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Abdominal Fat Necrosis in Sambar Deer (Cervus unicolor) in Brazil

Karin Werther, Márcio Botelho de Castro, Tianelen Malaquias Farias, and José Antonio Marciano

Universidade Estadual Paulista (UNESP) – Campus de Jaboticabal, Deptartmento de Veterinary Pathology, Via de Acesso Prof. Paulo Donate, Castellani s/nº, 14870-000 Jaboticabal/SP/Brazil (Werther), Zoológico de Brasília/DF/Brazil (de Castro), Tianelen Malaquias Farias, Zoológico de Brasília/DF/Brazil (Farias), and UNESP - Araçatuba/SP/Brazil (Marciano)

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Abstract. This paper presents two cases of abdominal fat necrosis in Sambar deer (Cervus unicolor) from the Zoological Garden in Brazil. The clinical changes, gross pathology findings, and histopathological alterations of this condition are described.

Key Words: Sambar deer, Cervus unicolor, fat necrosis

Introduction

Abdominal fat necrosis or abdominal lipomatosis, described by Bacon and coworkers,1 is a disease caused by ingestion of a tall fescue forage infected with the endophytic fungus Epichloe typhina. In 1982, Morgan-Jones reclassified this fungus as Acremonium coenophalium.2 Tall fescue forage (Festuca arundinacea) infected with the endophytic fungus came from New Zealand, and intoxication has occurred in many countries including New Zealand, the United States, Australia, Argentina, and Uruguay.3

Abdominal lipomatosis can occur in grade horses,3 quarterhorses,4 Swamp deer (Cervus duvaceli),5 Eld's deer (Cervus eldi thamin), Sika deer (C. nippon), and Sambar deer (C. unicolor).6 The principal clinical signs of disease are decreased weight gain and milk production, as well as a reduced rate of conception and heat dissipation in cattle.7 Intestinal obstruction may occur as the gut is compressed by firm lumps of necrotic fat. Affected animals also may exhibit anorexia, diarrhea, constipation, colic, or bloat. Emaciation is a common observation prior to death. Mares may have agalactia and thick placental membranes, while foals may exhibit weakness, inability to stand, lethargy, and progressive listlessness. Furthermore, foals may appear dysmature, as indicated by poor muscle tone, generalized weakness, and a silky coat with curling of the tips of the ears.4 In Swamp deer (Cervus duvauceli), severe dystocia is associated with narrowing of the pelvic canal.5 Large, firm, slightly mobile masses may be detected by rectal examination.

The presentation of fat necrosis also has been described in detail in Eld´s deer (Cervus eldi thamin).6 Anorexia, depression, and reluctance to stand have been observed. In addition, affected deer are easily handled. Palpation disclosed a firm subcutaneous mass (5 x 6 cm) overlying the right body of ilium. Loose tarry feces and blood were found on the tail and perineum. On abdominal palpation, a large, firm mass was found in right portion of the abdomen. Radiography also revealed two large radiopaque perirenal masses. At exploratory laparotomy, large firm white masses were adhered to most of the abdominal organs. The most important necropsy finding included an intensely bright yellow carcass fat and scattered, irregular, abdominal masses of very hard fat. The masses were a deep yellow color with chalky white and orange foci. The diameters of masses varied from 1 to 30 cm. Masses were observed most frequently in the small intestinal and rectal mesentery, where they often formed obstructive casts encircling the intestine or rectum. The masses also involved the kidney or heart. Another common site of formation was the ureter. Subsequent constriction of the ureter resulted in hydronephrosis. These lesions have been reported in cattle,8 Eld's deer (Cervus eldi thamin),6 and Swamp deer.5

Histologically, fat necrosis may be accompanied by foci of peripheral calcification and fibrosis.6 Some tissue specimens resemble a mixture of acute and chronic fat necrosis with few neutrophils, lymphocytes, and plasma cells, admixed with many macrophages and giants cells. Interstitial fibrosis also may be present.

