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CASE I – N99-909 (AFIP 2749408)
Signalment: Young adult, female baboon, Papio species
History: Baboons present clinically with solitary or multiple, raised, firm, often ulcerated skin lesions that tend to be on sparsely haired areas of the body such as the face, hands, feet, and tail areas. The lesions often recur following surgical excision and are refractory to medical therapy.
Gross Pathology: Lesions are usually confined to the skin and dermis but may involve subjacent bone and draining lymph nodes.
Laboratory Results: Generally unremarkable unless there is severe secondary infection of multiple skin lesions. The organisms are often easily found on skin scrapings (Wright stain). If not confident with the scraping, a surgical biopsy of the lesion is required.
Contributor’s Diagnosis and Comment: Haired skin: Dermatitis, granulomatous, multifocal, marked, with numerous intrahistiocytic yeasts, baboon (Papio sp.), primate.
Etiology: Histoplasma capsulatum var. duboisii (African histoplasmosis)
African or large-form histoplasmosis is a chronic granulomatous disease caused by the fungus Histoplasma capsulatum var. duboisii. Natural infection has been reported to occur only in baboons and humans. Human cases of African histoplasmosis have been reported in Africans and African immigrants in Madagascar and Canada. Spontaneous disease in animals is very rare. In 1956, the disease was diagnosed at the Pasteur Institute in Paris in a group of five baboons imported from Kindia, French Guinea. In 1960, two more cases were reported at the London School of Hygiene and Tropical Medicine in baboons imported from Gambia. In 1988, the first reported animal case in the United States was diagnosed in an adult red baboon at the Southwest Foundation for Biomedical Research in San Antonio, Texas. This animal had been imported from Senegal and was in the United States for about 2 years before disease occurred. In 1991, an epizootic of H. capsulatum var. duboisii, involving over 20 cases, was reported at the same Texas facility, occurring in both wild-caught and native-born baboons.
Soil is believed to be the natural reservoir of H. capsulatum var. duboisii, with inhalation, ingestion, and dermal contact as methods of transmission. It is generally believed that inhalation and ingestion of the organism result in a minor primary lesion in the lung or intestinal tract, with subsequent hematogenous spread to the skin, for which H. capsulatum var. duboisii seems to have a predilection. Some of the diseased baboons born in Texas had been housed on concrete without soil contact. In these animals, direct contact with affected baboons through grooming activities appears to be a viable mode of transmission. H. capsulatum var. duboisii appears to have a long incubation period of at least one year before clinical symptoms become apparent.
H. capsulatum var. duboisii infection results in a pyogranulomatous inflammatory reaction in the dermis and subcutaneous tissues with numerous macrophages, multi-nucleate giant cells (both Langhans and foreign-body types), and small aggregates of neutrophils distributed throughout. In cases with ulceration, neutrophils will be more numerous. Within the cytoplasm of giant cells and histiocytes, there are numerous, round to ovoid, pale-staining organisms measuring from 8 to 15 m m in diameter, with thick walls, and single, narrow-based buds. A single, small, round to elongate, basophilic-staining body can often be observed near the center of the yeast. The organisms, which stain well with Gomori’s methenamine silver or Gridley’s fungal stain, are often found in pairs and short chains. Lesions are typically nodular, ulcerated and exudative. Common sites of infection include the face, ears, hands, feet, tail, scrotum and buttocks. Regional lymph nodes that drain the infected areas are often enlarged. Extension of the skin lesions to the subjacent bone, with resultant osteomyelitis, has been observed. Discrete granulomatous lesions have been reported in liver and testis.
The identification of H. capsulatum var. duboisii generally can be made histologically by its unique morphologic appearance and resultant inflammation in tissue. Differential diagnoses for this disease might include several other fungal organisms. Histoplasma capsulatum var. capsulatum differs in that it measures only 2-4 m m in diameter. Cryptococcus neoformans, slightly smaller than H. capsulatum var. duboisii has a single bud, thin cell wall, and generally a wide, clear, unstained capsule that stains positive with mucicarmine stain. Immature or non-endosporulating spherules of Coccidioides immitis can be similar in shape but are often slightly larger (5-25 m m) than H. capsulatum var. duboisii; however, the presence of mature spherules containing endospores would clearly differentiate the two fungi. Blastomyces dermatitidis, which is very similar in size and shape to H. capsulatum var. duboisii, may be differentiated by its broad-based budding and lack of chain formation. Ultrastructurally, Blastomyces dermatitidis has multiple nuclei, whereas H. capsulatum var. duboisii has a single nucleus.
