AFIP Wednesday Slide Conference - No. 14
December 15, 1999

Conference Moderator:
LTC Denzel Frost, Diplomate, ACVP
Chief, Research Services Branch
Armed Forces Institute of Pathology
Washington, DC 20306-6000
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Case I - 27561-98 (AFIP 2680119)
Signalment: Five-month-old, female, Angus, bovine.
History: Acute onset of nervousness and ataxia progressing to recumbency with opisthotonus.
Gross Pathology: Grossly visible lesions were limited to the brain. There was a circumscribed area of malacia and discoloration approximately 3 cm in diameter involving the cerebellum, pons, and medulla.
Laboratory Results: Culture of the brain produced Mortierella wolfii. Routine cultures of the lung, liver, and kidney produced no significant bacteria. Fluorescent antibody tests produced negative results for BVD virus.
Contributor's Diagnosis and Comments: Cerebellum: Meningoencephalitis, necrotizing, chronic, focally extensive, severe, with vasculitis, thrombosis, and hyphae, Angus, bovine, etiology Mortierella wolfii.

Mortierella wolfii is a common cause of mycotic abortion in cattle in New Zealand and is reported as an infrequent cause in Great Britain and the United States. Under natural conditions, proposed routes of infection include skin wounds, the conjunctiva, and the respiratory, alimentary, and reproductive systems. The pathogenesis in some cases has been associated with the feeding of improperly handled silage. Mycotic pneumonia is often seen concurrently with or as a sequella to infection and placentitis in the cow.
Mycotic lesions are rarely found in cows in tissues other than the uterus and lungs, suggesting that cattle do not remain permanently infected following abortion and that only gravid cows develop lesions. Fetal lesions include focal encephalitis, hepatitis, and splenitis. In both the fetuses and cows, the lesions are characterized by necrosis, vasculitis, serofibrinous exudates, and neutrophil infiltrates with intra-lesional hyphae. In tissue sections the hyphae are nonseptate but may contain intra-hyphal vacuoles that appear similar to septa. Hyphae vary in width from about 2 to 12 mm and are often short and branched.
The case presented here had similar changes including severe encephalitis with necrosis of the neuropil, nonseptate hyphae, and infiltration by numerous neutrophils and mononuclear cells. Blood vessels often exhibited necrotizing vasculitis with thrombosis. This case is unusual in that it involved a 5-month-old calf. In addition to encephalitis, this calf had pneumonia and necrotizing splenitis with fungal hyphae. There was no history of silage feeding.
AFIP Diagnosis: Cerebellum and brain stem: Meningoencephalitis, subacute, focally extensive, severe, with necrotizing vasculitis, infarction and fungal hyphae, Angus, bovine, etiology consistent with a zygomycete.
Conference Note: Mortierella wolfii belongs in the mucormycosis group of zygomycotic fungi. This family is characterized by the presence of broad (3-25mm), non-septate or rarely septate hyphae, with non-parallel walls, and right angle, nondichotomous (unequal) branching. Although the H&E stained sections generally demonstrated the diagnostic features of this fungus, strong GMS positivity facilitated assessment of fungal morphology. Culture is required for specific identification of zygomycotic fungi.

The primary differential discussed in conference was aspergillosis. Histologic features of Aspergillus include thin (2-6mm), septate hyphae with parallel walls and dichotomous (equal) branching.
Contributor: University of Kentucky Livestock Disease Diagnostic Center, 1429 Newtown Pike, Lexington Kentucky 40511
1. Cordes DO, Carter ME, Di Menna ME: Mycotic pneumonia and placentitis caused by Mortierella wolfii. Vet Pathol 9:190-201, 1972
2. Done SH, Sharp MW, Lupson GR: Isolation of Mortierella wolfii from bovine lung. Vet Rec 134:194, 1994
3. McCausland IP, Slee KJ, Hirst FS: Mycotic abortion in cattle. Aust Vet J 64:129-132, 1987
4. Wohlgemuth K, Knudtson WU: Abortion associated with Mortierella wolfii in cattle. JAVMA 171:437-439, 1977
Case II - 99RA415 (AFIP 2681364)
Signalment: Adult, female, white-tailed deer (Odocoileus virginianus)
History: In March of 1999, an adult female white-tailed deer in Maine was observed to be very pruritic and in poor condition. The animal was destroyed humanely and necropsy was performed by the state veterinarian. Tissues were submitted to the National Veterinary Services Laboratory for surveillance for chronic wasting disease.
Gross Pathology: The animal was emaciated. Fat was present on heart and around kidneys. The skin had bilateral alopecia over large areas of the shoulders, lateral thorax, inguinal areas, and flanks with hyperpigmentation in many areas. There were some excoriations on neck and legs.
Laboratory Results: Histopathology of brain was negative for lesions of chronic wasting disease.