Case Report

Abdominal fat necrosis was observed in two Sambar deer (Cervus unicolor) housed at zoological gardens in Brazil. The Sambar deer is native to India, Southeast Asia, South China, Formosa, Malaysia, and Indonesia. Adults weigh approximately 100 to 150 kg.

The first incidence of fat necrosis occurred 1996 at the Zoological Garden of Brasilia City, Brazil. An adult female Sambar deer presented with abdominal enlargement suggestive of gestation. Apathy and dyspnea also were observed. The animal was in very bad condition and subsequently was euthanatized. At necropsy, a large, calcified, abdominal mass was observed. The mass had an irregular surface and weighed 19.8 kg. It encircled both the ovaries and uterus. In addition, hydronephrosis was present. This animal’s diet included a diversity of vegetables (including carrots and potatoes) and forage.

The second animal was nine-year-old, female, Sambar deer from the Zoological Garden of Ribeirão Preto, State of São Paulo, Brazil. This deer exhibited apathy, anorexia, And prostration, but was in good nutritional condition or perhaps slightly obese.

The diet consisted of forage (Panicum spp., Pennisetum sp., Cynodon sp.); carrots, cabbage, and other assorted vegetables; papaya; banana; equine extruded ration; pumpkin; and oats with peel. On physical examination, mucohemorrhagic vaginal secretions were observed. Abdominal radiographs revealed perirenal masses of high density. Following radiography, the deer died. At the necropsy, the heart valves appeared edematous instead of translucent. The trachea was congested and crepitus was palpated in the lungs. The liver was discolored and friable with areas of calcification. Sand was present in the digestive tract; however, the intestines contained a dark brown, fetid fluid. The feces were dry and covered with mucus. The kidneys were completely covered by calcificated masses that were adhered to the peritoneum. The perirenal masses measured 1-3 cm in diameter by 10 cm in length (Fig. 1). When the kidney was incised, abundant urine was obtained. The renal parenchyma had a more dense consistency than normally expected. The contralateral kidney also was encased by a calcificated mass that involved the adrenal gland and was adhered to the liver (Fig. 2). The urinary bladder was replete; urinary tract obstruction could not be documented. A large, firm, red mass that was adhered firmly to the vaginal wall near the cervix (Fig. 3). This vaginal mass was 15 cm in diameter and 30cm in length. Both ovaries were completely calcified, measuring 11.5 x 5 x 7.5 cm and 15 x 4.5 x 5.5 cm (Fig. 4 and 5).

 
Fig. 1: Calcified mass around the kidney.
 
Fig. 2: Calcificated mass around the kidney and adhered the liver.
Fig. 1: Calcified mass around the kidney. Fig. 2: Calcificated mass around the kidney and
adhered the liver.

 

 
Fig. 3: Fibroma in the vagina
Fig. 3: Fibroma in the vagina

 

 
Fig. 4: Periovarian calcification and necrosis of fat with yellow discoloration.
 
fig5.jpg (30885 bytes)
Fig. 4: Periovarian calcification and necrosis of fat
with yellow discoloration.
Fig. 5: Periovarian calcification and necrosis of fat.

 

Histologically, the intravaginal mass was a fibroma. Sections of kidney revealed tubular edema (Fig. 6), interstitial inflammation (Fig. 7), glomerular edema, and enlarged spaces within Bowman’s capsule (Fig. 8). The liver had lipid accumulation and hydropic degeneration with perivascular inflammatory foci (Fig. 9). Sections of lung disclosed atelectasis and emphysema. The ovarian and perirenal masses were composed of necrotic adipocytes with calcification (Fig. 10, 11,and 12). Some foci of fat necrosis also contained numerous inflammatory cells, including multinucleated giant cells.

 

 
Fig. 6: Photomicrograph of the kidney showing tubular edema (200x, H&E stain).
Fig. 6: Photomicrograph of the kidney showing
tubular edema (200x, H&E stain).

 

 
Fig. 7: Photomicrograph of the kidney with interstitial inflammation.
 
Fig. 8: Photomicrograph of the kidney showing enlarged spaces within Bowman’s capsule.
Fig. 7: Photomicrograph of the kidney with interstitial
inflammation (200 x, H&E stain).
Fig. 8: Photomicrograph of the kidney showing
enlarged spaces within Bowman’s capsule
(100 x, H&E stain).

