Abstract
One male and one female adult captive giant anteaters (Myrmecophaga tridactyla) were treated with a single dose of sulfadimethoxine 60 mg/kg p.o. Of these animals, one showed acute symptoms such as convulsions, apparently due to abdominal pain and vomiting. Treatment and recovery of this animal are described. Clinical examination suggests an impaired liver function or an idiopathic hypersensitivity as possible reasons for the unexpected reaction to the sulfadimethoxine.
Introduction
The giant anteater (Myrmecophaga tridactyla) belongs to the order of the Xenartra. They inhabit the neotropical regions of Central and South America. This order also includes the armadillos and sloths. Due to their exceptional biology and behavior the Xenartra represent a unique challenge to the zoo veterinarian. In comparison to the other Xenartra, very few anteaters are kept in zoological gardens and, therefore, very little is known about their management and reproduction. This lack of knowledge becomes apparent when information is needed, concerning the veterinary care of these animals. The aim of this case is to share the experience of a complication during the deworming of a giant anteater and the therapy used to save the animal.
Case Report
In 1995–1996, one male and one female adult giant anteaters arrived to Zurich Zoo from different zoos. The two animals were housed together during the day and separated during the night. They had an indoor and an outdoor enclosure. Their diet consisted of 1 L of a soup made from dog chow, minced meat, oats, fruits (e.g., kiwi, bananas, pears), and a vitamin and mineral supplement. Since their arrival, the animals appeared healthy. In October 1997 during a routine fecal parasitological examination it was found the both animals were shedding Capillaria spp. and Eimeria spp. Due to the fact that occasionally both animals had produced loose stool, it was decided to treat them against the parasites.
They were first treated with fenbendazole (Panacur® Suspension 10%, Hoechst) 15 mg/kg p.o. for 3 consecutive days. Nine days later, each animal was given sulfadimethoxine (Maxulvet®, Veterinaria) 60 mg/kg p.o. Approximately 6 hr later, the female animal showed symptoms of incoordination, which deteriorated within 1 hr. At the first clinical examination the animal was in lateral recumbency, vomiting, and had strong convulsions, apparently due to abdominal pain.
Differential diagnoses at this point were, in order of probability: an intoxication (sulfadimethoxine), a gastrointestinal obstruction (e.g., foreign body, parasites, enteritis), a reproductive disease, and a septic disease.
For the next 36 hr, the animal was treated with diazepam (Valium®, Roche), an anti-inflammatory drug metamizole (Vetalgin®, Veterinaria), vitamin K (Konakion®, Roche), enrofloxacin (Baytril® 10%, Bayer). The main aim of the treatment was to sedate the animal to a point were convulsions would disappear. Body temperature and heart rate were mildly elevated.
On the second day, an intravenous catheter was placed in the cephalic vein to initiate fluid therapy. Blood was collected from the animal for hematology and blood chemistry (Table 1). The most obvious finding was a moderate to strong increase in the serum enzyme activity of AST, ALT, GGT, and LDH. A blood gas analysis was also performed on day 2. It did not reveal any pathologic changes. An x-ray examination revealed a hyperostosis in the thoracolumbar spine. On the basis of these findings, differential diagnoses such as gastrointestinal obstruction, reproductive problem, and an infection were rejected. An intoxication, most likely due to the sulfadimethoxine, was considered the diagnosis.
Table 1. Blood values of a giant anteater (Myrmecophaga tridactyla) with suspected sulfadimethoxine intoxication
|
Parameter
|
Value
|
Reference range*
|
|
Hemoglobin g/dl
|
15.0
|
11.3–13.5
|
|
Red blood cell count (106/μl)
|
2.7
|
2.4–3.0
|
|
White cell count (103/μl)
|
9.5
|
5–10
|
|
Packed cell volume (%)
|
43
|
30–50
|
|
MCH (pg)
|
56
|
46–49
|
|
MCHC (g/dl)
|
35
|
31–35
|
|
MCV (fl)
|
159
|
135–137
|
|
Glucose (mmol/L)
|
2.7
|
1.6–4.7
|
|
Urea (mmol/L)
|
3.6
|
3.7–5.9
|
|
Creatinine (μmol/L)
|
107
|
79–106
|
|
Total protein (g/L)
|
69
|
52–74
|
|
Albumin (g/L)
|
32
|
12–33
|
|
Cholesterol (mmol/L)
|
1.5
|
2.2–3.2
|
|
Alkaline phosphatase (U/L)
|
16
|
74
|
|
AST (U/L)
|
102
|
19
|
|
ALT (U/L)
|
70
|
33
|
|
GGT (U/L)
|
119
|
13
|
|
LDH (U/L)
|
380
|
334
|
|
Na (mmol/L)
|
147
|
152
|
|
K (mmol/L)
|
5.0
|
5.8
|
|
Cl (mmol/L)
|
108
|
110
|
|
Ca (mmol/L)
|
2.8
|
2.1–2.5
|
|
P (mmol/L)
|
1.3
|
1.8–2.0
|
* Source: Ruempler (1995)
Table 2 gives the chronologic treatment and the course of the disease. The male, which was kept separate at all times, showed minor symptoms of incoordination 30 hr after treatment. The symptoms resolved within 2 hr without therapy. Approximately 48 hr after onset of symptoms the animal’s condition started to improve and within another 48 hr it returned to normal behavior. Since then the animal has been in good health.
