Results
AFIP Wednesday Slide Conference - No. 22
1 March 2000

Conference Moderator:
LTC Mark Martinez, Diplomate, ACVP
Pathology Division
U.S. Army Medical Research Institute of Infectious Disease
Ft. Detrick, Frederick, MD 21702-5011
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Case I - 1023-97 (AFIP 2593958 )
 
Signalment: Tissue from two adult female NCI Syrian hamsters.
 
History: One hamster was found recently dead while one in another cage was hunched and trembling prior to euthanasia. The second hamster had perineal fecal staining.
 
Gross Pathology: (For one of the animals) Body weight 117.8 grams. The amount of body fat is considered normal. Minimal postmortem autolysis is present. The glandular stomach and proximal duodenum are diffusely reddened. Moderate numbers of ecchymoses are present on the cecum, which is filled with green watery content. The colon contains a small amount of viscous liquid content.
 
Laboratory Results:
Cultures of cecal content resulted in 2+ growth of E. coli and failure to recover Citrobacter, Enterobacter, Klebsiella, Morganella, Proteus, Providencia, Pseudomonas or Salmonella from one animal. 1+ E. coli and Enterobacter were recovered from the other. Anaerobic cultures were not available. Campylobacter plates were negative.
 
ELISA tests for Sendai virus, PVM, reovirus 3, LCM, Encephalitozoon cuniculi, Tyzzer's bacillus and SV5 were negative. Clostridium difficile toxin A antigen capture ELISA was strongly positive for cecal contents of both hamsters.
 
Contributor's Diagnosis and Comments: Widespread, severe erosive enterocolitis, etiology Clostridium difficile.

This case was unusual in that there was no previous administration of antimicrobial drugs. This factor was important to the occurrence of the disease in rodents given clindamycin and other antibiotics. Clostridium difficile is also a common nosocomial infection in human beings, and has been reported in pigs, horses and dogs. Disease is thought to be the result of toxin production by the organism, and isolates that do not produce toxins are not pathogenic. Toxin A causes fluid secretion and enterocyte damage when injected into rodent intestine, while toxin B is not enterotoxic to animals, but cytocidal in cell culture. Isolation of the organism is time-consuming and sometimes inconsistent, so that antigen-capture ELISA to detect toxins in gut contents is the most often used method of confirming the diagnosis.
 
AFIP Diagnoses:
1. Ileocecal junction: Enterocolitis, erosive, subacute, diffuse, moderate, with crypt hyperplasia, submucosal edema, and numerous luminal bacilli, Syrian hamster, rodent.
2. Lymph node, mesenteric: Lymphadenitis, subacute, diffuse, moderate.

Conference Note: Clostridium difficile is a gram-positive anaerobic bacillus, that produces its pathogenic effects through two exotoxins, A (enterotoxin and proinflammatory agent) and B (cytotoxin). Toxins bind to receptors on gut epithelial cells resulting in inactivation of RhO cytoplasmic proteins, leading to disaggregation of actin microfilaments and cell retraction. Very young animals lack the epithelial receptors, and are thus tolerant of very high levels of toxin. Clostridium difficile has been associated with numerous disease syndromes in numerous species: Antibiotic associated pseudomembranous colitis in numerous species, colitis X and acute necrohemorrhagic enteritis in horses, ulcerative colitis in dogs, and toxic megacolon and colonic perforation in humans.
 
The differential diagnosis discussed in conference also included Campylobacter sp., Salmonella sp., E. coli, and Bacillus piliformis. Gram stains performed at the AFIP demonstrate numerous, monomorphic, Gram-positive bacilli.
 
Contributor: Department of Veterinary Pathobiology, University of Missouri, PO Box 6023, Columbia MO
 
References:
1. Barlett JG: Clostridium difficile: History of its role as an enteric pathogen and the current state of knowledge about the organism. Clin Inf Dis 18:S265-S272, 1994
2. Brazier JS: Role of the laboratory in investigations of Clostridium difficile diarrhea. Clin Inf Dis 16:S228-S233, 1993
3. Crawford JM: The gastrointestinal tract. In: Pathologic Basis of Disease, eds. Cotran RS, Kumar V, Collins T, pp. 809-810. WB Saunders, Philadelphia, PA, 1999
4. Kelly CP, Pothoulakis C, LaMont JT: Clostridium difficile colitis. New Eng J. Med 330:257-262, 1994
5. Knoop FC, Owens M, Crocker IC: Clostridium difficile: clinical disease and diagnosis. Clin Microb Rev 6:251-265, 1993
6. Liesenfeld O, Saeger F, Hahn H: Detection of Clostridium difficile by enzyme immunoassay, tissue culture test and culture. Infec 22:29-32, 1994
7. Lusk RH, Fekety R, Silva J, Browne RA, Ringler DH, Abrams GD. Clindamycin-induced enterocolitis in hamsters. J. Infectious Diseases 137:464-475, 1978
8. Wilson KH. The microecology of Clostridium difficile. Clin Inf Dis 16:S214-S218, 1993
 
