Results
AFIP Wednesday Slide Conference - No. 3
22 September 1999

Conference Moderator:
LTC Mark Mense
Diplomate, ACVP
Walter Reed Army Institute of Research
Division of Pathology
Washington, D.C. 20307-5100

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Case I - ND2 (AFIP2676133)

 

Signalment: Three 10 to 14-day-old budgerigar ( Melopsittacus undulatus) carcasses, gender unknown, were submitted to the North Dakota State University Veterinary Diagnostic Laboratory.

 

History: A budgerigar breeder began to experience losses in the adult population with subsequent spread to the newly hatched birds. New adults had recently been introduced to the aviary. Diet included oat groats soaked in water, commercial seed and water with a soluble vitamin added. Affected birds were treated with broad-spectrum antibiotics and acyclovir.

 

Gross Pathology: No significant gross abnormalities were observed.

 

Laboratory Results: Culture of small intestine and lung yielded Enterococcus fecalis and Enterobacter amnigenus. In situ hybridization tests performed on liver, kidney and heart were positive for avian polyomavirus.

 

Contributor's Diagnosis and Comments: Heart, myocardial hemorrhage, coalescing, acute, severe with multifocal cardiac myocyte degeneration and necrosis, and basophilic intranuclear inclusion bodies due to avian polyomavirus.

 

Avian polyomavirus (APV) is a member of the Papovaviridae that causes a variety of microscopic lesions in a number of different genera of psittacines and finches. Reported lesions include myocardial and hepatic necrosis, splenic lymphoid atrophy, nephritis, ballooning degeneration and acanthosis of the follicular epithelium, bone marrow necrosis, and cerebral vasculitis. Affected cells frequently contain characteristic, large, basophilic to amphophilic intranuclear inclusion bodies. Death is typically acute and can involve high numbers of birds; however, recovered individuals are thought to become carriers. The virus resides in a latent state until activated by periods of stress. The virus has a worldwide distribution, and asymptomatic intermittently shedding adults maintain it in avian populations. Molecular techniques such as PCR, DNA probes, and in situ hybridization are available and provide a rapid, sensitive, specific and economical means of providing diagnosis.

AFIP Diagnosis: Heart: Cardiomyocyte degeneration and necrosis, multifocal, moderate, with hemorrhage, karyomegaly, and amphophilic intranuclear inclusion bodies, budgerigar (Melopsittacus undulatus), avian.

Conference Note: Avian polyomavirus, also known as budgerigar fledging disease virus, is a 40-50nm diameter, non-enveloped, double stranded, DNA virus that is a member of the family Papovaviradae. The virus can be transmitted vertically and horizontally. Viral shedding occurs via secretions of the cloaca, skin, crop, respiratory tract and urinary tract. Recovered birds can shed virus intermittently, especially during periods of stress. Some birds have been known to shed virus even in the presence of high serum antibody titers. Embryos infected prior to the development of immunocompetence may develop severe, fatal disease or a tolerant carrier state.

 

Clinical signs generally depend on the age and condition of the bird but can include: sudden death in chicks less than 10 days of age, reduced formation of down and contour feathers, abdominal distention, subcutaneous hemorrhage, tremor of the head and neck, ataxia and bleeding from feather follicles. Infection has also been associated with decreased hatchability and embryonic death.

 

The most sensitive and specific method of diagnosis is identification of DNA sequences by polymerase chain reaction (PCR) testing and/or in situ hybridization. In the live bird, PCR can be performed on material collected from the cloaca. With necropsy specimens, liver and spleen are good tissues to test for viral DNA sequences.

The differential diagnosis for cardiomyocyte degeneration and necrosis in the budgerigar considered at the conference included hypovitaminosis E, aflatoxicosis, lead intoxication and infection with Chlamydia psittaci, avian polyomavirus, reovirus, adenovirus, herpesvirus or psittacine beak and feather disease virus. The presence of the large amphophilic intranuclear inclusions and karyomegalic cells is characteristic of polyomaviral infection, but similar inclusions may be seen in adenoviral infection. Specific tests, such as PCR with DNA probes, are needed for definitive diagnosis.

