energy
result in animals losing weight which lowers mineral requirements.

There are notable exceptions as to season of the year when mineral
supplementation is most critical. In the wet llanos of Venezuela,
Colombia and Bolivia, as water recedes in the dry season, cattle enter
the lowlands to graze a great variety of plant species. Under these
conditions, incidence of mineral deficiencies would not be expected to be
more prevalent during the wet season.

INCIDENCE OF MINERAL DEFICIENCIES AND TOXICITIES

Mineral deficiencies and imbalances for herbivores are reported from
almost all tropical regions of the world. Table 3 lists reports of
mineral deficiencies or toxicities in tropical countries of Africa, Latin
America and Asia. These reports include both confirmed and highly
suspected geographical areas of mineral deficiencies and toxicities in
cattle. Listing countries constitutes a very generalized approach, with
important geographical omissions inevitable, but it does indicate the
scope of the problem. The extent of affected areas is not generally
appreciated and it is logical that reports of mineral inadequacies will
greatly increase as more tropical countries undertake mineral research
and thereby improve their methods of detection.

The mineral elements most likely to be lacking under tropical
conditions are Ca, P, Na, Co, Cu, I, Se and Zn. In some regions, under
specific conditions, Mg, K, Fe, and Mn may be deficient and excesses of
F, Mo and Se are extremely detrimental.

CALCIUM AND PHOSPHORUS

Metabolism
Calcium and P have a vital function in almost all tissues in the
body and must be available to livestock in the proper quantities and
ratio. These elements make up over 70% of the total mineral elements in
the body. Ninety-nine percent of the Ca and 80% of the P in the entire
body are found in bones and teeth.

Approximately 1% of the body Ca is not in the skeleton and is widely
distributed in soft tissues, with the largest concentration in blood
plasma. Calcium is essential for skeletal formation, normal blood
clotting, rhythmic heart action, neuromuscular excitability, enzyme acti-
vation, and permeability of membranes. Approximately 20% of body P is
not in the skeleton and is distributed throughout the soft tissues, being
especially concentrated in red blood cells, muscle and nerve tissues. In










Table 3. GEOGRAPHICAL LOCATIONS OF MINERAL DEFICIENCIES OR TOXICITIES OF RUMINANTS
IN TROPICAL COUNTRIES OF LATIN AMERICA, AFRICA AND ASIAa

Required Elements
Calcium Argentina, Bolivia, Brazil, Colombia, Costa Rica, El Salvador, Guatemala, Guyana, India, Malawi, Mexico, Panama, Peru, Philippines, Senegal,
Surinam, Uganda, Venezuela, Zaire.
Magnesium Argentina, Brazil, Chile, Colombia, Costa Rica, Guatemala, Guyana, Haiti, Honduras, Jamaica, Kenya, Malawi, Peru, Surinam, Trinidad, Uganda,
Southern Africa, Uruguay, Venezuela.
Phosphorus Antigua, Argentina, Bolivia, Botswana, Brazil, Ceylon, Chile, Colombia, Costa Rica, Cuba, Dominican Republic, Ecuador, El Salvador, Egypt,
Ghana, Guatemala, Guyana, Haiti, Honduras, India, Indonesia, Jamaica, Kenya, Malagasy Republic, Malawi, Malaysia, Mexico, Nicaragua,
Nigeria, Panama, Paraguay, Peru, Philippines, Puerto Rico, Senegal, Somalia, Southern Africa, Surinam, Swaziland, Tanzania, Trinidad, Uganda,
Uruguay, Venezuela, Zaire, Zimbabwe.
Potassium Brazil, Haiti, Panama, Swaziland, Uganda, Venezuela.
Sodium Bolivia, Brazil, Chad, Colombia, Dominican Republic, Guatemala, Kenya, Malawi, New Guinea, Nigeria, Panama, Philippines, Senegal, Somalia,
Southern Africa, Surinam, Swaziland, Thailand, Uganda, Uruguay, Venezuela.
Sulfur Brazil, Colombia, Ecuador, Uganda.
Cobalt Argentina, Brazil, Colombia, Costa Rica, Cuba, Egypt, El Salvador, Guyana, Haiti, India, Indonesia, Katanga, Kenya, Malaysia, Mexico, Nicaragua,
Northern Africa, Peru, Philippines, South Africa, Surinam, Uganda, Uruguay, Zaire.
Copper (or Argentina, Bolivia, Brazil, Colombia, Costa Rica, Cuba, Dominican Republic, Ecuador, El Salvador, Ethiopia, Guatemala, Guyana, Haiti,
molybdenum Honduras, India, Indonesia, Kenya, Malaysia, Malawi, Mexico, Panama, Peru, Pnilippines, Senegal, Southern Africa, Sudan, Surinam, Swaziland,
toxicity) Tanzania, Trinidad, Uruguay, Venezuela, Zaire, Zimbabwe.
Iodine Worldwide.
Iron Brazil, Costa Rica, India, Panama.
Manganese Argentina, Brazil, Burma, Costa Rica, Panama, Southern Africa, Uganda.
Selenium Bahamas, Bolivia, Brazil, Columbia, Costa Rica, Dominican Republic, Ecuador, Guyana, Honduras, Indonesia, Malawi, Mexico, Paraguay, Peru,
Southern Africa, Swaziland, Thailand, Uganda, Uruguay, Venezuela.
Zinc Argentina, Bolivia, Brazil, Colombia, Costa Rica, Dominican Republic, Ecuador, El Salvador, Guatemala, Guyana, India, Indonesia, Kenya,
Malawi, Mexico, Panama, Peru, Philippines, Puerto Rica, South Africa, Sudan, Swaziland, Uganda, Uruguay, Venezuela.

Toxic Elements
Fluorine Algeria, Argentina, Ecuador, Guyana, India, Mexico, Morocco, Saudi Arabia, Southern Africa, Tanzania, Tunesia.
Manganese Brazil, Costa Rica, Indonesia, Peru, Surinam.
Selenium Argentina, Brazil, Central African Republic, Chad, Chile, Colombia, Ecuador, Honduras, India, Iran, Kenya, Madagascar, Mexico, Nigeria
Northern Africa, Peru, Puerto Rico, Southern Africa, Sudan, Upper Volta, Venezuela.


aMcDowell (1976); Fick et al. (1978); McDowell et al. (1983); Mtimuni (1982).









addition to skeletal formation, P is also essential for proper func-
tioning of rumen microorganisms, especially those which digest plant
cellulose, utilization of energy from feeds, buffering of blood and other
fluids, many enzyme systems, and protein metabolism.

Requirement
Adequate Ca and P nutrition depends not only on sufficient total
dietary supplies, but also on the chemical forms in which they occur in
the diet and on the Vitamin D status of the diet on the animal. The
dietary Ca:P ratio also can be important.

A dietary Ca:P ratio between 1:1 and 2:1 is assumed to be ideal for
growth and bone formation since this is approximately the ratio of the
two minerals in bone. Actually, ruminants can tolerate a wider range of
Ca:P particularly when their Vitamin D status is high. Nine Ca:P ratios
ranging from 0.41:1 to 14.3:1 were tested by Wise et al.(1963) with die-
tary ratios below 1:1 and over 7:1 growth and feed efficiency decreased
significantly. With excessive amounts of Ca or P in the ration, the
availability of certain trace elements may be decreased. On farms with
problems, it is not advisable to feed an excess of either element.

The requirements of beef cattle indicate that 0.18 1.04% Ca and
0.18 0.70% P are adequate for growing and fattening steers and heifers
(Table 4); 0.43 0.60% Ca and 0.31 0.40% P for lactating dairy cows
(Table 5); and 0.21 0.52% Ca and 0.16 0.37% P for sheep (Table 2).

Deficiency
Deficiency signs of borderline Ca and P deficiencies are not easily
distinguishable from other deficiencies. An inadequate intake of Ca may
cause weakened bones (Figures 3 & 4), slow growth, low milk production,
and tetany (convulsions) in severe deficiencies. Signs of P deficiencies
are not easily recognized except in severe cases when fragile bones, gen-
eral weakness, weight loss, emaciation, stiffness, reduced milk produc-
tion, and chewing of wood, rocks (Figure 5), bones (Figure 6) and other
objects may be noticed. Abnormal chewing of objects may also occur,
however, with other dietary deficiencies.

In cattle the most common mineral deficiency is lack of P (Table 3).
In most livestock grazing areas of tropical countries, soils and plants
are low in P. Many grass species containing over 0.3% P during early
stages of growth are available to grazing ruminants for only short
periods. For the greater part of the year, mature forages contain less
than 0.15% P. In many tropical countries, high amounts of soil Fe and Al
accentuate P deficiency by forming insoluble phosphate complexes.

In South Africa in the early 1900's, pioneer P supplementation
studies (Van Niekerk, 1978) revealed the cause of bovine botulism and
aphosphorosis. Both conditions were the result of a severe P deficiency,
with cattle exhibiting sub-normal growth and reproduction and a depraved
appetite or "pica" as illustrated by bone chewing. Besides South Africa,
other countries reporting death from botulism as a result of bone chewing
include Argentina (Figure 7, inside front cover), Brazil and Senegal. In
areas of Piaui, Brazil, an estimated 2 to 3% of approximately 100,000
cattle die annually of botulism.









addition to skeletal formation, P is also essential for proper func-
tioning of rumen microorganisms, especially those which digest plant
cellulose, utilization of energy from feeds, buffering of blood and other
fluids, many enzyme systems, and protein metabolism.

Requirement
Adequate Ca and P nutrition depends not only on sufficient total
dietary supplies, but also on the chemical forms in which they occur in
the diet and on the Vitamin D status of the diet on the animal. The
dietary Ca:P ratio also can be important.

A dietary Ca:P ratio between 1:1 and 2:1 is assumed to be ideal for
growth and bone formation since this is approximately the ratio of the
two minerals in bone. Actually, ruminants can tolerate a wider range of
Ca:P particularly when their Vitamin D status is high. Nine Ca:P ratios
ranging from 0.41:1 to 14.3:1 were tested by Wise et al.(1963) with die-
tary ratios below 1:1 and over 7:1 growth and feed efficiency decreased
significantly. With excessive amounts of Ca or P in the ration, the
availability of certain trace elements may be decreased. On farms with
problems, it is not advisable to feed an excess of either element.

The requirements of beef cattle indicate that 0.18 1.04% Ca and
0.18 0.70% P are adequate for growing and fattening steers and heifers
(Table 4); 0.43 0.60% Ca and 0.31 0.40% P for lactating dairy cows
(Table 5); and 0.21 0.52% Ca and 0.16 0.37% P for sheep (Table 2).

Deficiency
Deficiency signs of borderline Ca and P deficiencies are not easily
distinguishable from other deficiencies. An inadequate intake of Ca may
cause weakened bones (Figures 3 & 4), slow growth, low milk production,
and tetany (convulsions) in severe deficiencies. Signs of P deficiencies
are not easily recognized except in severe cases when fragile bones, gen-
eral weakness, weight loss, emaciation, stiffness, reduced milk produc-
tion, and chewing of wood, rocks (Figure 5), bones (Figure 6) and other
objects may be noticed. Abnormal chewing of objects may also occur,
however, with other dietary deficiencies.

In cattle the most common mineral deficiency is lack of P (Table 3).
In most livestock grazing areas of tropical countries, soils and plants
are low in P. Many grass species containing over 0.3% P during early
stages of growth are available to grazing ruminants for only short
periods. For the greater part of the year, mature forages contain less
than 0.15% P. In many tropical countries, high amounts of soil Fe and Al
accentuate P deficiency by forming insoluble phosphate complexes.

In South Africa in the early 1900's, pioneer P supplementation
studies (Van Niekerk, 1978) revealed the cause of bovine botulism and
aphosphorosis. Both conditions were the result of a severe P deficiency,
with cattle exhibiting sub-normal growth and reproduction and a depraved
appetite or "pica" as illustrated by bone chewing. Besides South Africa,
other countries reporting death from botulism as a result of bone chewing
include Argentina (Figure 7, inside front cover), Brazil and Senegal. In
areas of Piaui, Brazil, an estimated 2 to 3% of approximately 100,000
cattle die annually of botulism.






























Figu


Figures 3 and 4.


Figure 4





re 3

Both hips of cows shown above were broken (knocked down) as a result of a
low-calcium ration. Her skeletal reserve of calcium was depleted to the point
that her weakened bones were broken easily. Pelvic bones of a herdmate
(Figure 4) were broken in three places. (Florida Experiment Station Bulletin
262. R. Becker, W. M. Neal and A. L. Shealy, University of Florida, Gaines-
ville, Florida, U.S.A.).


Figure 5. Photo shows the contents of the
rumen of a cow that had exhibited
a "pica" condition of eating
stones and other objects. A large
number of stones (= 50 lb) were
found in the rumen of this animal
in La Libertad, Chiapas, Mexico.
(Courtesy Carlos Garcia Bojalil,
I.T.E.S.M., Queretaro, Qro.,
Mexico).


Figure 6. A cow chewing bone in a phos-
phorus-deficient area in southern
Mato Grosso, Brazil. Osteophagia
is a characteristic manifestation
of phosphorus deficiency and is
easily recognized, even at a dis-
tance, due to the typical position
of the distended neck. (Courtesy
Jurgen Dobereiner and Carlos H.
Tokarnia, EMBRAPA, Rio de
Janeiro, Brazil).









Table 4. CALCIUM AND PHOSPHORUS REQUIREMENTS FOR BEEF CATTLEa


Daily
gain
kg


Minimum
Daily
DM
kg


Calcium
In diet
Daily DM
g %


Phosphorus
In diet
Daily DM
g %


Growing finishing steer calves and yearlings


Pregnant yearling last third of pregnancy
350 0.4 7.3
400 0.4 8.0


0.18
0.24
0.47
0.18
0.22
0.27


0.27
0.28


Cows nursing calves, average milking ability, first 3-4 months postpartum
350 0.0 7.7 23 0.30 18
450 0.0 9.2 20 0.28 21

Cows nursing calves, superior milking ability, first 3-4 months postpartum, 10 kg milk/day
350 0.0 6.8 36 0.53 24
Aann n .0 39 0.43 26


0.18
0.22
0.37
0.18
0.20
0.23


0.21
0.20


0.36
0.29


aNRC (1976).


Weight
kg










Table 5. CALCIUM AND PHOSPHORUS REQUIREMENTS FOR LACTATING DAIRY COWSa

As a Percent of the Ration
Lactating Cow Rations
Cow wt, kg Daily Milk Yields, (kg)
<400 <8 8-13 13-18 >18
500 <11 11-17 17-23 >23 Dry Growing
600 <14 14-21 21-29 >29 Pregnant Mature Heifers
>700 <18 18-26 26-35 >35 Cows Bulls and Bulls
Calcium, % 0.43 0.48 0.54 0.60 0.37 0.24 0.40
Phosphorus, % 0.31 0.34 0.38 0.40 0.26 0.18 0.26

aNRC (1978).
Based on Daily Requirements
Calcium
The maintenance requirement for calcium is about 1.6 grams per 100 kg body weight. Lactation requirement for calcium is 2.7 grams of calcium per kg of
milk. This is based on one kg milk contains an average of 1.23 grams of calcium. The availability of calcium is estimated to be about 45 percent.
Phosphorus
The maintenance requirement for phosphorus is about 1.6 grams per 100 kg body weight. Lactation requirement for phosphorus is 1.8 grams of phosphorus
per kg of milk. This is based on one kg milk contains an average of 1.00 grams of phosphorus. The availability of phosphorus is estimated to be about 55 percent.









Under conditions of extreme P shortage, cattle may go for two or
three years without producing a calf or even coming into estrus. In P
deficient areas, if a calf is produced, cows may not come into regular
estrus again until body P levels are restored, either by feeding
supplementary P or by cessation of lactation.

The concentration of Ca in blood plasma or serum is influenced only
by severe deficiency whereas that of inorganic P is influenced by a
number of factors discussed under diagnosis of mineral deficiencies and
imbalances. These factors are difficult to control. Due to limitations
of serum Ca and P as an indicator of status, analysis of the ration and
bone composition and breaking strength are the best ways of assessing a
deficiency of Ca and P.

Prevention and Control
Calcium and P deficiencies can be prevented or overcome by direct
treatment of the animals through supplementation, in the diet or the
water supply, or indirectly by appropriate fertilizer treatment of the
soils on which the pastures to be consumed are grown.

The choice of supplementation procedure depends on the conditions of
husbandry. On sparse P deficient grazing the direct method is preferred
because the use of phosphate fertilizers involves high transport and
application cost, and herbage productivity is usually limited by climate
or soil problems. In more climatically favored and intensively farmed
areas phosphate applications designed primarily to increase pasture
yields also increase P concentrations. In extensive range conditions
where fertilizer applications are uneconomical, as in many areas of Latin
America, Asia and Africa, direct provision of additional P can be
achieved by the use of phosphate containing supplements or by treatment
of water supply with soluble phosphates. The easiest and cheapest proce-
dure is to provide a phosphatic mineral supplement in troughs or boxes
protected from the rain. Good sources of mineral phosphate are dicalcium
phosphate and superphosphate; ground rock phosphate is relatively unpala-
table and most sources are too high in F for safe use. Procedures that
require the use of water soluble phosphates, Na HPO or ammonium
polyphosphate are good but more expensive than the less soluble
phosphates. Many of the materials used as P supplements supply
significant amounts of Ca.

MAGNESIUM

Metabolism
Magnesium is abundant in most common feedstuffs relative to apparent
requirements by animals. It is widely distributed among plant and animal
tissues with some 70% of total body Mg present in the skeleton.
Magnesium is involved in the metabolism of carbohydrates and lipids as a
catalyst of a wide array of enzymes. It is required for cellular
oxidation and exerts a potent influence on neuromuscular activity.

Signs of hypomagnesemic tetany are encountered both in grazing
ruminants and in calves reared too long on milk without access to other
feeds. Susceptibility to grass tetany is increased in older ruminants
because of the decreased ability to mobilize skeletal Mg with increasing









Under conditions of extreme P shortage, cattle may go for two or
three years without producing a calf or even coming into estrus. In P
deficient areas, if a calf is produced, cows may not come into regular
estrus again until body P levels are restored, either by feeding
supplementary P or by cessation of lactation.

The concentration of Ca in blood plasma or serum is influenced only
by severe deficiency whereas that of inorganic P is influenced by a
number of factors discussed under diagnosis of mineral deficiencies and
imbalances. These factors are difficult to control. Due to limitations
of serum Ca and P as an indicator of status, analysis of the ration and
bone composition and breaking strength are the best ways of assessing a
deficiency of Ca and P.

Prevention and Control
Calcium and P deficiencies can be prevented or overcome by direct
treatment of the animals through supplementation, in the diet or the
water supply, or indirectly by appropriate fertilizer treatment of the
soils on which the pastures to be consumed are grown.

The choice of supplementation procedure depends on the conditions of
husbandry. On sparse P deficient grazing the direct method is preferred
because the use of phosphate fertilizers involves high transport and
application cost, and herbage productivity is usually limited by climate
or soil problems. In more climatically favored and intensively farmed
areas phosphate applications designed primarily to increase pasture
yields also increase P concentrations. In extensive range conditions
where fertilizer applications are uneconomical, as in many areas of Latin
America, Asia and Africa, direct provision of additional P can be
achieved by the use of phosphate containing supplements or by treatment
of water supply with soluble phosphates. The easiest and cheapest proce-
dure is to provide a phosphatic mineral supplement in troughs or boxes
protected from the rain. Good sources of mineral phosphate are dicalcium
phosphate and superphosphate; ground rock phosphate is relatively unpala-
table and most sources are too high in F for safe use. Procedures that
require the use of water soluble phosphates, Na HPO or ammonium
polyphosphate are good but more expensive than the less soluble
phosphates. Many of the materials used as P supplements supply
significant amounts of Ca.

MAGNESIUM

Metabolism
Magnesium is abundant in most common feedstuffs relative to apparent
requirements by animals. It is widely distributed among plant and animal
tissues with some 70% of total body Mg present in the skeleton.
Magnesium is involved in the metabolism of carbohydrates and lipids as a
catalyst of a wide array of enzymes. It is required for cellular
oxidation and exerts a potent influence on neuromuscular activity.

Signs of hypomagnesemic tetany are encountered both in grazing
ruminants and in calves reared too long on milk without access to other
feeds. Susceptibility to grass tetany is increased in older ruminants
because of the decreased ability to mobilize skeletal Mg with increasing









age. Grass tetany generally occurs during early spring, or a partic-
ularly wet autumn, among older cattle grazing grass or small grain
forages in cool weather. Clinical tetany is endemic in some countries,
affecting only a small proportion of cattle (1 to 2%). However, indi-
vidual herds may report incidence of tetany as high as 20%. Although not
characterized by death, incidence of nonclinical hypomagnesemia is far
greater than clinical tetany and economic consequences of lowered produc-
tion are substantial.

Requirement
The dietary Mg requirements of livestock vary with the species and
breed of animals, age and rate of growth or production and with bio-
logical availability in the diet. Dietary Mg requirements are influenced
by several other factors, including the protein content of the diet and
the Mg status of the animal. In mature ruminants the reticulorumen is
the principal site of Mg absorption (Thomas and Potter, 1976). Condi-
tions in the rumen, such as a high pH, which adversely affect Mg
absorption will therefore raise dietary requirements. High dietary
levels of Ca and P reduce Mg absorption.

Minimum needs of sheep and cattle for growth can generally be met by
pastures or rations containing 0.10%. A higher proportion, 0.18 to
0.20%, is considered necessary for lactating cows (Table 2). The dietary
availability of pasture Mg is generally assumed to be about 33%. This
may not always be the case, particularly with young spring grass heavy
fertilized with N and K.

Deficiency
In the past, Mg concentration of plasma or serum has been used as
follows to assess the status of adult cows: 2.0 3.5 mg/100 ml, usually
adequate; 1.0 2.0 mg/100 ml clear deficiency; less than 1.0 mg/100 ml,
severe deficiency, danger of tetany. Magnesium concentration in blood
plasma does not fall until there is a severe deficiency. In contrast, an
excess or a lack of Mg is immediately reflected in a higher or lower
daily excretion of Mg in urine. Hence, daily urinary excretion is a
better criterion of Mg supply than plasma concentration.

Tentative criteria for Mg in urine are as follows: more than 10.0
mg/100 ml, adequate to liberal; 2.0 10.0 mg/100 ml, inadequate; less
than 2.0 mg/100 ml, severe deficiency, danger of tetany. A rough
assessment of supply can be obtained from the content of Mg, N and K in
pasture. This approach is more accurate when the pasture is sampled
close to the date of grazing. If the dates are more than a week apart
the assessment is unreliable. This method can be used only for grazing
cattle, whereas the urine method is reliable on indoor rations as well as
pasture (NCMN, 1973). Magnesium deficiency in cattle is illustrated in
Figures 8 and 9.