 
Case II - 94263#10 ( AFIP 2694778)
 
Signalment: 16-year-old, female, cynomolgus macaque (Macaca fascicularis)
 
History: This monkey was imported from Indonesia on 7/15/94. During the animal's quarantine period, it was noted to have a draining cutaneous lesion on the cranial abdomen. Abdominal palpation revealed firm, large masses subjacent to the draining lesion. Euthanasia was elected approximately 6 weeks after importation and a complete necropsy was performed.
 
Gross Pathology: Presented for necropsy was a 3.8 kg, adult female monkey in good body condition with minimal post mortem autolysis. There was a 0.6 cm focus of dried yellow material 3 cm caudal to the sternum on the left cranial abdomen.

The capsular surface of the spleen was covered by a large (6 X 5 X 2.7 cm) abscess which was adherent to the left abdominal wall and communicated with the cutaneous draining lesion. On section, the white fibrous capsule of the abscess was up to 2 mm thick and the abscess contained numerous small 2 mm round to 2 X 1 cm elongate foci of yellow to greenish-yellow (purulent) material. The splenic parenchyma contained many pinpoint (1 mm) to coalescing (7 X 2 mm) abscesses. Lymphoid follicles were prominent in other regions of the spleen.
 
There was a 3 X 3 X 1.3 cm white firm mass on the capsule of the right lateral lobe of the liver, which was adhered to the body wall. The mass had a 2 mm thick fibrous capsule and contained purulent material similar to that seen in the splenic abscess. In the hepatic parenchyma subjacent to the abscess, there was an irregular pale focus (2.5 X 2.0 X 4.0 cm) containing pockets of purulent material. The left lateral lobe had a 2.5 X 2.0 X 1.0 cm abscess mainly involving the capsule of the liver and adherent to the diaphragm. The abdominal surface of the left diaphragm bore 2 raised white firm nodules (2.0 X 1.0 X 1.0 mm). All abdominal lymph nodes were moderately enlarged and bulged on cut surface.
 
Laboratory Results:
Clinical pathology:

 Test

 Value
  
 WBC  16,900  
 Segs  56%  
 Bands  0%  
 Monos  1%  
 Eos  0%  
 Basos  0%  
 Platelets  Normal  
 RBC  4.8  
 Hgb  7.9  
 MCV  61  
 Hct  29%  
 BUN  23 mg/dl  
 TSP  10.2 g/dl  

Moderate anisocytosis & poikilocytosis, slight polychromasia
Microbiology results:
Mycobacterial cultures of the spleen, liver and bone marrow revealed no growth after 48 days of incubation. Routine cultures initially interpreted as Pseudomonas aeruginosa, however, this was later recharacterized as Burkholderia (Pseudomonas) pseudomallei.
 
Virus status: Antibody-negative for SRV-1, SRV-2, SRV-5, SIV and
STLV.
 
Contributor's Diagnoses and Comments:
Gross Diagnoses:
1. Multifocal, chronic, hepatic abscesses with fibrous adhesion
2. Severe, chronic, multifocal to coalescing splenic abscess with cutaneous fistulous tract.
3. Moderate abdominal lymphadenopathy.
 
Histologic Diagnosis (this slide):
Spleen: Severe, multifocal to coalescing, chronic, suppurative splenitis with abscess formation
 
Other Histologic Diagnoses (slides not submitted)
1. Liver: Hepatic capsular abscess with peritoneal adhesion
2. Liver: Severe subacute to chronic cholangiohepatitis with biliary hyperplasia and fibrosis
3. Skin and body wall: Severe chronic suppurative dermatitis and panniculitis with fibrosis (fistulous tract)
4. Lymph nodes (multiple intra-abdominal): Mild to moderate diffuse follicular and paracortical lymphoid hyperplasia.
 
Etiology :
Burkholderia pseudomallei, the causative agent of Melioidosis, formerly known as Pseudomonas pseudomallei.
 
