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Title: Photosensitization in cattle grazing frosted common Bermudagrass
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Title: Photosensitization in cattle grazing frosted common Bermudagrass
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Creator: Kidder, Ralph W.
Publisher: University of Florida Agricultural Experiment Station
Publication Date: 1961
Copyright Date: 1961
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00
Bulletin 630

UNIVERSITY OF FLORIDA
AGRICULTURAL EXPERIMENT STATION
J. R. BECKENBACH, Director
GAINESVILLE, FLORIDA
(A contribution from the Everglades Experiment n)



"Photosensitization in Cattle Grazing

Frosted Common Bermudagrass

R. W. KIDDER, D. W. BEARDSLEY AND T. C. ERWIN
















a-,







Fig. 1.-Experimental steer No. 184, showing dejected appearance, the
earliest symptom of photosensitization. His dark pigmented skin did not
blister. This severe attack did not respond to treatment with sodium thio-
sulfate.

Single copies free to Florida residents upon request to
AGRICULTURAL EXPERIMENT STATION
GAINESVILLE, FLORIDA



















CONTENTS
Page

1. Introduction .............. .. ..... ........................ ......... ...... 3

2. Discovery in Florida .................. ----- ---. ..........-..-- ------- ......... 4

3. Sources of Economic Loss ................................ -- ... ................ 5

4. Conditions Which Produce this Disease .....................-- ....- ............ 5

5. Symptom s ......... .------..... ........-..... .........- -- .................. 6

6. Mold Relationships in Florida ............... ........- .........--.....- ......... 9

7. Experimental Results .............. ... ............... ......----- ....... 12

8. Treatments ..... ..----..- --.........----------.............-.... 18

9. Preventive Measures ...........--..... .--.. ----.-....--.. ---........... 19

10. Summary .....---------- ---......--....-- -----............... .....---..... 19

11. Acknowledgments ---..-...........-..--..-------.. ....... -........ 20

12. Literature Cited ......---- ......------------...........-...... 20


February 1961











Photosensitization in Cattle Grazing

Frosted Common Bermudagrass

R. W. KIDDER 1, D. W. BEARDSLEY 2, T. C. ERWIN 3

INTRODUCTION
Sunburn or sensitivity to sunlight is a common experience
for man but animals, under normal conditions, are not burned by
sunlight. Photosensitization is a type of hypersensitivity to sun-
light induced by some abnormality in the animal or in its feed
supply. The term should be defined to include the pathological
reaction of skin to light and also the condition which develops in
such sensitized skin when exposed to light. Thus the term photo-
sensitization includes that condition in which an animal has be-
come hypersensitive to sunlight as well as the syndrome or series
of reactions which develop when such an animal is exposed to
sunlight (2)4.
There are 4 general classes of photosensitization which affect
man and domestic animals. The administration of certain drugs
or chemicals can produce photosensitivity in animals. For ex-
ample, the drug phenothiazine occasionally causes keratitis in-
duced by light following administration as an anthelmintic (2).
A second type is inherited, commonly called congenital parphyria
or "pink tooth" of cattle (1).
A third type of photosensitization is produced when an animal
consumes a plant material containing an intense fluorescent com-
pound. When this is absorbed into the circulatory system, the
animal becomes sensitive to sunlight and becomes sunburned (1).
One of the plants producing this type of disease is St. Johnswort,
of the genus Hypericum. Hence, "Hypericism" is one name for
this type of sunburn. Buckwheat poisoning also produces a sim-
ilar response called "Fagopyrism". Lantana poisoning is in-
cluded in this type of photosensitization (15, 19), although it is
accompanied by icterus.
The fourth type of disease in animals caused by abnormal
sensitivity to sunlight is the result of a photosensitizing sub-
1 Animal Husbandman, Everglades Experiment Station, Belle Glade, Fla.
2 Formerly Assistant Animal Husbandman, Everglades Station; Present
address, Coastal Plain Experiment Station, Tifton, Georgia.
3Formerly Assistant Chemist, Everglades Station; Present address,
Orlando, Florida.
Figures in parentheses refer to Literature Cited.







