|
|
Signalment: Tissue is from an adult Holstein cow.
History: This cow died 3 days post-calving. The owners did not observe abnormal clinical signs prior to death.
Gross Pathology: The left caudal mammary gland was mildly reddened and somewhat firm.
Laboratory Results: Large numbers of Escherichia coli in pure culture were isolated from the mammary tissue.
Contributor’s Diagnosis and Comment: Mastitis, necrotizing and fibrinous, peracute, locally extensive, severe.
The epithelium lining both inter- and intralobular ducts is necrotic with thin strands of fibrin and intermixed cellular debris covering the underlying loose connective tissue. Numerous ducts and adjacent lymphatics are occluded with loose fibrin aggregates. There is widespread necrosis of epithelial cells that line bordering acini. Acini are filled with serous fluid, desquamated epithelial cells, and large numbers of rod-shaped bacteria. In most lobules, there are few leukocytic infiltrates; in rare lobules, acinar lumina are filled with moderate numbers of neutrophils that extend into bordering edematous interlobular septa. Multifocally, there is septal hemorrhage and moderate to severe congestion. In sections of lung (not included), alveolar septa have increased numbers of neutrophils and macrophages. No significant microscopic abnormalities are seen in sections of abomasum, liver and kidney. The clinical history, combined with bacteriological and histopathological findings, indicates a peracute coliform mastitis with secondary cardiovascular collapse as the probable cause of death.
The ductular orientation, with necrosis of the lining epithelium and preservation of basement membrane, matches that described for peracute coliform mastitis. Coliform mastitis is an important cause of acute mastitis and causes death in approximately 10% of affected animals, despite intensive antibiotic and electrolyte therapy. Although initial reports indicated that bacteremia is not present with E. coli infections of the mammary gland, more recent studies have demonstrated that bacteremia can be found in acutely infected animals. Death is classically attributed to the effects of endotoxin uptake from the infected quarter.
AFIP Diagnosis: Mammary gland: Mastitis, necrotizing, acute, diffuse, moderate, with interlobular edema, necrotizing lymphangitis, and intra-alveolar colonies of bacteria, Holstein cow, bovine.
Conference Comment: Coliform mastitis most often presents as a severe, acute infection, occurring with greatest frequency during the first two weeks of the dry period and the two weeks prior to calving. The occurrence of infections is greatest during these periods because of a lack of routine milking and, thus, udder washing and teat dipping. The relaxed teat sphincter and patent streak canal allow environmental pathogens, such as coliforms, to gain access to the mammary gland.
The mechanisms by which E. coli and its toxins produce disease are not completely understood. Neutrophil response is crucial in protection against and resolution of infections; delayed neutrophil chemotaxis into the gland, lack of inflammatory mediators, or decreased neutrophil function may allow the bacteria to multiply and release more endotoxin prior to the onset of the inflammatory reaction. Faster bacterial replication in early lactation also may be important in the pathogenesis.
Bacteremia may result following extensive damage to ductular epithelium by E. coli cytotoxins, and damage to secretory epithelium and basement membranes by engulfed organisms. Co-infections with other pathogens may aid in the destruction of basement membranes. Endotoxin has been shown to damage vascular endothelium and this may explain the edema, lymphangiectasia, and hemorrhage seen.
Contributor: University of Washington, Department of Veterinary Microbiology and Pathology, P.O. Box 647040, Pullman, WA 99164-7040
References: 1. Kennedy PC, Miller RB: The female genital system. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 3, pp. 460-462. Academic Press, Inc, San Diego, CA, 1993
2. Frost AJ, Brooker BE: Hyperacute Escherichia coli mastitis of cattle in the immediate post-partum period. Aust Vet J 63:327-331, 1986
3. Cebra CK, Garry FB, Dinsmore RP 1996. Naturally occurring acute coliform mastitis in Holstein cattle. J Vet Int Med 10:252-257, 1996
4. Anderson KL, Smithe AR, Gustafsson BK, Spahr SL, Whitmore HL: Diagnosis and treatment of acute mastitis in a large dairy herd. J Am Vet Med Assoc 181:690-693, 1982
5. Radostits OM, Blood DC, Gay CC: Major mastitides. In: Veterinary Medicine: A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses, 8th ed., pp. 584-594. Bailliere Tindall, Philadelphia, PA, 1994
CASE II – 99W12215 (AFIP 2739651)
Signalment: 6-month-old, male Shira’s moose, Alces alces shirasi
History: This free-ranging moose calf was darted near Pinedale, Wyoming, anesthetized, and transported with its dam to a captive wildlife facility near Wheatland, Wyoming in November, 1999. Approximately 1 month later, the calf was noted to be off by itself in the morning. By early afternoon, the calf was down and unable to rise. Bloody exudate was found on the perineum and in pools on the ground. The calf was euthanized and submitted to the Wyoming State Veterinary Laboratory for necropsy.