Prevention and Control
Several safe and practical means of raising the Mg intakes of
animals sufficient to sustain normal serum values and to prevent losses
from lactation tetany have been devised.









age. Grass tetany generally occurs during early spring, or a partic-
ularly wet autumn, among older cattle grazing grass or small grain
forages in cool weather. Clinical tetany is endemic in some countries,
affecting only a small proportion of cattle (1 to 2%). However, indi-
vidual herds may report incidence of tetany as high as 20%. Although not
characterized by death, incidence of nonclinical hypomagnesemia is far
greater than clinical tetany and economic consequences of lowered produc-
tion are substantial.

Requirement
The dietary Mg requirements of livestock vary with the species and
breed of animals, age and rate of growth or production and with bio-
logical availability in the diet. Dietary Mg requirements are influenced
by several other factors, including the protein content of the diet and
the Mg status of the animal. In mature ruminants the reticulorumen is
the principal site of Mg absorption (Thomas and Potter, 1976). Condi-
tions in the rumen, such as a high pH, which adversely affect Mg
absorption will therefore raise dietary requirements. High dietary
levels of Ca and P reduce Mg absorption.

Minimum needs of sheep and cattle for growth can generally be met by
pastures or rations containing 0.10%. A higher proportion, 0.18 to
0.20%, is considered necessary for lactating cows (Table 2). The dietary
availability of pasture Mg is generally assumed to be about 33%. This
may not always be the case, particularly with young spring grass heavy
fertilized with N and K.

Deficiency
In the past, Mg concentration of plasma or serum has been used as
follows to assess the status of adult cows: 2.0 3.5 mg/100 ml, usually
adequate; 1.0 2.0 mg/100 ml clear deficiency; less than 1.0 mg/100 ml,
severe deficiency, danger of tetany. Magnesium concentration in blood
plasma does not fall until there is a severe deficiency. In contrast, an
excess or a lack of Mg is immediately reflected in a higher or lower
daily excretion of Mg in urine. Hence, daily urinary excretion is a
better criterion of Mg supply than plasma concentration.

Tentative criteria for Mg in urine are as follows: more than 10.0
mg/100 ml, adequate to liberal; 2.0 10.0 mg/100 ml, inadequate; less
than 2.0 mg/100 ml, severe deficiency, danger of tetany. A rough
assessment of supply can be obtained from the content of Mg, N and K in
pasture. This approach is more accurate when the pasture is sampled
close to the date of grazing. If the dates are more than a week apart
the assessment is unreliable. This method can be used only for grazing
cattle, whereas the urine method is reliable on indoor rations as well as
pasture (NCMN, 1973). Magnesium deficiency in cattle is illustrated in
Figures 8 and 9.

Prevention and Control
Several safe and practical means of raising the Mg intakes of
animals sufficient to sustain normal serum values and to prevent losses
from lactation tetany have been devised.











W iA ..


Figure 8


r.r
. bi


US; U
i~~; ;s a


Figure 9


Figures 8 and 9.


Cow in collapse stage of tetany and death from tetany. Note area around
forelegs where ground has been thrashed during convulsions. (Courtesy
James A. Boling, Curtis W. Absher and Duane E. Miksch, University of Ken-
tucky, Lexington, Kentucky).


. .









Magnesium fertilizers calcinedd magnesite or Kieserite) can
significantly increase pasture concentrations. This method of control
has limitations on many soil types and usually has to be accompanied by
other means of supplying additional Mg. Foliar dusting of pastures with
calcined magnesite (MgO) before or during tetany prone periods is one
such means that has proven effective, provided it is applied at not less
than 17 kg/ha at not more than 10-day intervals (Rogers, 1979).

For calves and cows that are being fed concentrates, provision of
50g MgO/day in 300 400 g of concentrate mixture is adequate. Incor-
porating it into mineral mixes, drenches, molasses-based free choice
supplements or sprinkling the mineral on feed such as grains, chopped
roots or silage, have all proven satisfactory methods of supplementation.
There is general agreement that 50 60 g MgO/day is the minimum secure
prophylactic dose for adult cattle; 7 15 g/day for calves; and 7 g/day
for lactating ewes. These doses must be given to all stock continuously
during the tetany susceptible period. Addition to the water supply of
soluble Mg salts such as chloride, sulfate and acetate has been exten-
sively studied as a prophylactic measure with mostly beneficial results
(Rogers and Poole, 1976); however, water intake by drinking varies widely
between individuals.

Subcutaneous injection of a single dose of 400 ml of a 25% solution
of Mg sulfate or intravenous injection of a similar dose of Mg lactate
restores serum Mg of an affected cow to near normal within about 10
minutes. Serum Mg concentrations will fall again unless the cow is
immediately removed from the tetany producing pasture and fed Mg adequate
diets.

POTASSIUM

Metabolism
Potassium is the third most abundant mineral element in the animal
body and is the principal cation of intracellular fluid; it also is a
constituent of extra cellular fluid where it influences muscle activity.
Potassium is essential for life, being required for a variety of body
functions including osmotic balance, acid-base equilibrium, several
enzyme systems and water balance. An ionic balance exists between K, Na,
Ca and Mg.

Requirement
The requirement for K is higher for ruminants than for nonruminants.
For ruminant species the requirement is estimated to be between 0.5 -
0.8%. The potassium requirement appears to be increased for livestock
under stress. Excitement tends to increase urinary loss of K and
diseases with fever or diarrhea further increase K loss. A study from
Texas revealed increased weight gains for steers that had been stressed
by shipping when fed feedlot rations containing 1.0 1.5% K (Hutcheson,
1979). Recent Florida studies indicate that 0.8% K is not adequate under
heat stress, particularly with high producing dairy cows (Beede et al.,
1983).








































Figure 10. The lamb at top received a potassium-deficient ration (0.1 percent potassium),
whereas the lamb at bottom received sufficient dietary potassium (0.6 percent
potassium). (Courtesy of the University of Missouri and R. L. Preston).









Magnesium fertilizers calcinedd magnesite or Kieserite) can
significantly increase pasture concentrations. This method of control
has limitations on many soil types and usually has to be accompanied by
other means of supplying additional Mg. Foliar dusting of pastures with
calcined magnesite (MgO) before or during tetany prone periods is one
such means that has proven effective, provided it is applied at not less
than 17 kg/ha at not more than 10-day intervals (Rogers, 1979).

For calves and cows that are being fed concentrates, provision of
50g MgO/day in 300 400 g of concentrate mixture is adequate. Incor-
porating it into mineral mixes, drenches, molasses-based free choice
supplements or sprinkling the mineral on feed such as grains, chopped
roots or silage, have all proven satisfactory methods of supplementation.
There is general agreement that 50 60 g MgO/day is the minimum secure
prophylactic dose for adult cattle; 7 15 g/day for calves; and 7 g/day
for lactating ewes. These doses must be given to all stock continuously
during the tetany susceptible period. Addition to the water supply of
soluble Mg salts such as chloride, sulfate and acetate has been exten-
sively studied as a prophylactic measure with mostly beneficial results
(Rogers and Poole, 1976); however, water intake by drinking varies widely
between individuals.

Subcutaneous injection of a single dose of 400 ml of a 25% solution
of Mg sulfate or intravenous injection of a similar dose of Mg lactate
restores serum Mg of an affected cow to near normal within about 10
minutes. Serum Mg concentrations will fall again unless the cow is
immediately removed from the tetany producing pasture and fed Mg adequate
diets.

POTASSIUM

Metabolism
Potassium is the third most abundant mineral element in the animal
body and is the principal cation of intracellular fluid; it also is a
constituent of extra cellular fluid where it influences muscle activity.
Potassium is essential for life, being required for a variety of body
functions including osmotic balance, acid-base equilibrium, several
enzyme systems and water balance. An ionic balance exists between K, Na,
Ca and Mg.

Requirement
The requirement for K is higher for ruminants than for nonruminants.
For ruminant species the requirement is estimated to be between 0.5 -
0.8%. The potassium requirement appears to be increased for livestock
under stress. Excitement tends to increase urinary loss of K and
diseases with fever or diarrhea further increase K loss. A study from
Texas revealed increased weight gains for steers that had been stressed
by shipping when fed feedlot rations containing 1.0 1.5% K (Hutcheson,
1979). Recent Florida studies indicate that 0.8% K is not adequate under
heat stress, particularly with high producing dairy cows (Beede et al.,
1983).









Magnesium fertilizers calcinedd magnesite or Kieserite) can
significantly increase pasture concentrations. This method of control
has limitations on many soil types and usually has to be accompanied by
other means of supplying additional Mg. Foliar dusting of pastures with
calcined magnesite (MgO) before or during tetany prone periods is one
such means that has proven effective, provided it is applied at not less
than 17 kg/ha at not more than 10-day intervals (Rogers, 1979).

For calves and cows that are being fed concentrates, provision of
50g MgO/day in 300 400 g of concentrate mixture is adequate. Incor-
porating it into mineral mixes, drenches, molasses-based free choice
supplements or sprinkling the mineral on feed such as grains, chopped
roots or silage, have all proven satisfactory methods of supplementation.
There is general agreement that 50 60 g MgO/day is the minimum secure
prophylactic dose for adult cattle; 7 15 g/day for calves; and 7 g/day
for lactating ewes. These doses must be given to all stock continuously
during the tetany susceptible period. Addition to the water supply of
soluble Mg salts such as chloride, sulfate and acetate has been exten-
sively studied as a prophylactic measure with mostly beneficial results
(Rogers and Poole, 1976); however, water intake by drinking varies widely
between individuals.

Subcutaneous injection of a single dose of 400 ml of a 25% solution
of Mg sulfate or intravenous injection of a similar dose of Mg lactate
restores serum Mg of an affected cow to near normal within about 10
minutes. Serum Mg concentrations will fall again unless the cow is
immediately removed from the tetany producing pasture and fed Mg adequate
diets.

POTASSIUM

Metabolism
Potassium is the third most abundant mineral element in the animal
body and is the principal cation of intracellular fluid; it also is a
constituent of extra cellular fluid where it influences muscle activity.
Potassium is essential for life, being required for a variety of body
functions including osmotic balance, acid-base equilibrium, several
enzyme systems and water balance. An ionic balance exists between K, Na,
Ca and Mg.

Requirement
The requirement for K is higher for ruminants than for nonruminants.
For ruminant species the requirement is estimated to be between 0.5 -
0.8%. The potassium requirement appears to be increased for livestock
under stress. Excitement tends to increase urinary loss of K and
diseases with fever or diarrhea further increase K loss. A study from
Texas revealed increased weight gains for steers that had been stressed
by shipping when fed feedlot rations containing 1.0 1.5% K (Hutcheson,
1979). Recent Florida studies indicate that 0.8% K is not adequate under
heat stress, particularly with high producing dairy cows (Beede et al.,
1983).









Deficiency
Potassium deficiency results in nonspecific signs such as slow
growth, reduced feed and water intake, lowered feed efficiency, muscular
weakness, nervous disorders, stiffness and emaciation (Figure 10). Until
quite recently, it was believed that there was little possibility of K
deficiency since young forages generally contain considerably more K than
required by grazing livestock. However, the K content of many concen-
trates, which would be basic ingredients for feedlot cattle, is below the
requirement. Present information also indicates that mature winter
pastures which have weathered, or hay which has been exposed to rain and
sun or was overly mature when harvested, can have K levels which are less
than adequate for good nutrition. In tropical regions, it is possible
that K deficiencies could arise in view of the decreasing content of this
mineral with increasing forage maturity during the extended dry season
and the use of urea which supplies none of this element.

Evaluation of a K deficiency is difficult. Low serum K analyses
have some diagnostic value for establishing a deficiency but may be
caused also by malnutrition, negative nitrogen balance, gastrointestinal
losses and endocrine malfunction. Reduced feed consumption appears to be
an early sign of inadequate dietary K. Because reliable evaluations of K
deficiency based on tissue analyses are not available, dietary K concen-
tration appears to be the best indicator of K status.

Prevention and Control
Depending upon K levels in forages and other ingredients used, it
may be necessary to add supplemental K. This is particularly true when
grazing winter or dry season range pastures and when urea is substituted
for plant proteins. Several chemical forms of K, including the chloride,
carbonate, bicarbonate and orthophosphate sources, are approximately
equal in value, and K from forages also appears to be efficiently
utilized.

Toxicity
The maximum tolerable level for K is suggested to be 3% (NRC, 1980).
Because ingested K beyond the requirement is quickly excreted, K toxi-
cosis is not a practical problem under normal conditions. High K content
in forages during critical times of the year can be antagonistic to Mg
absorption and/or utilization and thus can influence the incidence of
grass tetany (see Mg section).

SODIUM AND CHLORINE (SALT)

Metabolism
Sodium and Cl, in addition to K, all function in maintaining osmotic
pressure and regulating acid-base equilibrium. These two mineral
elements function as electrolytes in body fluids and are specifically
involved at the cellular level in water metabolism, nutrient uptake and
transmission of nerve impulses. Chlorine is necessary for activation of
amylase and is essential for formation of gastric hydrochloric acid.

Requirement
The essential need for Na and Cl by livestock has been demonstrated
for thousands of years by a natural craving for common salt. Sodium is









Deficiency
Potassium deficiency results in nonspecific signs such as slow
growth, reduced feed and water intake, lowered feed efficiency, muscular
weakness, nervous disorders, stiffness and emaciation (Figure 10). Until
quite recently, it was believed that there was little possibility of K
deficiency since young forages generally contain considerably more K than
required by grazing livestock. However, the K content of many concen-
trates, which would be basic ingredients for feedlot cattle, is below the
requirement. Present information also indicates that mature winter
pastures which have weathered, or hay which has been exposed to rain and
sun or was overly mature when harvested, can have K levels which are less
than adequate for good nutrition. In tropical regions, it is possible
that K deficiencies could arise in view of the decreasing content of this
mineral with increasing forage maturity during the extended dry season
and the use of urea which supplies none of this element.

Evaluation of a K deficiency is difficult. Low serum K analyses
have some diagnostic value for establishing a deficiency but may be
caused also by malnutrition, negative nitrogen balance, gastrointestinal
losses and endocrine malfunction. Reduced feed consumption appears to be
an early sign of inadequate dietary K. Because reliable evaluations of K
deficiency based on tissue analyses are not available, dietary K concen-
tration appears to be the best indicator of K status.

Prevention and Control
Depending upon K levels in forages and other ingredients used, it
may be necessary to add supplemental K. This is particularly true when
grazing winter or dry season range pastures and when urea is substituted
for plant proteins. Several chemical forms of K, including the chloride,
carbonate, bicarbonate and orthophosphate sources, are approximately
equal in value, and K from forages also appears to be efficiently
utilized.

Toxicity
The maximum tolerable level for K is suggested to be 3% (NRC, 1980).
Because ingested K beyond the requirement is quickly excreted, K toxi-
cosis is not a practical problem under normal conditions. High K content
in forages during critical times of the year can be antagonistic to Mg
absorption and/or utilization and thus can influence the incidence of
grass tetany (see Mg section).

SODIUM AND CHLORINE (SALT)

Metabolism
Sodium and Cl, in addition to K, all function in maintaining osmotic
pressure and regulating acid-base equilibrium. These two mineral
elements function as electrolytes in body fluids and are specifically
involved at the cellular level in water metabolism, nutrient uptake and
transmission of nerve impulses. Chlorine is necessary for activation of
amylase and is essential for formation of gastric hydrochloric acid.

Requirement
The essential need for Na and Cl by livestock has been demonstrated
for thousands of years by a natural craving for common salt. Sodium is









Deficiency
Potassium deficiency results in nonspecific signs such as slow
growth, reduced feed and water intake, lowered feed efficiency, muscular
weakness, nervous disorders, stiffness and emaciation (Figure 10). Until
quite recently, it was believed that there was little possibility of K
deficiency since young forages generally contain considerably more K than
required by grazing livestock. However, the K content of many concen-
trates, which would be basic ingredients for feedlot cattle, is below the
requirement. Present information also indicates that mature winter
pastures which have weathered, or hay which has been exposed to rain and
sun or was overly mature when harvested, can have K levels which are less
than adequate for good nutrition. In tropical regions, it is possible
that K deficiencies could arise in view of the decreasing content of this
mineral with increasing forage maturity during the extended dry season
and the use of urea which supplies none of this element.

Evaluation of a K deficiency is difficult. Low serum K analyses
have some diagnostic value for establishing a deficiency but may be
caused also by malnutrition, negative nitrogen balance, gastrointestinal
losses and endocrine malfunction. Reduced feed consumption appears to be
an early sign of inadequate dietary K. Because reliable evaluations of K
deficiency based on tissue analyses are not available, dietary K concen-
tration appears to be the best indicator of K status.

Prevention and Control
Depending upon K levels in forages and other ingredients used, it
may be necessary to add supplemental K. This is particularly true when
grazing winter or dry season range pastures and when urea is substituted
for plant proteins. Several chemical forms of K, including the chloride,
carbonate, bicarbonate and orthophosphate sources, are approximately
equal in value, and K from forages also appears to be efficiently
utilized.

Toxicity
The maximum tolerable level for K is suggested to be 3% (NRC, 1980).
Because ingested K beyond the requirement is quickly excreted, K toxi-
cosis is not a practical problem under normal conditions. High K content
in forages during critical times of the year can be antagonistic to Mg
absorption and/or utilization and thus can influence the incidence of
grass tetany (see Mg section).

SODIUM AND CHLORINE (SALT)

Metabolism
Sodium and Cl, in addition to K, all function in maintaining osmotic
pressure and regulating acid-base equilibrium. These two mineral
elements function as electrolytes in body fluids and are specifically
involved at the cellular level in water metabolism, nutrient uptake and
transmission of nerve impulses. Chlorine is necessary for activation of
amylase and is essential for formation of gastric hydrochloric acid.

Requirement
The essential need for Na and Cl by livestock has been demonstrated
for thousands of years by a natural craving for common salt. Sodium is









Deficiency
Potassium deficiency results in nonspecific signs such as slow
growth, reduced feed and water intake, lowered feed efficiency, muscular
weakness, nervous disorders, stiffness and emaciation (Figure 10). Until
quite recently, it was believed that there was little possibility of K
deficiency since young forages generally contain considerably more K than
required by grazing livestock. However, the K content of many concen-
trates, which would be basic ingredients for feedlot cattle, is below the
requirement. Present information also indicates that mature winter
pastures which have weathered, or hay which has been exposed to rain and
sun or was overly mature when harvested, can have K levels which are less
than adequate for good nutrition. In tropical regions, it is possible
that K deficiencies could arise in view of the decreasing content of this
mineral with increasing forage maturity during the extended dry season
and the use of urea which supplies none of this element.

Evaluation of a K deficiency is difficult. Low serum K analyses
have some diagnostic value for establishing a deficiency but may be
caused also by malnutrition, negative nitrogen balance, gastrointestinal
losses and endocrine malfunction. Reduced feed consumption appears to be
an early sign of inadequate dietary K. Because reliable evaluations of K
deficiency based on tissue analyses are not available, dietary K concen-
tration appears to be the best indicator of K status.

Prevention and Control
Depending upon K levels in forages and other ingredients used, it
may be necessary to add supplemental K. This is particularly true when
grazing winter or dry season range pastures and when urea is substituted
for plant proteins. Several chemical forms of K, including the chloride,
carbonate, bicarbonate and orthophosphate sources, are approximately
equal in value, and K from forages also appears to be efficiently
utilized.

Toxicity
The maximum tolerable level for K is suggested to be 3% (NRC, 1980).
Because ingested K beyond the requirement is quickly excreted, K toxi-
cosis is not a practical problem under normal conditions. High K content
in forages during critical times of the year can be antagonistic to Mg
absorption and/or utilization and thus can influence the incidence of
grass tetany (see Mg section).

SODIUM AND CHLORINE (SALT)

Metabolism
Sodium and Cl, in addition to K, all function in maintaining osmotic
pressure and regulating acid-base equilibrium. These two mineral
elements function as electrolytes in body fluids and are specifically
involved at the cellular level in water metabolism, nutrient uptake and
transmission of nerve impulses. Chlorine is necessary for activation of
amylase and is essential for formation of gastric hydrochloric acid.

Requirement
The essential need for Na and Cl by livestock has been demonstrated
for thousands of years by a natural craving for common salt. Sodium is









Deficiency
Potassium deficiency results in nonspecific signs such as slow
growth, reduced feed and water intake, lowered feed efficiency, muscular
weakness, nervous disorders, stiffness and emaciation (Figure 10). Until
quite recently, it was believed that there was little possibility of K
deficiency since young forages generally contain considerably more K than
required by grazing livestock. However, the K content of many concen-
trates, which would be basic ingredients for feedlot cattle, is below the
requirement. Present information also indicates that mature winter
pastures which have weathered, or hay which has been exposed to rain and
sun or was overly mature when harvested, can have K levels which are less
than adequate for good nutrition. In tropical regions, it is possible
that K deficiencies could arise in view of the decreasing content of this
mineral with increasing forage maturity during the extended dry season
and the use of urea which supplies none of this element.

Evaluation of a K deficiency is difficult. Low serum K analyses
have some diagnostic value for establishing a deficiency but may be
caused also by malnutrition, negative nitrogen balance, gastrointestinal
losses and endocrine malfunction. Reduced feed consumption appears to be
an early sign of inadequate dietary K. Because reliable evaluations of K
deficiency based on tissue analyses are not available, dietary K concen-
tration appears to be the best indicator of K status.

Prevention and Control
Depending upon K levels in forages and other ingredients used, it
may be necessary to add supplemental K. This is particularly true when
grazing winter or dry season range pastures and when urea is substituted
for plant proteins. Several chemical forms of K, including the chloride,
carbonate, bicarbonate and orthophosphate sources, are approximately
equal in value, and K from forages also appears to be efficiently
utilized.

Toxicity
The maximum tolerable level for K is suggested to be 3% (NRC, 1980).
Because ingested K beyond the requirement is quickly excreted, K toxi-
cosis is not a practical problem under normal conditions. High K content
in forages during critical times of the year can be antagonistic to Mg
absorption and/or utilization and thus can influence the incidence of
grass tetany (see Mg section).

SODIUM AND CHLORINE (SALT)

Metabolism
Sodium and Cl, in addition to K, all function in maintaining osmotic
pressure and regulating acid-base equilibrium. These two mineral
elements function as electrolytes in body fluids and are specifically
involved at the cellular level in water metabolism, nutrient uptake and
transmission of nerve impulses. Chlorine is necessary for activation of
amylase and is essential for formation of gastric hydrochloric acid.

