• TABLE OF CONTENTS
HIDE
 Experiment
 Discussion
 Conclusion
 Table I - Hemic changes and serum...
 Fig. 1 - Iditol dehydrogenase responses...
 Fig. 2 - Iditol dehydrogenase (ID)...














Group Title: Department of Animal Science research report - Florida Agricultural Experiment Station ; AL-1980-10
Title: Experimentally induced equine aflatoxicosis
CITATION PAGE IMAGE ZOOMABLE
Full Citation
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Permanent Link: http://ufdc.ufl.edu/UF00073119/00001
 Material Information
Title: Experimentally induced equine aflatoxicosis
Series Title: Department of Animal Science research report
Physical Description: 2, 3 p. : ill. ; 28 cm.
Language: English
Creator: Asquith, Richard L
University of Florida -- Dept. of Animal Science
University of Florida -- Agricultural Experiment Station
Publisher: Florida Agricultural Experiment Station
Place of Publication: Gainesville Fla
Publication Date: 1980
 Subjects
Subject: Horses -- Diseases and pests -- Florida   ( lcsh )
Aflatoxins -- Research -- Florida   ( lcsh )
Genre: government publication (state, provincial, terriorial, dependent)   ( marcgt )
non-fiction   ( marcgt )
 Notes
Statement of Responsibility: R.L. Asquith.
General Note: Caption title.
General Note: "September, 1980."
Funding: Animal science research report (University of Florida. Dept. of Animal Science) ;
 Record Information
Bibliographic ID: UF00073119
Volume ID: VID00001
Source Institution: University of Florida
Rights Management: All rights reserved by the source institution and holding location.
Resource Identifier: oclc - 80753071

Table of Contents
    Experiment
        Page 1
    Discussion
        Page 2
    Conclusion
        Page 2
    Table I - Hemic changes and serum enzyme levels after administering a single dose of purified aflatoxin B1 at 5 mg/kg of body weight to a pony
        Page 3
    Fig. 1 - Iditol dehydrogenase responses in young ponies to aflatoxin B1
        Page 4
    Fig. 2 - Iditol dehydrogenase (ID) responses in young ponies to aflatoxin B1 (post-dosing means, square root transformation vs time)
        Page 5
Full Text

Department of Animal Science Florida Agricultural
Research Report AL-1980-10 Experiment Station
September, 1980 Gainesville, Florida

EXPERIMENTALLY INDUCED EQUINE AFLATOXICOSIS

R. L. Asquith1


Moldy feed toxicosis has been recognized as a biohazard for domestic animals
for many years, but it was not until 1961 that the toxins elaborated by Aspergillus
flavus and Aspergillus parasiticus were identified as the causitive agenftof
"Turkey-X" disease in the United Kingdom. This disease syndrome characterized
by stunting, icterus and deaths has been reported in other species of animals and
in other countries. Later these toxins became recognized as secondary metabolites
of fungal origin known as the aflatoxins. They are one of the larger groups of
toxic mold byproducts known collectively as mycotoxins.

Considerable research has been completed in aflatoxicosis in animals other
than the horse; one finds very little work done with this species other than Shurg
and Noon's report on experiments where cotton seed meal was fed to adult horses, and
the work by the author of this paper. Some of the known effects of aflatoxins on
livestock, poultry, and man are as follows: anorexia, reduced growth rate, liver
damage, nephropathy, carcinogenesis, teratogenesis, hemorrhagic enteritis, prolonged
clotting time, abortion, and both acute and chronic death losses. It is always
dangerous to extrapolate data from one species to another, but even more so concern-
ing the effects of aflatoxins as they may vary with age, nutritional plane, sex,
and even breeds within the species. This lack of information on aflatoxicosis in
horses and the discovery of aflatoxin contaminated feed in Florida rations at
the Horse Research Center prompted earlier and present investigations.

Experiment
A preliminary trial using a six month old pony was necessary to establish the
toxic range of dose levels and to observe clinical signs. Blood samples were taken
prior to treatment and again at 24, 30, and 33 hours after dosing. A single dose of
purified aflatoxin B, 5mg/Kg of body weight was administered via a stomach tube.
The pony died after 68 hours. Table I depicts the hematological values obtained
and the serum enzyme determinations.

A controlled experiment to demonstrate aflatoxicosis was performed. Twelve clin-
ically normal Shetland ponies, from 6 to 8 months of age, were allocated to 4 treat-
ment groups. Aflatoxin B1 was administered at a level of 2 mg/Kg body weight to
Group A, 1 mg/Kg to Group B. 0.5 mg/Kg to Group C and a placebo was given to Group D
(controls). Plasma samples were assayed at 4 hour intervals for ID levels to deter-
mine the degree of hepatic damage.

Two ponies in Group A died within 76 hours after dosing; the third animal in
Group A died on day 32 after exposure to the aflatoxin; all other animals survived
the experiment. The significant ID peak mean values were: Group A 1514.0 IU/L
(P<0.05), Group B 192.6 IU/L (P<0.05), Group C 8.5 IU/L (P<0.05), and Group D
(controls) 2.7.IU/L. .(Fig..1)...


DVM, Associate Professor of Equine Health








A square root transformation analysis of the post-dosing response of ID
levels in relation to time, demonstrated that the mean of Group A became signi-
ficantly higher (P<0.05) than the Control Group at 5 6 hours; the mean of
Group B at 12 16 hours, and Group C at 20 24 hours. (Fig. 2)

Discussion

Monitoring vital signs throughout the preliminary trial revealed an elevation
of body temperature from 100.80F up to 1040F within 4 hours after dosing. The
temperature peaked at 106.60F at 29 hours and then regressed to 100.20F just prior
to death. The heart rate remained normal, 44 60/min. for the first 24 hours and
then accelerated to 140/min. and became erratic prior to death. The respiratory
rate also remained normal, 16 20/min., for 24 hours then rapidly increased to
116/min. and became irregular. The appetite remained good until the temperature
peaked; the pony then became lethargic and reluctant to move around the stall.
Approximately 19 hours after dosing, the pony became ataxic and exhibited general-
ized muscle tremors. Within minutes the animal went down into a lateral recumbent
position and exhibited tetanic convulsions. Later, the pony became comatose and
died 80 minutes after recumbency.