We have seen melioidosis in 7 cynomolgus macaques imported from Indonesia over a 5-year period. Of these animals, most developed hepatic and/or splenic abscesses, some with draining skin lesions. We have seen one case each of epididymitis and meningoencephalitis.
 
This particular animal is one of three from this shipment to have multiple abdominal abscesses (primarily splenic and hepatic). The other two cases cultured out B. pseudomallei, while this one initially cultured P. aeruginosa. Because of the history of the other 2 animals, the culture was questioned. Further analysis revealed Burkholderia pseudomallei.
 
B. pseudomallei is a gram-negative, obligate anaerobe. It is a soil and water saprophyte indigenous to Southeast Asia. Melioidosis may present as septicemia, soft tissue abscesses, pneumonitis, suppurative pneumonia, myocarditis, pericarditis, lymphadenitis, infections of the male urogenital tract, and meningoencephalitis. Many species have been affected by this disease, including man, several species of nonhuman primates, horses, camels, goats, cockatoos, and wallabies. Transmission to laboratory workers has been documented.

AFIP Diagnosis:
1. Spleen and splenic capsule: Abscesses, multiple and coalescing, chronic. cynomolgus macaque (Macaca fascicularis), non-human primate.
2. Splenic capsule and pancreas: Adhesion, chronic, with inflammation, pancreatic parenchymal atrophy, ductular hyperplasia, and regeneration.

Conference Note: Burkholderia pseudomallei (melioidosis) has been referred to as the "remarkable imitator" because of it's long clinical course and extremely variable clinical signs. The organism also has the ability to emerge after remaining latent in wild caught primates for up to 10 years. Recrudescence has been attributed to environmental stress and/or compromise of host defense mechanisms. The broad species range, zoonotic potential and ability to spread insidiously through animal colonies make this disease a significant problem. Frequently, the only way to eradicate B. pseudomallei is through enzyme linked immunosorbent assay testing for antibodies and euthanasia of all positive animals.
 
Although most conference participants favored B. pseudomallei, the following causes of multisystemic abscesses and splenitis were also included in the differential diagnosis: Nocardia, Mycoplasma sp., Corynebacterium pseudotuberculosis, Yersinia sp., Francisella tularensis, Pseudomonas mallei, Listeria monocytogenes, Mycobacterium and fungi.
 
Contributor: Wake Forest University School of Medicine, Department of Pathology, Section on Comparative Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1040.
 
References:
1. Ladds PW, Thomas AD, Pott B. Melioidosis with acute meningoencephalitis in a horse. Aust Vet J 57:306-307, 1978
2. Schlech WF, Turchik JB, Westlake RE, Klein GC, Band JD, Weaver RE: Laboratory-acquired infection with Pseudomonas pseudomallei (Melioidosis). N Eng J Med 305:1133-1135, 1981
3. Thomas AD, Wilson AJ, Aubrey JN: Melioidosis in a sulphur-crested cockatoo (Cacatua galerita). Aust Vet J 54:306-307, 1978
 
 
Case III -970666 (AFIP 2596110)
 
Signalment: Dog, German shepherd, female, 12-years-old
 
History: This dog was presented at consultation with anorexia, discordance, polypnea and weakness. Radiographs of the thorax indicated the presence of a large volume of thoracic fluid. A sample of this fluid was submitted for analysis to our laboratory. An echography was performed and a thoracic mass located cranial to the heart was suspected. After the diagnosis, the dog was euthanatized at the owner's request.
 
Gross Pathology: No complete necropsy was performed, but opening of the pleural cavity showed numerous small nodules distributed on all pleural surfaces within the thorax. Some nodules were transmitted to our laboratory for histologic examination.
 
Laboratory results: The pleural fluid was collected twice. The first time, the thorax was drained of 1.3 liters of pale, yellow, mildly opaque fluid. It had 14440 cells/ cubic mm and 34 g/l of total proteins (estimated by refractometry). The following day, the pleural fluid (only a few milliliters) was serosanguineous and showed 29350 cells/ cubic mm and 29 g/l of total proteins.
 
Thoracic fluid cytology revealed numerous and irregular cellular clusters associated with many inflammatory cells. The clusters were composed of very irregular atypical vacuolated mesothelial cells close together and which resemble carcinoma cells. The cells present distinctive features of malignancy such a marked variation in size, anisokaryosis, coarse chromatin pattern and numerous prominent nucleoli. However, there were few mitotic figures.
 