Requirement
The essential need for Na and Cl by livestock has been demonstrated
for thousands of years by a natural craving for common salt. Sodium is









Deficiency
Potassium deficiency results in nonspecific signs such as slow
growth, reduced feed and water intake, lowered feed efficiency, muscular
weakness, nervous disorders, stiffness and emaciation (Figure 10). Until
quite recently, it was believed that there was little possibility of K
deficiency since young forages generally contain considerably more K than
required by grazing livestock. However, the K content of many concen-
trates, which would be basic ingredients for feedlot cattle, is below the
requirement. Present information also indicates that mature winter
pastures which have weathered, or hay which has been exposed to rain and
sun or was overly mature when harvested, can have K levels which are less
than adequate for good nutrition. In tropical regions, it is possible
that K deficiencies could arise in view of the decreasing content of this
mineral with increasing forage maturity during the extended dry season
and the use of urea which supplies none of this element.

Evaluation of a K deficiency is difficult. Low serum K analyses
have some diagnostic value for establishing a deficiency but may be
caused also by malnutrition, negative nitrogen balance, gastrointestinal
losses and endocrine malfunction. Reduced feed consumption appears to be
an early sign of inadequate dietary K. Because reliable evaluations of K
deficiency based on tissue analyses are not available, dietary K concen-
tration appears to be the best indicator of K status.

Prevention and Control
Depending upon K levels in forages and other ingredients used, it
may be necessary to add supplemental K. This is particularly true when
grazing winter or dry season range pastures and when urea is substituted
for plant proteins. Several chemical forms of K, including the chloride,
carbonate, bicarbonate and orthophosphate sources, are approximately
equal in value, and K from forages also appears to be efficiently
utilized.

Toxicity
The maximum tolerable level for K is suggested to be 3% (NRC, 1980).
Because ingested K beyond the requirement is quickly excreted, K toxi-
cosis is not a practical problem under normal conditions. High K content
in forages during critical times of the year can be antagonistic to Mg
absorption and/or utilization and thus can influence the incidence of
grass tetany (see Mg section).

SODIUM AND CHLORINE (SALT)

Metabolism
Sodium and Cl, in addition to K, all function in maintaining osmotic
pressure and regulating acid-base equilibrium. These two mineral
elements function as electrolytes in body fluids and are specifically
involved at the cellular level in water metabolism, nutrient uptake and
transmission of nerve impulses. Chlorine is necessary for activation of
amylase and is essential for formation of gastric hydrochloric acid.

Requirement
The essential need for Na and Cl by livestock has been demonstrated
for thousands of years by a natural craving for common salt. Sodium is









the critical nutrient in salt and evidence of a naturally occurring
dietary deficiency of Cl, as distinct from Na, has not been established.
However, the requirement is often expressed as salt (NaC1). The recom-
mended Na requirement for grazing ruminants is between 0.04 0.18%, with
the higher level recommended for lactating dairy cows.

Deficiency
The initial sign of Na and Cl deficiency is a craving for salt,
demonstrated by the avid licking of wood, soil and sweat from other
animals and drinking water. A prolonged deficiency causes loss of
appetite, decreased growth, unthrifty appearance, reduced milk production
and loss of weight (Figure 11).

Most grazing livestock in tropical countries either receive
insufficient salt or have only very limited access to salt at certain
times of the year. According to SUtmoller et al. (1966), the insuf-
ficiency of Na is the most widespread mineral deficiency in the Amazon
Busin of Brazil (Z 3.5 million sq. km). Livestock deprived of salt may
be so voracious that they often injure each other in attempting to reach
salt. Sodium deficiency is most likely to occur: 1) during lactation,
due to secretion of Na in milk; 2) in rapidly growing animals; 3) under
tropical or hot semi-arid conditions where large losses of water and Na
occur in the sweat and where pastures are low in Na; 4) in animals
grazing pastures heavily fertilized with K which depresses herbage Na
levels. Even after prolonged severe deficiency, NaC1 (salt) levels
secreted in milk remain high. Thus, lactating animals suffer most from
lack of salt in the diet (Loosli, 1978).

Because of animals' rapid reaction to deficiency long before
clinical signs appear, the best criterion for assessment of Na status is
concentration of Na and K in saliva. Deficiency causes a fall in Na and
a rise in K.

Prevention and Control
Tropical forages normally do not contain sufficient quantities of Na
to meet the requirements of grazing livestock throughout the year. This
inadequacy is easily overcome by the practice of providing common salt ad
libitum. The salt needs of grazing cattle, for example, can easily be
met with mineral mixtures containing 20 to 35% salt and consumed at a
rate of 0.1 lb (45 g) per head daily. It is recommended that feedlot
rations contain 0.25% added salt, one-half the 0.5% level recommended a
few years past. An advantage of the lower salt level in modern feedlot
rations is the prevention of salt buildup in feedlot waste, lessening
problems in waste treatment and its utilization as a fertilizer.

Toxicity
Most animals can tolerate large quantities of dietary salt when an
adequate supply of water is available. Clinical signs following
consumption of water with more than 7000 ppm of dissolved salt include
low consumption of feed and water, mild digestive disturbances, low rates
of gain and diarrhea.









the critical nutrient in salt and evidence of a naturally occurring
dietary deficiency of Cl, as distinct from Na, has not been established.
However, the requirement is often expressed as salt (NaC1). The recom-
mended Na requirement for grazing ruminants is between 0.04 0.18%, with
the higher level recommended for lactating dairy cows.

Deficiency
The initial sign of Na and Cl deficiency is a craving for salt,
demonstrated by the avid licking of wood, soil and sweat from other
animals and drinking water. A prolonged deficiency causes loss of
appetite, decreased growth, unthrifty appearance, reduced milk production
and loss of weight (Figure 11).

Most grazing livestock in tropical countries either receive
insufficient salt or have only very limited access to salt at certain
times of the year. According to SUtmoller et al. (1966), the insuf-
ficiency of Na is the most widespread mineral deficiency in the Amazon
Busin of Brazil (Z 3.5 million sq. km). Livestock deprived of salt may
be so voracious that they often injure each other in attempting to reach
salt. Sodium deficiency is most likely to occur: 1) during lactation,
due to secretion of Na in milk; 2) in rapidly growing animals; 3) under
tropical or hot semi-arid conditions where large losses of water and Na
occur in the sweat and where pastures are low in Na; 4) in animals
grazing pastures heavily fertilized with K which depresses herbage Na
levels. Even after prolonged severe deficiency, NaC1 (salt) levels
secreted in milk remain high. Thus, lactating animals suffer most from
lack of salt in the diet (Loosli, 1978).

Because of animals' rapid reaction to deficiency long before
clinical signs appear, the best criterion for assessment of Na status is
concentration of Na and K in saliva. Deficiency causes a fall in Na and
a rise in K.

Prevention and Control
Tropical forages normally do not contain sufficient quantities of Na
to meet the requirements of grazing livestock throughout the year. This
inadequacy is easily overcome by the practice of providing common salt ad
libitum. The salt needs of grazing cattle, for example, can easily be
met with mineral mixtures containing 20 to 35% salt and consumed at a
rate of 0.1 lb (45 g) per head daily. It is recommended that feedlot
rations contain 0.25% added salt, one-half the 0.5% level recommended a
few years past. An advantage of the lower salt level in modern feedlot
rations is the prevention of salt buildup in feedlot waste, lessening
problems in waste treatment and its utilization as a fertilizer.

Toxicity
Most animals can tolerate large quantities of dietary salt when an
adequate supply of water is available. Clinical signs following
consumption of water with more than 7000 ppm of dissolved salt include
low consumption of feed and water, mild digestive disturbances, low rates
of gain and diarrhea.









the critical nutrient in salt and evidence of a naturally occurring
dietary deficiency of Cl, as distinct from Na, has not been established.
However, the requirement is often expressed as salt (NaC1). The recom-
mended Na requirement for grazing ruminants is between 0.04 0.18%, with
the higher level recommended for lactating dairy cows.

Deficiency
The initial sign of Na and Cl deficiency is a craving for salt,
demonstrated by the avid licking of wood, soil and sweat from other
animals and drinking water. A prolonged deficiency causes loss of
appetite, decreased growth, unthrifty appearance, reduced milk production
and loss of weight (Figure 11).

Most grazing livestock in tropical countries either receive
insufficient salt or have only very limited access to salt at certain
times of the year. According to SUtmoller et al. (1966), the insuf-
ficiency of Na is the most widespread mineral deficiency in the Amazon
Busin of Brazil (Z 3.5 million sq. km). Livestock deprived of salt may
be so voracious that they often injure each other in attempting to reach
salt. Sodium deficiency is most likely to occur: 1) during lactation,
due to secretion of Na in milk; 2) in rapidly growing animals; 3) under
tropical or hot semi-arid conditions where large losses of water and Na
occur in the sweat and where pastures are low in Na; 4) in animals
grazing pastures heavily fertilized with K which depresses herbage Na
levels. Even after prolonged severe deficiency, NaC1 (salt) levels
secreted in milk remain high. Thus, lactating animals suffer most from
lack of salt in the diet (Loosli, 1978).

Because of animals' rapid reaction to deficiency long before
clinical signs appear, the best criterion for assessment of Na status is
concentration of Na and K in saliva. Deficiency causes a fall in Na and
a rise in K.

Prevention and Control
Tropical forages normally do not contain sufficient quantities of Na
to meet the requirements of grazing livestock throughout the year. This
inadequacy is easily overcome by the practice of providing common salt ad
libitum. The salt needs of grazing cattle, for example, can easily be
met with mineral mixtures containing 20 to 35% salt and consumed at a
rate of 0.1 lb (45 g) per head daily. It is recommended that feedlot
rations contain 0.25% added salt, one-half the 0.5% level recommended a
few years past. An advantage of the lower salt level in modern feedlot
rations is the prevention of salt buildup in feedlot waste, lessening
problems in waste treatment and its utilization as a fertilizer.

Toxicity
Most animals can tolerate large quantities of dietary salt when an
adequate supply of water is available. Clinical signs following
consumption of water with more than 7000 ppm of dissolved salt include
low consumption of feed and water, mild digestive disturbances, low rates
of gain and diarrhea.











-r -
\~


Figure 11. Salt deficiency in a dairy cow. Illustrates before and after one year of salt depriva-
tion (Cornell Bulletin 938, courtesy S. E. Smith, Cornell University, Ithaca, New
York, U.S.A.).









SULFUR

Metabolism
Sulfur is an important element in the synthesis of protein since two
important amino acids, methionine and cysteine contain S. Likewise, S is
a part of the vitamins thiamin and biotin and of sulfated polysaccha-
rides, including chondroitin. Chondroitin is a key component of
cartilage, bone, tendons and blood vessel walls. Body functions that
involve S include protein synthesis and metabolism, fat and carbohydrate
metabolism, blood clotting, endocrine function and intra- and extra-
cellular fluid acid-base balance.

Requirement
Sulfur requirements of ruminants are not well defined. Between 0.10
and 0.32% S is the estimated requirement for grazing ruminants (Table 2).
Since the S requirement for optimum microbial action appears to be the
highest need for S of ruminants, the effect of S on rumen function is
studied. The optimum S level for cellulose digestion in vitro has been
reported to be 0.16 0.24% of dry matter. The S requirement of rumi-
nants can be approached from a consideration of the N to S ratio.
Tissues of cattle contain a N:S ration of 15:1, and it has been shown
that dietary ratios of 12 to 15:1 are excellent for cattle. Due to
requirements of S for wool, a ratio of 10:1 is commonly recommended for
sheep rations.

Deficiency
Signs of S deficiency have been described as loss of weight,
weakness, lacrimation, dullness and death (Figure 12). In a S defi-
ciency, microbial protein synthesis is reduced and the animal shows signs
of protein malnutrition. A lack of S also results in a microbial popu-
lation that does not utilize lactate; therefore, lactate accumulates in
the rumen, blood and urine. It is difficult to diagnose a deficiency,
especially a borderline one. Serum sulfate levels have been suggested as
an indicator of S deficiency, but blood lactate and dietary S levels may
be the most reliable indicators of S status.

A recent review (Miles and McDowell, 1983) summarized four cattle
supplementation trials where control diets contained between 0.04 and
0.10% S. Intake by S-supplemented cattle increased from 7 to 260% and
production of milk and meat increased by 6 to more than 400% according to
these studies. Some reports from tropical regions indicate that S
fertilization may increase forage intake by improving palatability of
less palatable species. Further S supplementation studies for grazing
livestock are warranted.

Prevention and Control
Sulfur supplementation will most likely be needed to meet the
requirements of ruminants when poor quality roughages grown on
S-deficient soils or feeds combined with non-protein nitrogen (NPN) such
as urea are fed. Since there is no S in urea, the element may need to be
added when high levels of urea are fed.

Sulfur may be provided in the diet by both organic and inorganic
sources. Ruminants may utilize the S in methionine, methionine hydroxy









SULFUR

Metabolism
Sulfur is an important element in the synthesis of protein since two
important amino acids, methionine and cysteine contain S. Likewise, S is
a part of the vitamins thiamin and biotin and of sulfated polysaccha-
rides, including chondroitin. Chondroitin is a key component of
cartilage, bone, tendons and blood vessel walls. Body functions that
involve S include protein synthesis and metabolism, fat and carbohydrate
metabolism, blood clotting, endocrine function and intra- and extra-
cellular fluid acid-base balance.

Requirement
Sulfur requirements of ruminants are not well defined. Between 0.10
and 0.32% S is the estimated requirement for grazing ruminants (Table 2).
Since the S requirement for optimum microbial action appears to be the
highest need for S of ruminants, the effect of S on rumen function is
studied. The optimum S level for cellulose digestion in vitro has been
reported to be 0.16 0.24% of dry matter. The S requirement of rumi-
nants can be approached from a consideration of the N to S ratio.
Tissues of cattle contain a N:S ration of 15:1, and it has been shown
that dietary ratios of 12 to 15:1 are excellent for cattle. Due to
requirements of S for wool, a ratio of 10:1 is commonly recommended for
sheep rations.

Deficiency
Signs of S deficiency have been described as loss of weight,
weakness, lacrimation, dullness and death (Figure 12). In a S defi-
ciency, microbial protein synthesis is reduced and the animal shows signs
of protein malnutrition. A lack of S also results in a microbial popu-
lation that does not utilize lactate; therefore, lactate accumulates in
the rumen, blood and urine. It is difficult to diagnose a deficiency,
especially a borderline one. Serum sulfate levels have been suggested as
an indicator of S deficiency, but blood lactate and dietary S levels may
be the most reliable indicators of S status.

A recent review (Miles and McDowell, 1983) summarized four cattle
supplementation trials where control diets contained between 0.04 and
0.10% S. Intake by S-supplemented cattle increased from 7 to 260% and
production of milk and meat increased by 6 to more than 400% according to
these studies. Some reports from tropical regions indicate that S
fertilization may increase forage intake by improving palatability of
less palatable species. Further S supplementation studies for grazing
livestock are warranted.

Prevention and Control
Sulfur supplementation will most likely be needed to meet the
requirements of ruminants when poor quality roughages grown on
S-deficient soils or feeds combined with non-protein nitrogen (NPN) such
as urea are fed. Since there is no S in urea, the element may need to be
added when high levels of urea are fed.

Sulfur may be provided in the diet by both organic and inorganic
sources. Ruminants may utilize the S in methionine, methionine hydroxy









SULFUR

Metabolism
Sulfur is an important element in the synthesis of protein since two
important amino acids, methionine and cysteine contain S. Likewise, S is
a part of the vitamins thiamin and biotin and of sulfated polysaccha-
rides, including chondroitin. Chondroitin is a key component of
cartilage, bone, tendons and blood vessel walls. Body functions that
involve S include protein synthesis and metabolism, fat and carbohydrate
metabolism, blood clotting, endocrine function and intra- and extra-
cellular fluid acid-base balance.

Requirement
Sulfur requirements of ruminants are not well defined. Between 0.10
and 0.32% S is the estimated requirement for grazing ruminants (Table 2).
Since the S requirement for optimum microbial action appears to be the
highest need for S of ruminants, the effect of S on rumen function is
studied. The optimum S level for cellulose digestion in vitro has been
reported to be 0.16 0.24% of dry matter. The S requirement of rumi-
nants can be approached from a consideration of the N to S ratio.
Tissues of cattle contain a N:S ration of 15:1, and it has been shown
that dietary ratios of 12 to 15:1 are excellent for cattle. Due to
requirements of S for wool, a ratio of 10:1 is commonly recommended for
sheep rations.

Deficiency
Signs of S deficiency have been described as loss of weight,
weakness, lacrimation, dullness and death (Figure 12). In a S defi-
ciency, microbial protein synthesis is reduced and the animal shows signs
of protein malnutrition. A lack of S also results in a microbial popu-
lation that does not utilize lactate; therefore, lactate accumulates in
the rumen, blood and urine. It is difficult to diagnose a deficiency,
especially a borderline one. Serum sulfate levels have been suggested as
an indicator of S deficiency, but blood lactate and dietary S levels may
be the most reliable indicators of S status.

A recent review (Miles and McDowell, 1983) summarized four cattle
supplementation trials where control diets contained between 0.04 and
0.10% S. Intake by S-supplemented cattle increased from 7 to 260% and
production of milk and meat increased by 6 to more than 400% according to
these studies. Some reports from tropical regions indicate that S
fertilization may increase forage intake by improving palatability of
less palatable species. Further S supplementation studies for grazing
livestock are warranted.

Prevention and Control
Sulfur supplementation will most likely be needed to meet the
requirements of ruminants when poor quality roughages grown on
S-deficient soils or feeds combined with non-protein nitrogen (NPN) such
as urea are fed. Since there is no S in urea, the element may need to be
added when high levels of urea are fed.

Sulfur may be provided in the diet by both organic and inorganic
sources. Ruminants may utilize the S in methionine, methionine hydroxy









SULFUR

Metabolism
Sulfur is an important element in the synthesis of protein since two
important amino acids, methionine and cysteine contain S. Likewise, S is
a part of the vitamins thiamin and biotin and of sulfated polysaccha-
rides, including chondroitin. Chondroitin is a key component of
cartilage, bone, tendons and blood vessel walls. Body functions that
involve S include protein synthesis and metabolism, fat and carbohydrate
metabolism, blood clotting, endocrine function and intra- and extra-
cellular fluid acid-base balance.

Requirement
Sulfur requirements of ruminants are not well defined. Between 0.10
and 0.32% S is the estimated requirement for grazing ruminants (Table 2).
Since the S requirement for optimum microbial action appears to be the
highest need for S of ruminants, the effect of S on rumen function is
studied. The optimum S level for cellulose digestion in vitro has been
reported to be 0.16 0.24% of dry matter. The S requirement of rumi-
nants can be approached from a consideration of the N to S ratio.
Tissues of cattle contain a N:S ration of 15:1, and it has been shown
that dietary ratios of 12 to 15:1 are excellent for cattle. Due to
requirements of S for wool, a ratio of 10:1 is commonly recommended for
sheep rations.

Deficiency
Signs of S deficiency have been described as loss of weight,
weakness, lacrimation, dullness and death (Figure 12). In a S defi-
ciency, microbial protein synthesis is reduced and the animal shows signs
of protein malnutrition. A lack of S also results in a microbial popu-
lation that does not utilize lactate; therefore, lactate accumulates in
the rumen, blood and urine. It is difficult to diagnose a deficiency,
especially a borderline one. Serum sulfate levels have been suggested as
an indicator of S deficiency, but blood lactate and dietary S levels may
be the most reliable indicators of S status.

A recent review (Miles and McDowell, 1983) summarized four cattle
supplementation trials where control diets contained between 0.04 and
0.10% S. Intake by S-supplemented cattle increased from 7 to 260% and
production of milk and meat increased by 6 to more than 400% according to
these studies. Some reports from tropical regions indicate that S
fertilization may increase forage intake by improving palatability of
less palatable species. Further S supplementation studies for grazing
livestock are warranted.

Prevention and Control
Sulfur supplementation will most likely be needed to meet the
requirements of ruminants when poor quality roughages grown on
S-deficient soils or feeds combined with non-protein nitrogen (NPN) such
as urea are fed. Since there is no S in urea, the element may need to be
added when high levels of urea are fed.

Sulfur may be provided in the diet by both organic and inorganic
sources. Ruminants may utilize the S in methionine, methionine hydroxy









SULFUR

Metabolism
Sulfur is an important element in the synthesis of protein since two
important amino acids, methionine and cysteine contain S. Likewise, S is
a part of the vitamins thiamin and biotin and of sulfated polysaccha-
rides, including chondroitin. Chondroitin is a key component of
cartilage, bone, tendons and blood vessel walls. Body functions that
involve S include protein synthesis and metabolism, fat and carbohydrate
metabolism, blood clotting, endocrine function and intra- and extra-
cellular fluid acid-base balance.

Requirement
Sulfur requirements of ruminants are not well defined. Between 0.10
and 0.32% S is the estimated requirement for grazing ruminants (Table 2).
Since the S requirement for optimum microbial action appears to be the
highest need for S of ruminants, the effect of S on rumen function is
studied. The optimum S level for cellulose digestion in vitro has been
reported to be 0.16 0.24% of dry matter. The S requirement of rumi-
nants can be approached from a consideration of the N to S ratio.
Tissues of cattle contain a N:S ration of 15:1, and it has been shown
that dietary ratios of 12 to 15:1 are excellent for cattle. Due to
requirements of S for wool, a ratio of 10:1 is commonly recommended for
sheep rations.

Deficiency
Signs of S deficiency have been described as loss of weight,
weakness, lacrimation, dullness and death (Figure 12). In a S defi-
ciency, microbial protein synthesis is reduced and the animal shows signs
of protein malnutrition. A lack of S also results in a microbial popu-
lation that does not utilize lactate; therefore, lactate accumulates in
the rumen, blood and urine. It is difficult to diagnose a deficiency,
especially a borderline one. Serum sulfate levels have been suggested as
an indicator of S deficiency, but blood lactate and dietary S levels may
be the most reliable indicators of S status.

A recent review (Miles and McDowell, 1983) summarized four cattle
supplementation trials where control diets contained between 0.04 and
0.10% S. Intake by S-supplemented cattle increased from 7 to 260% and
production of milk and meat increased by 6 to more than 400% according to
these studies. Some reports from tropical regions indicate that S
fertilization may increase forage intake by improving palatability of
less palatable species. Further S supplementation studies for grazing
livestock are warranted.

Prevention and Control
Sulfur supplementation will most likely be needed to meet the
requirements of ruminants when poor quality roughages grown on
S-deficient soils or feeds combined with non-protein nitrogen (NPN) such
as urea are fed. Since there is no S in urea, the element may need to be
added when high levels of urea are fed.

Sulfur may be provided in the diet by both organic and inorganic
sources. Ruminants may utilize the S in methionine, methionine hydroxy




















-q~ ~Pt


Figure 12. Lambs fed a low-sulfur diet. The lamb on the left received 3 g of sulfur per pound
of ration, whereas the lamb on the right received none. Note the excessive saliva-
tion lacrimation, and shedding of wool by the lamb on the right. (Courtesy U.S.
Garrigus, University of Illinois, Urbana-Champaign, Illinois, U.S.A.).









analog, Na, Ca, Mg, K or ammonium sulfate salts or elemental S. Sulfur
as the highly insoluble elemental S or lignin sulfonate is much less
available and it is suggested that elemental S (flowers of sulfur) is
utilized about one-third as efficiently as the sulfate or methionine
forms. Sulfur in corn and corn silage has been found to be less
available than that in sodium sulfate, methionine and methionine hydroxy
analog.