Contributor's Diagnoses and Comments:
1) Skin: hair follicle and sebaceous gland parasitism, Demodex odocoilei, severe.
2) Skin: dermatitis, pustular and ulcerative (some sections), subacute, with acanthosis, orthokeratotic hyperkeratosis, hyperpigmentation, and hair loss, mild to moderate.

Anagen follicles are abundant in the section, but intact hairs are scarce. The mites that are present in the hair follicles are consistent with previous records of demodicosis in white-tailed deer. The mites are present in all developmental stages, not only in the follicle lumen, but also in sebaceous gland ducts, within sebaceous glands, and occasionally on the surface. Adults and nymphs are recognized by 4 pairs of evenly spaced legs that are segmented in adults. Larvae and protonymphs are also present. This species has been reported to invade dermis and even venules, but none were identified outside of follicles in this specimen.
The mites are thought to first occupy hair follicles with intact hairs and then move into sebaceous glands to feed and reproduce. Increasing numbers of mites cause distention of glands and follicles eventually causing hair loss. Hairs typically are in anagen at this stage. The exact cause of the hair loss is not known, and a mite induced retardation of hair growth has been proposed. Inflammation is present in some areas but is typically weak even when the dermis is invaded. The superficial inflammation in this case may be secondary to pruritus, excoriation, and bacteria. The cause of this animal's debilitation is not known, but the demodecosis is likely secondary.
Thanks to Dr. C. W. Ridky of the Maine Department of Agriculture, Department of Inland Fisheries and Wildlife for submission of the case and Dr. Tom Gidlewski of the National Veterinary Services Laboratory, Department of Pathobiology, Ames, Iowa for the referral.
AFIP Diagnoses:
1. Haired skin: Epidermal hyperplasia, diffuse, moderate, with superficial and follicular orthokeratotic hyperkeratosis, follicular ectasia, minimal multifocal chronic dermatitis, and numerous mites, white-tailed deer (Odocoileus virginianus), cervid.
2. Dermis, vessels: Vasculitis, necrotizing and fibrinous, multifocal, with overlying subepidermal hemorrhage and focal ulceration.
Conference Note: The key features for identification of mites in tissue section are chitinous exoskeleton, jointed appendages, skeletal muscle, and a hemocoelom. Most animals are parasitized by a Demodex species. They are generally considered normal inhabitants of the hair follicle and sebaceous glands.