4 Florida Agricultural Experiment Stations

stance called "phylloerythrin" produced within the digestive
tract of the animal from plant material containing chlorophyll
(1, 3). In the Karoo veldt of South Africa this disease was
described in sheep in 1934 (1) as "geeldikkop" which may be
translated from the Dutch as "yellow thick head." It was be-
lieved to be caused by grazing on Tribulus terrestris. However,
many cases developed in sheep grazing grasses and alfala in the
absence of this weed. In New Zealand a similar disease was
identified in sheep in 1938 (2) and was named "facial eczema".
The photosensitizing agent was identified by Clare in 1944 (3,
4) as phylloerythrin.
This type of photosensitization was identified in 1950 (7, 8,
9) as the disease affecting cattle in South Florida while grazing
common bermudagrass, Cynodon dactylon, following periods
when the top growth had been frosted.

DISCOVERY IN FLORIDA
The most widespread occurrences of photosensitization in cat-
tle in Florida were during the winters of 1948, 1949 and 1950.
Following the extensive flooding of 1947, many St. Augustine-
grass and other improved grass pastures were drowned. Fol-
lowing subsidence these pastures recovered quickly with common
bermudagrass, from seed scattered by the flood water. Close
observation of the disease showed that it occurred mostly on
these and similar bermudagrass pastures. A few cases were seen
in the summer months but the severe outbreaks reached epidemic
proportions in the winter and early spring.
During these 3 years between 20 and 30 herds of cattle were
affected in the Everglades area and the number of cases in each
herd varied from less than 10 to 500-600 head. In some herds
almost 100 percent of the animals were affected, while in others
only 10 to 20 percent became sick. Death losses varied from
less than 2 percent to more than 20 percent. Affected cattle lost
so much weight and condition that often a year was required for
complete recovery. Many cattle carried the scars of their burns
permanently (Fig. 8). Some animals lost ears or portions of
ears which marked them permanently (Fig. 7).
A few cases of this type of photosensitization occur each year
in Florida if certain conditions of weather and forage growth
develop. Similar experiences have been reported from Texas
(18) and other areas in the Southern states.








Photosensitization in Cattle Grazing Bermudagrass 5

SOURCES OF ECONOMIC LOSS
Economic losses resulting from photosensitization varied con-
siderably from herd to herd. In some instances every animal in
the herd was affected to some degree. Many that died in the
early stages of the disease were dark-colored animals. After
the blisters appeared there was more danger of death loss from
secondary infections in the open wounds caused by second and
third degree burns. These burns were more severe on white or
light-colored animals and on the white spots of spotted animals.
Much of the economic loss came from the extreme weight
losses of affected animals. Animals with recorded weights lost
an average of 3 to 9.5 pounds per day for 2 to 3 weeks (Table 1).

TABLE 1.-RESULTS OF EXPERIMENT 3 SHOWING TIME INTERVAL BETWEEN
DATE OF FROST AND FIRST APPEARANCE OF SYMPTOMS OF PHOTOSENSITI-
ZATION WITH WEIGHT LOSS OF EXPERIMENTAL ANIMALS.
1 Days j Weight
Steer I Steers Interval Weight Lost/
No. Frost Symp- Frost to Lost IDay
In toms Out Illness (Lbs.) (Lbs.)
184 Apr. 8 Apr. 24 May 11 May 16 33 130 6
179 Apr. 8 Apr. 24 May 8 May 16 30 65 3
178 IApr. 8 May 3 May 13 May 16 35 75 6
183 Apr. 8 May 3 May 18 June 6 40 35 1
181 Apr. 8 May 9 May 18 May 25 40 130 9.5
182 Apr. 8 May 9 May 18 June 6 40 95 3.5
No
symp-
toms
180 Apr. 8 May 16 observed June 6 20 1
185 Apr. 8 May 16 May 29 June 6 50 0 0


Recovery was slow after the animal regained its appetite. A few
animals which apparently had recovered were observed lame 8
to 10 months later when their hoof growth moved the weakened
growth rings toward their toes and the toes broke off (Fig. 10).