To date, treatment of baboons with antifungal agents has proven to be expensive and generally unsuccessful. Surgical excision of the lesions was effective in eliminating the infection from some baboons.
AFIP Diagnosis: Haired skin: Dermatitis, granulomatous, nodular, multifocal and coalescing, moderate, with ulceration, epidermal hyperplasia, and numerous intrahistiocytic yeasts, baboon (Papio sp.), nonhuman primate.
Conference Comment: Despite the increased incidence of HIV-positive patients in Africa, there does not appear to be a concomitant increase in cases of African histoplasmosis due to H. capsulatum var. duboisii. Only a few cases of disseminated disease are reported each year. In the United States, however, disseminated histoplasmosis due to H. capsulatum var. capsulatum is reported with relative frequency in HIV-positive patients.
Contributor: Air Force Research Laboratory/HEDV, Comparative Pathology, 2509 Kennedy Circle, Brooks AFB, TX, 78235
References: 1. Bennett BT, Abee CR, and Henrickson R: Bacterial and mycotic diseases. In: Nonhuman Primates in Biomedical Research: Diseases, pp. 95-96. Academic Press, New York, NY, 1998
2. Butler TM, Hubbard GB: An epizootic of Histoplasma duboisii (African histoplasmosis) in an American baboon colony. Lab Anim Sci 41(5):407-410, 1991
3. Eichmann A, Schar G: African histoplasmosis in a patient with HIV-2 infection. J Swiss Med 126(18):765-769, 1996
4. Hubbard GB, Migaki G, Butler TM, Warner RA: Diagnostic exercise: cutaneous papules in a baboon. Lab Anim Sci 41:370-371, 1991
5. Migaki G, Hubbard GB, Butler TM: Histoplasma capsulatum var. duboisii infection, baboon. In: Nonhuman Primates II: Monographs on Pathology of Laboratory Animals, ed. Jones TC, Mohr U, Hunt RD, Springer-Verlag, New York, NY 1993
CASE II – UFSM-2 (AFIP 2741036)
Signalment: 2-year-old, mixed breed cow, bovine
History: The owner found the cow in sternal recumbence. It was not seen within the preceding 3 day period. The cow was sent to the Veterinary Teaching Hospital. It looked bright-eyed and alert with head and ears erect. There was moderate drooling, tail paralysis, and ascending skin anesthesia was apparent. Since the cow came from an area where an outbreak of vampire bat-transmitted rabies in cattle was diagnosed in 1998, and since other cattle in the area were affected with similar clinical signs, a tentative clinical diagnosis of rabies was made. The cow was euthanized to confirm the diagnosis, two days after admittance in lateral recumbency. Further investigation revealed that 25 bovine died with similar clinical signs in the area within a month period. One of those necropsied had a similar diagnosis as the cow of this report. Examination of the skin of non-affected cattle in the area showed high incidence of vampire bat inflicted bites.
Gross Pathology: Necropsy findings were absent with the exception of small foci of brown discoloration (hemorrhages) seen in the cut surface of segments of the cervical cord examined after formalin fixation.
Laboratory Results: Fluorescent antibody technique performed on fresh brain and spinal cord showed positivity for rabies antigen.
Contributor’s Diagnosis and Comment: Morphologic diagnosis: Spinal cord, moderate nonsuppurative poliomyelitis, perivascular hemorrhage and intracytoplasmic eosinophilic inclusion bodies in neurons.
Etiologic diagnosis: Viral myelitis
Etiology: Rabies virus
Four blocks of different sites in the spinal cord were sectioned so that the lesions, although present in every section, vary markedly in intensity among sections. Additionally, sections of the brain (not included) showed similar lesions mainly in the medulla, pons, colliculi, thalamus and cerebellum.
Rabies is an acute, bite-transmitted, almost invariably fatal, viral infection of the central nervous system manifested as a nonsuppurative encephalomyelitis with variable neurologic signs in cattle. The causative agent is an enveloped, RNA, highly neurotropic virus belonging to the family Rhabdoviridae, genus Lyssavirus. The disease is of great concern because it is a zoonosis. Estimated losses in cattle due to vampire bat-transmitted rabies worldwide are over 50 million American dollars.