Toxicity and Interrelationships
The interrelationship of S with Cu and Mo is discussed (see Cu and
Mo) with Cu requirements increased by both S and Mo. Likewise, the
interrelationship between Se and S is due in part to their similar
structures. Selenium can replace S in some organic compounds but the
metabolic activity of the seleno-compound is less than that of the normal
S-containing compound. Sulfur has been used to counteract the effects of
Se when fed in toxic concentrations.

Maximum tolerable level for S is reported to be 0.40% (NRC, 1980),
but is less well defined than the maximum requirement. Ruminants can
tolerate more S from natural feed ingredients than from added sulfate.
Excessive dietary S levels may cause acute toxicity resulting in clinical
signs of abdominal pain, muscle twitching, diarrhea, severe dehydration,
strong odor of sulfide on the breath, congested lungs and acute enteritis
(Miller, 1979).

COBALT

Metabolism
Cobalt is required by rumen microorganisms for the synthesis of
vitamin B12. Although Co was recognized as an essential microelement for
ruminants, the nutritional function of Co was not discovered until the
discovery of vitamin B12 in 1948. The production of vitamin B. in the
rumen depends on the Co, the roughage content of the diet and te total
dietary intake. There is no evidence that vitamin B synthesis is
possible within body tissues. The ruminant is therefore ultimately
dependent on the synthetic capacity of its rumen organisms. Rumen
microorganisms produce many Co-containing vitamin B12-like compounds
which have no true vitamin B activity for body tissues. Information
exists which shows that Co-deficient sheep convert at least 60 percent of
their limited supply of dietary Co into compounds that cannot be absorbed
and used. True vitamin B 2 (5,6-dimethyl benzimidazolylcobamide cyanide
or DMBC) is frequently re erred to as cobalamin.

The main source of energy to ruminants is not glucose but primarily
acetic and propionic acids. Vitamin B12 is necessary for the normal
functioning of a number of enzyme systems in energy utilization. Thus,
vitamin B12 deficient ruminants fail to convert propionate efficiently to
succinate. The main route of Co excretion and control of metabolic
balance is largely achieved by excretion in the urine.

Requirement
Cobalt requirements have been established as 0.1 ppm of dietary dry
matter intake for grazing ruminant animals. Under grazing conditions,
lambs are the most sensitive to Co deficiency, followed by mature sheep,









analog, Na, Ca, Mg, K or ammonium sulfate salts or elemental S. Sulfur
as the highly insoluble elemental S or lignin sulfonate is much less
available and it is suggested that elemental S (flowers of sulfur) is
utilized about one-third as efficiently as the sulfate or methionine
forms. Sulfur in corn and corn silage has been found to be less
available than that in sodium sulfate, methionine and methionine hydroxy
analog.

Toxicity and Interrelationships
The interrelationship of S with Cu and Mo is discussed (see Cu and
Mo) with Cu requirements increased by both S and Mo. Likewise, the
interrelationship between Se and S is due in part to their similar
structures. Selenium can replace S in some organic compounds but the
metabolic activity of the seleno-compound is less than that of the normal
S-containing compound. Sulfur has been used to counteract the effects of
Se when fed in toxic concentrations.

Maximum tolerable level for S is reported to be 0.40% (NRC, 1980),
but is less well defined than the maximum requirement. Ruminants can
tolerate more S from natural feed ingredients than from added sulfate.
Excessive dietary S levels may cause acute toxicity resulting in clinical
signs of abdominal pain, muscle twitching, diarrhea, severe dehydration,
strong odor of sulfide on the breath, congested lungs and acute enteritis
(Miller, 1979).

COBALT

Metabolism
Cobalt is required by rumen microorganisms for the synthesis of
vitamin B12. Although Co was recognized as an essential microelement for
ruminants, the nutritional function of Co was not discovered until the
discovery of vitamin B12 in 1948. The production of vitamin B. in the
rumen depends on the Co, the roughage content of the diet and te total
dietary intake. There is no evidence that vitamin B synthesis is
possible within body tissues. The ruminant is therefore ultimately
dependent on the synthetic capacity of its rumen organisms. Rumen
microorganisms produce many Co-containing vitamin B12-like compounds
which have no true vitamin B activity for body tissues. Information
exists which shows that Co-deficient sheep convert at least 60 percent of
their limited supply of dietary Co into compounds that cannot be absorbed
and used. True vitamin B 2 (5,6-dimethyl benzimidazolylcobamide cyanide
or DMBC) is frequently re erred to as cobalamin.

The main source of energy to ruminants is not glucose but primarily
acetic and propionic acids. Vitamin B12 is necessary for the normal
functioning of a number of enzyme systems in energy utilization. Thus,
vitamin B12 deficient ruminants fail to convert propionate efficiently to
succinate. The main route of Co excretion and control of metabolic
balance is largely achieved by excretion in the urine.

Requirement
Cobalt requirements have been established as 0.1 ppm of dietary dry
matter intake for grazing ruminant animals. Under grazing conditions,
lambs are the most sensitive to Co deficiency, followed by mature sheep,









analog, Na, Ca, Mg, K or ammonium sulfate salts or elemental S. Sulfur
as the highly insoluble elemental S or lignin sulfonate is much less
available and it is suggested that elemental S (flowers of sulfur) is
utilized about one-third as efficiently as the sulfate or methionine
forms. Sulfur in corn and corn silage has been found to be less
available than that in sodium sulfate, methionine and methionine hydroxy
analog.

Toxicity and Interrelationships
The interrelationship of S with Cu and Mo is discussed (see Cu and
Mo) with Cu requirements increased by both S and Mo. Likewise, the
interrelationship between Se and S is due in part to their similar
structures. Selenium can replace S in some organic compounds but the
metabolic activity of the seleno-compound is less than that of the normal
S-containing compound. Sulfur has been used to counteract the effects of
Se when fed in toxic concentrations.

Maximum tolerable level for S is reported to be 0.40% (NRC, 1980),
but is less well defined than the maximum requirement. Ruminants can
tolerate more S from natural feed ingredients than from added sulfate.
Excessive dietary S levels may cause acute toxicity resulting in clinical
signs of abdominal pain, muscle twitching, diarrhea, severe dehydration,
strong odor of sulfide on the breath, congested lungs and acute enteritis
(Miller, 1979).

COBALT

Metabolism
Cobalt is required by rumen microorganisms for the synthesis of
vitamin B12. Although Co was recognized as an essential microelement for
ruminants, the nutritional function of Co was not discovered until the
discovery of vitamin B12 in 1948. The production of vitamin B. in the
rumen depends on the Co, the roughage content of the diet and te total
dietary intake. There is no evidence that vitamin B synthesis is
possible within body tissues. The ruminant is therefore ultimately
dependent on the synthetic capacity of its rumen organisms. Rumen
microorganisms produce many Co-containing vitamin B12-like compounds
which have no true vitamin B activity for body tissues. Information
exists which shows that Co-deficient sheep convert at least 60 percent of
their limited supply of dietary Co into compounds that cannot be absorbed
and used. True vitamin B 2 (5,6-dimethyl benzimidazolylcobamide cyanide
or DMBC) is frequently re erred to as cobalamin.

The main source of energy to ruminants is not glucose but primarily
acetic and propionic acids. Vitamin B12 is necessary for the normal
functioning of a number of enzyme systems in energy utilization. Thus,
vitamin B12 deficient ruminants fail to convert propionate efficiently to
succinate. The main route of Co excretion and control of metabolic
balance is largely achieved by excretion in the urine.

Requirement
Cobalt requirements have been established as 0.1 ppm of dietary dry
matter intake for grazing ruminant animals. Under grazing conditions,
lambs are the most sensitive to Co deficiency, followed by mature sheep,









analog, Na, Ca, Mg, K or ammonium sulfate salts or elemental S. Sulfur
as the highly insoluble elemental S or lignin sulfonate is much less
available and it is suggested that elemental S (flowers of sulfur) is
utilized about one-third as efficiently as the sulfate or methionine
forms. Sulfur in corn and corn silage has been found to be less
available than that in sodium sulfate, methionine and methionine hydroxy
analog.

Toxicity and Interrelationships
The interrelationship of S with Cu and Mo is discussed (see Cu and
Mo) with Cu requirements increased by both S and Mo. Likewise, the
interrelationship between Se and S is due in part to their similar
structures. Selenium can replace S in some organic compounds but the
metabolic activity of the seleno-compound is less than that of the normal
S-containing compound. Sulfur has been used to counteract the effects of
Se when fed in toxic concentrations.

Maximum tolerable level for S is reported to be 0.40% (NRC, 1980),
but is less well defined than the maximum requirement. Ruminants can
tolerate more S from natural feed ingredients than from added sulfate.
Excessive dietary S levels may cause acute toxicity resulting in clinical
signs of abdominal pain, muscle twitching, diarrhea, severe dehydration,
strong odor of sulfide on the breath, congested lungs and acute enteritis
(Miller, 1979).

COBALT

Metabolism
Cobalt is required by rumen microorganisms for the synthesis of
vitamin B12. Although Co was recognized as an essential microelement for
ruminants, the nutritional function of Co was not discovered until the
discovery of vitamin B12 in 1948. The production of vitamin B. in the
rumen depends on the Co, the roughage content of the diet and te total
dietary intake. There is no evidence that vitamin B synthesis is
possible within body tissues. The ruminant is therefore ultimately
dependent on the synthetic capacity of its rumen organisms. Rumen
microorganisms produce many Co-containing vitamin B12-like compounds
which have no true vitamin B activity for body tissues. Information
exists which shows that Co-deficient sheep convert at least 60 percent of
their limited supply of dietary Co into compounds that cannot be absorbed
and used. True vitamin B 2 (5,6-dimethyl benzimidazolylcobamide cyanide
or DMBC) is frequently re erred to as cobalamin.

The main source of energy to ruminants is not glucose but primarily
acetic and propionic acids. Vitamin B12 is necessary for the normal
functioning of a number of enzyme systems in energy utilization. Thus,
vitamin B12 deficient ruminants fail to convert propionate efficiently to
succinate. The main route of Co excretion and control of metabolic
balance is largely achieved by excretion in the urine.

Requirement
Cobalt requirements have been established as 0.1 ppm of dietary dry
matter intake for grazing ruminant animals. Under grazing conditions,
lambs are the most sensitive to Co deficiency, followed by mature sheep,









calves, and mature cattle in that order. Field experience suggests that
only small species differences exist among ruminants in Co requirements.
Two of the factors which contribute to the relatively high Co requirement
of the ruminant are (1) its inefficient use of dietary Co for the produc-
tion of vitamin B12 in the rumen and (2) the absorption of this vitamin
from the alimentary tract.

Deficiency
Cobalt deficiency occurs most frequently in grazing ruminants and is
widespread throughout large areas of most countries in the tropics. It
ranks with Na, P and Cu as one of the most severe limitations to grazing
ruminants. The deficiency is found on soils of diverse origin including
coarse, volcanic, sandy loams and leached sands. Raising the pH by
liming reduces the Co uptake by the plant and may increase the severity
of the deficiency. Severe forms of Co deficiency in grazing ruminants
have been given a variety of local names which describe a wasting
disease. Most severe deficiencies can occur in luxuriant pastures, but
horses grazing the same pastures are unaffected.

Visual manifestations of a Co deficiency are not specific and are
similar to those found in malnutrition due to low intakes of energy and
protein. Animals on Co deficient pastures gradually lose appetite and
failure of growth or loss of weight is followed by extreme loss of
appetite, rapid muscular wasting, depraved appetite, severe anemia and
death. If the deficiency is mild or marginal, the above clinical signs
may never occur and only the young, most susceptible animals may exhibit
signs of unthriftiness which are indistinguishable from the effects of
parasitism or low feed intake. Cobalt deficiency in cattle is illus-
trated in Figure 13 (below) and Figure 14 (latter inside front cover).

Mild forms of Co deficiency in grazing ruminants are difficult to
diagnose on the basis of clinical and pathological signs because the only
indications may be a state of unthriftiness and no anemia. Consequently,
the only sure way of establishing that a Co deficiency is present is by
observing and measuring the response following the administration of oral
Co or vitamin B injections in terms of increased appetite and weight
gain. Liver Co levels below 0.07 ppm on dry basis are indicative of low
dietary Co levels. Pasture Co levels below 0.1 ppm on the dry basis will
likely produce a deficiency in lambs and calves while prolonged access to
pastures containing below 0.07 ppm of Co can be expected to produce a
widespread deficiency.

Prevention and Control
Cobalt deficiency in grazing ruminants can best be prevented by
direct oral administration of Co through mineral supplements containing
at least 0.002 percent Co. Large and frequent injections of vitamin B12
can effectively prevent or cure Co deficiency but are much more expen-
sive. Oral dosing or drenching with dilute Co solutions are satisfactory
if the doses are regular and frequent. Oral administration of vitamin
B12 is relatively ineffective. Placing a Co containing pellet in the
rumen with a grinder, to prevent coating of the pellet, is effective for
many months but this technique has one of its greatest values as an aid
in diagnosing Co deficiency.









calves, and mature cattle in that order. Field experience suggests that
only small species differences exist among ruminants in Co requirements.
Two of the factors which contribute to the relatively high Co requirement
of the ruminant are (1) its inefficient use of dietary Co for the produc-
tion of vitamin B12 in the rumen and (2) the absorption of this vitamin
from the alimentary tract.

Deficiency
Cobalt deficiency occurs most frequently in grazing ruminants and is
widespread throughout large areas of most countries in the tropics. It
ranks with Na, P and Cu as one of the most severe limitations to grazing
ruminants. The deficiency is found on soils of diverse origin including
coarse, volcanic, sandy loams and leached sands. Raising the pH by
liming reduces the Co uptake by the plant and may increase the severity
of the deficiency. Severe forms of Co deficiency in grazing ruminants
have been given a variety of local names which describe a wasting
disease. Most severe deficiencies can occur in luxuriant pastures, but
horses grazing the same pastures are unaffected.

Visual manifestations of a Co deficiency are not specific and are
similar to those found in malnutrition due to low intakes of energy and
protein. Animals on Co deficient pastures gradually lose appetite and
failure of growth or loss of weight is followed by extreme loss of
appetite, rapid muscular wasting, depraved appetite, severe anemia and
death. If the deficiency is mild or marginal, the above clinical signs
may never occur and only the young, most susceptible animals may exhibit
signs of unthriftiness which are indistinguishable from the effects of
parasitism or low feed intake. Cobalt deficiency in cattle is illus-
trated in Figure 13 (below) and Figure 14 (latter inside front cover).

Mild forms of Co deficiency in grazing ruminants are difficult to
diagnose on the basis of clinical and pathological signs because the only
indications may be a state of unthriftiness and no anemia. Consequently,
the only sure way of establishing that a Co deficiency is present is by
observing and measuring the response following the administration of oral
Co or vitamin B injections in terms of increased appetite and weight
gain. Liver Co levels below 0.07 ppm on dry basis are indicative of low
dietary Co levels. Pasture Co levels below 0.1 ppm on the dry basis will
likely produce a deficiency in lambs and calves while prolonged access to
pastures containing below 0.07 ppm of Co can be expected to produce a
widespread deficiency.

Prevention and Control
Cobalt deficiency in grazing ruminants can best be prevented by
direct oral administration of Co through mineral supplements containing
at least 0.002 percent Co. Large and frequent injections of vitamin B12
can effectively prevent or cure Co deficiency but are much more expen-
sive. Oral dosing or drenching with dilute Co solutions are satisfactory
if the doses are regular and frequent. Oral administration of vitamin
B12 is relatively ineffective. Placing a Co containing pellet in the
rumen with a grinder, to prevent coating of the pellet, is effective for
many months but this technique has one of its greatest values as an aid
in diagnosing Co deficiency.








































Figure 13. Cobalt deficiency. The top photograph shows a cobalt-deficient heifer that had
access to an iron-copper-salt supplement. Note the severe emaciation. Her blood
contained 6.6 g of hemoglobin per 100 ml on February 25, 1937. The bottom
photograph is the same heifer fully recovered with an iron-copper-cobalt salt supple-
ment while on the same pasture. (Florida Experiment Station Bulletin 699. 1965.
R. B. Becker, J. R. Henderson and R. B. Leighty, University of Florida, Gainesville,
Florida, U.S.A.).









Cobalt supplementation of Co deficient diets will markedly increase
the vitamin B 2 content of milk and particularly colostrum. Cow's
colostrum is lour to ten times higher in Co than regular milk.

Toxicity
Cobalt has a low order of toxicity in all species studied. Daily
doses of 3 mg Co/kg body weight or approximately 150 ppm Co (1,000 times
normal levels) can be tolerated by sheep for many weeks without visible
toxic effects. Doses of 4 to 10 mg Co/kg body weight will severely
depress appetite and body weight as well as produce anemia. Some deaths
occur at the higher level.

COPPER AND MOLYBDENUM

Metabolism
Copper is essential in hemoglobin production, the functioning of
enzyme systems, as a component of various body pigments and is involved
in the central nervous system, bone metabolism and heart function.
Copper is interrelated with other dietary factors including Mo, S, Zn,
protein, Fe and other trace elements. These interactions are important
to understand and recognize when considering dietary Cu requirements.
Molybdenum has been shown to be an essential component of certain enzyme
systems within the body but the Mo problem, insofar as ruminants are
concerned, is usually one of toxicosis.

Requirement
The Cu requirements of ruminant animals are so powerfully influenced
by interactions between other dietary components, especially Mo and S,
that it is necessary to specify the conditions in which the requirements
are to apply. Ideal conditions are those in which all the dietary
factors affecting Cu absorption and utilization in the animal are at
optimum levels. Where applications of Ca carbonate to pastures are high,
the Cu requirement of Merino sheep has been placed at 10 ppm, whereas in
Western Australia where no such application occurs and the Mo contents of
the pastures are generally below 1.5 ppm, 6 ppm Cu was found adequate
(Camargo et al., 1962).

The Cu requirements of cattle for growth and health are higher than
those of sheep. Even when Mo intakes were low, as in the critical
experiments of Mills et al. (1976) with Friesian calves, 8 ppm Cu/kg dry
diet did not entirely meet their needs and 10 ppm was suggested as the
minimum requirement. The Mo requirement of grazing livestock is esti-
mated to be 0.01 ppm or less and no Mo deficiencies have been reported or
identified in grazing ruminants.

Deficiency
With the exception of P, deficiency of Cu is the most severe mineral
limitation to grazing livestock throughout extensive regions of the
tropics (Table 3). Copper deficiencies in ruminants occur mainly under
grazing conditions, with gross signs of the deficiency being rare when
concentrate feeds are fed. The majority of world reports are concerned
with a "conditioned" Cu deficiency where normal amounts of Cu (6-16 ppm)
are inadequate due to higher than normal amounts of other elements such
as Mo, S and other factors which block the utilization of Cu by the body.









Cobalt supplementation of Co deficient diets will markedly increase
the vitamin B 2 content of milk and particularly colostrum. Cow's
colostrum is lour to ten times higher in Co than regular milk.

Toxicity
Cobalt has a low order of toxicity in all species studied. Daily
doses of 3 mg Co/kg body weight or approximately 150 ppm Co (1,000 times
normal levels) can be tolerated by sheep for many weeks without visible
toxic effects. Doses of 4 to 10 mg Co/kg body weight will severely
depress appetite and body weight as well as produce anemia. Some deaths
occur at the higher level.

COPPER AND MOLYBDENUM

Metabolism
Copper is essential in hemoglobin production, the functioning of
enzyme systems, as a component of various body pigments and is involved
in the central nervous system, bone metabolism and heart function.
Copper is interrelated with other dietary factors including Mo, S, Zn,
protein, Fe and other trace elements. These interactions are important
to understand and recognize when considering dietary Cu requirements.
Molybdenum has been shown to be an essential component of certain enzyme
systems within the body but the Mo problem, insofar as ruminants are
concerned, is usually one of toxicosis.

Requirement
The Cu requirements of ruminant animals are so powerfully influenced
by interactions between other dietary components, especially Mo and S,
that it is necessary to specify the conditions in which the requirements
are to apply. Ideal conditions are those in which all the dietary
factors affecting Cu absorption and utilization in the animal are at
optimum levels. Where applications of Ca carbonate to pastures are high,
the Cu requirement of Merino sheep has been placed at 10 ppm, whereas in
Western Australia where no such application occurs and the Mo contents of
the pastures are generally below 1.5 ppm, 6 ppm Cu was found adequate
(Camargo et al., 1962).

The Cu requirements of cattle for growth and health are higher than
those of sheep. Even when Mo intakes were low, as in the critical
experiments of Mills et al. (1976) with Friesian calves, 8 ppm Cu/kg dry
diet did not entirely meet their needs and 10 ppm was suggested as the
minimum requirement. The Mo requirement of grazing livestock is esti-
mated to be 0.01 ppm or less and no Mo deficiencies have been reported or
identified in grazing ruminants.

Deficiency
With the exception of P, deficiency of Cu is the most severe mineral
limitation to grazing livestock throughout extensive regions of the
tropics (Table 3). Copper deficiencies in ruminants occur mainly under
grazing conditions, with gross signs of the deficiency being rare when
concentrate feeds are fed. The majority of world reports are concerned
with a "conditioned" Cu deficiency where normal amounts of Cu (6-16 ppm)
are inadequate due to higher than normal amounts of other elements such
as Mo, S and other factors which block the utilization of Cu by the body.









Cobalt supplementation of Co deficient diets will markedly increase
the vitamin B 2 content of milk and particularly colostrum. Cow's
colostrum is lour to ten times higher in Co than regular milk.

Toxicity
Cobalt has a low order of toxicity in all species studied. Daily
doses of 3 mg Co/kg body weight or approximately 150 ppm Co (1,000 times
normal levels) can be tolerated by sheep for many weeks without visible
toxic effects. Doses of 4 to 10 mg Co/kg body weight will severely
depress appetite and body weight as well as produce anemia. Some deaths
occur at the higher level.

COPPER AND MOLYBDENUM

Metabolism
Copper is essential in hemoglobin production, the functioning of
enzyme systems, as a component of various body pigments and is involved
in the central nervous system, bone metabolism and heart function.
Copper is interrelated with other dietary factors including Mo, S, Zn,
protein, Fe and other trace elements. These interactions are important
to understand and recognize when considering dietary Cu requirements.
Molybdenum has been shown to be an essential component of certain enzyme
systems within the body but the Mo problem, insofar as ruminants are
concerned, is usually one of toxicosis.