 

 
Figure 9: Photomicrograph of the liver showing lipidosis and hydropic degeneration.
Figure 9: Photomicrograph of the liver showing
lipidosis and hydropic degeneration (200x, H&E stain).

 

 
Figure 10: Photomicrograph of adipose tissue showing necrosis and calcification
 
Figure 11: Photomicrograph of adipose tissue showing necrosis and calcification
Figure 10: Photomicrograph of adipose tissue showing
necrosis and calcification (40x, H&E stain).
Figure 11: Photomicrograph of adipose tissue showing
necrosis and calcification (40x, H&E stain).
(100 x, H&E stain).

 

 
Figure 12: Photomicrograph of the adipose tissue showing necrosis and calcification.
Figure 12: Photomicrograph of the adipose tissue
showing necrosis and calcification (200x, H&E stain).

 

 

Discussion

The principal cause of abdominal fat necrosis is chronic ingestion of endophyte-infected tall fescue, although genetic predisposition, obesity, and sex are likely to be contributing factors.6 Consumption of endophyte-infected fescue seed, combined with elevated environmental temperature, increases body fat mobilization and reduces apparent nutrient digestion in rats.9

Based on the literature, clinical histories, radiographic results, and pathological (macroscopic and microscopic) findings, these two Sambar deer had classical abdominal fat necrosis. The etiology of the fat necrosis in these deer is not completely clear, but it is possible that the forage could have been contaminated with endophyte fungus that produced mycotoxins causing fat necrosis. The prognosis for affected animals is usually poor because large calcificated masses often compromise normal organ function by the time clinical signs of disease are first observed. Therefore, preventive management is crucial to control or eliminate fat necrosis in ruminants. Such preventive measures include removing the animals from the endophyte contaminated fescue pastures or changing the diet to prevent mycotoxin exposure. Frequent examination of the quality of the food and forage is important to try to control fungal growth or decrease exposure to mycotoxins.

References

1. Bacon CW, Porter J., Robbins JD, Luttrell ES: Epichloe typhina from toxic tall fescue grasses. Appl Environ Microbio. 34:576, 1977.

2. Morgan-Jones G, Gams W: Notes on Hypomycetes XLI. An endophyte of Festuca arundinacea and the anamorph of Epichloe typhina, new taxa in one of two sections of Acremonium. Mycotaxon 15:311, 1982.

3. Riet-Correa F: Intoxicação por Festuca arundinacea. In: Riet-Correa, Mendez, Schild (eds.). Intoxicações por plantas e micotoxicoses em animais domésticos, Editorial Agropecuária Hemisfério Sur S.R.L., Montevideo, pp. 240-245, 1993.

4. Mirza MH, Costa LRR, Paccamonti D, Seahorn PL: Theriogenology question of the month. J Am Vet Med Assoc 213:1405-1406, 1998.

5. Ashton DG, Appleby EC, Jones DM: Abdominal lipomatosis in swamp deer (Cervus duvauceli)-a preliminary report. Verh Berl Erkr Zootiere 24:455-458, 1982.

6. Wolfe BA, Bush M, Monfort SL, Mumford SL, Pessier A, Montali RJ: Abdominal lipomatosis attributed to tall fescue toxicosis in deer. J Am Vet Med Assoc 213:1783-1785, 1998.

7. Paterson J, Forsheriu C, Larson B, Samford M, Kerley M: The effects of fescue toxicosis on beef cattle productivity. J Anim Sci 73:889-898, 1995.

8. Williams DJ, Tyler DE, Pappi E: Abdominal fat necrosis as a herd problem in Georgia cattle. J Am Vet Med Assoc 154:1017-1021, 1969.

9. Larson BD, Paterson JA, Kerley MS, Bell SC: Endophyte-infected tall fescue ingestion and stress of environmental heat affects bodycomposition in the rat model. J Anim Sci 70 (Suppl. 1):86, 1992.

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