Incubation period in cattle is 10 to 60 days but longer periods have been documented. The clinical course usually lasts 1-2 days, but can be as long as 8-10 days. Signs of rabies in cattle, as in other species, are extremely variable. Early signs are subtle, usually go undetected, and include depression, anorexia and a drop in milk yield. In cattle, the paralytic form of the disease is the common presentation. There is knuckling, ataxia, hypoesthesia, and sinking of the hindquarters, and flaccid tail, followed by paralysis and collapse. Cattle with furious rabies present continuous hoarse bellowing, violent activity and hyperesthesia.
Morphological lesions of rabies in the central nervous system of infected animals are of varying intensity and location. They are generally microscopic, although a few cases of gross lesions with malacia and hemorrhage have been documented. Necropsy findings, such as evidence of injury and self-mutilation, and the presence of alimentary foreign bodies, are pointed out as important clues for the diagnosis. However, in our experience with rabies in cattle, these findings were rarely, if ever, present.
Pathological changes of importance in rabies are microscopic and include nonsuppurative polioencephalomyelitis and ganglioneuritis of the craniospinal ganglia. The severity of these lesions varies greatly and can be minimal in cattle dying from rabies. Neuronal degeneration is usually absent or mild. Reportedly, in 70% to 85% of the cases of rabies infection with the street virus, characteristic intracytoplasmic inclusion bodies (Negri bodies) will be observed, as was the case of the cow of this report. Negri bodies are usually round and 2-8 um in diameter, but can assume elongated forms when located in neuronal processes (axons or dendrites). They may contain internal basophilic stippling and a peripheral halo. Spongiform changes, similar to those found in the transmissible spongiform encephalopathies, were reported in skunks, foxes, sheep, horses, and cattle. However, we did not observe such changes in a large series of brains from rabid cattle.
Rabies virus is usually inoculated through the bite of a rabid animal. Following inoculation, there is replication in muscle cells and the virus passes to axon terminals of motor neurons and to neuromuscular spindles. The virus moves, then, by retrograde axoplasmic flow to the spinal cord or brain stem. From the brain and spinal cord there is centrifugal spread along peripheral nerves to many organs. In salivary glands, the virus replicates in the acinar epithelium and buds into the lumen, being shed in saliva. Insectivorous and fructivorous bat species can transmit rabies. Transmission of rabies by vampire bats to cattle, and less so to other species, is important in South America, including Brazil, where this type of rabies transmission occurs in most regions. In a recent survey performed in our laboratory, 552 out of 6,021 necropsied cattle (9.16%) had a diagnosis of neurological disease. One hundred and fifty one of those 552 cases (27.35%) were diagnosed as rabies.
Rabies diagnosis is carried out by immunofluorescence procedures and by transmission to neonatal mice by intracerebral inoculation. Immunohistochemistry can be used to demonstrate the rabies viral antigen in formalin-fixed brain.
AFIP Diagnosis: Spinal cord: Myelitis, nonsuppurative, multifocal, mild, with perivascular hemorrhage, and neuronal, eosinophilic, intracytoplasmic inclusion (Negri) bodies, cow, mixed breed, bovine.
Conference Comment: Negri bodies are found, with variable frequency, most consistently in cerebellar Purkinje cells in ruminants, and hippocampal neurons in carnivores. Concern over the recent detection of bovine spongiform encephalopathy (BSE) in the United Kingdom and other European countries has resulted in increased surveillance of bovine neurologic cases in the United States to assess local occurrence. Although spongiform changes in the medulla oblongata, with a history of nervous signs, are considered pathognomonic for BSE, processing artifact, toxins, metabolic diseases, and rabies virus infection may induce spongiform change in the brain, as well. In addition to the diagnostic methods mentioned by the contributor, cell culture technology is also employed in the laboratory detection of rabies virus.