Requirement
The Cu requirements of ruminant animals are so powerfully influenced
by interactions between other dietary components, especially Mo and S,
that it is necessary to specify the conditions in which the requirements
are to apply. Ideal conditions are those in which all the dietary
factors affecting Cu absorption and utilization in the animal are at
optimum levels. Where applications of Ca carbonate to pastures are high,
the Cu requirement of Merino sheep has been placed at 10 ppm, whereas in
Western Australia where no such application occurs and the Mo contents of
the pastures are generally below 1.5 ppm, 6 ppm Cu was found adequate
(Camargo et al., 1962).

The Cu requirements of cattle for growth and health are higher than
those of sheep. Even when Mo intakes were low, as in the critical
experiments of Mills et al. (1976) with Friesian calves, 8 ppm Cu/kg dry
diet did not entirely meet their needs and 10 ppm was suggested as the
minimum requirement. The Mo requirement of grazing livestock is esti-
mated to be 0.01 ppm or less and no Mo deficiencies have been reported or
identified in grazing ruminants.

Deficiency
With the exception of P, deficiency of Cu is the most severe mineral
limitation to grazing livestock throughout extensive regions of the
tropics (Table 3). Copper deficiencies in ruminants occur mainly under
grazing conditions, with gross signs of the deficiency being rare when
concentrate feeds are fed. The majority of world reports are concerned
with a "conditioned" Cu deficiency where normal amounts of Cu (6-16 ppm)
are inadequate due to higher than normal amounts of other elements such
as Mo, S and other factors which block the utilization of Cu by the body.









Cobalt supplementation of Co deficient diets will markedly increase
the vitamin B 2 content of milk and particularly colostrum. Cow's
colostrum is lour to ten times higher in Co than regular milk.

Toxicity
Cobalt has a low order of toxicity in all species studied. Daily
doses of 3 mg Co/kg body weight or approximately 150 ppm Co (1,000 times
normal levels) can be tolerated by sheep for many weeks without visible
toxic effects. Doses of 4 to 10 mg Co/kg body weight will severely
depress appetite and body weight as well as produce anemia. Some deaths
occur at the higher level.

COPPER AND MOLYBDENUM

Metabolism
Copper is essential in hemoglobin production, the functioning of
enzyme systems, as a component of various body pigments and is involved
in the central nervous system, bone metabolism and heart function.
Copper is interrelated with other dietary factors including Mo, S, Zn,
protein, Fe and other trace elements. These interactions are important
to understand and recognize when considering dietary Cu requirements.
Molybdenum has been shown to be an essential component of certain enzyme
systems within the body but the Mo problem, insofar as ruminants are
concerned, is usually one of toxicosis.

Requirement
The Cu requirements of ruminant animals are so powerfully influenced
by interactions between other dietary components, especially Mo and S,
that it is necessary to specify the conditions in which the requirements
are to apply. Ideal conditions are those in which all the dietary
factors affecting Cu absorption and utilization in the animal are at
optimum levels. Where applications of Ca carbonate to pastures are high,
the Cu requirement of Merino sheep has been placed at 10 ppm, whereas in
Western Australia where no such application occurs and the Mo contents of
the pastures are generally below 1.5 ppm, 6 ppm Cu was found adequate
(Camargo et al., 1962).

The Cu requirements of cattle for growth and health are higher than
those of sheep. Even when Mo intakes were low, as in the critical
experiments of Mills et al. (1976) with Friesian calves, 8 ppm Cu/kg dry
diet did not entirely meet their needs and 10 ppm was suggested as the
minimum requirement. The Mo requirement of grazing livestock is esti-
mated to be 0.01 ppm or less and no Mo deficiencies have been reported or
identified in grazing ruminants.

Deficiency
With the exception of P, deficiency of Cu is the most severe mineral
limitation to grazing livestock throughout extensive regions of the
tropics (Table 3). Copper deficiencies in ruminants occur mainly under
grazing conditions, with gross signs of the deficiency being rare when
concentrate feeds are fed. The majority of world reports are concerned
with a "conditioned" Cu deficiency where normal amounts of Cu (6-16 ppm)
are inadequate due to higher than normal amounts of other elements such
as Mo, S and other factors which block the utilization of Cu by the body.









Cobalt supplementation of Co deficient diets will markedly increase
the vitamin B 2 content of milk and particularly colostrum. Cow's
colostrum is lour to ten times higher in Co than regular milk.

Toxicity
Cobalt has a low order of toxicity in all species studied. Daily
doses of 3 mg Co/kg body weight or approximately 150 ppm Co (1,000 times
normal levels) can be tolerated by sheep for many weeks without visible
toxic effects. Doses of 4 to 10 mg Co/kg body weight will severely
depress appetite and body weight as well as produce anemia. Some deaths
occur at the higher level.

COPPER AND MOLYBDENUM

Metabolism
Copper is essential in hemoglobin production, the functioning of
enzyme systems, as a component of various body pigments and is involved
in the central nervous system, bone metabolism and heart function.
Copper is interrelated with other dietary factors including Mo, S, Zn,
protein, Fe and other trace elements. These interactions are important
to understand and recognize when considering dietary Cu requirements.
Molybdenum has been shown to be an essential component of certain enzyme
systems within the body but the Mo problem, insofar as ruminants are
concerned, is usually one of toxicosis.

Requirement
The Cu requirements of ruminant animals are so powerfully influenced
by interactions between other dietary components, especially Mo and S,
that it is necessary to specify the conditions in which the requirements
are to apply. Ideal conditions are those in which all the dietary
factors affecting Cu absorption and utilization in the animal are at
optimum levels. Where applications of Ca carbonate to pastures are high,
the Cu requirement of Merino sheep has been placed at 10 ppm, whereas in
Western Australia where no such application occurs and the Mo contents of
the pastures are generally below 1.5 ppm, 6 ppm Cu was found adequate
(Camargo et al., 1962).

The Cu requirements of cattle for growth and health are higher than
those of sheep. Even when Mo intakes were low, as in the critical
experiments of Mills et al. (1976) with Friesian calves, 8 ppm Cu/kg dry
diet did not entirely meet their needs and 10 ppm was suggested as the
minimum requirement. The Mo requirement of grazing livestock is esti-
mated to be 0.01 ppm or less and no Mo deficiencies have been reported or
identified in grazing ruminants.

Deficiency
With the exception of P, deficiency of Cu is the most severe mineral
limitation to grazing livestock throughout extensive regions of the
tropics (Table 3). Copper deficiencies in ruminants occur mainly under
grazing conditions, with gross signs of the deficiency being rare when
concentrate feeds are fed. The majority of world reports are concerned
with a "conditioned" Cu deficiency where normal amounts of Cu (6-16 ppm)
are inadequate due to higher than normal amounts of other elements such
as Mo, S and other factors which block the utilization of Cu by the body.









Copper deficiencies usually occur when forage Mo exceeds 3 ppm and the Cu
level is below 5 ppm. Ward (1977) categorized Cu deficiency into four
groups where the feed contained: 1) high levels of Mo (more than 20
ppm); 2) low Cu but significant amounts of Mo (i.e., ratio <2:1); 3)
deficient Cu (less than 5 ppm); and 4) normal Cu and low Mo, with high
levels of soluble protein. It is suggested that the latter situation is
the result of high intakes of soluble protein from fresh pasture which
increases the amounts of sulfide produced in the rumen, thus resulting in
unavailable Cu sulfide.

Clinical signs of Cu deficiency include scours, pale membranes of
the eyes and mouth, rough and bleached hair (Figures 15 [inside front
cover], 16 and 17), slow growth and loss of body weight. However, many
Cu deficient animals may be fat, have a smooth, normal-appearing hair
coat and not be anemic. Another sign is the development of fragile
bones, particularly the long bones, which break easily, sometimes without
apparent cause. Cattle that show these skeletal abnormalities move like
a pacing horse rather than like normal cattle. Copper-deficient cattle
may die suddenly when exerted and post-mortem examination may reveal
small lesions of the heart. Not all of these signs necessarily occur in
every Cu-deficient animal, and many may be due to other causes.

Determination of Cu in the diet or pasture has limited diagnostic
value and can in fact be seriously misleading unless other elements with
which Cu interacts, particularly Mo and S, are determined also. The
criterion most widely used for Cu deficiency are the concentration of Cu
in the liver. The liver is the main storage organ of the body for Cu, so
liver Cu concentrations would be expected to provide an useful index of
the Cu status of the animal. Liver Cu values vary greatly with species
and age of the animal, certain disease states and nature of the diet.
Among domestic livestock, liver Cu values in healthy sheep and cattle
have a normal range of 100 400 ppm on a dry basis. In sheep and
cattle, liver concentrations vary slightly from birth to maturity. Liver
Cu concentrations reflect the dietary status (Mills et al., 1976) but
they are influenced by the dietary proportions of Mo and S, by high
intakes of Zn and Ca carbonate and other dietary compounds. They must
therefore be used with caution as diagnostic aids. Evidence suggests
that the Cu values of 25 to 75 ppm of liver dry matter should be used to
differentiate deficient from normal animals.

Whole blood or plasma concentrations also reflect the dietary Cu
status although the normal range is wide. For sheep, cattle and goats
the normal range is 0.6 to 1.5 pg Cu/ml. The values are influenced by
age, pregnancy and disease as well as by the intakes of Cu, Mo and S. It
is widely accepted that whole blood or plasma Cu values consistently
below 0.5 pg/ml are indicative of deficiency in sheep and cattle.

Changes in the activities of a number of Cu metalloenzymes in the
blood and tissues occur during the development of Cu deficiency in
livestock and offer diagnostic possibilities. It has been shown by Todd
(1970) that ceruloplasmin (ferroxidase I) estimations on blood serum
provide advantages over whole blood or plasma Cu determinations because
of the relative stability of the enzyme, the small size of the serum
sample required and the technical convenience of the assay.




























Figure 16. Illustrates normal hair and color around the eye of a cow in Argentina.


Figure 17. Shows the animal with a copper deficiency as illustrated by loss of hair (ring around
the eye). (Courtesy Bernardo Jorge Carrillo, C.I.C.V., INTA, Castelar, Argentina).









Prevention and Control
Under range conditions in the tropics, deficiency can be prevented
by the provision of Cu-containing supplements, by dosing or drenching the
animals at intevals with Cu compounds or by injection of organic com-
plexes of Cu. Mineral supplements containing 0.1 to 0.2% Cu sulfate are
generally consumed voluntarily by grazing animals in amounts sufficient
to maintain adequate and safe total Cu intakes.

Subcutaneous or intramuscular injection of some safe and slowly
absorbed forms of Cu constitute satisfactory means of treating animals in
Cu deficient areas where the pasture Mo contents are moderate, even at
intervals as long as three months (Sutherland et al., 1955). Copper
glycinate, Cu-EDTA and Dicuprene can be used in doses of 30 40 mg for
cattle (Cunningham, 1959; Camargo et al., 1962).

The application of Cu containing fertilizers can be an effective
means of raising the Cu content of pasture to levels adequate for grazing
livestock and increasing pasture yields. The amounts required vary with
the soil type and climatic conditions. Australian experience indicates
that a single dressing of 5 7 kg/ha of Cu sulfate or its Cu equivalent
in the form of cheaper Cu ores is usually sufficient for three or four
years except on calcareous soils.

Toxicity
In reviewing Cu toxicity, it is noted that chronic Cu toxicity in
ruminants is almost entirely confined to sheep. A Cu content over 20 ppm
in feed can cause chronic poisoning in sheep. Also, literature suggests
that normal Cu combined with low levels of Mo and S may result in Cu
toxicity in sheep.

Both Mo toxicity and Cu deficiency are generally corrected by
providing additional Cu in the animals' diet. In severe Mo toxic areas,
injections of Cu compounds are often the preferred method of adminis-
tration since the primary site for Cu x Mo interaction is the gut.

It has been known since 1938 that Mo excess in forages causes a
clinical condition in cattle that is difficult to distinguish from acute
Cu deficiency in general appearance. Diarrhea (Figure 18), loss of hair
and coat color, dry skin, stiff joints, emaciation and anemia charac-
teristic of this condition may occur when Mo levels are in excess.

IODINE

Metabolism
The primary physiological requirement for I is the synthesis of
hormones by the thyroid gland which regulates energy metabolism. Thyroid
hormones have an active role in thermoregulation, intermediary metabo-
lism, reproduction, growth and development, circulation and muscle
function.

Requirement
Estimated I requirements for ruminants have varied from 0.05 to 0.8
ppm. The I requirements for growth are not necessarily identical with
those for reproduction and lactation or for maintenance of the integrity









Prevention and Control
Under range conditions in the tropics, deficiency can be prevented
by the provision of Cu-containing supplements, by dosing or drenching the
animals at intevals with Cu compounds or by injection of organic com-
plexes of Cu. Mineral supplements containing 0.1 to 0.2% Cu sulfate are
generally consumed voluntarily by grazing animals in amounts sufficient
to maintain adequate and safe total Cu intakes.

Subcutaneous or intramuscular injection of some safe and slowly
absorbed forms of Cu constitute satisfactory means of treating animals in
Cu deficient areas where the pasture Mo contents are moderate, even at
intervals as long as three months (Sutherland et al., 1955). Copper
glycinate, Cu-EDTA and Dicuprene can be used in doses of 30 40 mg for
cattle (Cunningham, 1959; Camargo et al., 1962).

The application of Cu containing fertilizers can be an effective
means of raising the Cu content of pasture to levels adequate for grazing
livestock and increasing pasture yields. The amounts required vary with
the soil type and climatic conditions. Australian experience indicates
that a single dressing of 5 7 kg/ha of Cu sulfate or its Cu equivalent
in the form of cheaper Cu ores is usually sufficient for three or four
years except on calcareous soils.

Toxicity
In reviewing Cu toxicity, it is noted that chronic Cu toxicity in
ruminants is almost entirely confined to sheep. A Cu content over 20 ppm
in feed can cause chronic poisoning in sheep. Also, literature suggests
that normal Cu combined with low levels of Mo and S may result in Cu
toxicity in sheep.

Both Mo toxicity and Cu deficiency are generally corrected by
providing additional Cu in the animals' diet. In severe Mo toxic areas,
injections of Cu compounds are often the preferred method of adminis-
tration since the primary site for Cu x Mo interaction is the gut.

It has been known since 1938 that Mo excess in forages causes a
clinical condition in cattle that is difficult to distinguish from acute
Cu deficiency in general appearance. Diarrhea (Figure 18), loss of hair
and coat color, dry skin, stiff joints, emaciation and anemia charac-
teristic of this condition may occur when Mo levels are in excess.

IODINE

Metabolism
The primary physiological requirement for I is the synthesis of
hormones by the thyroid gland which regulates energy metabolism. Thyroid
hormones have an active role in thermoregulation, intermediary metabo-
lism, reproduction, growth and development, circulation and muscle
function.

Requirement
Estimated I requirements for ruminants have varied from 0.05 to 0.8
ppm. The I requirements for growth are not necessarily identical with
those for reproduction and lactation or for maintenance of the integrity









Prevention and Control
Under range conditions in the tropics, deficiency can be prevented
by the provision of Cu-containing supplements, by dosing or drenching the
animals at intevals with Cu compounds or by injection of organic com-
plexes of Cu. Mineral supplements containing 0.1 to 0.2% Cu sulfate are
generally consumed voluntarily by grazing animals in amounts sufficient
to maintain adequate and safe total Cu intakes.

Subcutaneous or intramuscular injection of some safe and slowly
absorbed forms of Cu constitute satisfactory means of treating animals in
Cu deficient areas where the pasture Mo contents are moderate, even at
intervals as long as three months (Sutherland et al., 1955). Copper
glycinate, Cu-EDTA and Dicuprene can be used in doses of 30 40 mg for
cattle (Cunningham, 1959; Camargo et al., 1962).

The application of Cu containing fertilizers can be an effective
means of raising the Cu content of pasture to levels adequate for grazing
livestock and increasing pasture yields. The amounts required vary with
the soil type and climatic conditions. Australian experience indicates
that a single dressing of 5 7 kg/ha of Cu sulfate or its Cu equivalent
in the form of cheaper Cu ores is usually sufficient for three or four
years except on calcareous soils.

Toxicity
In reviewing Cu toxicity, it is noted that chronic Cu toxicity in
ruminants is almost entirely confined to sheep. A Cu content over 20 ppm
in feed can cause chronic poisoning in sheep. Also, literature suggests
that normal Cu combined with low levels of Mo and S may result in Cu
toxicity in sheep.

Both Mo toxicity and Cu deficiency are generally corrected by
providing additional Cu in the animals' diet. In severe Mo toxic areas,
injections of Cu compounds are often the preferred method of adminis-
tration since the primary site for Cu x Mo interaction is the gut.

It has been known since 1938 that Mo excess in forages causes a
clinical condition in cattle that is difficult to distinguish from acute
Cu deficiency in general appearance. Diarrhea (Figure 18), loss of hair
and coat color, dry skin, stiff joints, emaciation and anemia charac-
teristic of this condition may occur when Mo levels are in excess.

IODINE

Metabolism
The primary physiological requirement for I is the synthesis of
hormones by the thyroid gland which regulates energy metabolism. Thyroid
hormones have an active role in thermoregulation, intermediary metabo-
lism, reproduction, growth and development, circulation and muscle
function.

Requirement
Estimated I requirements for ruminants have varied from 0.05 to 0.8
ppm. The I requirements for growth are not necessarily identical with
those for reproduction and lactation or for maintenance of the integrity


































Figure 18. The animals pictured above exhibit severe diarrhea as a result of excess dietary
molybdenum and too little copper. (Courtesy Bernardo Jorge Carrillo, C.I.C.V.,
INTA, Castelar, Argentina).


c.
5 \~
?I









of thyroid structure and function. Although I deficiency results
primarily from low intake of I, its incidence is greatly enhanced by
intake of goitrogens that interfere with I utilization (Underwood, 1977).
The net effect of goitrogens in most instances is to increase the I
requirement. Perhaps the presence of goitrogenic substances is of equal
or greater importance than low dietary I as a contributing factor toward
I deficiencies. Goitrogenic substances are much more prevalent in feeds
than is generally recognized and include Brassica species (i.e., rape,
kale and turnips) as well as soybean meal. If the diet contains as much
as 25% strongly goitrogenic feeds, supplemental I should be at least
doubled.

Deficiency
Iodine deficiency in man and farm animals as endemic goiter is one
of the most prevalent deficiency diseases and occurs in almost every
country in the world (Figure 19). The incidence of deficiency has
declined in many countries as a result of the widespread use of iodized
salt. However, in many tropical countries of the world, endemic goiter
remains an exceedingly serious human and livestock problem.

Deficiency of I results in a lack of thyroxin and is manifested by
general weakness, stunted growth or stillborn animals with goiter
(Figures 20 & 21). Iodine deficiency in breeding animals results in
suppression of estrus periods in the female and lack of libido in the
male (Church, 1971). Studies indicate that cattle fed insufficient I are
less able to resist stress.

Severe I deficiency can be diagnosed on the clinical evidence of
goiter alone. Less severe forms of goiter or I deficiency are more
difficult to diagnose and thus weight and histological structure of the
thyroid gland, as well as serum I (largely thyroxine), are used to
establish status of this element. Milk I concentration is extremely
responsive to changes in dietary intakes and is used to establish the
status of animals (See table 6).

Prevention and Control
For grazing livestock, the use of iodized salt has eliminated I
deficiency in many parts of the world. Availability studies on various I
compounds indicate that several sources are relatively equal in availa-
bility (See Table 10). Potassium iodide, sodium iodide and calcium
iodate are readily available to ruminants but will leach or evaporate
from salt blocks under wet tropical conditions. Potassium iodate, stabi-
lized potassium iodide or pentacalcium orthoperiodate are equally
available to livestock but are much more stable forms of I and not as
rapidly lost from salt blocks.

Toxicity
Iodine toxicosis may result when high levels of I are used over long
periods to correct or prevent diseases such as "footrot" and "lumpy jaw."
Toxicosis signs include depressed appetite, dull, listless appearance,
scaliness and sloughing of the skin, difficulty in swallowing, hacking
cough and excessive tears from eyes. Recovery from I toxicity is rapid
after the excess I is eliminated from the diet.









of thyroid structure and function. Although I deficiency results
primarily from low intake of I, its incidence is greatly enhanced by
intake of goitrogens that interfere with I utilization (Underwood, 1977).
The net effect of goitrogens in most instances is to increase the I
requirement. Perhaps the presence of goitrogenic substances is of equal
or greater importance than low dietary I as a contributing factor toward
I deficiencies. Goitrogenic substances are much more prevalent in feeds
than is generally recognized and include Brassica species (i.e., rape,
kale and turnips) as well as soybean meal. If the diet contains as much
as 25% strongly goitrogenic feeds, supplemental I should be at least
doubled.

Deficiency
Iodine deficiency in man and farm animals as endemic goiter is one
of the most prevalent deficiency diseases and occurs in almost every
country in the world (Figure 19). The incidence of deficiency has
declined in many countries as a result of the widespread use of iodized
salt. However, in many tropical countries of the world, endemic goiter
remains an exceedingly serious human and livestock problem.

Deficiency of I results in a lack of thyroxin and is manifested by
general weakness, stunted growth or stillborn animals with goiter
(Figures 20 & 21). Iodine deficiency in breeding animals results in
suppression of estrus periods in the female and lack of libido in the
male (Church, 1971). Studies indicate that cattle fed insufficient I are
less able to resist stress.

Severe I deficiency can be diagnosed on the clinical evidence of
goiter alone. Less severe forms of goiter or I deficiency are more
difficult to diagnose and thus weight and histological structure of the
thyroid gland, as well as serum I (largely thyroxine), are used to
establish status of this element. Milk I concentration is extremely
responsive to changes in dietary intakes and is used to establish the
status of animals (See table 6).

Prevention and Control
For grazing livestock, the use of iodized salt has eliminated I
deficiency in many parts of the world. Availability studies on various I
compounds indicate that several sources are relatively equal in availa-
bility (See Table 10). Potassium iodide, sodium iodide and calcium
iodate are readily available to ruminants but will leach or evaporate
from salt blocks under wet tropical conditions. Potassium iodate, stabi-
lized potassium iodide or pentacalcium orthoperiodate are equally
available to livestock but are much more stable forms of I and not as
rapidly lost from salt blocks.

Toxicity
Iodine toxicosis may result when high levels of I are used over long
periods to correct or prevent diseases such as "footrot" and "lumpy jaw."
Toxicosis signs include depressed appetite, dull, listless appearance,
scaliness and sloughing of the skin, difficulty in swallowing, hacking
cough and excessive tears from eyes. Recovery from I toxicity is rapid
after the excess I is eliminated from the diet.









of thyroid structure and function. Although I deficiency results
primarily from low intake of I, its incidence is greatly enhanced by
intake of goitrogens that interfere with I utilization (Underwood, 1977).
The net effect of goitrogens in most instances is to increase the I
requirement. Perhaps the presence of goitrogenic substances is of equal
or greater importance than low dietary I as a contributing factor toward
I deficiencies. Goitrogenic substances are much more prevalent in feeds
than is generally recognized and include Brassica species (i.e., rape,
kale and turnips) as well as soybean meal. If the diet contains as much
as 25% strongly goitrogenic feeds, supplemental I should be at least
doubled.