CONDITIONS WHICH PRODUCE THIS DISEASE
As an animal consumes green forage-such as grass, clover
or alfalfa-a large quantity of the green coloring material, chlor-
ophyll, is ingested. During the normal digestion process this







6 Florida Agricultural Experiment Stations

chlorophyll is changed into several compounds, one of which is
a porphyrin called phylloerythrin (6, 10). Normally this phyllo-
erythrin is removed from the circulatory system by the liver
and excreted in bile through the bile duct into the small intestine.
From this point it is excreted with the feces.
When this normal method of excretion is inhibited, the excess
phylloerythrin in the blood becomes a photosensitizing agent and
causes the thin-skinned and non-pigmented skin areas to become
sensitive to the sunlight. Under these conditions phylloerythrin
is excreted in the urine, causing it to appear a dark reddish-
brown color, which at first sight might suggest hematinuria or
bloody urine (6, 10).
The metabolic changes which inhibit this normal excretion
of phylloerythrin are still a mystery to some extent. When
phylloerythrin is extracted artificially and injected into the
circulatory system experimentally, the animal becomes photo-
sensitized without icterus. When the bile duct is ligated experi-
mentally in a normal animal, the phylloerythrin is taken up by
the blood stream, producing photosensitization, with icterus.
These facts indicate that icterus is the cause of the photosensiti-
zation since icterus was not a result of the presence of phylloery-
thrin in the circulation (1).
Numerous workers in New Zealand have accepted this theory
and some investigators are studying the facial eczema situation
under the terminology of "hepatogenous photosensitivity" (2).
Others have found that guinea pigs are satisfactoy experimental
animals for determining if a forage is toxic and then preserving
hay from these toxic pastures for later studies with sheep (17).
Another important step in these studies was the development
of a chemical test, "beaker test", for determining forage toxicity
and its capacity to produce facial eczema when fed to lambs
(14, 16, 18). Histological studies of the livers of sheep affected
with facial eczema showed that a cholangitis (inflammation of
the bile ducts) developed in which the ducts became occluded
with a fibrous growth or connective tissue. Cirrhosis and icterus
develop from this retention of bile, and photosensitization fol-
lows if the animal is on pasture or a ration of green feed (12).

SYMPTOMS
The earliest noticeable symptoms of photosensitization in
cattle are an empty, dejected appearance combined with excessive
salivation, sometimes lacrimation and usually diarrhea (Fig. 1).







Photosensitization in Cattle Grazing Bermudagrass 7

During the next 24 to 48 hours, animals can be observed licking
themselves more than usual and switching their tails. The third
or fourth day from the first appearance of illness they reach the
violent head-shaking stage. In addition to shaking their heads,
they repeatedly scratch their horns or polls with their hind feet
(Fig. 2) or rub their heads on fence posts, fence wires, watering
troughs or any solid object. Sunburned tissues may show up on
the muzzle, nostrils or eyelids coincident with the head-shaking
stage or immediately following it (Fig. 4). During the next 2
or 3 days, blistering will appear on the ears, anus, flank, udder or
scrotum or any white spots or thin-skinned areas (Fig. 3). Blis-
tered ears usually curl inward and become more or less covered
inside and out with scab. Discolored urine may be observed at
any stage after the first or second day of the violent head-shaking
stage and even after the blisters and broken skin are evident.
Some animals, especially those with dark pigmented skin, in the
absence of treatment, have died before the sunburned symptoms
could be observed.
Autopsy findings show varying degrees of icterus, with the
liver having a granular appearance and an excess of yellow-

Fig. 2.-Experimental steer No. 184, in the characteristic pose scratch-
ing horns with hind foot. This is part of the violent head-shaking stage.





















H i ii lNIN







8 Florida Agricultural Experiment Stations

colored fluid when the organ is cut. The gallbladder is distended
with yellow bile and some animals show excessive yellow fluids
in the peritoneal cavity.
Observations of slaughtered cattle apparently recovered from
the disease have shown permanently hard, coarsely granular and
cirrhotic livers. The livers often have thin edges and thickened
centers, shaping them like a turtle shell or tropical sun helmet
(Fig. 10). These livers are not suitable for food.
Liver specimens from experimental steer No. 178 (Fig. 4)
were studied and described by Bailey 5 as follows: "Cloudy swell-
ing with a rather marked increase in size of the hepatic cells; the
section from the center of the liver showed some increase in con-
nective tissue around the triads but no general increase. In some
sections, however, (these must have been from near the edge)

"Personal communication from W. S. Bailey, Head, Dept. of Pathology
and Parasitology, School of Vet. Med., A.P.I. (now Auburn U.), Auburn,
Alabama. Feb. 1951.