Table 2. Chronologic course of a giant anteater (Myrmecophaga tridactyla) with suspected sulfadimethoxine intoxication. (The animal’s weight was 63 kg.)
|
Time
|
Therapy
|
Symptoms
|
|
Day 1
|
|
15.00 h
|
Diazepam 20 mg i.m.
Metamizole 1,000 mg i.m.
Scopolamine 8 mg i.m.
|
Onset of symptoms: colic, vomiting, and lateral recumbency.
Following medication → calm in lat. recumb.
|
|
21.00 h
|
Diazepam 20 mg i.m.
Metamizole 1,000 mg i.m.
Scopolamine 8 mg i.m.
|
Again colic
|
|
Day 2
|
|
07.00 h
|
Diazepam 20 mg i.m.
Metamizole 2,000 mg i.m.
|
Again colic and vomiting
|
|
09.00 h
|
1 l of lactated Ringer’s solution and 250 ml of NaCl/glucose i.v. over 7 h
Vitamin K 10 mg i.m.
Enrofloxacin 300 mg i.m.
|
Calm in lat. recumb., placement of i.v.-catheter. Collection of blood samples.
|
|
16.00 h
|
Diazepam 10 mg i.m.
|
Calm in lat. recumb.
|
|
Day 3
|
|
07.00 h
|
|
First lat. recumb.; wakes up and eats 1 dl of yogurt. Starts walking around. Then sleeps for several hours.
|
|
19.00 h
|
|
Active, eats
|
|
Day 4/5
|
|
|
|
Steady improvement, apparently healthy
|
Discussion
This case reports the symptoms and treatment of a suspected intoxication with sulfadimethoxine in a captive giant anteater. The finding that this drug could lead to an adverse reaction in this animal was surprising. Sulfadimethoxine is a long-acting sulfonamide, which is known for its broad activity against gram positive and negative bacteria as well as coccidia, and its low toxicity. It has been used in a wide range of species including exotic mammals, birds, and reptiles.3 In most species, sulfadimethoxine is acetylated in the liver to acetylsulfadimethoxine and excreted unchanged in the liver. Sulfadimethoxine’s long elimination half-lives are a result of its appreciable reabsorption in the renal tubules. Sulfadimethoxine is therefore contraindicated in patients with impaired liver and/or kidney function. In humans, adverse effects to sulfonamides include gastrointestinal disorders (e.g., nausea, vomiting, diarrhea), hypersensitivity reactions, neurotoxicity, allergic and toxic hepatic disease. To the author’s knowledge such symptoms related to sulfonamide therapy have not been previously described in Xenarthra. Sulfonamides have been used in captive giant anteaters before without adverse effect (Osmann, personal communication). Possible explanations for the occurrence of this reaction only in one of the two animals, might be an inhibited function of the liver or an idiopathic hypersensitivity to sulfadimethoxine. Blood biochemistry results suggested a possible liver disease. In the literature, liver disease, such as liver cell necrosis, have been reported in giant anteaters.2,4 A chronic impaired liver function in this animal and, therefore, a reduced metabolization of the medicament could have been the cause that led to these symptoms. The body weight of this animal was 63 kg, which is considerably higher than body weights of anteaters given in the literature (30–40 kg).4 The animal does not make an obese appearance, but some degree of fatty liver degeneration may be present. A conclusive diagnosis of liver disease could have only been possible on the basis of a liver biopsy, which in this case was not available.
The vertebral hyperostosis, which was diagnosed in the radiologic examination, was considered to be of nutritional origin. In anteaters (Tamandua tetradactyla and T. mexicana), similar changes have been found and it was suggested that they might be caused due to a hypervitaminosis A and/or D.1 As a result, an evaluation and improvement of the diet has been initiated. As has been demonstrated with the present case, further clinical and pathologic research is needed to improve the management of giant anteaters in captivity.
Acknowledgments
The authors thank Heinz Kohler from Zurich Zoo for his assistance.
Literature Cited
1. Crawshaw, G. J. and S. E. Oyarzun. 1996. Vertebral hyperostosis in anteaters (Tamandua tetradactyla and Tamandua mexicana): probable hypervitaminosis A and/or D. J. Zoo Wildl. Med. 27:158–169.
2. Diniz, L. S. M., E. O. Costa, and P. M. A. Oliveira. 1995. Clinical disorders observed in anteaters (Myrmecophagidae, Edentata) in captivity. Vet. Res. Comm. 19:409–415.
3. Marx, K. L., and M. A. Roston (eds.). 1996. The Exotic Animal Drug Compendium. Veterinary Learning Systems, Trenton, New Jersey.
4. Ruempler, G. 1995. Nebengelenktiere (Zahnarme), Schuppentiere, Erdferkel. In: Göltenboth, R., and H.-G. Klös (eds.). Krankheiten der Zoo- und Wildtiere. Blackwell Wissenschafts-Verlag, Berlin.