Cytological examination of the second fluid presented the same aspect associated with a highly hemorrhagic background.
 
Contributor's Diagnosis and Comments: Malignant mesothelioma, pleural cavity, dog.
Light microscopic examination demonstrates within the fibrofatty connective tissue of the pleura a papillary proliferation of mesothelial cells. The papillary structures are supported by fibrovascular stroma covered by one or several layers of cuboidal or columnar neoplastic mesothelial cells. In some areas, there is a sharp transition from normal to neoplastic tissue.

In several regions, nests and cords of tumor cells extend below the surface and form a less organised proliferation, which is associated with a fibrocellular stroma containing isolated spindle-shaped cells or large anaplastic cells.

The neoplastic mesothelial cells have an eosinophilic cytoplasm with distinct borders and often contain vacuoles. Nuclei have multiple prominent nucleoli. There are marked anisokaryosis and anisocytosis. Scattered mitotic figures are present. In all areas, a large number of inflammatory cells are mixed with neoplastic cells.
 
Mesotheliomas are rare tumors arising from the mesothelium lining the pleural, pericardial or peritoneal cavities. Cases of involvement of the tunica vaginalis of the testis have been reported also. In domestic animals, two distribution patterns can be observed: cattle and sheep develop tumors in fetal, newborn and young animals whereas in others species, adult or aged animals are affected. In dogs, the pleura is the main site of development after the pericardium and the peritoneal cavity. The clinical sign associated with pleural mesothelioma is essentially dyspnea caused by accumulation of fluid in the pleural cavity. Collapse of lung lobes can be a consequence of the effusion also. Analysis of the effusion fluid usually shows a milky or bloody color, low protein content, may show free erythrocytes and a moderate number of nucleated cells. These latter cells are sometimes only leukocytes but tumor cells can be found also.
 
On gross examination, tumors are formed either by small nodules, sessile or pedunculated, from a few millimeters to 10 centimeters in diameter or by villous projections arising from the serosal surface. Depending of the amount of hemorrhage, the color varies from gray-white to red. Some fibrous or sclerosing forms have been reported more rarely.
 
Mesotheliomas present three main histological patterns: a form resembling fibrosarcoma with spindle-shape cells, a sclerosing pattern and, the most common, an epithelioid type. In this latter form, cuboidal epithelioid cells cover papillary projections made of spindle-shape cells and conjunctivo-vascular stroma. Sometimes cells can form tubules or rosettes and mitoses are usually not numerous. Sclerosing mesotheliomas are composed of large anaplastic cells with sometimes multinucleated giant cells. On histologic examination, mesotheliomas can be either benign or malignant. The malignant type is more common and frequently leads to local extension into the coelomic cavities. Involvement of local lymph nodes can occur, but hematogenous metastatic dissemination is extremely rare. Concerning the epithelioid pattern differential diagnosis must be made with metastasis from an adenocarcinoma located in another site, mammary gland or ovary for example. Lipomas, liposarcomas and more rare tumors such as ganglioneuromas can also develop from the serous membranes.
 
In humans, an association between malignant mesothelioma and asbestos exposure has been well established. In domestic animals, however, few tumors have been examined for asbestos fibers but there is little evidence for a relationship between asbestos inhalation and mesothelioma. Concerning newborn cattle, a congenital origin has been found for mesotheliomas.
 
AFIP Diagnosis: Malignant mesothelioma, German shepherd dog, canine.
 
Conference Note: Mesotheliomas occur with the greatest frequency in cattle and dogs, but have been reported in most domestic species. In cattle, they occur most often as a congenital neoplasm in fetuses or young calves. Mesothelioma arising from the tunica vaginalis is one of the most common tumors of the male Fischer 344 rat.
 
The tumors may cause the accumulation of large amounts of fluid, resulting in ascites, cardiac insufficiency, cardiac tamponade, or respiratory distress depending upon the location of the tumor. Adhesions are often formed between the affected serosal surface and adjacent organs.
 
Ultrastructurally, neoplastic mesothelial cells have a prominent basal lamina, well-developed microvilli, desmosomes, abundant rough endoplasmic reticulum, and mitochondria.
 
The mucicarmine stain with and without hyaluronidase can help distinguish mesothelioma from adenocarcinoma. The presence of mucicarminophilic, hyaluronidase resistant material within cytoplasmic vacuoles supports adenocarcinoma. By immunohistochemistry, neoplastic cells of mesothelioma are typically positive for both keratin and vimentin. Carcinomas are usually keratin positive and vimentin negative.
 