Fig. 3.-A light-colored steer in the characteristic pose of scratching
his head with his hind foot. This steer was thoroughly blistered, indicating
that he had been in the head-shaking stage for 5 to 8 days.



SI.












~itF~c~18







Photosensitization in Cattle Grazing Bermudagrass 9

there was a marked proliferation of interlobular connective tis-
sue, presenting a characteristic picture of cirrhosis. In these
areas there was some increase in the number of bile ducts. An-
other section (edge) showed almost complete replacement of the
hepatic tissue with connective tissue."
Experimental steer No. 511, which died suddenly several
weeks following apparent recovery from the disease, had a liver
which consisted mostly of connective tissue.
McFarlane et al in New Zealand (12) describe the lesions of
facial eczema in sheep as follows: "The essential pathology of
facial eczema in the sheep is an acute cholangitis which in se-
vere, acute, or chronic cases proceeds to obliteration of the duct
by fibrous tissue. This latter phenomenon is immediately fol-
lowed by ductule hyperplasia, canalicular infarction and hepato-
cellular necrosis and later by cicatrisation of those areas drained
by obliterated bile ducts and compensatory hyperplasia of the
non-affected portions of the liver." McFarlane has shown that
the icterus and cirrhosis in the liver are produced by the occlu-
sion of the bile ducts. Thus the normal excretion of phylloery-
thrin is prevented and it is taken up by the blood, causing photo-
sensitization. The kidneys then remove the phylloerythrin from
the blood, producing the reddish-brown color in the urine which
makes it appear bloody.

MOLD RELATIONSHIPS IN FLORIDA
A close study of epidemic outbreaks in Florida revealed that
they occurred from 3 to 8 weeks following a frost which killed
the top growth of bermudagrass. Frost-killed grass at first be-
comes standing hay. As the hay starts to deteriorate, several
molds appear on the dead material. One of these is especially
prominent at about the time regrowth of new green blades of
grass is ready for grazing. This mold is visible but can be seen
more clearly with the aid of a 12-X hand lens. When bermuda-
grass is cut and left in bunches on the ground, mold having this
appearance nearly always can be found as the dead grass ap-
proaches one stage of decomposition.
In January 1957 photosensitization appeared, following a
frost, in cattle on one Experiment Station pasture in which the
predominant forage was common bermudagrass. A mold growth
and green forage appeared simultaneously and 4 animals de-
veloped typical cases of photosensitization. This mold was ident-








10 Florida Agricultural Experiment Stations

ified by Van Nostran 6 as a species of Periconia. It appeared
to be the same mold as that found in pastures of the area where
photosensitization has occurred. It is supposed that this is a
normal organism associated with decaying vegetation. However,
when cattle consume this moldy grass prior to, or along with,
the new growth of green grass they become affected by icterus
and photosensitization. An illustration is shown in Fig. 11.
































Fig. 4-Experimental steer No. 178 as the blistering effect
was first fully evident.

In May 1960 a sample of dead bermudagrass with mold growth
of this description on it was submitted to the office of National

"Dr. F. L. Van Nostran, formerly assistant Plant Pathologist, Ever-
glades Experiment Station. Present address, Plant Pathology Dept., South
Dakota State College, Brookings, S. D.








Photosensitization in Cattle Grazing Bermudagrass 11

Fungus Collections where it was identified by Lack 7 as Periconia
minutissima Cla.
At the Raukura research station in New Zealand, Percival
recognized a saprophytic fungus identified as Sporodesmium
bakeri Syd. on the lower blades of some grass samples (13).
This fungus occurred on toxic forage but was absent when the
forage was not toxic. Facial eczema occurred on lambs grazing
these toxic pastures. The grass was toxic when fed to guinea
pigs. A spore sample gave a positive "beaker test" (16) and
cultures of this fungus fed to lambs and guinea pigs produced
the characteristic lesions of facial eczema, as well as icterus and
photosensitivity in the lambs. Mycelia as well as conidia were
toxic. Highly sporulating cultures were more toxic than poorly
sporulating cultures.
Since mold which, when magnified, looks like Periconia minu-
tissima Cla. has been found regularly on dead bermudagrass in
Florida pastures where this type of photosensitization has oc-
curred and since the type of icterus produced is very similar to
SDr. Marie L. (Farr) Lack, Plant Industry Station, Beltsville, Maryland.