Deficiency
Iodine deficiency in man and farm animals as endemic goiter is one
of the most prevalent deficiency diseases and occurs in almost every
country in the world (Figure 19). The incidence of deficiency has
declined in many countries as a result of the widespread use of iodized
salt. However, in many tropical countries of the world, endemic goiter
remains an exceedingly serious human and livestock problem.

Deficiency of I results in a lack of thyroxin and is manifested by
general weakness, stunted growth or stillborn animals with goiter
(Figures 20 & 21). Iodine deficiency in breeding animals results in
suppression of estrus periods in the female and lack of libido in the
male (Church, 1971). Studies indicate that cattle fed insufficient I are
less able to resist stress.

Severe I deficiency can be diagnosed on the clinical evidence of
goiter alone. Less severe forms of goiter or I deficiency are more
difficult to diagnose and thus weight and histological structure of the
thyroid gland, as well as serum I (largely thyroxine), are used to
establish status of this element. Milk I concentration is extremely
responsive to changes in dietary intakes and is used to establish the
status of animals (See table 6).

Prevention and Control
For grazing livestock, the use of iodized salt has eliminated I
deficiency in many parts of the world. Availability studies on various I
compounds indicate that several sources are relatively equal in availa-
bility (See Table 10). Potassium iodide, sodium iodide and calcium
iodate are readily available to ruminants but will leach or evaporate
from salt blocks under wet tropical conditions. Potassium iodate, stabi-
lized potassium iodide or pentacalcium orthoperiodate are equally
available to livestock but are much more stable forms of I and not as
rapidly lost from salt blocks.

Toxicity
Iodine toxicosis may result when high levels of I are used over long
periods to correct or prevent diseases such as "footrot" and "lumpy jaw."
Toxicosis signs include depressed appetite, dull, listless appearance,
scaliness and sloughing of the skin, difficulty in swallowing, hacking
cough and excessive tears from eyes. Recovery from I toxicity is rapid
after the excess I is eliminated from the diet.


































Figure 19. World map showing occurrence of endemic goiter. Black areas indicate areas where
endemic goiter has been found. (Courtesy Chilean Iodine Educational Bureau,
Chile House, 20 Ropemaker Street, London E.C.2.)























7j






















Figure 20. Goiter caused by iodine deficiency in calves and goats in Minas Gerais, Brazil.
(Courtesy Francisco Megale, Federal University of Minas Gerais, Belo Horizonte,
Brazil).




















































Figure 21. Goiter in goats as a result of iodine deficiency in Yogyakarta, Indonesia (top); in
calves in Rondonapolis, Mato Grosso, Brazil (lower left) and Mindanao, Philippines
(lower right) (L. R. McDowell, University of Florida, Gainesville).









IRON AND MANGANESE

Metabolism
Iron plays a vital role in animal metabolism, mainly confined to the
process of cellular respiration, as a component of hemoglobin, myoglobin
and cytochrome and in certain enzymes. Manganese is needed in the body
for normal bone structure, reproduction and the normal functioning of the
central nervous system. Manganese is a metal cofactor for many enzymes
involved in carbohydrate metabolism and in mucopolysaccharide synthesis.

Requirement
Iron requirements of ruminants are not well established; however, it
is known that young animals have higher requirements than adults. For
adult ruminant species, the Fe requirement is estimated to range from 20
- 50 ppm (Table 2) while the requirement for calves is thought to be 100
ppm. Calves fed on an exclusively whole milk diet (milk is low in Fe)
will develop Fe deficiency anemia within two to three months.

The minimum dietary Mn requirements of ruminants are not precisely
known but likely range between 20 to 40 ppm. Manganese requirements are
substantially lower for growth than for optimal reproductive performance
and they are increased by high intakes of Ca and P.

Deficiency
Iron deficiency seldom occurs in adult livestock, unless there is
considerable blood loss from parasites or disease. Signs of a lack of
Fe, in addition to anemia and related blood changes, include lower weight
gains, listlessness, inability to withstand circulatory strain, labored
breathing after mild exercise, reduced appetite and decreased resistance
to infection (Miller, 1979). General clinical signs of Mn deficiency are
degenerative reproductive failure in both sexes, bone malformations and
crippling, ataxia, depigmentation, deterioration of the central nervous
system, impaired growth and skeletal abnormalities. Although rarely
reported for tropical regions, clinical signs suggesting a Mn deficiency
have been observed in Costa Rica (C. Lang, personal communication) and
Mato Grosso, Brazil (Mendes, 1977).

Determination of Mn deficiency status is assisted by liver
concentration and Fe by hemoglobin and percent saturation of transferring
(Table 6). Percent saturation of transferring is most sensitive to an
early detection of Fe deficiency.

Prevention and Control
Supplementation with Fe and Mn is much less important than for other
trace minerals. The majority of tropical soils are acid, resulting in
forage levels of Fe and Mn generally in excess of requirements. In
addition, soil consumption will provide substantial quantities of these
minerals to grazing livestock diets, particularly Fe. Iron supple-
mentation is most warranted for grazing livestock when forages contain
less than 100 ppm Fe and/or if insects or parasites are causing
substantial blood loss.

Generally, Fe from ferrous sulfate and ferric citrate are more
available than that in ferrous carbonate and much more available than in









IRON AND MANGANESE

Metabolism
Iron plays a vital role in animal metabolism, mainly confined to the
process of cellular respiration, as a component of hemoglobin, myoglobin
and cytochrome and in certain enzymes. Manganese is needed in the body
for normal bone structure, reproduction and the normal functioning of the
central nervous system. Manganese is a metal cofactor for many enzymes
involved in carbohydrate metabolism and in mucopolysaccharide synthesis.

Requirement
Iron requirements of ruminants are not well established; however, it
is known that young animals have higher requirements than adults. For
adult ruminant species, the Fe requirement is estimated to range from 20
- 50 ppm (Table 2) while the requirement for calves is thought to be 100
ppm. Calves fed on an exclusively whole milk diet (milk is low in Fe)
will develop Fe deficiency anemia within two to three months.

The minimum dietary Mn requirements of ruminants are not precisely
known but likely range between 20 to 40 ppm. Manganese requirements are
substantially lower for growth than for optimal reproductive performance
and they are increased by high intakes of Ca and P.

Deficiency
Iron deficiency seldom occurs in adult livestock, unless there is
considerable blood loss from parasites or disease. Signs of a lack of
Fe, in addition to anemia and related blood changes, include lower weight
gains, listlessness, inability to withstand circulatory strain, labored
breathing after mild exercise, reduced appetite and decreased resistance
to infection (Miller, 1979). General clinical signs of Mn deficiency are
degenerative reproductive failure in both sexes, bone malformations and
crippling, ataxia, depigmentation, deterioration of the central nervous
system, impaired growth and skeletal abnormalities. Although rarely
reported for tropical regions, clinical signs suggesting a Mn deficiency
have been observed in Costa Rica (C. Lang, personal communication) and
Mato Grosso, Brazil (Mendes, 1977).

Determination of Mn deficiency status is assisted by liver
concentration and Fe by hemoglobin and percent saturation of transferring
(Table 6). Percent saturation of transferring is most sensitive to an
early detection of Fe deficiency.

Prevention and Control
Supplementation with Fe and Mn is much less important than for other
trace minerals. The majority of tropical soils are acid, resulting in
forage levels of Fe and Mn generally in excess of requirements. In
addition, soil consumption will provide substantial quantities of these
minerals to grazing livestock diets, particularly Fe. Iron supple-
mentation is most warranted for grazing livestock when forages contain
less than 100 ppm Fe and/or if insects or parasites are causing
substantial blood loss.

Generally, Fe from ferrous sulfate and ferric citrate are more
available than that in ferrous carbonate and much more available than in









IRON AND MANGANESE

Metabolism
Iron plays a vital role in animal metabolism, mainly confined to the
process of cellular respiration, as a component of hemoglobin, myoglobin
and cytochrome and in certain enzymes. Manganese is needed in the body
for normal bone structure, reproduction and the normal functioning of the
central nervous system. Manganese is a metal cofactor for many enzymes
involved in carbohydrate metabolism and in mucopolysaccharide synthesis.

Requirement
Iron requirements of ruminants are not well established; however, it
is known that young animals have higher requirements than adults. For
adult ruminant species, the Fe requirement is estimated to range from 20
- 50 ppm (Table 2) while the requirement for calves is thought to be 100
ppm. Calves fed on an exclusively whole milk diet (milk is low in Fe)
will develop Fe deficiency anemia within two to three months.

The minimum dietary Mn requirements of ruminants are not precisely
known but likely range between 20 to 40 ppm. Manganese requirements are
substantially lower for growth than for optimal reproductive performance
and they are increased by high intakes of Ca and P.

Deficiency
Iron deficiency seldom occurs in adult livestock, unless there is
considerable blood loss from parasites or disease. Signs of a lack of
Fe, in addition to anemia and related blood changes, include lower weight
gains, listlessness, inability to withstand circulatory strain, labored
breathing after mild exercise, reduced appetite and decreased resistance
to infection (Miller, 1979). General clinical signs of Mn deficiency are
degenerative reproductive failure in both sexes, bone malformations and
crippling, ataxia, depigmentation, deterioration of the central nervous
system, impaired growth and skeletal abnormalities. Although rarely
reported for tropical regions, clinical signs suggesting a Mn deficiency
have been observed in Costa Rica (C. Lang, personal communication) and
Mato Grosso, Brazil (Mendes, 1977).

Determination of Mn deficiency status is assisted by liver
concentration and Fe by hemoglobin and percent saturation of transferring
(Table 6). Percent saturation of transferring is most sensitive to an
early detection of Fe deficiency.

Prevention and Control
Supplementation with Fe and Mn is much less important than for other
trace minerals. The majority of tropical soils are acid, resulting in
forage levels of Fe and Mn generally in excess of requirements. In
addition, soil consumption will provide substantial quantities of these
minerals to grazing livestock diets, particularly Fe. Iron supple-
mentation is most warranted for grazing livestock when forages contain
less than 100 ppm Fe and/or if insects or parasites are causing
substantial blood loss.

Generally, Fe from ferrous sulfate and ferric citrate are more
available than that in ferrous carbonate and much more available than in









IRON AND MANGANESE

Metabolism
Iron plays a vital role in animal metabolism, mainly confined to the
process of cellular respiration, as a component of hemoglobin, myoglobin
and cytochrome and in certain enzymes. Manganese is needed in the body
for normal bone structure, reproduction and the normal functioning of the
central nervous system. Manganese is a metal cofactor for many enzymes
involved in carbohydrate metabolism and in mucopolysaccharide synthesis.

Requirement
Iron requirements of ruminants are not well established; however, it
is known that young animals have higher requirements than adults. For
adult ruminant species, the Fe requirement is estimated to range from 20
- 50 ppm (Table 2) while the requirement for calves is thought to be 100
ppm. Calves fed on an exclusively whole milk diet (milk is low in Fe)
will develop Fe deficiency anemia within two to three months.

The minimum dietary Mn requirements of ruminants are not precisely
known but likely range between 20 to 40 ppm. Manganese requirements are
substantially lower for growth than for optimal reproductive performance
and they are increased by high intakes of Ca and P.

Deficiency
Iron deficiency seldom occurs in adult livestock, unless there is
considerable blood loss from parasites or disease. Signs of a lack of
Fe, in addition to anemia and related blood changes, include lower weight
gains, listlessness, inability to withstand circulatory strain, labored
breathing after mild exercise, reduced appetite and decreased resistance
to infection (Miller, 1979). General clinical signs of Mn deficiency are
degenerative reproductive failure in both sexes, bone malformations and
crippling, ataxia, depigmentation, deterioration of the central nervous
system, impaired growth and skeletal abnormalities. Although rarely
reported for tropical regions, clinical signs suggesting a Mn deficiency
have been observed in Costa Rica (C. Lang, personal communication) and
Mato Grosso, Brazil (Mendes, 1977).

Determination of Mn deficiency status is assisted by liver
concentration and Fe by hemoglobin and percent saturation of transferring
(Table 6). Percent saturation of transferring is most sensitive to an
early detection of Fe deficiency.

Prevention and Control
Supplementation with Fe and Mn is much less important than for other
trace minerals. The majority of tropical soils are acid, resulting in
forage levels of Fe and Mn generally in excess of requirements. In
addition, soil consumption will provide substantial quantities of these
minerals to grazing livestock diets, particularly Fe. Iron supple-
mentation is most warranted for grazing livestock when forages contain
less than 100 ppm Fe and/or if insects or parasites are causing
substantial blood loss.

Generally, Fe from ferrous sulfate and ferric citrate are more
available than that in ferrous carbonate and much more available than in









IRON AND MANGANESE

Metabolism
Iron plays a vital role in animal metabolism, mainly confined to the
process of cellular respiration, as a component of hemoglobin, myoglobin
and cytochrome and in certain enzymes. Manganese is needed in the body
for normal bone structure, reproduction and the normal functioning of the
central nervous system. Manganese is a metal cofactor for many enzymes
involved in carbohydrate metabolism and in mucopolysaccharide synthesis.

Requirement
Iron requirements of ruminants are not well established; however, it
is known that young animals have higher requirements than adults. For
adult ruminant species, the Fe requirement is estimated to range from 20
- 50 ppm (Table 2) while the requirement for calves is thought to be 100
ppm. Calves fed on an exclusively whole milk diet (milk is low in Fe)
will develop Fe deficiency anemia within two to three months.

The minimum dietary Mn requirements of ruminants are not precisely
known but likely range between 20 to 40 ppm. Manganese requirements are
substantially lower for growth than for optimal reproductive performance
and they are increased by high intakes of Ca and P.

Deficiency
Iron deficiency seldom occurs in adult livestock, unless there is
considerable blood loss from parasites or disease. Signs of a lack of
Fe, in addition to anemia and related blood changes, include lower weight
gains, listlessness, inability to withstand circulatory strain, labored
breathing after mild exercise, reduced appetite and decreased resistance
to infection (Miller, 1979). General clinical signs of Mn deficiency are
degenerative reproductive failure in both sexes, bone malformations and
crippling, ataxia, depigmentation, deterioration of the central nervous
system, impaired growth and skeletal abnormalities. Although rarely
reported for tropical regions, clinical signs suggesting a Mn deficiency
have been observed in Costa Rica (C. Lang, personal communication) and
Mato Grosso, Brazil (Mendes, 1977).

Determination of Mn deficiency status is assisted by liver
concentration and Fe by hemoglobin and percent saturation of transferring
(Table 6). Percent saturation of transferring is most sensitive to an
early detection of Fe deficiency.

Prevention and Control
Supplementation with Fe and Mn is much less important than for other
trace minerals. The majority of tropical soils are acid, resulting in
forage levels of Fe and Mn generally in excess of requirements. In
addition, soil consumption will provide substantial quantities of these
minerals to grazing livestock diets, particularly Fe. Iron supple-
mentation is most warranted for grazing livestock when forages contain
less than 100 ppm Fe and/or if insects or parasites are causing
substantial blood loss.

Generally, Fe from ferrous sulfate and ferric citrate are more
available than that in ferrous carbonate and much more available than in









ferric oxide and iron phytate. Forms of Mn as sulfate, carbonate, oxide
or chloride have been shown to be effective sources for ruminants.

Toxicity
Manganese and Fe are among the least toxic of the essential trace
elements. For both Fe and Mn the maximum tolerable level is approxi-
mately 1000 ppm. Iron toxicity is characterized by reduced feed intake,
lowered daily gain, diarrhea, hypothermia and metabolic acidosis. The
first observed effects of excessive dietary Mn are depressed blood
hemoglobin, reduced feed consumption and slower growth.

Mineral imbalances typified by excesses of Fe and Mn, often
associated with tropical forages, may interfere with metabolism of other
minerals (Lebdosoekojo et al., 1980). In a region of Costa Rica charac-
terized by volcanic soils, high Mn concentrations in forages which
resulted in low reproductive rates of cattle have been observed (Lang,
1971).

SELENIUM

Metabolism
Selenium has been considered an essential element since it was
demonstrated that it was the effective component of "factor-3" (Schwarz,
1957) in preventing exudative diathesis in chicks and nutritional
muscular dystrophy in calves and lambs. The duodenum is the main site of
Se absorption and there is no absorption from the rumen or abomasum.
Absorbed Se is carried mainly in the plasma where it undergoes a chemical
transformation prior to being bound by the plasma proteins. Selenium
then becomes a part of the protein portion of many animal tissues.
Glutathione peroxidase (GSH-Px), an enzyme, contains Se and is associated
with S containing amino acids. Since GSH-Px was identified as a seleno-
protein, its activity has been demonstrated in a wide range of body
tissues and fluids. Likewise, the dramatic dependence of the GSH-Px
activity of the tissues on dietary Se intakes has been shown from
numerous studies with several species. Feeding a low Se diet has been
shown to decrease GSH-Px activity of tissues in the following relative
order: plasma > kidney > heart > liver > lung > red blood cells >
testes.

Requirement
A dietary intake of 0.1 ppm Se provides a satisfactory margin of
safety against dietary variables likely to be encountered by grazing
sheep and cattle. Minimum Se requirements vary some with the form of the
Se ingested and other dietary factors. Selenium is relatively unstable
so losses can occur during drying and storing. High sulfate intakes are
known to reduce Se availability to animals so that Se requirements are
likely to be greater when sulfate intakes are high than when they are
low. There is a complex nutritional interrelationship between Se and
vitamin E so that each can spare or alter the requirement of the other,
but not completely replace each other.

Deficiency
Signs of a pronounced dietary Se deficiency in ruminants include
reduced growth and nutritional muscular dystrophy, often referred to as









ferric oxide and iron phytate. Forms of Mn as sulfate, carbonate, oxide
or chloride have been shown to be effective sources for ruminants.

Toxicity
Manganese and Fe are among the least toxic of the essential trace
elements. For both Fe and Mn the maximum tolerable level is approxi-
mately 1000 ppm. Iron toxicity is characterized by reduced feed intake,
lowered daily gain, diarrhea, hypothermia and metabolic acidosis. The
first observed effects of excessive dietary Mn are depressed blood
hemoglobin, reduced feed consumption and slower growth.

Mineral imbalances typified by excesses of Fe and Mn, often
associated with tropical forages, may interfere with metabolism of other
minerals (Lebdosoekojo et al., 1980). In a region of Costa Rica charac-
terized by volcanic soils, high Mn concentrations in forages which
resulted in low reproductive rates of cattle have been observed (Lang,
1971).

SELENIUM

Metabolism
Selenium has been considered an essential element since it was
demonstrated that it was the effective component of "factor-3" (Schwarz,
1957) in preventing exudative diathesis in chicks and nutritional
muscular dystrophy in calves and lambs. The duodenum is the main site of
Se absorption and there is no absorption from the rumen or abomasum.
Absorbed Se is carried mainly in the plasma where it undergoes a chemical
transformation prior to being bound by the plasma proteins. Selenium
then becomes a part of the protein portion of many animal tissues.
Glutathione peroxidase (GSH-Px), an enzyme, contains Se and is associated
with S containing amino acids. Since GSH-Px was identified as a seleno-
protein, its activity has been demonstrated in a wide range of body
tissues and fluids. Likewise, the dramatic dependence of the GSH-Px
activity of the tissues on dietary Se intakes has been shown from
numerous studies with several species. Feeding a low Se diet has been
shown to decrease GSH-Px activity of tissues in the following relative
order: plasma > kidney > heart > liver > lung > red blood cells >
testes.

Requirement
A dietary intake of 0.1 ppm Se provides a satisfactory margin of
safety against dietary variables likely to be encountered by grazing
sheep and cattle. Minimum Se requirements vary some with the form of the
Se ingested and other dietary factors. Selenium is relatively unstable
so losses can occur during drying and storing. High sulfate intakes are
known to reduce Se availability to animals so that Se requirements are
likely to be greater when sulfate intakes are high than when they are
low. There is a complex nutritional interrelationship between Se and
vitamin E so that each can spare or alter the requirement of the other,
but not completely replace each other.

Deficiency
Signs of a pronounced dietary Se deficiency in ruminants include
reduced growth and nutritional muscular dystrophy, often referred to as









ferric oxide and iron phytate. Forms of Mn as sulfate, carbonate, oxide
or chloride have been shown to be effective sources for ruminants.

Toxicity
Manganese and Fe are among the least toxic of the essential trace
elements. For both Fe and Mn the maximum tolerable level is approxi-
mately 1000 ppm. Iron toxicity is characterized by reduced feed intake,
lowered daily gain, diarrhea, hypothermia and metabolic acidosis. The
first observed effects of excessive dietary Mn are depressed blood
hemoglobin, reduced feed consumption and slower growth.

Mineral imbalances typified by excesses of Fe and Mn, often
associated with tropical forages, may interfere with metabolism of other
minerals (Lebdosoekojo et al., 1980). In a region of Costa Rica charac-
terized by volcanic soils, high Mn concentrations in forages which
resulted in low reproductive rates of cattle have been observed (Lang,
1971).

SELENIUM

Metabolism
Selenium has been considered an essential element since it was
demonstrated that it was the effective component of "factor-3" (Schwarz,
1957) in preventing exudative diathesis in chicks and nutritional
muscular dystrophy in calves and lambs. The duodenum is the main site of
Se absorption and there is no absorption from the rumen or abomasum.
Absorbed Se is carried mainly in the plasma where it undergoes a chemical
transformation prior to being bound by the plasma proteins. Selenium
then becomes a part of the protein portion of many animal tissues.
Glutathione peroxidase (GSH-Px), an enzyme, contains Se and is associated
with S containing amino acids. Since GSH-Px was identified as a seleno-
protein, its activity has been demonstrated in a wide range of body
tissues and fluids. Likewise, the dramatic dependence of the GSH-Px
activity of the tissues on dietary Se intakes has been shown from
numerous studies with several species. Feeding a low Se diet has been
shown to decrease GSH-Px activity of tissues in the following relative
order: plasma > kidney > heart > liver > lung > red blood cells >
testes.

Requirement
A dietary intake of 0.1 ppm Se provides a satisfactory margin of
safety against dietary variables likely to be encountered by grazing
sheep and cattle. Minimum Se requirements vary some with the form of the
Se ingested and other dietary factors. Selenium is relatively unstable
so losses can occur during drying and storing. High sulfate intakes are
known to reduce Se availability to animals so that Se requirements are
likely to be greater when sulfate intakes are high than when they are
low. There is a complex nutritional interrelationship between Se and
vitamin E so that each can spare or alter the requirement of the other,
but not completely replace each other.