The only gross lesions seen upon necropsy were petechial hemorrhages on the
mucosa of the small intestine and surfaces of the liver. Tissue sections were
taken from various organs; the only significant lesion was generalized and massive
necrosis from all sections of the liver.

In the controlled trial the macroscopic lesions presented at necropsy varied
from animal to animal. In general, there were visceral petechial hemorrhages,
focal lesions in the liver, some hemorrhage in skeletal muscle and evidence of
patchy pneumonia. Histopathologic findings in these animals and in our other trial:
invariably demonstrated some degree of liver damage. Massive and focal necrosis, b
duct proliferation, and vacuolation was seen, but again not necessarily in each
animal.

Clinical signs observed while monitoring every hour throughout this trial
were as follows: anorexia, elevated temperature (1030F 1060F), increased heart
and respiratory rates, ataxia, convulsions, icterus, colic, bloody feces, abdomina
straining and both acute and delayed deaths.

Conclusion

These findings indicate that the possibility of field cases of equine aflatoxi-
cosis exists and the awareness of this disease should be considered in a differentia
diagnosis. Results of this experiment may provide some guidelines in assessment of
clinical toxicity in horses exposed to aflatoxins.








A square root transformation analysis of the post-dosing response of ID
levels in relation to time, demonstrated that the mean of Group A became signi-
ficantly higher (P<0.05) than the Control Group at 5 6 hours; the mean of
Group B at 12 16 hours, and Group C at 20 24 hours. (Fig. 2)

Discussion

Monitoring vital signs throughout the preliminary trial revealed an elevation
of body temperature from 100.80F up to 1040F within 4 hours after dosing. The
temperature peaked at 106.60F at 29 hours and then regressed to 100.20F just prior
to death. The heart rate remained normal, 44 60/min. for the first 24 hours and
then accelerated to 140/min. and became erratic prior to death. The respiratory
rate also remained normal, 16 20/min., for 24 hours then rapidly increased to
116/min. and became irregular. The appetite remained good until the temperature
peaked; the pony then became lethargic and reluctant to move around the stall.
Approximately 19 hours after dosing, the pony became ataxic and exhibited general-
ized muscle tremors. Within minutes the animal went down into a lateral recumbent
position and exhibited tetanic convulsions. Later, the pony became comatose and
died 80 minutes after recumbency.

The only gross lesions seen upon necropsy were petechial hemorrhages on the
mucosa of the small intestine and surfaces of the liver. Tissue sections were
taken from various organs; the only significant lesion was generalized and massive
necrosis from all sections of the liver.

In the controlled trial the macroscopic lesions presented at necropsy varied
from animal to animal. In general, there were visceral petechial hemorrhages,
focal lesions in the liver, some hemorrhage in skeletal muscle and evidence of
patchy pneumonia. Histopathologic findings in these animals and in our other trial:
invariably demonstrated some degree of liver damage. Massive and focal necrosis, b
duct proliferation, and vacuolation was seen, but again not necessarily in each
animal.

Clinical signs observed while monitoring every hour throughout this trial
were as follows: anorexia, elevated temperature (1030F 1060F), increased heart
and respiratory rates, ataxia, convulsions, icterus, colic, bloody feces, abdomina
straining and both acute and delayed deaths.

Conclusion

These findings indicate that the possibility of field cases of equine aflatoxi-
cosis exists and the awareness of this disease should be considered in a differentia
diagnosis. Results of this experiment may provide some guidelines in assessment of
clinical toxicity in horses exposed to aflatoxins.


















HOURS AFTER DOSING


0 ...


Hct (%)

Hb (g/100ml)
3
WBC (10 i/l)
6
RBC (10 /il)

BUN (mg/dl)

Prothrombin
Time (Sec.)

ALP (Iu/l)

GGT (Iu/l)

GOT (lu/1)

ID (Iu/1)


37.1

13.1

10.147

9.32

16.0

12.0


211

14

156

4.5


.. . 2 4 . .


37.5

12.9

11.039

9.19

12.1

15.9


247

19

172

452


30 ...... 33


33.5

12.0

9.375

8.36

11.6

22.1


213

32

894

1800


37.7

13.4

8.25

9.44

12.4

25.2

231

32

1260

3677


Table I. Hemic changes and serum enzyme levels after

dose of purified aflatoxin B1 at 5 mg/Kg of


administering a single

body weight to a pony.













1800


1600


1400


1200


1000
,..I


800 o.


600


400


200




Group A GroupB Group C Group D
(2.0mg/kg) (1.0mg/kg) 10.5 mg/kg) (control)









Fig 1 Iditol dehydrogenase responses in young ponies to aflatoxin B1 (mean peak

responses + SEM). Figure reproduced by the courtesy of the Editor of the American

Journal of Veterinary Research.




















40


35


30


25


S 20 $t-


15


10 7


5 group C.0.5mg/kg)

/kg) Croup D crtntrof

10 20 30 40 50 60 70 80 90 100

Time After Treatment In Hours













Fig 2 Iditol dehydrogenase (ID) responses in young ponies to aflatoxin B1 (post-

dosing means, square toot transformation vs time). Figure reproduced by the courtesy

of the Editor of the American Journal of Veterinary Research.


O-




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