Fig. 5.-Experimental steer No. 178 showing the peeling of thin-skinned
areas 30 days after the blistering took place (June 1950).




















*" '^S ..-. --* P.LC .
gil


WA W_,
r 2-r








12 Florida Agricultural Experiment Stations

that found in cases of facial eczema in New Zealand, it is highly
probable that in some way this mold establishes the sequence
which causes the bile ducts to become obstructed, thus producing
the icterus and cholangitis which inhibits the normal excretion
of phylloerythrin with the resulting photosensitization. This
hypothesis promotes the idea or possibility that the disease in-
volved essentially is a mold toxicity, with the cholangitis, icterus
and photosensitization being effects or symptoms.

EXPERIMENTAL RESULTS
Following a conference of Experiment Station personnel and
cattlemen late in January 1950, a series of experiments was con-
ducted to study the relationship between the prevalence of moldy
bermudagrass and the occurrence of symptoms of photosensiti-
zation in cattle. A bermudagrass pasture on which several ani-
mals had contracted severe cases of photosensitization was se-
lected for experimental studies. A 1-acre area of this pasture
was fenced so that cattle could not graze any weeds in the fence
row and all weeds were removed manually from within the plot.

Fig. 6.-Experimental steer No. 178 just before he was slaughtered
for the autopsy (December 1950).




















-- 4
.,4.~







Photosensitization in Cattle Grazing Bermudagrass 13

Several experiments were conducted in succession on this pas-
ture.
On November 27, 1949, a heavy frost killed tender vegetables
and pastures in the Everglades area. The first cases of photo-
sensitization were reported by cattlemen on January 10, 1950,
and within 10 days additional reports indicated between 500 and
600 cattle affected in the area. Thus, the first cases were evident
approximately 6 weeks following the frost. Pastures remained
toxic from January 10 until February 8-about 4 weeks. Rec-
ords of other periods indicated that pastures became toxic about
4 to 5 weeks after the frost and remained dangerous for about
4 weeks. Cool weather following the frost apparently retarded
the development of mold on the dead grass and thus delayed the
occurrence of symptoms of photosensitization in cattle on these
pastures.
Experiment 1.-Five yearling steers with no previous ex-
posure to bermudagrass were put into the 1-acre test pasture on
January 26. On February 6 steer No. 123 showed dark-colored
urine, depression and loss of appetite. On February 8 all 5

Fig. 7.-Ears were permanently curled on steer No. 178.













1. .I
"\ "
-- .








14 Florida Agricultural Experiment Stations

steers showed irritation by scratching their heads with their hind
feet and shaking their heads. Three days later all of these cat-
tle showed improvement in appetite and appearance, indicating
that the forage had outgrown its toxic stage. The steers were
removed following a frost on February 18.

























Fig. 8.-Burn scars show plainly about a year after this steer
was photosensitized.

Experiment 2.-The 5 steers were returned to the experi-
mental pasture on March 16, when mold growth was plentiful
on the bermudagrass and green leaves were growing through
the dead grass. All weeds were again removed manually. On
March 23-7 days after being placed in the pasture-No. 120
was scratching his head with his hind feet and was inflamed
on muzzle and nostrils. The next day all the steers showed the
same symptoms. One steer was observed passing discolored
urine on March 30, and had ear tips burned and curled on April
8. Steers No. 120 and 121 also passed dark-colored urine April 8.
Another frost on this date killed the grass and made it necessary
to remove the cattle April 12. Results of this trial demonstrated
the interval of 34 days between the frost and the first day the