Gross Pathology: The moose calf was in fair body condition. Bloody fluid was present on the perineum. There was marked pulmonary edema and a mild increase in clear fluid in the thoracic cavity. Acute hemorrhage was noted on the serosa and mucosa of the small intestine, cecum, and spiral colon, with the most severe lesions in the spiral colon. Bloody contents were found in the lumen.
Laboratory Results:
Parasitology: Small trichostrongyles, 2 eggs per gram of feces.
Bacteriology: Escherichia coli was isolated from the spiral colon, small intestine, and mesenteric lymph node. No organisms were isolated from the lung.
Serology: Negative at <1:4 to bovine virus diarrhea virus type 1 and 2, infectious bovine rhinotracheitis virus, parainfluenza-3 virus, and bovine respiratory syncytial virus. Negative at <1:100 to Leptospira interrogans serovars canicola, icterohemorrhagiae, and pomona. Positive at 1:100 for antibodies against L. interrogans serovars grippotyphosa and hardjo.
Fluorescent antibody tests: The spiral colon and mesenteric lymph node were negative for the following: bovine respiratory syncytial virus, parainfluenza-3 virus, infectious bovine rhinotracheitis virus, bluetongue virus, epizootic hemorrhagic disease virus, and bovine adenovirus 3. The tissues were fluorescent antibody test positive for bovine adenovirus 5.
Electron microscopy: Adenovirus was observed by negative stain electron microscopy in small intestine, spiral colon, and lung.
Virus isolation: Adenovirus was isolated on white-tailed deer umbilical endothelium, and the presence of virus was confirmed by negative stain electron microscopy.
Contributor’s Diagnosis and Comment: 1. Cecum and large intestine: Typhlocolitis, hemorrhagic, associated with diffuse vasculitis, moose.
2. Lung: Diffuse vasculitis, with interlobular edema, moose.
Etiology: Adenovirus
Vasculitis was widespread, but especially severe in the lung, cecum, and spiral colon. The endothelium of vessels, ranging in size from capillaries to large arteries and veins, was swollen or had sloughed into lumina. Scattered endothelial cells contained large basophilic to amphophilic intranuclear inclusion bodies. Occasionally, fibrinoid necrosis and mixed cellular infiltrates were present in vessel walls and in perivascular areas. Affected vessels were most common in lung and portions of the large intestine. Acute edema and hemorrhage were common in association with affected vessels, and there was a relatively light, mixed inflammatory cell infiltrate in these areas.
Adenoviral hemorrhagic disease (or systemic adenoviral infection) has caused significant mortality in free-ranging mule deer (Odocoileus hemionus) and black-tailed deer (Odocoileus hemionus columbianus) in California, and it has been experimentally reproduced in mule deer yearlings and fawns. Systemic adenovirus infection was recently identified in several captive moose calves in Ontario, Canada (Smith et. al., 1999). Duration of clinical disease in systemic adenoviral disease in cervids is hours to a few days. Lesions in the reported deer and moose cases were essentially identical to the lesions observed in the Shira’s moose calf: systemic vasculitis, with prominent pulmonary edema, and hemorrhagic typhlocolitis. The adenovirus isolated from the deer in California was characterized as being closely related to bovine adenovirus-3. Systemic adenovirus infections in ruminants is typically seen in young animals and often associated with stress or immunosuppression. The factors leading to the high mortality observed in deer in California was not determined. The affected moose calf likely was stressed, considering it had been recently captured from the wild and was adjusting to captivity. Adenoviral disease was not observed in other moose or deer at the wildlife facility. The source of the adenovirus affecting this moose was not determined; however, adenoviruses in cervids clearly are more widely distributed than previously thought. Systemic adenoviral infection should be considered as a differential diagnosis when investigating hemorrhagic disease in cervids.
AFIP Diagnoses: 1. Large intestine: Vasculitis, necrotizing, acute, diffuse, moderate, with endothelial basophilic intranuclear inclusion bodies, hemorrhage and edema, Shira’s moose (Alces alces shirasi), cervid.
2. Lung: Vasculitis, necrotizing, acute, diffuse, with interstitial edema, hemorrhage, rare fibrin thrombi, and rare endothelial basophilic intranuclear inclusion bodies.
Conference Comment: The lack of a competent immune system is considered an important factor in fatal adenoviral infections in many species. The tropism of the deer adenoviral strain for endothelium results in vascular damage, most notably resulting in pulmonary edema and hemorrhagic enteropathy. Localized vasculitis can result in extensive ulceration and abscessation in the mouth and forestomachs through opportunistic infections that then spread systemically. Immunosuppression in older animals, or an underdeveloped immune system in neonates, is usually required for clinical expression of disease with adenoviral infection.
Many of the deer in the reports referenced by the contributor had viral-induced oral and ruminal abscesses from which Fusobacterium necrophorum and Arcanobacterium pyogenes were cultured. Similarities between these animals and the pronghorn antelope in the following case (Case III) were discussed. Although the oral abscesses would not be directly fatal, subsequent chronic wasting due to starvation, or septicemia resulting from stomatitis or osteomyelitis, were suggested in the reports as possible sequelae to prior nonfatal adenovirus infection in these deer.