Contributor: Universidade Federal de Santa Maria, Departamento de Patologia, 97105-900, Santa Maria, RS, Brazil
References: 1. Foley GL, Zachary JF: Rabies-induced spongiform change and encephalitis in a heifer. Vet Pathol 32: 309-311, 1995
2. Heuschele WP: Rabies and other viral diseases. Vet Clin North Am – Food Anim Pract 3(1):45-59, 1987
3. Hudson LC, Weinstock D, Jordan T, Bold-Fletcher NO: Clinical features of experimentally induced rabies in cattle and sheep. J Vet Med B 43:85-95, 1996
4. Jones TC, Hunt RD, King NW: Diseases caused by viruses. In: Veterinary Pathology, 6th ed., pp. 325-329. Williams & Wilkins, Baltimore, MD, 1997
5. Jubb KVF, Huxtable CR: The nervous system. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 1, pp. 403-406. Academic Press, San Diego, CA, 1993
6. King AA, Turner GS: Rabies: a review. J Comp Path 108:1-39, 1993
7. Martínez-Burnes J, López A, Medellín J, Haines D, Loza E, Martinez M: An outbreak of vampire bat-transmitted rabies in cattle in northeastern Mexico. Can Vet J 38:175-177, 1997
8. O’Toole D, Mills K, Ellis J, Welch V, Fillerup M: Poliomyelomalacia and ganglioneuritis in a horse with paralytic rabies. J Vet Diagn Invest 5:94-97, 1993
9. Summers BA, Cummings JF, De Lahunta A: Inflammatory diseases of the central nervous system. In: Veterinary Neuropathology, pp. 95-99. Mosby, Inc., Baltimore, MD, 1995
CASE III – N00-250 (AFIP 2749411)
Signalment: Adult, female Spanish-cross goat
History: This goat exhibited weakness and reluctance to stand that progressed to paresis over the course of six days. The animal was not febrile, and no joint or other musculoskeletal abnormalities were detected on clinical examination.
Gross Pathology: There were well demarcated, firm, pinkish-white nodules up to 1.5 cm diameter disseminated throughout all lobes of the liver. The nodules had caseous white centers on cut surface. A few similar, but smaller, nodules were observed in the spleen and mesenteric lymph nodes.
Laboratory Results: Laboratory testing revealed anemia (Hct=17%) and mild leukocytosis (WBC count=25.7 x 103). Serum chemistries and electrolytes were normal. Cultures taken of liver lesions produced a heavy growth of Rhodococcus equi, which was subsequently confirmed by a gas chromatography profile of microbe fatty acids. Stained sections of liver tissue revealed numerous Gram-positive coccobacilli in the granulomas. Acid-fast stains of liver sections were negative for organisms.
Contributor’s Diagnoses and Comment: 1. Liver: Granulomas, multifocal, random with numerous coccobacilli.
2. Liver, portal areas: Inflammation, chronic, with fibrosis and bile duct proliferation.
3. Liver, hepatocytes: Vacuolar change, diffuse, moderate.
4. Liver: Extramedullary hematopoiesis, multifocal.
Similar in its gross appearance to caseous lymphadenitis caused by Corynebacterium ovis, Rhodococcus equi has become an increasingly reported cause of disseminated abscesses and mortality in goats. The most consistent and striking gross lesion in affected goats is caseous abscessation of the liver, but lesions have also been described in the spleen, lung, mesenteric lymph nodes and bone. Typical clinical signs reported in goats include weight loss, anorexia, prolonged febrile illness and high mortality. As the bacteria have an apparent predilection for bone, R. equi should also be considered in any goats presenting with paresis or single leg lameness without other obvious causes. Vertebral osteomyelitis has been reported in several infected goats and was considered the most likely cause of paresis in the submitted case.
R. equi is a pleomorphic, facultative, intracellular, Gram-positive coccobacillus found readily in the soil and recovered from the feces of birds and herbivores. Normal routes of infection are thought to be either by inhalation or ingestion, leading to the two most common clinical forms of the disease, pneumonia and enterocolitis, respectively.
R. equi is best known as a cause of pyogranulomatous pneumonia with abscessation, enterocolitis, and osteomyelitis in foals. It is a sporadic cause of lymphadenitis in swine, sheep, cats, llamas and cattle, and a commonly recognized opportunistic pathogen of immunosuppressed people, particularly AIDS patients. In people, the lung is the primary site of infection, where it causes pulmonary abscesses with cavitating pneumonia similar to that seen in foals.
Virulence factors have been well described for strains of R. equi isolated from horses. These strains contain an 85 to 90 kb plasmid that encodes a 15-17 kd virulence associated protein referred to as VapA. While R. equi-infected goats have not been shown to harbor any underlying immunosuppressive disease, they are typically infected with nonvirulent strains of R. equi, lacking the VapA virulence factor. This suggests that goats may have an inherent susceptibility to this intracellular pathogen, or that additional virulence factors important to goats remain unrecognized. Infection with a VapA-negative Rhodococcus equi has also been reported in a dog and in some HIV patients and other immunocompromised individuals. Chronic R. equi pneumonia in people has been associated with the development of pulmonary malakoplakia, a rare condition characterized by the accumulation of macrophages that contain concentrically laminated intracytoplasmic basophilic inclusions (Michaelis-Gutmann bodies).