Photosensitization in Cattle Grazing Bermudagrass 15

animals showed positive symptoms of photosensitization. The
5 steers lost an average of 42 pounds in 27 days on pasture.
Experiment 3.-The previous trials had shown that the mold
should appear in 3 to 4 weeks. A new group of steers was pur-
chased from an area free from bermudagrass pasture or exposure
to this type of disease. Two of these steers, Nos. 184 and 179,
were put in the experimental pasture on April 24-16 days after
frost and before any new mold growth appeared. Green blades
of grass were just showing through the dead grass. On May 3
2 more steers, Nos. 178 and 183, were put into the pasture as the
mold growth had become heavy on the dead grass. On May 9
2 more steers, Nos. 181 and 182, were added, making a total of 6.
On May 11 steer No. 179 had started shaking his head and had
"a sore muzzle, while steer No. 184 was gaunt and dejected, with
"a dry muzzle. By May 13 both steers were shaking their heads
vigorously or violently. Two days later No. 178 showed the same
symptoms. On May 16 these 3 steers were removed from the
pasture for treatment. The remaining steers on the pasture
developed the head shaking symptoms May 18-20. Of 4 other
steers added to the pasture in this trial, only 1 failed to become
ill before the toxic stage of the pasture had passed. All were
removed on June 6. These results, along with the loss in weight
of each steer while in the experimental pasture, are shown in
Table 1.
Records indicate that animals will develop symptoms in 7
to 14 days after first exposure. Steer No. 185 did not appear ill

Fig. 9.-Turtle-shaped cirrhotic liver from experimental steer No. 178
7 months after he suffered photosensitization.








16 Florida Agricultural Experiment Stations

until the 13th day of exposure. All steers in experiment No. 2
became affected by the 8th day on the pasture.
Experiment 4.-Moldy bermudagrass was cut daily in the 10-
acre field where the experimental pasture was located and fed
to a steer (No. 511) in dry lot. This steer ate 20 to 25 pounds
of this grass daily. The first feeding period of 28 days was be-
tween frosts and no toxic effects were produced. A second feed-
ing period of 16 days was carried on when the pasture was pro-
ducing photosensitization in the grazing cattle. No trouble was
obvious in this steer in the dry lot while feeding on dead moldy
bermudagrass. However, when he was turned out to pasture
he developed a very severe attack of photosensitization. Tempo-
rary relief was produced with treatments but death came sud-
denly several weeks later. None of these trials were conducted
in a barn.
Experiment 5.-A weed common in many of the pastures
(Parietaria floridana) was fed at a rate of 40-50 pounds per day

Fig. 10.-Hoof growth rings, steer 178. Such a condition often causes
severe lameness about 10 months after recovery following photosensitiza-
tion.









"" -







Photosensitization in Cattle Grazing Bermudagrass 17

to a cow. Although she lost 65 pounds during a 28-day feeding
period, no signs of photosensitization appeared.
Experiment 6.-Seven steers affected with photosensitization
on a neighboring ranch were brought to dry lot pens at the Ex-
periment Station and fed a ration reasonably free from chloro-
phyll. Seven days on this chlorophyll-free diet produced suffi-
cient curative effects that they were again returned to pasture
without further evidence of photosensitization. Untreated cat-
tle on the ranch from the same group were still critically ill.
Experiment 7.-Washings containing mold spores from 20
to 25 pounds of moldy bermudagrass were fed daily to a cow for
15 days. It was necessary to pass a stomach tube to get this
material into the cow. No signs of photosensitization were pro-
duced in this cow by this procedure.
Experiment 8.-Mold spores were collected with a vacuum
cleaner from moldy grass in the pasture. A 12-ounce drench

Fig. 11.-A photomicrograph of a blade of bermudagrass showing mold
growth tentatively identified as Periconia minutissima Cla. (X140).



it '







18 Florida Agricultural Experiment Stations

containing a suspension of these mold spores was given twice
daily for 7 days to a steer but no symptoms of photosensitiza-
tion were observed.
Experiment 9.-Post mortem records of autopsied animals
and of slaughtered animals that seemed to have recovered from
photosensitization indicated a need for a more complete record
of autopsy findings from an apparently recovered animal with a
known case history. Steer No. 178 from experiment No. 3 was
slaughtered for specimens on December 5, 6 months after re-
covery (Figs. 5, 6, 7). The important autopsy findings were re-
corded photographically and are presented in Figures 7, 9 and 10.
Some of the discussion of symptoms on page 5 is based on the
findings from this experimental animal.