Deficiency
Signs of a pronounced dietary Se deficiency in ruminants include
reduced growth and nutritional muscular dystrophy, often referred to as









ferric oxide and iron phytate. Forms of Mn as sulfate, carbonate, oxide
or chloride have been shown to be effective sources for ruminants.

Toxicity
Manganese and Fe are among the least toxic of the essential trace
elements. For both Fe and Mn the maximum tolerable level is approxi-
mately 1000 ppm. Iron toxicity is characterized by reduced feed intake,
lowered daily gain, diarrhea, hypothermia and metabolic acidosis. The
first observed effects of excessive dietary Mn are depressed blood
hemoglobin, reduced feed consumption and slower growth.

Mineral imbalances typified by excesses of Fe and Mn, often
associated with tropical forages, may interfere with metabolism of other
minerals (Lebdosoekojo et al., 1980). In a region of Costa Rica charac-
terized by volcanic soils, high Mn concentrations in forages which
resulted in low reproductive rates of cattle have been observed (Lang,
1971).

SELENIUM

Metabolism
Selenium has been considered an essential element since it was
demonstrated that it was the effective component of "factor-3" (Schwarz,
1957) in preventing exudative diathesis in chicks and nutritional
muscular dystrophy in calves and lambs. The duodenum is the main site of
Se absorption and there is no absorption from the rumen or abomasum.
Absorbed Se is carried mainly in the plasma where it undergoes a chemical
transformation prior to being bound by the plasma proteins. Selenium
then becomes a part of the protein portion of many animal tissues.
Glutathione peroxidase (GSH-Px), an enzyme, contains Se and is associated
with S containing amino acids. Since GSH-Px was identified as a seleno-
protein, its activity has been demonstrated in a wide range of body
tissues and fluids. Likewise, the dramatic dependence of the GSH-Px
activity of the tissues on dietary Se intakes has been shown from
numerous studies with several species. Feeding a low Se diet has been
shown to decrease GSH-Px activity of tissues in the following relative
order: plasma > kidney > heart > liver > lung > red blood cells >
testes.

Requirement
A dietary intake of 0.1 ppm Se provides a satisfactory margin of
safety against dietary variables likely to be encountered by grazing
sheep and cattle. Minimum Se requirements vary some with the form of the
Se ingested and other dietary factors. Selenium is relatively unstable
so losses can occur during drying and storing. High sulfate intakes are
known to reduce Se availability to animals so that Se requirements are
likely to be greater when sulfate intakes are high than when they are
low. There is a complex nutritional interrelationship between Se and
vitamin E so that each can spare or alter the requirement of the other,
but not completely replace each other.

Deficiency
Signs of a pronounced dietary Se deficiency in ruminants include
reduced growth and nutritional muscular dystrophy, often referred to as









ferric oxide and iron phytate. Forms of Mn as sulfate, carbonate, oxide
or chloride have been shown to be effective sources for ruminants.

Toxicity
Manganese and Fe are among the least toxic of the essential trace
elements. For both Fe and Mn the maximum tolerable level is approxi-
mately 1000 ppm. Iron toxicity is characterized by reduced feed intake,
lowered daily gain, diarrhea, hypothermia and metabolic acidosis. The
first observed effects of excessive dietary Mn are depressed blood
hemoglobin, reduced feed consumption and slower growth.

Mineral imbalances typified by excesses of Fe and Mn, often
associated with tropical forages, may interfere with metabolism of other
minerals (Lebdosoekojo et al., 1980). In a region of Costa Rica charac-
terized by volcanic soils, high Mn concentrations in forages which
resulted in low reproductive rates of cattle have been observed (Lang,
1971).

SELENIUM

Metabolism
Selenium has been considered an essential element since it was
demonstrated that it was the effective component of "factor-3" (Schwarz,
1957) in preventing exudative diathesis in chicks and nutritional
muscular dystrophy in calves and lambs. The duodenum is the main site of
Se absorption and there is no absorption from the rumen or abomasum.
Absorbed Se is carried mainly in the plasma where it undergoes a chemical
transformation prior to being bound by the plasma proteins. Selenium
then becomes a part of the protein portion of many animal tissues.
Glutathione peroxidase (GSH-Px), an enzyme, contains Se and is associated
with S containing amino acids. Since GSH-Px was identified as a seleno-
protein, its activity has been demonstrated in a wide range of body
tissues and fluids. Likewise, the dramatic dependence of the GSH-Px
activity of the tissues on dietary Se intakes has been shown from
numerous studies with several species. Feeding a low Se diet has been
shown to decrease GSH-Px activity of tissues in the following relative
order: plasma > kidney > heart > liver > lung > red blood cells >
testes.

Requirement
A dietary intake of 0.1 ppm Se provides a satisfactory margin of
safety against dietary variables likely to be encountered by grazing
sheep and cattle. Minimum Se requirements vary some with the form of the
Se ingested and other dietary factors. Selenium is relatively unstable
so losses can occur during drying and storing. High sulfate intakes are
known to reduce Se availability to animals so that Se requirements are
likely to be greater when sulfate intakes are high than when they are
low. There is a complex nutritional interrelationship between Se and
vitamin E so that each can spare or alter the requirement of the other,
but not completely replace each other.

Deficiency
Signs of a pronounced dietary Se deficiency in ruminants include
reduced growth and nutritional muscular dystrophy, often referred to as









white muscle disease, in lambs and calves (Figures 22 24) and poor
reproductive performance in older animals. Nutritional muscular
dystrophy is a degenerative disease of the striated muscles that occurs,
without neural involvement, in a wide range of animal species. In lambs
it can occur at birth or at any age up to twelve months, but it is most
common between three and six weeks of age. Lambs affected at birth
usually die within a few days while lambs affected later show a stiff and
stilted gait and an arched back. They are reluctant to move about, lose
condition, become prostrate and die. Animals with severe heart involve-
ment may die suddenly without showing any external signs described above.
White muscle disease has received most attention in lambs and calves and
is characterized biochemically by subnormal Se and GSH-Px concentrations
in the blood and tissues and by abnormally high levels of serum glutamic
oxaloacetic transaminase (SGOT).

Selenium-responsive unthriftiness, known as "ill thrift", occurs in
lambs on pasture in parts of New Zealand and can occur in beef and dairy
cattle of all ages. The condition varies from subnormal growth rate to
unthriftiness with rapid loss of weight and sometimes mortality. Ill
thrift can be prevented by Se treatment accompanied by striking increases
in growth and wool yield in some instances. Neither vitamin E nor
ethoxyquin (an antioxidant) has any effect on the unthriftiness.

Impaired reproductive performance has been produced by Se deficien-
cies in all species studied. A high seasonal incidence of infertility in
ewes occurs in parts of New Zealand in association with white muscle
disease. In certain areas, 30 percent of ewes may be infertile and
losses of lambs are high. The infertility results from high embryonic
mortality occurring between three and four weeks after conception, which
is about the time of implantation. This mortality can be prevented by
Se, but by neither vitamin E nor an antioxidant.

High incidences of retained placentas in cattle has been greatly
reduced by the administration of adequate dietary levels of Se as shown
by research in the United States, Scotland and Brazil.

Prevention and Control
The early interest in Se related primarily to the toxic mani-
festations of selenosis in grazing livestock in parts of the Great Plains
of North America. These localized seleniferous areas produced conditions
referred to as "alkali disease" and "blind staggers." In these areas,
toxic Se intakes result from the consumption of Se accumulator plants or
normal forages with relatively high Se concentrations due to the presence
of above normal levels of available Se in the soils. Other localized
seleniferous areas have been identified in Argentina, Australia,
Colombia, Ireland, Israel, Mexico, Soviet Union and South Africa.

All degrees of Se poisoning exist. Chronic Se poisoning is charac-
terized by dullness, emaciation, rough hair coat, loss of hair from the
mane and tail of horses, soreness and elongated hoof growth, stiffness
and lameness due to erosion of the joints and long bones, atrophy of the
heart and cirrhosis of the liver (Figures 25 & 26). In acute Se
poisoning, the animals suffer from blindness, abdominal pain, salivation,
grating of the teeth and some degree of paralysis.
























Figure 22


Figure 23 Figure 24


Figures 22, 23 and 24. White muscle disease. The calf in the top photograph is about 3
months old. Lameness and generalized weakness of muscles can be
seen. Photographs below show abnormal white areas in the heart mus-
cles. (Courtesy O. H. Muth, School of Veterinary Medicine, Oregon
State University, Corvallis, Oregon).





























Figure 25. Selenium toxicity in the selenium-toxic region of Puerto Boyaca, Colombia. Miss-
hapen hoof due to selenium injury. (L. R. McDowell, University of Florida,
Gainesville).


Figure 26. Selenium toxicity in Holstein cattle'in the region of Saltillo, Mexico. Misshapen
hooves were found frequently, particularly in older animals (L. R. McDowell, Uni-
versity of Florida, Gainesville).









The toxicity of Se can be modified by the dietary levels of As, Ag,
Hg, Cu and Cd. Arsenic has been used to successfully alleviate some
levels of Se poisoning in cattle. Three possibilities to prevent or
reduce Se poisoning include (1) soil treatment to reduce Se uptake by
plants; (2) treatment of animals to reduce absorption or increase
excretion (As); and (3) modify diet of animal by dilution or rotating the
animal to non-seleniferous grazing areas.

ZINC

Metabolism
The levels and activities of Zn metalloenzymes and Zn dependent
enzymes have been extensively studied. Zinc is involved primarily in
nucleic acid and protein metabolism and, therefore, in the fundamental
processes of cell replication. The utilization of amino acids in the
synthesis of protein is impaired in Zn deficiency.

About one-third of the Zn absorption in cattle is from the abomasum,
with the remainder occurring throughout the small intestine. Absorbed Zn
from the intestine is carried to the liver, which is the major organ of
Zn metabolism. Zinc leaves the body primarily by way of the feces but
significant quantities are lost in the sweat, especially in the tropics.

Requirements
The minimum Zn requirement of ruminants varies with the chemical
form or combination in which the element occurs with other components of
the diet. The suggested Zn requirement for dairy cattle is 40 ppm
compared to 30 ppm for beef cattle. Zinc deficiency has been reported
under field conditions when forage contained from 18 to 83 ppm. Legg and
Sears (1960) demonstrated a parakeratosis skin disorder in cattle in
Guyana which were consuming forage containing 18 to 42 ppm Zn.

Deficiency
A Zn deficiency for grazing livestock was once thought unlikely
under practical conditions. A field case of Zn deficiency in cattle was
first reported in Guyana (Legg and Sears, 1960). More recently, 16 other
Latin American countries, three from Europe, South Africa and the U.S.A.
have confirmed Zn deficiencies in grazing cattle when the ration con-
tained less than 40 ppm. Low levels of Zn in soils, plants and animal
tissues have been reported throughout much of Latin America.

Early effects of Zn deficiency include reduced feed intake, growth
rate and feed efficiency, followed by skin disorders (Figures 27 [inside
front cover] & 28). Visual signs of severe Zn deficiency include dry,
scaly and cracked skin on the head, neck, stomach, scrotum and legs.
Intact young male animals may often show skin lesions first. Other
clinical signs include inflammation of the nose and mouth, stiffness of
joints, hair loss and rough hair coat. The important effects of Zn
deficiency occur in borderline cases where clinical signs may not be
expressed. Spermatogensis, testicular growth and the development of the
primary and secondary sex organs in the male, and all phases of the
reproductive process in the female from estrus to parturition and
lactation, can be adversely affected in Zn deficiency.









The toxicity of Se can be modified by the dietary levels of As, Ag,
Hg, Cu and Cd. Arsenic has been used to successfully alleviate some
levels of Se poisoning in cattle. Three possibilities to prevent or
reduce Se poisoning include (1) soil treatment to reduce Se uptake by
plants; (2) treatment of animals to reduce absorption or increase
excretion (As); and (3) modify diet of animal by dilution or rotating the
animal to non-seleniferous grazing areas.

ZINC

Metabolism
The levels and activities of Zn metalloenzymes and Zn dependent
enzymes have been extensively studied. Zinc is involved primarily in
nucleic acid and protein metabolism and, therefore, in the fundamental
processes of cell replication. The utilization of amino acids in the
synthesis of protein is impaired in Zn deficiency.

About one-third of the Zn absorption in cattle is from the abomasum,
with the remainder occurring throughout the small intestine. Absorbed Zn
from the intestine is carried to the liver, which is the major organ of
Zn metabolism. Zinc leaves the body primarily by way of the feces but
significant quantities are lost in the sweat, especially in the tropics.

Requirements
The minimum Zn requirement of ruminants varies with the chemical
form or combination in which the element occurs with other components of
the diet. The suggested Zn requirement for dairy cattle is 40 ppm
compared to 30 ppm for beef cattle. Zinc deficiency has been reported
under field conditions when forage contained from 18 to 83 ppm. Legg and
Sears (1960) demonstrated a parakeratosis skin disorder in cattle in
Guyana which were consuming forage containing 18 to 42 ppm Zn.

Deficiency
A Zn deficiency for grazing livestock was once thought unlikely
under practical conditions. A field case of Zn deficiency in cattle was
first reported in Guyana (Legg and Sears, 1960). More recently, 16 other
Latin American countries, three from Europe, South Africa and the U.S.A.
have confirmed Zn deficiencies in grazing cattle when the ration con-
tained less than 40 ppm. Low levels of Zn in soils, plants and animal
tissues have been reported throughout much of Latin America.

Early effects of Zn deficiency include reduced feed intake, growth
rate and feed efficiency, followed by skin disorders (Figures 27 [inside
front cover] & 28). Visual signs of severe Zn deficiency include dry,
scaly and cracked skin on the head, neck, stomach, scrotum and legs.
Intact young male animals may often show skin lesions first. Other
clinical signs include inflammation of the nose and mouth, stiffness of
joints, hair loss and rough hair coat. The important effects of Zn
deficiency occur in borderline cases where clinical signs may not be
expressed. Spermatogensis, testicular growth and the development of the
primary and secondary sex organs in the male, and all phases of the
reproductive process in the female from estrus to parturition and
lactation, can be adversely affected in Zn deficiency.









The toxicity of Se can be modified by the dietary levels of As, Ag,
Hg, Cu and Cd. Arsenic has been used to successfully alleviate some
levels of Se poisoning in cattle. Three possibilities to prevent or
reduce Se poisoning include (1) soil treatment to reduce Se uptake by
plants; (2) treatment of animals to reduce absorption or increase
excretion (As); and (3) modify diet of animal by dilution or rotating the
animal to non-seleniferous grazing areas.

ZINC

Metabolism
The levels and activities of Zn metalloenzymes and Zn dependent
enzymes have been extensively studied. Zinc is involved primarily in
nucleic acid and protein metabolism and, therefore, in the fundamental
processes of cell replication. The utilization of amino acids in the
synthesis of protein is impaired in Zn deficiency.

About one-third of the Zn absorption in cattle is from the abomasum,
with the remainder occurring throughout the small intestine. Absorbed Zn
from the intestine is carried to the liver, which is the major organ of
Zn metabolism. Zinc leaves the body primarily by way of the feces but
significant quantities are lost in the sweat, especially in the tropics.

Requirements
The minimum Zn requirement of ruminants varies with the chemical
form or combination in which the element occurs with other components of
the diet. The suggested Zn requirement for dairy cattle is 40 ppm
compared to 30 ppm for beef cattle. Zinc deficiency has been reported
under field conditions when forage contained from 18 to 83 ppm. Legg and
Sears (1960) demonstrated a parakeratosis skin disorder in cattle in
Guyana which were consuming forage containing 18 to 42 ppm Zn.

Deficiency
A Zn deficiency for grazing livestock was once thought unlikely
under practical conditions. A field case of Zn deficiency in cattle was
first reported in Guyana (Legg and Sears, 1960). More recently, 16 other
Latin American countries, three from Europe, South Africa and the U.S.A.
have confirmed Zn deficiencies in grazing cattle when the ration con-
tained less than 40 ppm. Low levels of Zn in soils, plants and animal
tissues have been reported throughout much of Latin America.

Early effects of Zn deficiency include reduced feed intake, growth
rate and feed efficiency, followed by skin disorders (Figures 27 [inside
front cover] & 28). Visual signs of severe Zn deficiency include dry,
scaly and cracked skin on the head, neck, stomach, scrotum and legs.
Intact young male animals may often show skin lesions first. Other
clinical signs include inflammation of the nose and mouth, stiffness of
joints, hair loss and rough hair coat. The important effects of Zn
deficiency occur in borderline cases where clinical signs may not be
expressed. Spermatogensis, testicular growth and the development of the
primary and secondary sex organs in the male, and all phases of the
reproductive process in the female from estrus to parturition and
lactation, can be adversely affected in Zn deficiency.









The toxicity of Se can be modified by the dietary levels of As, Ag,
Hg, Cu and Cd. Arsenic has been used to successfully alleviate some
levels of Se poisoning in cattle. Three possibilities to prevent or
reduce Se poisoning include (1) soil treatment to reduce Se uptake by
plants; (2) treatment of animals to reduce absorption or increase
excretion (As); and (3) modify diet of animal by dilution or rotating the
animal to non-seleniferous grazing areas.

ZINC

Metabolism
The levels and activities of Zn metalloenzymes and Zn dependent
enzymes have been extensively studied. Zinc is involved primarily in
nucleic acid and protein metabolism and, therefore, in the fundamental
processes of cell replication. The utilization of amino acids in the
synthesis of protein is impaired in Zn deficiency.

About one-third of the Zn absorption in cattle is from the abomasum,
with the remainder occurring throughout the small intestine. Absorbed Zn
from the intestine is carried to the liver, which is the major organ of
Zn metabolism. Zinc leaves the body primarily by way of the feces but
significant quantities are lost in the sweat, especially in the tropics.

Requirements
The minimum Zn requirement of ruminants varies with the chemical
form or combination in which the element occurs with other components of
the diet. The suggested Zn requirement for dairy cattle is 40 ppm
compared to 30 ppm for beef cattle. Zinc deficiency has been reported
under field conditions when forage contained from 18 to 83 ppm. Legg and
Sears (1960) demonstrated a parakeratosis skin disorder in cattle in
Guyana which were consuming forage containing 18 to 42 ppm Zn.

Deficiency
A Zn deficiency for grazing livestock was once thought unlikely
under practical conditions. A field case of Zn deficiency in cattle was
first reported in Guyana (Legg and Sears, 1960). More recently, 16 other
Latin American countries, three from Europe, South Africa and the U.S.A.
have confirmed Zn deficiencies in grazing cattle when the ration con-
tained less than 40 ppm. Low levels of Zn in soils, plants and animal
tissues have been reported throughout much of Latin America.

Early effects of Zn deficiency include reduced feed intake, growth
rate and feed efficiency, followed by skin disorders (Figures 27 [inside
front cover] & 28). Visual signs of severe Zn deficiency include dry,
scaly and cracked skin on the head, neck, stomach, scrotum and legs.
Intact young male animals may often show skin lesions first. Other
clinical signs include inflammation of the nose and mouth, stiffness of
joints, hair loss and rough hair coat. The important effects of Zn
deficiency occur in borderline cases where clinical signs may not be
expressed. Spermatogensis, testicular growth and the development of the
primary and secondary sex organs in the male, and all phases of the
reproductive process in the female from estrus to parturition and
lactation, can be adversely affected in Zn deficiency.



































Figure 28. Zinc deficiency lesions in sheep (Sudan) which responded to supplementation.
(Courtesy 0. M. Mahmoud, University of Khartoum, Sudan).









Prevention and Control
Supplemental Zn can be provided by feeding mineral salts containing
0.50% Zn. Under tropical conditions it seems logical to add 20 to 30 ppm
of supplemental Zn to ruminant diets, unless forage analyses suggest
adequate to high levels of this element. This level of Zn should be
adequate to correct any likely borderline deficiency. A majority of
trace mineral mixtures indicate some Zn on the tag but most commercial
trace mineral salt mixtures contain an insignificant amount of Zn
relative to the animal's requirement.

Toxicity
Cattle, sheep and most mammals exhibit considerable tolerance to
high intakes of Zn. The extent of the tolerance depends mainly on the
relative contents of Ca, Cu, Fe, and Cd with which Zn interacts in the
processes of absorption and utilization. Consumption by lambs of diets
containing 1,000 ppm Zn as the oxide reduced weight gains and decreased
feed efficiency, 1,500 ppm depressed feed consumption and 1,700 ppm
induced a depraved appetite and wood chewing. Dietary Zn levels in
excess of 500 ppm are necessary to adversely affect ruminant livestock
performance.

NEWER TRACE ELEMENTS

Additional trace elements for which there is evidence concerning
their essentiality include F, V, Ni, Cr, Sn, Si, Cd and As. These
minerals are sometimes referred to as the "newer trace elements" because
the evidence for their essentiality has been obtained in recent years.
However, in contrast, for many years in humans the beneficial effects on
teeth for added F in water has been known. Chromium has been reported to
be involved in maintaining normal serum cholesterol status and to be an
integral part of the glucose tolerance factor in humans. Nickel was
observed to be essential for liver integrity and necessary for optimum
function of the enzyme urease. Between 1970 and 1977, it was reported
that Sn, V, Si, As and Cd were necessary for normal growth in rats. The
latter studies were conducted with highly purified diets and dust-free
environments. Arsenic had been shown to improve growth and feed effi-
ciency in swine and poultry as early as 1955, but this response is
generally considered not to be a nutritional effect.

Deficiencies of these elements have not been verified in domestic
animals; consequently, supplementation is not considered necessary at
present. It is important, however, that additional information be
accumulated with regard to these elements for domestic animals to assure
that these "newer trace elements" continue to be available in adequate
amounts for the animal.

TOXIC ELEMENTS

All mineral elements, whether considered to be essential or poten-
tially toxic, can have an adverse effect upon the animal if included in
the diet at excessively high levels. Many factors, including age,
function of the animals (growing, producing milk, etc.) and levels of
other nutrients in the diet, affect the level at which a mineral becomes
toxic.









Prevention and Control
Supplemental Zn can be provided by feeding mineral salts containing
0.50% Zn. Under tropical conditions it seems logical to add 20 to 30 ppm
of supplemental Zn to ruminant diets, unless forage analyses suggest
adequate to high levels of this element. This level of Zn should be
adequate to correct any likely borderline deficiency. A majority of
trace mineral mixtures indicate some Zn on the tag but most commercial
trace mineral salt mixtures contain an insignificant amount of Zn
relative to the animal's requirement.

Toxicity
Cattle, sheep and most mammals exhibit considerable tolerance to
high intakes of Zn. The extent of the tolerance depends mainly on the
relative contents of Ca, Cu, Fe, and Cd with which Zn interacts in the
processes of absorption and utilization. Consumption by lambs of diets
containing 1,000 ppm Zn as the oxide reduced weight gains and decreased
feed efficiency, 1,500 ppm depressed feed consumption and 1,700 ppm
induced a depraved appetite and wood chewing. Dietary Zn levels in
excess of 500 ppm are necessary to adversely affect ruminant livestock
performance.