AFIP Diagnoses: 1. Liver: Granulomas, many, with intrahistiocytic coccobacilli, Spanish-cross goat, caprine.
2. Liver: Hepatitis, portal, lymphoplasmacytic, chronic, diffuse, with biliary hyperplasia.
3. Liver, sinusoids: Extramedullary granulopoiesis and erythropoiesis, multifocal, mild.
Conference Comment: The contributor has provided an excellent, concise summary of the entity.
Contributor: Department of Pathobiology, Clinical Research, Wilford Hall Medical Center, 1255 Wilford Hall Loop, Lackland AFB, TX 78236
References: 1. Cantor GH, Byrne BA, Hines SA, Richards HM, III: VapA-negative Rhodococcus equi in a dog with necrotizing pyogranulomatous hepatitis, osteomyelitis, and myositis. J Vet Diagn Invest 10(3):297-300, 1998
2. Davis WP, Steficek BA, Watson GL, Yamini B, Madarame H, Takai S, Render JA: Disseminated Rhodococcus equi infection in two goats. Vet Pathol 36:336-339, 1999
3. Fairley RA, Rairley NM: Rhodococcus equi infection of cats. Vet Derm 10:43-46, 1999
4. Fernandez Guerrero ML, Ramos JM, Renedo G, Gadea I, Alix A: Pulmonary malacoplakia associated with Rhodococcus equi infection in patients with AIDS: case report and review. Clin Inf Dis 28:1334-1336, 1999
5. Fitzgerald SD: Emerging, Evolving and Re-emerging Veterinary Diseases. CL Davis Syllabi, www.afip.org, 1997
6. Scott MA, Graham BS, Verrall R, Dixon R, Schaffner W, Tham KT: Rhodococcus equi – an increasingly recognized opportunistic pathogen. Am J Clin Pathol 103:649-655, 1995
7. Tkachuk-Saad O, Lusis P, Welsh RD, Prescott JF: Rhodococcus equi infections in goats. Vet Rec 143:311-312, 1998
CASE IV – 99N1262 (AFIP 2741895)
Signalment: 6-week-old, male Holstein calf
History: This calf was presented with a history of depression and lameness that had persisted for three weeks. Clinical examination revealed polyarthritis, wheezes in dependent lung fields, and apparent deficits in cranial nerves VII, VIII and IX. The farm from which this calf originated has a history of Mycoplasma-associated mastitis and the farm manager feeds mastitic milk to the calves. Multiple calves reportedly had similar signs, and joint aspirates or bronchoalveolar lavages from these animals were culture positive for Mycoplasma bovis.
Gross Pathology: The external auditory meatus of both right and left ears contains white, viscous pus. Both tympanic bullae are filled by caseous, green-yellow pus, and the bony structures of the left bulla are very soft. The right frontal sinus and the right nasal cavity also contain abundant pus. A 3.0 x 4.0 x 0.2 cm aggregate of fibrin is present over the ventral aspect of the cervical spinal cord. Approximately 3 ml of cloudy, reddish cerebrospinal fluid is present. Multiple joints contain abundant yellow, cloudy fluid with fibrin clots. Affected joints include the right and left scapulohumeral joints, the right and left elbow joints, and the left stifle. The cranioventral one-half of the lungs is dark red and slightly firm. The abdominal cavity contains three, unattached, firm, yellow masses from 2 cm in diameter to 1 x 2 x 2 cm (presumably fibrin rich with leukocytes).
Laboratory Results: Bacterial culture of joint fluid yielded large numbers of Mycoplasma bovis only. Cultures of bulla contents revealed large numbers of Mycoplasma bovis, as well as Bacteroides stercosis and Prevotella heparinolyticus-like bacteria.