TREATMENTS
An effective treatment for this condition was developed
through the cooperation of 2 practicing veterinarians, Dr. C. A.
Forman of Fort Lauderdale and Dr. R. D. Henthorne of Lake
Worth. Sodium thiosulfate injected intravenously or given
orally alleviated the symptoms of photosensitization successfully
(7, 8, 9). When used as an intravenous injection, only reagent
grade sodium thiosulfate was recommended at the rate of 1
ounce per 100 pounds live weight. In practice 1/4 pound of sodium
thiosulfate was dissolved in 500 cubic centimeters distilled water
and given intravenously to a mature animal. This treatment can
be repeated daily for 2 or 3 days if necessary. Commercial grade
sodium thiosulfate was satisfactory for oral administration at
the rate 2 ounces per 100 pounds live weight, or double the
amount used intravenously. Some cases were treated success-
fully by giving both oral and intravenous treatments simulta-
neously. Some cases developed secondary infections which re-
quired treatments with intravenous sulfa drugs. The removal
of green feed from the ration was an aid in recovery of affected
animals.
Losses have been controlled by veterinarians and cattlemen
of the area to a great extent by the sodium thiosulfate treatment.
Very few animals treated in the early stages have died. Nearly
all fatalities were advanced cases when treated. In the early
trials, 108 of 524 untreated cattle in 1 herd died-a mortality
rate of 20.61 percent. Only 5 died of 231 cattle treated in an-
other herd-a mortality rate of 2.11 percent. Convalescence
or return to normal forage consumption for treated cattle re-







Photosensitization in Cattle Grazing Bermudagrass 19

quired only 2 to 4 weeks, against 6 to 12 weeks or longer for
untreated cattle that recovered. The majority of the cattle
treated in this series received only the intravenous injections,
but it was observed in other herds that concurrent oral therapy
expedited recovery.

PREVENTIVE MEASURES
Since it is possible to observe the development of mold on
frozen bermudagrass and, by relating this to the appearance of
new growth, predict the time of appearance of the disease, it
is also possible to break this cycle by destroying the dead ber-
mudagrass after a frost, before the mold has developed, and
allow the cattle access to the new growth alone. Mowing ber-
mudagrass very closely following a frost will help to avoid the
moldy stage on the dead grass. A rotary mower is satisfactory
for this purpose.
A better plan is to replace the bermudagrass with pangola-
grass, St. Augustinegrass, caribgrass or paragrass, because any
of these will provide at least twice as much forage as common
bermudagrass in South Florida. These preferred grasses have
growth habits which do not produce new growth with moldy
dead grass.
A regular program of pasture fertilization will help bring
out the new growth more quickly following a frost.
Supplementary feed such as grass silage, sugar cane or tempo-
rary pastures will provide forage, following a frost, so that cattle
will not have to consume moldy grass.

SUMMARY
A disease of cattle appeared in southern Florida following
the flood of 1947. This disease was observed almost exclusively
on bermudagrass pastures as an epidemic. Studies indicated
that sunburn or some abnormal sensitivity to sunlight was in-
volved. Reports from New Zealand and from South Africa de-
scribed a similar disease in sheep and established a hypothesis
for further study.
One of the normal by-products from the digestion of chloro-
phyll is a porphyrin called phylloerythrin. This is removed nor-
mally from the circulation by the liver and excreted with the bile.
Whenever some factor inhibits the normal excretion of phylloery-
thrin, it accumulates in the blood and produces sensitivity to sun-
light in the non-pigmented and thin-skinned areas of the animal.








20 Florida Agricultural Experiment Stations

A jaundice or icterus caused by liver damage is involved in this
disease and may precede the factors or sequence which inhibits
the normal excretion of phylloerythrin.
Occurrence of photosensitization in South Florida followed
periods when bermudagrass had been frosted. Several molds ap-
peared on the dead grass in 3 to 5 weeks after a frost. The most
prominent of these molds has been identified as Periconia min-
utissima Cla. Re-growth of green grass becomes available for
grazing at about the time this mold sporulates on the dead grass.
Cattle obtaining their forage from such pastures developed photo-
sensitization.
In New Zealand, research has shown that facial eczema, a
similar photosensitization disease of sheep, is produced when a
fungus identified as Sporodesmium bakeri Syd. is present on the
forage.
Since both icterus and photosensitization follow the consump-
tion of moldy grass along with new green grass, the disease may
be a mold toxicity, with icterus and photosensitization as effects
or symptoms.
By following approved cultural practices and eliminating com-
mon bermudagrass, cattlemen in South Florida have successfully
controlled photosensitization for a period of nearly 10 years.
When cases occur, the treatment with sodium thiosulfate either
intravenously or orally has alleviated the symptoms and reduced
economic losses.
ACKNOWLEDGMENTS
Our present level of understanding of this disease was made possible
only in consequence of the prompt and generous cooperation of the stock-
men and veterinarians of this area. It is indeed a pleasure to acknowledge
their assistance and to commend them as they successfully control this dis-
ease by using the treatments and preventive measures which they helped
so graciously to develop.