Contributor: North Dakota State University, Veterinary Diagnostic Laboratory, Fargo, ND

 

References:
1. Garcia AP, Latimer KS, Niagro FD, et al: Diagnosis of polyomavirus-induced hepatic necrosis in psittacine birds using DNA probes. J Vet Diag Invest. 6:308-314, 1994

2. Phalen DN, Wilson VG, Graham DL: Organ distribution of avian polyomavirus DNA and virus-neutralizing antibody titers in healthy adult budgerigars. Am J Vet Res. 54:2040-2047 1993

3. Ritchie BW, Harrison GJ, Harrison LR: Disease etiologies. In: Avian Medicine Principles and Application. pp. 888-892, Wingers Publishing Inc., Lake Worth Florida, 1994

4. Ritchie BW, Niagro FD, Latimer KS, et al: Avian polyomavirus: An overview. JAAV. 5:147-153 1991

5. Ritchie BW, Niagro FD, Latimer KS, et al: Polyomavirus infections in adult psittacine birds. JAAV. 5:202-206, 1991

 

 

Case II - 99-1141 (AFIP 2679497)

 

Signalment: A three-day-old, female, Quarterhorse foal.

History: The foal was presented for abdominal distension and umbilical edema. On physical exam, the foal had a capillary refill time >3 seconds, was 8-10% dehydrated, and had abdominal distension and umbilical edema. The foal was observed to urinate normally. Abdominal radiographs showed a fluid density within the peritoneal cavity and abdominal ultrasound showed a urine filled bladder and free fluid within the peritoneal cavity. Two liters of a turbid serosanguineous fluid was removed from the peritoneal cavity. The foal died acutely.

Gross Pathology: A 20 cm in diameter, firm, irregular mass was present in the peritoneal cavity associated with the left liver lobe. The ventral aspect of the mass had an area of capsular rupture with associated blood clots and necrotic neoplastic tissue. On cut surface, the mass was mottled tan/red and friable. Other findings included:

-Four liters of a red, watery, opaque fluid with multiple blood clots present on peritoneal surfaces (hemoabdomen).
-Icterus.
-Umbilical edema.
-Acute pulmonary congestion and edema (agonal).

 

Laboratory Results: The foal had a PCV of 15%, hypochloremia, hyponatremia and azotemia (BUN=64, Cr=6.8).

The peritoneal fluid had a PCV of 7%, TP of 3.0 mg/dl, BUN of 62 and a Cr of 7.4.

 

Contributor's Diagnosis and Comments: Liver, Hepatoblastoma with hemorrhage and central necrosis.

 

The hepatic mass consisted of two populations of cells arranged in either tubules or trabeculae and pseudo-rosette formations. The cell population within the well-developed tubular structures was tall cuboidal with abundant eosinophilic cytoplasm, apical brush borders, basilar vesicular nuclei with stippled chromatin and occasional mitotic figures (< 1 per 20x field). This population of cells was interpreted to have undergone ductal differentiation. The second population of cells, which is more frequent, is arranged in trabecular to pseudo-rosette structures. The cells are cuboidal with lightly eosinophilic abundant cytoplasm with vesicular nuclei, stippled chromatin and multiple nucleoli. Mitotic figures are rare (1 per 20 field). The trabecular structures are separated by a fine fibrous stroma. These cells are interpreted as "fetal hepatic cells". There are multifocal areas of hemorrhage and central necrosis within the mass. The neoplastic cell populations were variably positive for cytokeratin (AE1/3) and neuron-specific enolase (NSE) immunohistochemically. PAS staining with and without diastase treatment revealed varying degrees of glycogen accumulation within the neoplastic cells. There was no evidence of neuroendocrine granules in either cell population by histochemistry (Churukian-Schenk stain) or by electron microscopy.