NEWER TRACE ELEMENTS

Additional trace elements for which there is evidence concerning
their essentiality include F, V, Ni, Cr, Sn, Si, Cd and As. These
minerals are sometimes referred to as the "newer trace elements" because
the evidence for their essentiality has been obtained in recent years.
However, in contrast, for many years in humans the beneficial effects on
teeth for added F in water has been known. Chromium has been reported to
be involved in maintaining normal serum cholesterol status and to be an
integral part of the glucose tolerance factor in humans. Nickel was
observed to be essential for liver integrity and necessary for optimum
function of the enzyme urease. Between 1970 and 1977, it was reported
that Sn, V, Si, As and Cd were necessary for normal growth in rats. The
latter studies were conducted with highly purified diets and dust-free
environments. Arsenic had been shown to improve growth and feed effi-
ciency in swine and poultry as early as 1955, but this response is
generally considered not to be a nutritional effect.

Deficiencies of these elements have not been verified in domestic
animals; consequently, supplementation is not considered necessary at
present. It is important, however, that additional information be
accumulated with regard to these elements for domestic animals to assure
that these "newer trace elements" continue to be available in adequate
amounts for the animal.

TOXIC ELEMENTS

All mineral elements, whether considered to be essential or poten-
tially toxic, can have an adverse effect upon the animal if included in
the diet at excessively high levels. Many factors, including age,
function of the animals (growing, producing milk, etc.) and levels of
other nutrients in the diet, affect the level at which a mineral becomes
toxic.









Prevention and Control
Supplemental Zn can be provided by feeding mineral salts containing
0.50% Zn. Under tropical conditions it seems logical to add 20 to 30 ppm
of supplemental Zn to ruminant diets, unless forage analyses suggest
adequate to high levels of this element. This level of Zn should be
adequate to correct any likely borderline deficiency. A majority of
trace mineral mixtures indicate some Zn on the tag but most commercial
trace mineral salt mixtures contain an insignificant amount of Zn
relative to the animal's requirement.

Toxicity
Cattle, sheep and most mammals exhibit considerable tolerance to
high intakes of Zn. The extent of the tolerance depends mainly on the
relative contents of Ca, Cu, Fe, and Cd with which Zn interacts in the
processes of absorption and utilization. Consumption by lambs of diets
containing 1,000 ppm Zn as the oxide reduced weight gains and decreased
feed efficiency, 1,500 ppm depressed feed consumption and 1,700 ppm
induced a depraved appetite and wood chewing. Dietary Zn levels in
excess of 500 ppm are necessary to adversely affect ruminant livestock
performance.

NEWER TRACE ELEMENTS

Additional trace elements for which there is evidence concerning
their essentiality include F, V, Ni, Cr, Sn, Si, Cd and As. These
minerals are sometimes referred to as the "newer trace elements" because
the evidence for their essentiality has been obtained in recent years.
However, in contrast, for many years in humans the beneficial effects on
teeth for added F in water has been known. Chromium has been reported to
be involved in maintaining normal serum cholesterol status and to be an
integral part of the glucose tolerance factor in humans. Nickel was
observed to be essential for liver integrity and necessary for optimum
function of the enzyme urease. Between 1970 and 1977, it was reported
that Sn, V, Si, As and Cd were necessary for normal growth in rats. The
latter studies were conducted with highly purified diets and dust-free
environments. Arsenic had been shown to improve growth and feed effi-
ciency in swine and poultry as early as 1955, but this response is
generally considered not to be a nutritional effect.

Deficiencies of these elements have not been verified in domestic
animals; consequently, supplementation is not considered necessary at
present. It is important, however, that additional information be
accumulated with regard to these elements for domestic animals to assure
that these "newer trace elements" continue to be available in adequate
amounts for the animal.

TOXIC ELEMENTS

All mineral elements, whether considered to be essential or poten-
tially toxic, can have an adverse effect upon the animal if included in
the diet at excessively high levels. Many factors, including age,
function of the animals (growing, producing milk, etc.) and levels of
other nutrients in the diet, affect the level at which a mineral becomes
toxic.









Prevention and Control
Supplemental Zn can be provided by feeding mineral salts containing
0.50% Zn. Under tropical conditions it seems logical to add 20 to 30 ppm
of supplemental Zn to ruminant diets, unless forage analyses suggest
adequate to high levels of this element. This level of Zn should be
adequate to correct any likely borderline deficiency. A majority of
trace mineral mixtures indicate some Zn on the tag but most commercial
trace mineral salt mixtures contain an insignificant amount of Zn
relative to the animal's requirement.

Toxicity
Cattle, sheep and most mammals exhibit considerable tolerance to
high intakes of Zn. The extent of the tolerance depends mainly on the
relative contents of Ca, Cu, Fe, and Cd with which Zn interacts in the
processes of absorption and utilization. Consumption by lambs of diets
containing 1,000 ppm Zn as the oxide reduced weight gains and decreased
feed efficiency, 1,500 ppm depressed feed consumption and 1,700 ppm
induced a depraved appetite and wood chewing. Dietary Zn levels in
excess of 500 ppm are necessary to adversely affect ruminant livestock
performance.

NEWER TRACE ELEMENTS

Additional trace elements for which there is evidence concerning
their essentiality include F, V, Ni, Cr, Sn, Si, Cd and As. These
minerals are sometimes referred to as the "newer trace elements" because
the evidence for their essentiality has been obtained in recent years.
However, in contrast, for many years in humans the beneficial effects on
teeth for added F in water has been known. Chromium has been reported to
be involved in maintaining normal serum cholesterol status and to be an
integral part of the glucose tolerance factor in humans. Nickel was
observed to be essential for liver integrity and necessary for optimum
function of the enzyme urease. Between 1970 and 1977, it was reported
that Sn, V, Si, As and Cd were necessary for normal growth in rats. The
latter studies were conducted with highly purified diets and dust-free
environments. Arsenic had been shown to improve growth and feed effi-
ciency in swine and poultry as early as 1955, but this response is
generally considered not to be a nutritional effect.

Deficiencies of these elements have not been verified in domestic
animals; consequently, supplementation is not considered necessary at
present. It is important, however, that additional information be
accumulated with regard to these elements for domestic animals to assure
that these "newer trace elements" continue to be available in adequate
amounts for the animal.

TOXIC ELEMENTS

All mineral elements, whether considered to be essential or poten-
tially toxic, can have an adverse effect upon the animal if included in
the diet at excessively high levels. Many factors, including age,
function of the animals (growing, producing milk, etc.) and levels of
other nutrients in the diet, affect the level at which a mineral becomes
toxic.









Mineral toxicities are more difficult to control than deficiencies,
especially under grazing conditions. Molybdenosis is controlled by
additional doses of Cu, fluorosis by avoidance of high F phosphates and
water and selenosis by rotational grazing to avoid continuous access to
high Se forages or by diluting the ration with low Se feeds.

In addition to the elements already discussed, there is reason for
concern about toxicity of certain other minerals, including Pb, Ni, Hg,
Cd and V. In general, mineral toxicosis problems in domestic animals
occur on an area basis as influenced either by the type of soil or by the
location of a source of industrial pollution. The levels of some mine-
rals in plant tissues vary greatly due to certain soil factors and the
quantity of the mineral present in the soil. Manganese, Se and Mo can
occur at elevated levels in forages for this reason. Forages also become
contaminated on the leaf surface with minerals such as F, Pb, Hg and Cd
from industrial pollution. The use of sewage sludge as a soil amendment
may result in elevated levels of Cd in plant tissue. Natural water
supplies can also contain excessive levels of S, F, Na, Mn and Fe.
Mineral supplements contain elements other than those of primary interest
and on occasion will contribute significant levels of certain minerals to
the diet. The use of animal wastes as a feedstuff contribute to higher
dietary intakes of minerals.

FLUORINE

The three elements most frequently causing toxicity problems are F,
Mo and Se, with Mo and Se discussed in previous sections.

Essentiality
In limited amounts, F has been demonstrated to increase resistance
of teeth to cavities in humans and experimental animals. It also has
been reported to benefit mice by reducing anemia and improving fertility
as well as increasing growth of rats. However, if it is an essential
element for most animals, the requirements are exceedingly low.

Toxicity
Although apparently essential for most species, only toxic effects
of F are likely to be of importance to grazing livestock. Chronic
fluorosis is generally observed under three conditions: 1) continuous
consumption of high F mineral supplements; 2) drinking water high in F (3
to 15 ppm or more); and 3) grazing F contaminated forages adjacent to
industrial plants which emit F fumes or dust. With notable exceptions,
the F content of plants is seldom more than 1 to 2 ppm since most plants
have a limited capacity to absorb this element. The most common inci-
dence of fluorosis results from consumption of high F mineral supplements
or contaminated forages near industrial plants.

Toxicity of F is a reflection of amount and duration of ingestion,
solubility of fluorides ingested, age of animal, nutrition, stress
factors and individual animal differences. If animals are young the
teeth may become modified in shape, size and color. The incisors may
become pitted and the molars may show cavities due to fracture or wear,
especially if excess F has been consumed prior to development of the
permanent teeth. Jaw and long bones develop exostosis and joints may









Mineral toxicities are more difficult to control than deficiencies,
especially under grazing conditions. Molybdenosis is controlled by
additional doses of Cu, fluorosis by avoidance of high F phosphates and
water and selenosis by rotational grazing to avoid continuous access to
high Se forages or by diluting the ration with low Se feeds.

In addition to the elements already discussed, there is reason for
concern about toxicity of certain other minerals, including Pb, Ni, Hg,
Cd and V. In general, mineral toxicosis problems in domestic animals
occur on an area basis as influenced either by the type of soil or by the
location of a source of industrial pollution. The levels of some mine-
rals in plant tissues vary greatly due to certain soil factors and the
quantity of the mineral present in the soil. Manganese, Se and Mo can
occur at elevated levels in forages for this reason. Forages also become
contaminated on the leaf surface with minerals such as F, Pb, Hg and Cd
from industrial pollution. The use of sewage sludge as a soil amendment
may result in elevated levels of Cd in plant tissue. Natural water
supplies can also contain excessive levels of S, F, Na, Mn and Fe.
Mineral supplements contain elements other than those of primary interest
and on occasion will contribute significant levels of certain minerals to
the diet. The use of animal wastes as a feedstuff contribute to higher
dietary intakes of minerals.

FLUORINE

The three elements most frequently causing toxicity problems are F,
Mo and Se, with Mo and Se discussed in previous sections.

Essentiality
In limited amounts, F has been demonstrated to increase resistance
of teeth to cavities in humans and experimental animals. It also has
been reported to benefit mice by reducing anemia and improving fertility
as well as increasing growth of rats. However, if it is an essential
element for most animals, the requirements are exceedingly low.

Toxicity
Although apparently essential for most species, only toxic effects
of F are likely to be of importance to grazing livestock. Chronic
fluorosis is generally observed under three conditions: 1) continuous
consumption of high F mineral supplements; 2) drinking water high in F (3
to 15 ppm or more); and 3) grazing F contaminated forages adjacent to
industrial plants which emit F fumes or dust. With notable exceptions,
the F content of plants is seldom more than 1 to 2 ppm since most plants
have a limited capacity to absorb this element. The most common inci-
dence of fluorosis results from consumption of high F mineral supplements
or contaminated forages near industrial plants.

Toxicity of F is a reflection of amount and duration of ingestion,
solubility of fluorides ingested, age of animal, nutrition, stress
factors and individual animal differences. If animals are young the
teeth may become modified in shape, size and color. The incisors may
become pitted and the molars may show cavities due to fracture or wear,
especially if excess F has been consumed prior to development of the
permanent teeth. Jaw and long bones develop exostosis and joints may









Mineral toxicities are more difficult to control than deficiencies,
especially under grazing conditions. Molybdenosis is controlled by
additional doses of Cu, fluorosis by avoidance of high F phosphates and
water and selenosis by rotational grazing to avoid continuous access to
high Se forages or by diluting the ration with low Se feeds.

In addition to the elements already discussed, there is reason for
concern about toxicity of certain other minerals, including Pb, Ni, Hg,
Cd and V. In general, mineral toxicosis problems in domestic animals
occur on an area basis as influenced either by the type of soil or by the
location of a source of industrial pollution. The levels of some mine-
rals in plant tissues vary greatly due to certain soil factors and the
quantity of the mineral present in the soil. Manganese, Se and Mo can
occur at elevated levels in forages for this reason. Forages also become
contaminated on the leaf surface with minerals such as F, Pb, Hg and Cd
from industrial pollution. The use of sewage sludge as a soil amendment
may result in elevated levels of Cd in plant tissue. Natural water
supplies can also contain excessive levels of S, F, Na, Mn and Fe.
Mineral supplements contain elements other than those of primary interest
and on occasion will contribute significant levels of certain minerals to
the diet. The use of animal wastes as a feedstuff contribute to higher
dietary intakes of minerals.

FLUORINE

The three elements most frequently causing toxicity problems are F,
Mo and Se, with Mo and Se discussed in previous sections.

Essentiality
In limited amounts, F has been demonstrated to increase resistance
of teeth to cavities in humans and experimental animals. It also has
been reported to benefit mice by reducing anemia and improving fertility
as well as increasing growth of rats. However, if it is an essential
element for most animals, the requirements are exceedingly low.

Toxicity
Although apparently essential for most species, only toxic effects
of F are likely to be of importance to grazing livestock. Chronic
fluorosis is generally observed under three conditions: 1) continuous
consumption of high F mineral supplements; 2) drinking water high in F (3
to 15 ppm or more); and 3) grazing F contaminated forages adjacent to
industrial plants which emit F fumes or dust. With notable exceptions,
the F content of plants is seldom more than 1 to 2 ppm since most plants
have a limited capacity to absorb this element. The most common inci-
dence of fluorosis results from consumption of high F mineral supplements
or contaminated forages near industrial plants.

Toxicity of F is a reflection of amount and duration of ingestion,
solubility of fluorides ingested, age of animal, nutrition, stress
factors and individual animal differences. If animals are young the
teeth may become modified in shape, size and color. The incisors may
become pitted and the molars may show cavities due to fracture or wear,
especially if excess F has been consumed prior to development of the
permanent teeth. Jaw and long bones develop exostosis and joints may









become thickened, causing the animal to become stiff and lame. A level
of 20 to 30 ppm of total F in the diet will cause dental mottling; above
50 ppm, it will cause a significant incidence of lameness and decreased
milk production in lactating cows. Cattle frequently have decreased feed
intake when F is greater than 50 ppm in the diet. Figures 29-31 show
teeth and metatarsal bones of cattle suffering from fluorosis.

Suttie et al. (1957) observed that lactating cows could tolerate 30
ppm F with no apparent difficulty and that 50 ppm would result in
fluorosis within three to five years. Cattle are less tolerant to F
toxicity than other grazing livestock and some reports indicate that
general undernutrition enhances the deleterious effects of F toxicosis.

Intake of F in water containing 1 ppm by cattle has been estimated
to provide 0.01 1.0 mg F per kg body weight per day, which is not of
health significance. However, mottled teeth have been observed in cows
drinking water that contained 4 to 5 ppm of the element. In total intake
calculations, the F present in water should be taken into account.

Chemical Forms
The chemical form of F is significant since F in sodium fluoride is
much more available than in calcium fluoride or rock phosphate. It is
apparent that phosphorus sources manufactured by the furnace process are
relatively free of fluorides. Those manufactured from defluorinated
phosphoric acid will contain safe levels when added to feed supplements
and salt mixtures for livestock and meet the recommendation of having not
more than one part F per 100 parts of P. Soft rock phosphate and ground
raw rock phosphate generally exceed this ratio by about ten-fold and for
this reason should be closely monitored as to both the quantity of F
provided and the length of time provided to livestock. Bone meal, fish
meal and poultry by-product meals may at times have considerable F
present and this should be taken into account for total F intake when
fed.

Prevention and Control
For the prevention of fluorosis, F content of water and supplemental
phosphates should be determined along with visual observations to detect
early signs of fluorosis. Under some circumstances, exceeding the upper
recommendation of 30 50 ppm F for grazing livestock may be justified.
When defluorinated phosphates are unavailable or prohibitively expensive,
fertilizer or untreated phosphates would be recommended but only for
short periods of time. As an example, higher F-containing phosphates
would be more appropriately provided to feedlot cattle than to animals
retained in the breeding herd.

DIAGNOSIS OF MINERAL DEFICIENCIES AND IMBALANCES

Mineral nutrition disorders range from acute mineral deficiencies or
toxicities characterized by well-marked clinical signs and pathological
changes to mild and transient conditions difficult to diagnose and
expressed as a vague unthriftiness or unsatisfactory growth and produc-
tion. These latter conditions assume great importance because they occur
over large areas and affect a large number of animals in addition to the
fact that they can be confused with the effects of energy and/or protein
deficiencies and various types of parasitism (Underwood, 1977).









become thickened, causing the animal to become stiff and lame. A level
of 20 to 30 ppm of total F in the diet will cause dental mottling; above
50 ppm, it will cause a significant incidence of lameness and decreased
milk production in lactating cows. Cattle frequently have decreased feed
intake when F is greater than 50 ppm in the diet. Figures 29-31 show
teeth and metatarsal bones of cattle suffering from fluorosis.

Suttie et al. (1957) observed that lactating cows could tolerate 30
ppm F with no apparent difficulty and that 50 ppm would result in
fluorosis within three to five years. Cattle are less tolerant to F
toxicity than other grazing livestock and some reports indicate that
general undernutrition enhances the deleterious effects of F toxicosis.

Intake of F in water containing 1 ppm by cattle has been estimated
to provide 0.01 1.0 mg F per kg body weight per day, which is not of
health significance. However, mottled teeth have been observed in cows
drinking water that contained 4 to 5 ppm of the element. In total intake
calculations, the F present in water should be taken into account.

Chemical Forms
The chemical form of F is significant since F in sodium fluoride is
much more available than in calcium fluoride or rock phosphate. It is
apparent that phosphorus sources manufactured by the furnace process are
relatively free of fluorides. Those manufactured from defluorinated
phosphoric acid will contain safe levels when added to feed supplements
and salt mixtures for livestock and meet the recommendation of having not
more than one part F per 100 parts of P. Soft rock phosphate and ground
raw rock phosphate generally exceed this ratio by about ten-fold and for
this reason should be closely monitored as to both the quantity of F
provided and the length of time provided to livestock. Bone meal, fish
meal and poultry by-product meals may at times have considerable F
present and this should be taken into account for total F intake when
fed.

Prevention and Control
For the prevention of fluorosis, F content of water and supplemental
phosphates should be determined along with visual observations to detect
early signs of fluorosis. Under some circumstances, exceeding the upper
recommendation of 30 50 ppm F for grazing livestock may be justified.
When defluorinated phosphates are unavailable or prohibitively expensive,
fertilizer or untreated phosphates would be recommended but only for
short periods of time. As an example, higher F-containing phosphates
would be more appropriately provided to feedlot cattle than to animals
retained in the breeding herd.

DIAGNOSIS OF MINERAL DEFICIENCIES AND IMBALANCES

Mineral nutrition disorders range from acute mineral deficiencies or
toxicities characterized by well-marked clinical signs and pathological
changes to mild and transient conditions difficult to diagnose and
expressed as a vague unthriftiness or unsatisfactory growth and produc-
tion. These latter conditions assume great importance because they occur
over large areas and affect a large number of animals in addition to the
fact that they can be confused with the effects of energy and/or protein
deficiencies and various types of parasitism (Underwood, 1977).









become thickened, causing the animal to become stiff and lame. A level
of 20 to 30 ppm of total F in the diet will cause dental mottling; above
50 ppm, it will cause a significant incidence of lameness and decreased
milk production in lactating cows. Cattle frequently have decreased feed
intake when F is greater than 50 ppm in the diet. Figures 29-31 show
teeth and metatarsal bones of cattle suffering from fluorosis.

Suttie et al. (1957) observed that lactating cows could tolerate 30
ppm F with no apparent difficulty and that 50 ppm would result in
fluorosis within three to five years. Cattle are less tolerant to F
toxicity than other grazing livestock and some reports indicate that
general undernutrition enhances the deleterious effects of F toxicosis.

Intake of F in water containing 1 ppm by cattle has been estimated
to provide 0.01 1.0 mg F per kg body weight per day, which is not of
health significance. However, mottled teeth have been observed in cows
drinking water that contained 4 to 5 ppm of the element. In total intake
calculations, the F present in water should be taken into account.

Chemical Forms
The chemical form of F is significant since F in sodium fluoride is
much more available than in calcium fluoride or rock phosphate. It is
apparent that phosphorus sources manufactured by the furnace process are
relatively free of fluorides. Those manufactured from defluorinated
phosphoric acid will contain safe levels when added to feed supplements
and salt mixtures for livestock and meet the recommendation of having not
more than one part F per 100 parts of P. Soft rock phosphate and ground
raw rock phosphate generally exceed this ratio by about ten-fold and for
this reason should be closely monitored as to both the quantity of F
provided and the length of time provided to livestock. Bone meal, fish
meal and poultry by-product meals may at times have considerable F
present and this should be taken into account for total F intake when
fed.

Prevention and Control
For the prevention of fluorosis, F content of water and supplemental
phosphates should be determined along with visual observations to detect
early signs of fluorosis. Under some circumstances, exceeding the upper
recommendation of 30 50 ppm F for grazing livestock may be justified.
When defluorinated phosphates are unavailable or prohibitively expensive,
fertilizer or untreated phosphates would be recommended but only for
short periods of time. As an example, higher F-containing phosphates
would be more appropriately provided to feedlot cattle than to animals
retained in the breeding herd.

DIAGNOSIS OF MINERAL DEFICIENCIES AND IMBALANCES

Mineral nutrition disorders range from acute mineral deficiencies or
toxicities characterized by well-marked clinical signs and pathological
changes to mild and transient conditions difficult to diagnose and
expressed as a vague unthriftiness or unsatisfactory growth and produc-
tion. These latter conditions assume great importance because they occur
over large areas and affect a large number of animals in addition to the
fact that they can be confused with the effects of energy and/or protein
deficiencies and various types of parasitism (Underwood, 1977).















Figure 29. Incisors from four-year old bovine with severe dental fluorosis. Lesions include
enamel hypoplasia, hypocalcification, staining and abnormal wear and reflect a
near constant elevated fluoride intake during the period of tooth formation.


Ik


Figure 30. Incisors from five-year old bovine with severe dental fluorosis reflect intermittent
periods of elevated fluoride ingestion during the period of tooth formation.


Figure 31. Bovine metatarsals. Left; normal. Right: osteo-fluorosis with severe periosteal
hyperostosis with roughened irregular surface consisting of disorganized and poorly
mineralized bone. Note that the articultating surfaces are unaffected. (All figures
courtesy of J. L. Shupe and A. E. Olson, Utah State University, Logan, Utah.
Reproduced with permission of the National Academy of Sciences).


K J




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