Factors predisposing to development of generalized demodicosis are not fully understood; some of the more significant factors include: immune status, breed and breeding line, age, length of hair coat, nutritional status, stage of estrus cycle, parturition, stress, endoparasitism and debilitating disease. Immunity is thought to be the most significant. Both immunodeficiency and immune-mediated injury to the skin may play roles in the disease. The cause of the vasculitis that was present in some sections was not evident, but conference participants considered the possibility of epizootic hemorrhagic disease of deer.
Contributor: Department of Veterinary Pathology, Iowa State University, Ames, Iowa 50011-1250
1. Barker IK, Van Dreumel AA, Palmer N: The Alimentary System. In: Pathology of Domestic Animals, eds. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 2, pp.173-174. Academic Press, San Diego, CA, 1993
2. Desch CE and Nutting WB: Demodex odocoilei sp nov. from the white-tailed deer, Odocoileus virginianus. Can J Zool 52:785-789. 1974.
3. Yager JA, Scott Danny: The Skin and Appendages. In: Pathology of Domestic Animals, eds Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 1, pp. 686-690. Academic Press, San Diego, CA, 1993
Case III - 1968406 (AFIP 2679046)
Signalment: Adult, ovine, male, bighorn sheep, Ovis canadenis
History: This adult ram was observed to be depressed for 2 days, had watery diarrhea, and subsequently died. The animal had been purchased and shipped in from Colorado to this mixed herd in Michigan which consisted of bighorn sheep, mule deer and elk.
Gross Pathology: On necropsy, this ram was in good body condition. The mucosal linings throughout the abomasum, small intestine and colon were diffusely congested and thickened. No other gross lesions were noted.
Laboratory Results: Yersinia pseudotuberculosis was isolated in high numbers from abomasum, small intestine and liver.
Contributor's Diagnosis and Comments: Small intestine: moderate acute necrotizing enteritis with numerous microabscesses and bacterial colonies.
The histologic appearance of the intestinal tract with necrosis, suppurative infiltrates, and presence of bacterial colonies supports a bacterial etiology in this case. The extremely prominent colonies of small gram-negative bacilli, associated with microabscess formation in the intestinal mucosa are highly suggestive of infection with Yersinia spp.5 Isolation of high numbers of Y. pseudotuberculosis confirmed the diagnosis in this case.
Cases of acute enterocolitis due to Yersinia spp. infection, frequently associated with septicemia and high mortality, have been reported frequently in sheep, goats, and farmed deer in New Zealand and Australia.4,6 In addition, many different species of mammals and over 50 species of birds, including both captive and free-living, have been reported with Yersinia spp. infection from throughout the world.3 In North America, outbreaks of yersiniosis have been more sporadic than in Europe or Australia, 2,3 however, several outbreaks of yersiniosis have been recently reported in North American deer ranches, wildlife parks, and in free-ranging wildlife.1,5,7 It is believed that wild birds and rodents serve as reservoirs of infection for captive and wild mammals.3
AFIP Diagnosis: Small intestine: Enteritis, erosive, subacute, diffuse, moderate, with microabcesses containing numerous large colonies of bacteria, bighorn sheep (Ovis canadenis), ovine.
Conference Note: Yersinia pseudotuberculos is is a gram negative, facultative, nonmotile, psychrophilic (able to replicate at 4° C), coccobacillus. It is difficult to isolate on routine culture; cold enrichment and culture at 20° C are required for isolation. The organism is considered to be commensal in many species; therefore, isolation of the organism from deeper tissues, such as blood, urine, lymph nodes, wounds or abscesses is more meaningful.
The genus Yersinia contains six species: Y. pestis, Y. pseudotuberculosis, Y. enterocolitica, Y. frederiksenii, Y. intermedia and Y. ruckerii (fish). Y. pestis, the etiologic agent of human plague, Y. pseudotuberculosis and Y. enterocolitica are the major species of this genus; Y. pseudotuberculosis and Y. enterocolitica are considered primarily enteric pathogens. Y. frederiksenii, Y. intermedia tend to cause skin and wound infections. Y. pseudotuberculosis and Y. enterocolitica have little host specificity and infect many avian and mammalian species; differentiation between the two requires culture.

Infection generally occurs following orogastric inoculation, in which the bacteria enter the lamina propria of the distal ileum, cecum and colon with subsequent necrosis of Peyer's patches and eventual mucosal ulceration; extension to mesenteric lymph nodes and septicemia may also occur. If septicemia develops, suppurative lesions may develop in various organs (e.g. liver, spleen, lungs, meninges). Yersiniosis is frequently associated with a triad of gross lesions; hepatosplenomegaly and distended bowel. Infection is precipitated by changes in environmental conditions, such as a decrease in temperature, poor nutrition or overcrowding. Epizootics in domestic species are frequently preceded by outbreaks in rodents or birds.