Hepatoblastoma is a rare neoplasm in all species and has been reported in young and adult sheep, mice, pigs, cattle and horses. In humans, the neoplasm occurs usually within the first 2-3 years of life. In general, hepatic neoplasia in the equine is quite rare. Hepatoblastoma in the equine has been reported twice previously in the literature (a 3-year-old Appaloosa gelding and a male Thoroughbred fetus). The current theory of hepatoblastoma histogenesis states that the neoplasm is derived from a hepatic pluripotential stem cell. The stem cells can then undergo differentiation to primarily embryonal hepatic cell types or occasionally to cartilage, muscle, bone or neural tissue. Embryonal hepatic cell types are described as polygonal cells with scanty basophilic cytoplasm, large nuclei, a single prominent nucleolus, clumped chromatin and numerous mitotic figures. These embryonal hepatic cells can then undergo differentiation to fetal hepatic cell types or ductal and/or squamous differentiation. Fetal hepatic cell types are described as appearing similar to hepatocytes, but smaller with eosinophilic and lightly granular cytoplasm, small oval nuclei, 1 to 2 small nucleoli and fine granular chromatin which are arranged in trabecular structures. Ductal differentiation of embryonal hepatic cells results in small duct formation, reminiscent of bile ducts.

 

AFIP Diagnosis: Liver: Hepatoblastoma, Quarterhorse, equine.

 

Conference Note: Conference participants and the Department of Hepatic Pathology of the Armed Forces Institute of Pathology concurred with the contributor's diagnosis of hepatoblastoma based on the histomorphologic characteristics. In addition, immunohistochemistry performed at the AFIP demonstrated that neoplastic cells are multifocally positive for human hepatocyte antigen indicating variable hepatic differentiation within the tumor. The differential diagnosis discussed in conference included hepatoblastoma, cholangiocellular carcinoma and metastatic carcinoma. In humans, prognosis is based on the stage of disease. In the two reported equine cases, thoracic metastasis was present. In mice, N-nitrosodiethylamine has been shown to induce hepatoblastomas.

 

Contributor: Department of Veterinary Biosciences, The Ohio State University, 1925 Coffey Road, Columbus, OH 43210

 

References:
1. Craig JR, Peters RL and Edmondson HA: Atlas of Tumor Pathology, Tumors of the Liver and Intrahepatic Bile Ducts, Fascicle 26; AFIP Washington D.C.: pp.190-7, 1988

2. Neu SM: Hepatoblastoma in an equine fetus. J Vet Diagn Invest 5:634-637, 1993

3. Nonoyama T et al: Mouse hepatoblastomas: a histologic, ultrastructural, and immunohistochemical study. Vet Pathol 25: 286-296, 1988

4. Nonoyama T et al: Hepatoblastoma with squamous differentiation in a B6C3F1 mouse. Vet Pathol 23: 619-622, 1986

5. Prater PE, Patton CS, Held JP; Pleural effusion resulting from malignant hepatoblastoma in a horse. JAVMA 194(3): 383-385, 1989

6. Shida T, Yamada T and Nomura Y: Hepatoblastoma in a dog. J Vet Med Sci 59(12): 1167-1170, 1997

7. Shiga A, Shirota K, 2. Haas JE et al: Histopathology and prognosis in childhood hepatoblastoma and hepatocarcinoma. Cancer 64: 1082-1095, 1989

 

 

Case III - 96-2667 (AFIP 2683734)

 

Signalment: Porcine, Yorkshire X Landrace

 

History: 7 live pigs, 5-10 weeks of age, males and females included.

Herd is porcine reproductive and respiratory syndrome (PRRS) negative. Many other animals showing similar clinical signs in herd. Early post-weaning period some of the piglets show poor growth relative to herdmates. Develop pallor and heavy breathing. Eventually pigs become icteric, emaciated and many die.