This neoplasm did not stain with mucicarmine. Immunohistochemically, the neoplastic cells are diffusely positive for keratin and multifocally positive for vimentin. Thus, histomorphology and immunohistochemistry support mesothelioma.
 
Contributor: Ecole Vétérinaire dAlfort, Laboratoire dAnatomie Pathologique, 7, Avenue du Général de Gaulle, 94704 Maisons Alfort - France.
 
References:
1. Barker IK: The peritoneum and retroperitoneum in Pathology of Domestic Animals, vol. 2, eds. Jubb, KVF, Kennedy, PC, Palmer, 4th ed., pp. 31-35. Academic Press, Inc., San Diego, CA, 1993
2. Forbes DC, Matthews BR: Abdominal mesothelioma in a dog. Can Vet J 32:176-177, 1991
3. Foumel C, Magnol JP, Guelfi JF: Color atlas of cancer cytology of the dog and cat, PMCAC Ed, pp.82-83, 1994
4. Harbison ML, Godleski JJ: Malignant mesothelioma in urban dogs. Vet. Path., 20:531-540,1983.
5. Head KW: Tumors of the alimentary tract. In: Moulton JE: Tumors in domestic animals, 3rd ed., pp. 422-427. University of California Press, San Diego, CA, 1990
6. McDonough SP, MacLachlan NJ, Tobias AH: Canine pericardial mesothelioma. Vet Path 29:256-260, 1992
7. Smith DA, Hill FWG: Metastatic malignant mesothelioma in a dog.
J Comp Pathol 100:98-101,1989
 
 
Case IV - G5594-99 (AFIP2715642)
 
Signalment: Adult, male, golden-headed lion tamarin (Leontopithecus chrysomelas)
 
History: This animal was from a group of 11 animals separately housed in a zoo. All animals showed clinical symptoms of conjunctivitis, blepharitis, and ulceration of muco-cutaneous junctions of the lips. Eight animals died, three recovered after severe illness. Antibodies against measles virus and herpes simplex virus (HSV 1,2) were negative in one tested animal. One of the dead animals was submitted to the German Primate Centre for diagnostic purposes.
 
Gross Pathology: The animal showed severe ulcerative stomatitis and inflammation of muco-cutaneous junctions of the lips. Furthermore an erosive to ulcerative conjunctivitis, esophagitis and gastritis were found. Within the liver there were multiple foci of necrosis.
 
Laboratory Results:
Staphylococcus aureus, Streptococcus pneumoniae viridans-group and Streptococcus bovis II D were cultured from the mucous membranes of the eyes and oropharynx.

Contributor's Diagnoses and Comments:
1. Hepatitis, necrotizing, acute to subacute, multifocal, moderate, histiocytic with few lymphocytes and granulocytes with hemorrhage and hepatocytic amphophilic to eosinophilic intranuclear inclusions with and without halo.
2. Glossitis, ulcerative, subacute, multifocal moderate to severe, granulocytic and histiolymphocytic, with ballooning degeneration of epithelial cells, multinucleate giant cells with amphophilic to eosinophilic intranuclear inclusions, focal necrotizing vasculitis in the muscle and superficial bacterial growth.
3. Conjunctivitis/Cheilitis, ulcerative, acute to subacute, focal, moderate, granulocytic and histiolymphocytic, with ballooning degeneration, spongiotic vesicles, multinucleate giant cells, amphophilic to eosinophilic intranuclear inclusions in epithelial cells, focal sebaceous adenitis, mineralization and superficial bacterial growth.
 
Electron microscopy of liver tissue revealed numerous viral particles with nucleocapsid and characteristic symmetry within nuclei of hepatocytes in the periphery of the necrotic foci. The viral particles measured approximately 100 nm in diameter. Occasionally virions, 150 to 200 nm in diameter, obtaining an envelope from the inner membrane of the nucleus could be seen. Histologic and electron microscopic findings are consistent with alphaherpesvirus infection (Herpes simplex or Herpes tamarinus).
 
Erosive to ulcerative stomatitis with multinucleated giant cells containing intranuclear inclusions in connection with necrotizing hepatitis, where inclusion bodies can be seen also, are characteristic for an alphaherpesvirus infection induced by human herpesvirus 1,2 (H. simplex) or saimirine herpesvirus 1 (Herpesvirus tamarinus syn. H. platyrrhinae). Both viruses lead to systemic infection with identical gross and microscopic lesions. Furthermore, they can not be distinguished by electron microscopy.
 