Contributor’s Diagnosis and Comment: Auditory bulla: severe, subacute to chronic, suppurative, otitis media
Air spaces within the auditory bulla are filled by necrotic debris and the ulcerated mucosa is lined by neutrophils, most of which are degenerate. The submucosa is expanded by a moderate number of plasma cells, lymphocytes and macrophages, as well as numerous fibroblasts. The mucosa, submucosa and bony partitions lining many air spaces are completely necrotic. The surfaces of necrotic bony septa and intact bone adjacent to inflammatory infiltrates are heavily scalloped with numerous osteoclasts seated in deep lacunae. Many small cocci and coccobacilli are scattered throughout the necrotic debris. The medullary cavity of the bone adjacent to the bulla contains wispy connective tissue and moderate numbers of scattered, neutrophils, plasma cells and occasional lymphocytes. The trabeculae of this bone are lined by cuboidal osteoblasts. Some sections include portions of the semicircular canals, which have small numbers of lymphocytes and plasma cells.
Mycoplasma bovis is a well-known agent of mastitis, pneumonia, arthritis, synovitis and genital infections in cattle. Recently, it has also been associated with otitis media in dairy calves. There is a correlation with the practice of feeding mastitic milk, and, according to one report, the incidence of otitis paralleled a transient failure to pasteurize the mastitic milk used as a feed source. Pigs inoculated intranasally with Mycoplasma hyorhinis developed eustachitis that progressed to otitis media, and this is a proposed pathogenesis of the disease in calves.
Secondary invasion by opportunistic bacteria has been reported in Mycoplasma-associated pneumonia and otitis media, though, in many instances, a pure culture of Mycoplasma was reported. A single joint aspirate from this calf yielded a pure culture of Mycoplasma bovis (sample submitted by referring clinician) but Bacteroides stercosis and a bacterium similar to Prevotella heparinolyticus were also isolated from the tympanic bulla. Both are obligate anaerobes that likely became established due to favorable conditions created by the Mycoplasma infection. Tympanic bulla swabs of additional calves necropsied from the same herd yielded pure cultures of M. bovis.
AFIP Diagnosis: Trabecular bone, epithelial-lined spaces, connective tissue, and stratified squamous epithelium: Necrosis and inflammation, suppurative, chronic, focally extensive, severe, with reactive woven bone formation, Holstein calf, bovine.
Conference Comment: There was some difficulty in tissue identification with this case, but most conference participants managed to narrow down the location to somewhere near the respiratory passages. The variability of epithelial components present in tissue sections made identification more challenging, with rare sections containing ciliated respiratory epithelium.
Purulent otitis media due to Mycoplasma spp. is an occasional problem in the laboratory setting, too. Mycoplasma pulmonis is a cause of otitis media in certain laboratory rat colonies, particularly in older animals. The organism has been isolated from the middle ear of normal rats, suggesting that this may be one reservoir for the organism. Other organisms isolated from the middle ear of clinically normal rats may play a synergistic role in the development of otitis media.
Contributor: University of California, Davis, Veterinary Medical Teaching Hospital, Department of Veterinary Pathology, 1 Garrod Drive, Davis, California 95616
References: 1. Adgeboye DS, Halbur PG, Nutsch RG, Kadlec RG, Rosenbusch RF: Mycoplasma bovis-associated pneumonia and arthritis complicated with pyogranulomatous tenosynovitis in calves. J Am Vet Med Assoc 209:647-649, 1996
2. Brown MB, Dechant GM, Donovan GA, Hutchison J, Brown DR: Association of Mycoplasma bovis with otitis media in dairy calves. Abstracts of the General Meeting of the American Society for Microbiology 98(G7):274, 1998
3. Eamens GJ: Bacterial and mycoplasmal flora of the middle ear of laboratory rats with otitis media. Lab Anim Sci 34:480-483, 1984
4. Morita T, Ohiwa S, Shimada A, Kazama S, Yagihashi T, Umemura T: Intranasally inoculated Mycoplasma hyorhinis causes eustachitis in pigs. Vet Pathol 36:174-178, 1999
5. Pfutzner H, Sachse K: Mycoplasma bovis as an agent of mastitis, pneumonia, arthritis and genital disorders in cattle. Rev Sci Tech Off Int Epiz 15:1477-1494, 1996
6. Rodriguez F, Bryson DG, Ball HJ, Forster F: Pathological and immunohistochemical studies of natural and experimental Mycoplasma bovis pneumonia in calves. J Comp Path 115:151-162, 1996
7. Walz PH, Mullaney TP, Render JA, Walker RD, Mosser T, Baker
JC: Otitis media in preweaned Holstein dairy calves in Michigan
due to Mycoplasma bovis. J Vet Diagn Invest 9:250-254,
1997
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
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