 

Gross Pathology: Pigs in this submission showed a wide range of lesions. All pigs were in poor body condition. Most lymph nodes were enlarged, and lungs did not collapse. Multifocal areas of lungs, especially cranioventrally, were mottled or red and firm. Thymus of many pigs was small or could not be identified. Kidneys were moderately to markedly enlarged. In one pig, the kidneys were estimated to be approximately 15 times normal size. Kidneys were soft, pale gray and appeared waxy. One pig showed thinning of the wall of the small intestine, edema of the mesentery, and the lumen contained a watery material.

 

Laboratory Results: Positive for porcine circovirus by immunohistochemistry.

 

Contributor's Diagnoses and Comments:

1. Lymph node, follicular hyperplasia with histiocytosis and eosinophil infiltration.

2. Lymph node, lymphocytolysis, moderate.

In many of the histologic sections, syncytial cells containing amphophilic and occasionally basophilic intracytoplasmic inclusion bodies can be seen in the cortex of the lymph node. The inclusion bodies are most frequently noted in B-cell follicles (also see kodachrome). Follicles are dominated by large lymphoblasts with a decrease in the number of small lymphocytes found. Other lesions in this group of pigs were: Lymphohistiocytic interstitial nephritis, granulomatous lymphadenitis, interstitial pneumonia (often granulomatous) with lymphoid hyperplasia, single cell necrosis in the exocrine pancreas, and lymphohistiocytic infiltrates within the stomach wall.

Immunohistochemistry positively identified porcine circovirus type 2 in these tissues.

Porcine circovirus was first described as a contaminant in PK-15 cell lines. Antibodies to this virus are widespread in the pig industry, and it has only been recently that this virus has been implicated as a cause of significant disease. Postweaning multisystemic wasting syndrome (PMWS) affects weaned pigs and is a progressive disease with vague clinical signs including poor hair coat, weight loss, jaundice, and dyspnea. Post mortem lesions are characteristic for this disease and include generalized lymphadenopathy and interstitial pneumonia. Histology of this disease is variable with the stage. Early in the disease course, there is hyperplasia of lymphoid tissue. As the disease progresses, infiltration of lymphoid tissues with histiocytic cells, and gradual loss of mature lymphocytes is seen. Syncytial cells are occasionally seen within lymphoid tissues. Lymphohistiocytic infiltrates are seen in multiple organs, including kidney, liver, lung, heart, and intestine. Basophilic intracytoplasmic inclusion bodies characteristic of circovirus are seen in many cases of PMWS. These are found in histiocytic cells most frequently in B-cell follicles.

Porcine circovirus-associated disease is occasionally found in conjunction with PRRS virus infection, and lesions produced by these two viruses may be similar, particularly in the lungs. Lymph node lesions seen in cases of PRRS tend to be more proliferative and lack histiocytic infiltration. Lesions similar to naturally occurring cases of PMWS have recently been reproduced by infection of gnotobiotic pigs, and provide strong evidence that Porcine circovirus is the cause of PMWS.

 

AFIP Diagnosis: Lymph node: Lymphadenitis, granulomatous, diffuse, moderate, with mild lymphoid hyperplasia and rare intrahistiocytic polymorphous eosinophilic to amphophilic cytoplasmic inclusion bodies, Yorkshire/Landrace cross, porcine.

 

Conference Note: PMWS is an important emerging disease in North America and Europe, consistently infecting pigs around 42 days of age. The disease is believed to be multifactorial. Porcine circovirus (PCV) is a consistent factor in the development of clinical disease; however, recent evidence suggests that porcine parvovirus may also play a role. PCV is a non- enveloped, 15-24nm diameter, single stranded, DNA virus of the family Circoviridae, that replicates within the cytoplasm of the cell. Circoviruses are the smallest viruses that infect vertebrates. Other member of this family are chicken anemia virus, beak and feather disease of psittacine birds and numerous viruses that infect plants. There is little DNA homology among the three viruses that infect vertebrates.