LITERATURE CITED
1. Blum, H. F. Photodynamic Action and Diseases Caused by Light.
Reinhold Publishing Corp., New York, N. Y. 1941.
2. Clare, N. T. Photosensitization in diseases of domestic animals. Com-
monwealth Agricultural Bureaux, Farnham Royal, Bucks, England.
1952.
3. Clare, N. T. Photosensitivity disease in New Zealand. III. The
photosensitizing agent in facial eczema N. Z. Jour. of Sci. and Tech.
25(5) 202A. 1944.








Photosensitization in Cattle Grazing Bermudagrass 21

4. Clare, N. T. Photosensitivity diseases in New Zealand. IV. The
photosensitizing agent in Southdown photosensitivity. N. Z. Jour. of
Sci. and Tech. 27(1): 23. 1945.
5. Filmer, J. F. Facial eczema and other photosensitivity conditions.
Ann. Report Animal Res. Division N. Z. Dept. of Agr. p. 12. 1949-50.
6. Harrow, Benjamin. Textbook of Biochemistry 5th Ed. W. B. Sanders
Co. Philadelphia and London. 1950.
7. Kidder, R. W., D. W. Beardsley and T. C. Erwin. Photosensitization
control is now possible. Florida Cattleman, May 1950.
8. Kidder, R. W., D. W. Beardsley and T. C. Erwin. Photosensitization
in cattle grazing bermudagrass. 1951. U. of Fla. E.E.S. Mimeo 51-1.
9. Kidder, R. W., D. W. Beardsley and T. C. Erwin. Abstract-photosensi-
tization in cattle grazing bermudagrass. Proc. Assn. of Southern Agr.
Workers, Memphis, Tenn. Feb. 1951.
10. Lemberg, Phil R., and J. W. Legge (Australia). Hematin compounds
and bile pigments. Interscience Publishers, Inc., New York, N. Y.
1949.
11. Levy, E. Bruce, and P. W. Smallfield. Photosensitivity diseases in New
Zealand. II. Facial eczema, the influence of soil, climate, pasture com-
position and management. N. Z. Jour. of Sci. and Tech. 24(4): 198A.
1942.
12. McFarland, D., J. V. Evans and C. S. W. Reid. Photosensitivity dis-
eases in New Zealand. XIV. The pathogenesis of facial eczema. N. Z.
Jour. Agr. Res. 2(1): 194. 1959.
13. Percival, J. C. Photosensitivity diseases in New Zealand. XVII. The
association of Sporodesmium bakeri Syd. with facial eczema. N. Z.
Jour. of Agr. Res. 2(5): 1041. 1959.
14. Perrin, D. D. Photosensitivity diseases in N. Z. XV. A chemical test
for the detection of facial eczema toxicity in pasture. N. Z. Jour. Agr.
Res. 2(2): 266. 1959.
15. Sanders, D. A. Lantana poisoning in cattle. Jour. A.V.M.A. 119:
139-141. 1946.
16. Sandos, Jean, N. T. Clare, and E. P. White. Photosensitivity diseases
in N. Z. XVI. Improved procedure for the beaker test for facial eczema
toxicity. N. Z. Jour. of Agr. Res. Sec. A 2(3): 623. 1959.
17. Simpson, J. E. V., D. P. Sinclair, J. B. Swan, J. F. Filmer. Photosensi-
tivity diseases in New Zealand. XI. Collection and preservation of
pasture that produces facial eczema. N. Z. Jour. of Sci. and Tech. Sec.
A 38(9): 947. 1957.
18. Sperry, O. E., R. D. Turk, G. O. Hoffman and F. B. Stroud. Photosen-
sitization of cattle in Texas. Texas Agr. Exp. Sta. Bul. 812. July,
1955.
19. West, Erdman, and M. W. Emmel. Poisonous Plants in Florida. Fla.
Agr. Exp. Sta. Bul. 510. 1952.













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