Several species of marmosets and tamarins are susceptible to certain herpesviruses asymptomatically carried by squirrel monkeys, macaques and humans. In the case of H. simplex humans are the natural host or reservoir, and infected people like zoo visitors or technicians can excrete the virus in the absence of visible lesions. H. tamarinus is carried by squirrel monkeys (Saimiri sciureus), in which clinical disease is rarely reported. Because of the detection of neutralizing antibodies, cinnamon ring-tailed monkeys (Cebus albifrons) and spider monkeys (Ateles spp.) are considered to be natural reservoir hosts, too. Infection of marmosets, tamarins, owl monkeys and tree shrews induces sporadic episodes of generalized fatal infection with high morbidity and mortality eg. in zoos.
 
In this case anamnestical investigations showed that the group of golden-headed lion tamarins could have had contact with zoo visitors or transmission of H. tamarinus from other cebids could have occurred via zoo technicians. A retrospective diagnostic differentiation of both viruses can only be carried out by PCR techniques in necropsy material or by antibody analysis of the surviving animals.
 
Case 22-4. Liver (per contributor) TEM. Scattered within the nucleus are multiple, 100nm diameter, viral particles (central nucleoid surrounded by a capsid = [nucleocapsid]). Occasional virions, 150-200nm in diameter, are acquiring an envelope from the inner nuclear membrane.
 
AFIP Diagnoses:
1. Liver: Hepatitis, necrotizing, acute to subacute, subcapsular, multifocal, moderate, with syncytia and eosinophilic intranuclear inclusion bodies, golden headed tamarin (Leontopithecus chrysomelas), nonhuman primate.
2. Lip and eyelid: Inflammation, necrotizing, acute, multifocal, moderate to severe, with ulceration, syncytia and eosinophilic intranuclear inclusion bodies.

Conference Note: A number of alpha-herpesviruses naturally infect nonhuman primates, including Herpes T of squirrel monkeys, H. simiae (B virus) of macaques, SA-8 of African green monkeys and simian varicella. Human alpha-herpesviruses are HSV-1, HSV-2 and H. varicella/H. zoster. Herpes simplex infection in marmosets, tamarins and owl monkeys cannot be differentiated clinically, grossly or histologically from herpesvirus T infection. Specific immunohistochemical staining, virus isolation or specific molecular techniques are necessary for precise identification of the causative virus. When infected with HSV or Herpes T, marmosets, tamarins and owl monkeys may develop a generalized disease, often with encephalitis and death. Accordingly, all macaques should be handled with appropriate caution, species of monkeys should not be mixed, and persons with active HSV infections should be precluded from contact with susceptible nonhuman species.
 
Contributor: German Primate Centre, Department of Veterinary Medicine and Primate Husbandry, Kellnerweg 4, 37077 Göttingen, Germany.
 
References:
1. Bruno SF, Liebhold MM, Mätz-Rensing K, Romao MAP, Didier A, Brandes F, Bressan ACS, Kaup FJ: Herpesvirus-Infektion bei freilebenden Schwarzpinseläffchen (Callithrix penicillata, E. Geoffroyi 1812) im Parque Estadual da Serra Tiririca Niterói, Rio de Janeiro, Brasilien. BMTW 110:427-430, 1997.
2. Hunt RD: Herpes simplex Infection. In: Nonhuman Primates I, eds. Jones TC, Mohr U, Hunt RD, pp. 82-86. Springer-Verlag, Berlin, New York, 1993
3. Hunt RD, Blake BJ: Herpes platyrrhinae Infection. In: Nonhuman Primates I, eds. Jones TC, Mohr U, Hunt RD, pp. 100-103. Springer-Verlag, Berlin, New York, 1993
4. Juan-Sallés C, Ramos-Vara JA, Prats N, Solé-Nicolás J, Segalés J, Marco AJ: Spontaneous herpes simplex virus infection in common marmosets (Callithrix jacchus). J Vet Diagn Invest 9:341-345, 1997
5. Mansfield K, King N: Viral Diseases. In: Nonhuman Primates in Biomedical Research: Diseases, eds. Bennett BT, Abee CR, Hendrickson R, pp. 5-12. Academic Press, San Diego, New York, 1998
 
 
J Scot Estep, DVM
Captain, United States Army
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
Internet: estep@afip.osd.mil
 
* 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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