 

Clinical signs: Wasting, dyspnea, enlarged lymph nodes, diarrhea (profuse watery), pallor, and jaundice. Although jaundice is a sporadic clinical sign, its presence is useful in differentiating PMWS from PRRS.

 

Gross lesions: Lesions vary somewhat based on the stage of the disease, but commonly include: Lymph node enlargement (particularly inguinal, mesenteric, bronchial, and mediastinal), pallor or icterus of skin and mucous membranes, noncollapsing to atelectatic lungs, diffuse atrophy and mottling of liver, gastric ulceration, thin-walled edematous intestines, and occasionally enlarged edematous kidneys.

 

Histologic signs: The presence of polymorphous, botryoid, basophilic intracytoplasmic inclusions within histiocytes (occasionally multinucleate) that completely replace the B-cell region of lymph node follicles is considered a unique feature of this disease. Other lesions include: interstitial pneumonia; lymphohistiocytic periportal hepatitis with hepatocyte degeneration; edema and lymphohistiocytic, lymphoblastic peripelvic nephritis; lymphoid depletion of spleen with replacement by histiocytes; lymphohistiocytic gastroenteritis; and lymphohistiocytic pancreatitis.

Contributor: Department of Veterinary Pathology, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, SK, S7N 5B4 Canada

 

References:
1. Allan GM, Kennedy S, McNeilly F, et al: Experimental reproduction of severe wasting disease by co-infection of pigs with porcine circovirus and porcine parvovirus. J Comp Path 121:1-11, 1999

2. Ellis J, Krakowka S, LairmoreM, Haines D, et al: Reproduction of lesions of postweaning multisystemic wasting syndrome in gnotobiotic piglets. J Vet Diagn Invest 11:3-14, 1999

3. Harding JCS, Clark EG: Recognizing and diagnosing postweaning multisystemic wasting syndrome (PMWS). Swine Health and Production 5(5):201-203, 1997.
4. Harding JCS, Clark EG, Strokappe JH, Willson PI, Ellis JA: Postweaning multisystemic wasting syndrome: epidemiology and clinical presentation. Swine Health and Production 6(6):249-254, 1998

5. Rosell C, Segales J, et al: Pathological, immunohistochemical and in-situ hybridization studies of natural cases of postweaning multisystemic wasting syndrome (PMWS) in pigs. J Comp Path 120: 59-78 1999

 

 

Case IV - 99-2 (AFIP 2680556)

 

Signalment: Adult (1-2 years/age), wild-type zebrafish (Brachydanio rerio)

 

History: The fish was from a facility that contains about 3,000 - 5,000 zebrafish housed in three independent, recirculating freshwater systems. There was no previous history of clinically observable infectious disease within the facility. A relatively closed colony management system was in place with only bleached embryos admitted into the facility.

Peracute gas-bubble disease (GBD) due to mechanical failure was diagnosed three months earlier, which resulted in approximately 40% mortality of the fish within one life support system. Multiple fish (survivors of GBD incident) began spontaneously developing variably-sized ulcerative skin lesions along the flank caudal to the opercula. Affected fish became progressively lethargic and emaciated. There were no clinical signs among the fish in the other two recirculating water systems. The following water quality parameters were routinely measured and found to be within normal limits: pH, temperature, ammonia, nitrite, nitrate, and conductivity.

 

Gross Pathology: Several fish demonstrated variably-sized, spherical, ulcerative skin lesions along the flank caudal to the opercula. Skin lesions ranged from superficial erosions to deep ulcers. Affected fish also demonstrated pin-point hemorrhages at the base of the fins and around the anal pore.

 

Laboratory Results: Culture of liver, kidney, and spleen from multiple fish on LJ (Lowenstein-Jensen) and 7H11 media were positive for Mycobacterium spp. Cultures exhibited growth on the selective media between 10 - 21 days.

 

Contributor's Diagnoses and Comments:

1. Oophoritis and peritonitis, severe, chronic, granulomatous with caseous necrosis, egg necrosis, and intralesional acid-fast bacilli, etiology: Mycobacterium.