Contributor: Animal Health Diagnostic Laboratory, PO Box 30076, Lansing, MI 48909-7576
1. Blake JE, McLean BD, Gunn A: Yersiniosis in free-ranging muskoxen on Banks Island, Northwest Territories, Canada. J. Wildl Dis 27:527-533, 1991
2. Hubbert WT: Yersiniosis in mammals and birds in the United States: case reports and review. Am J Trop Med Hyg 21:458-463, 1972
3. Mair NS: Yersiniosis in wildlife and its public health implications. J Wildl Dis 9:64-71, 1973
4. Philbey AW, Glastonbury JRW, Links IJ, Mathew LM: Yersinia species isolated from sheep with enterocolitis. Aust Vet J 68:108-110, 1991
5. Sanford KJ: Outbreaks of yersiniosis caused by Yersinia pseudotuberculosis in farmed cervids. J Vet Diagn Invest 7:78-81, 1995
6. Slee KJ, Skilbeck NW: Epidemiology of Yersinia pseudotuberculosis and Y. enterocolitica infections in sheep in Australia. J Clin Microbiol 30:712-715, 1992
7. Welsh RD, Ely RW, Holland RJ: Epizootic of Yersinia pseudotuberculosis in a wildlife park. J Amer Vet Med Assoc 201:142-144, 1992
Case IV - 99-08 (AFIP 2679432)
Signalment: Owl monkey, Aotus vociferans, adult, female
History: This monkey was splenectomized and inoculated with Plasmodium cynoniologi ten months prior to death. It developed alopecia and thickened scaly skin on the tail. It also developed a bloody nose and mucopurulent discharge over the left eye. The monkey was treated with SMZ -TMP, and the eye im-proved but the tail did not. The monkey went into respiratory arrest and died during recovery from surgery to amputate the tail.
Gross Pathology: Necropsy revealed a moderately enlarged heart.
Contributor's Diagnoses and Comments:
1) Liver, vacuolar degeneration (lipidosis), mild-moderate.
2) Kidney, membranoproliferative glomerulopathy, multifocal, severe, with multifocal tubular degeneration, mild.
It has been recognized for many years that renal disease occurs in association with malarial infection. In recent years, P. falciparum infections have been reported to produce circulating immune complexes, which deposit in the glomeruli. The occurrence of renal disease in Aotus monkeys infected with P. malaria and P. falciparum and clinical courses are similar to those of humans. In P. falciparum infection, large immune complexes tend to be taken up by the mesangium rather than passed through the basement membrane. Because of this activity, the mesangium may expand.
Histologically, there is glomerular hypercellularity, infiltration by polymorphonuclear leukocytes, mild thickening of the glomerular basement membrane, and glomerular mesangial expansion. There may also be mild tubular degeneration. Glomerulopathies and interstitial nephritis are common causes of death in Aotus monkeys. Differential diagnosis for glomerular disease includes Herpesvirus saimiri, Pasteurella pseudotuberculosis, and rheumatoid arthritis.
AFIP Diagnosis:
1. Kidney: Glomerulopathy, global, diffuse, moderate, with mesangial proliferation, synechia and obsolescence, owl monkey (Aotus vociferans), non-human primate.
2. Kidney: Nephritis, tubulointerstitial, chronic-active, multifocal, moderate.
Conference Note: Malarial parasites of animals belong to the genera Plasmodium, Hepatocystis, Hemoproteus and Leucocytozoon; the genus Plasmodium is the cause of malaria in man, and also parasitizes a number of non-human primates, rodents, birds (most often canaries, cockatoos, pigeons and penguins) and reptiles. The 4 species of Plasmodium that infect man are P. falciparum (highest morbidity and mortality), P. vivax, P. ovale and P. malariae. The main species in rats and mice are P. berghei and P. vinckei. The rodent species are endemic in South Africa, and have been extensively studied as animal models. Malaria occurs in all major families of lizards and occasionally in snakes, but not in crocodiles, turtles or tuataras.
Mammalian malarias of the genus Plasmodium are transmitted by mosquito hosts of various species of Anopheles. Avian malarial parasites are mainly transmitted by mosquitoes of the genera Aedes and Culex. The owl monkey is not a natural host of any of the plasmodia, but is of great research interest because it can be experimentally infected with the three human malarial parasites, and most importantly, P. falciparum. The common glomerulonephritis and interstitial nephritis of owl monkeys complicates its use in studies of Plasmodium-associated renal disease.

Contributor: Emory University, Division of Animal Resources, G70 Rollins Research Center, 1510 Clifton Road, Atlanta, GA. 30322
1. Aikawa M, Broderson JR, Igarashi I, Jacobs G, Pappaioanou M, Collins WE, Campbell CC: Atlas of renal disease in Aotus monkeys with experimental plasmodial infec-tion, pp. 1, 10-11, 86-89. American Institute of Biological Sciences, 1988
2. Benirschke, Garner & Jones: Pathology of Laboratory Animals, Vols 1 & 2, pp. 1001-1008, 1610-1613. Springer-Verlag. 1978
3. Cotran RS, Kumar V, Collins T: Pathologic Basis of Disease, 6th ed., pp. 943-968. Saunders, Philadelphia, PA. 1999
4. Michael AF: The glomerular mesangium. Kid. Int., 7:141-154, 1980
5. Nagatake N: Renal pathology in Owl monkeys vaccinated with Plasmodium falciparum asexual blood-stage synthetic peptide antigens. Am. J. Trop. Med. Hug., 47(5):614-20, 1992
6. Samuelson J: Infectious Diseases. In: Pathologic Basis of Disease, eds. Cotran RS, Kumar V, Collins T, 6th ed., pp. 389-390. Saunders, Philadelphia, PA, 1999
J Scot Estep, DVM
Captain, VC, USA
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
* The American Veterinary Medical Association and the American College of Veterinary Pathologists are co-sponsors of the Registry of Veterinary Pathology. The C.L. Davis Foundation also provides substantial support for the Registry.
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