2. Skeletal muscle necrosis and mineralization, mild-moderate, multifocal.

Microscopic lesions in the zebrafish (Brachydanio rerio) consisted of multifocal granulomatous oophoritis with necrosis and areas of peritonitis. The ovary had variably-sized (approximately 0.1 to 1 mm-diameter) well-delimited granulomas as well as poorly organized infiltrates of macrophages. Granulomas consisted of closely spaced collections of macrophages, including numerous epithelioid and foamy macrophages, and peripheral circumferential bands of fibrosis. Many granulomas had necrotic centers with coagulated anucleate or karyopyknotic cells, amorphous granular debris, and, in large granulomas, remnants of collapsed egg walls admixed with hypereosinophilic coagulum. Occasionally, extracellular brown pigment accumulation and mineralization were also evident in necrotic areas. Ziehl-Neelson staining demonstrated numerous, intracellular and extracellular acid fast bacilli within most granulomas. However, some granulomas lacked both acid fast bacilli and areas of central necrosis, and others had central necrosis with no discernible bacteria. Also present were unorganized infiltrates of large, epithelioid macrophages in the ovary between or within necrotic eggs. Multinucleate giant cells were infrequent. Similar granulomatous inflammation was present within the peritoneal connective tissue around portions of the intestine. Sporadic skeletal muscle necrosis and mineralization were also seen.

 

Atypical mycobacterial infections of fish are most commonly associated with Mycobacterium marinum, M. fortuitum, or M. chelonae. Due to its long incubation period and chronic, subclinical form, this insidious disease can remain undetected within established facilities for extended periods of time. Mycobacterial infections of fish have been identified worldwide in over 150 species of salt and fresh water fish. (Talaat et al, 1997). Once established, Mycobacterium spp. can become a resident of the microbial flora within the water system.

 

The clinical signs of mycobacteriosis in zebrafish can be highly variable since both acute and chronic forms of infection have been characterized (Talaat et al, 1998). Chronically diseased animals usually manifest by having a poor growth rate, chronic wasting, and emaciation. There is usually an associated decrease in reproductive rates and a slightly increased mortality rate within the affected colony. Acutely diseased animals often demonstrate the generalized clinical condition known as "dropsy syndrome" which consists of abdominal distention, and scale edema. This edema results in a lifting or "porcupine-like" effect to the scales. Petechiation or ulceration of scales and fin erosion are often evident.

 

Preliminary diagnosis of mycobacteriosis is based on the identification of clinical signs consistent with the disease. Histologic examination of affected kidney, liver, and splenic tissue often yields acid-fast positive staining, rod shaped bacteria in affected tissues. The atypical aquatic Mycobacterium species may display staining characteristics similar to gram-positive bacteria. However, definitive confirmation of Mycobacterium infection is currently made only by culture of the organisms on LJ (Lowenstein-Jensen) and 7H11 media and subsequent biochemical analysis. Atypical Mycobacterium spp. are extremely slow growing organisms in culture and may require 30-60 days for definitive culture results to be obtained. Frequently, acid fast bacteria may not be readily identified histologically in affected tissues but yield positive culture results when tested.

 

Unfortunately, effective treatment of infected facilities can only be accomplished by eradication of infected stocks and subsequent disinfection of all substrates within the facility. Various attempts at treatment with a number of antibiotics have had limited success in controlling the infection but not eliminating it. Since various Mycobacterium species have been isolated from the environmental biofilms which form within water systems (Schultze-Röbbecke et al, 1992), disinfection of the tank and filter system is necessary. Prior to sanitation of the water system, all associated filter material and disposable equipment should be discarded. Disinfection of the water system and surfaces should be conducted with a bleach solution. The outer surfaces of all tanks and related hardware should be treated with the same bleach solution. Restock the system and culture fish after several months to monitor for re-infection of the system. It is important to realize that once an infection has occurred within a facility, it is very difficult to completely sanitize effectively.

 

Atypical cutaneous mycobacterial infections of humans have been well documented. Known as "fish handler's granuloma" or "swimmer's granuloma," these infections are usually self-limiting and result only in a localized area of erythema and swelling on the affected extremity. However, more serious clinical disease such as persistent cutaneous granulomas, osteomyelitis, and tenosynovitis have been reported (Chang et al., 1999; Gatt, 1998; Murry, 1998; Shih et al., 1997) as a result of trauma with infected surfaces or concurrent immunosuppression... Life-threatening and fatal disease due to M. marinum and M. fortuitum have also been documented (Lessing et al., 1993). Zoonotic transmission of M. marinum and M. fortuitum to fish handlers or persons in close contact with infected fish or aquaria has been documented. Frequently, resolution of these persistent infections involves lengthy systemic antibiotic treatment regimes (Hoyen et al., 1998; Levendoglu-Tugal et al., 1998). All laboratory personnel in contact with the fish or associated hardware should be aware of the potential health risk. Precautionary measures, such as the wearing of latex gloves, should be implemented when treating outbreaks.

Case 3-4.Gross

AFB stain, 40x obj.

Case 3-4.

 

AFIP Diagnosis: Celom and ovary: Inflammation, granulomatous, diffuse, moderate, with multiple granulomas, rupture of oocytes and multiple colonies of bacilli, wild-type zebrafish (Brachydanio rerio), pieces.

 

Conference Note: Differential diagnosis discussed for this case included infection by mycobacteria and nocardia. Culture or other specific techniques are needed for definitive diagnosis.

 

Contributor: Massachusetts Institute of Technology , 77 Massachusetts Avenue, Cambridge, MA. 02139

References:
1. Chang WJ, Tse DT, Rosa RH Jr., Miller D: Periocular atypical mycobacterial infections. Ophthalmology. 106:86-90, 1999

2. Conroy G, Conroy D: Acid-fast bacterial infection and its control in guppies (Lesbistes reticulatus) reared on an ornamental fish farm in Venezuela. Vet Rec. 13:177-178, 1999

3. Gatt R, Cushieri P, Scibberras C: An unusual case of flexor sheath tenosynovitis. J Hand Surg. 23:689-690, 1998

4. Hoyen HA, Lacey SH, Graham TJ: Atypical hand infections. Hand Clin. 4:613-634, 1998

5. Lessing MP, Walker DD: Fatal pulmonary infection due to Mycobacterium fortuitum. J Clin Pathol. 46:271, 1993

6. Levendoglu-Tugal O, Munoz J, Brudnicki A, Fevzi Ozkaynak M, Sandoval C, Jayabose S: Infections due to nontuberculous mycobacteria in children with leukemia. Clin Infect Dis. 27:1227-1230, 1998

7. Murry PM: Septic arthritis of the hand and wrist. Hand Clin. 4:579-587, 1998

8. Schulze-Robbecke R, Janning B, Fischeder R: Occurrence of mycobacteria in biofilm samples. Tuber Lung Dis. 73:141-144,1992

9. Stoskopf M: Fish Medicine. W.B. Saunders. Philadelphia, PA. 1993

10. Shih JY, Hsueh PR, Chang YL, Chen MT, Yang PC, Luh KT: Osteomyelitis and tenosynovitis due to Mycobacterium marinum in a fish dealer. J Formos Med Assoc. 96:913-916, 1997

11. Talaat AM, Reimschuessel R, Wasserman SS, Trucksis M: Goldfish, Carassius auratus, a novel animal model for the study of Mycobacterium marinum pathogenesis. Infection and Immunity. 66:2938-2942, 1998

12. Talaat AM, Reimschuessel R, Trucksis M: Identification of mycobacteria infecting fish to the species level using polymerase chain reaction and restriction enzyme analysis. Vet Microbiol. 58:229-237, 1997

 

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
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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