The presence of transmural, filamentous Gram negative bacteria within the sections of large intestine generated discussion during the conference as to whether the bacteria represented postmortem overgrowth, or were the result of a peracute bacteremia since no autolytic changes were observed within the mucosal epithelium. The lack of an inflammatory response and lack of bacteria in the lung sections argued in favor of postmortem overgrowth.
Contributor: University of Wyoming, Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, 1174 Snowy Range Road, Laramie, Wyoming 82070
References: 1. Lapointe JM, Hedges JF, Woods LW, Reubel GH, MacLachlan NJ: The adenovirus that causes hemorrhagic disease of black-tailed deer is closely related to bovine adenovirus-3. Arch Virol 144(2):393-396, 1999
2. Woods LW, Swift PK, Barr BC, Horzinek MC, Nordhausen RW, Stillian MH, Patton JF, Oliver MN, Jones KR, MacLachlan NJ: Systemic adenovirus infection associated with high mortality in mule deer (Odocoileus hemionus) in California. Vet Pathol 33:125-132, 1996
3. Woods LW, Hanley RS, Chiu PHW, Burd M, Nordhausen RW, Stillian MH, Swift PK: Experimental adenovirus hemorrhagic disease in yearling black-tailed deer. J Wildlife Dis 33:801-811, 1997
4. Woods LW, Hanley RS, Chiu PH, Lehmkuhl HD, Nordhausen RW, Stillian MH, Swift PK: Lesions and transmission of experimental adenovirus hemorrhagic disease in black-tailed deer fawns. Vet Pathol 36:100-110, 1999
CASE III – TAMU-1 (AFIP 2740378)
Signalment: Adult, female pronghorn antelope (Antilocapra americana)
History: 36 pronghorns were found dead over a 6-week period in a pen on a research farm. Some animals died with signs of lameness and swelling of a limb. Others, such as this one, were found dead without clinical signs.
Gross Pathology: Grey-white “dry” lesions, 1-2 cm in diameter, with a red border were seen in the tongue and rumen.
Laboratory Results: Not available.
Contributor’s Diagnosis and Comment: Acute, focally extensive, necrotizing glossitis and necrosis; acute, focally extensive rumenitis and necrosis; numerous, intralesional, filamentous bacteria.
Submitted are typical lesions of systemic necrobacillosis as it occurred in a captive herd. The animals had no cases of necrobacillosis until 5 days after the first rain that followed a protracted drought. Initial cases had necrobacillosis of the feet, with spread to several viscera, including liver, rumen, omentum, lung, and cecum. Later, cases such as that submitted began to occur about a week into the outbreak. Animals had oral lesions (tongue, gingiva, palate and cheek) with systemic spread, but without pododermatitis. The pasture could not be drained adequately, and it remained wet with some standing pools. The animals preferred to drink from pools on the ground rather than from waterers provided. The outbreak continued until all animals were lost. Fusobacterium necrophorum was isolated, often with Arcanobacterium pyogenes, from oral and pedal lesions. Fusobacterium necrophorum was isolated from all systemic lesions. Lesions grossly look like infarcts, but their dry nature is due to the local production of bacterial toxins that cause coagulative necrosis. Inflammation is minimal and ends at the border of these acute lesions. The filamentous organisms are visible and readily stained. It is believed that the initial cases with draining foot lesions contaminated the groundwater pools, and that minor lesions of the mouth provided entry of the organisms. This is typical of the pathogenesis observed in pedal fusobacteriosis of sheep. Identical outbreaks have been observed in captive or crowded deer and elk. In the old days before antibiotics, fusobacteriosis was common in teenagers and young adults (relation to tooth eruption?) as a fulminant septicemia going from primary jaw lesions to the lungs, especially (Lemierre’s Syndrome). Our case resembles this disease. The organism was presumed to be biotype A because of its virulence.
AFIP Diagnoses: 1. Buccal mucosa, salivary glands, and haired skin: Stomatitis, necrotizing, acute, focally extensive, severe, with mineralization, and myriad filamentous bacilli and colonies of cocci, pronghorn antelope (Antilocapra americana), antilocapridae.
2. Rumen: Rumenitis, necrotizing, acute, focally extensive, severe, with myriad filamentous bacilli.
Conference Comment: F. necrophorum is a normal inhabitant of the oral cavity that can cause necrosis, edema, and inflammation following mucosal injury. In calves with necrotic stomatitis, lesions are restricted to the oral cavity and death is usually due to edema and inflammation causing laryngeal obstruction, or due to an apparent toxemia. Usually only a small proportion of calves in a group are affected. Immunosuppression or age-related humoral and cellular immune deficiencies are likely very important in the clinical outcome of infection.
Conference participants considered the death of 36 adult antelope over 6 weeks as a result of Fusobacterium necrophorum contamination of water leading to systemic toxemia to be unusual. The possibility of viral co-infection or prior immunosuppression was discussed.
Contributor: Texas A&M University, College of Veterinary Medicine, Department of Veterinary Pathobiology, College Station, TX 77843-4467
References: 1. Fowler ME, Jacobsen N, Erb L, McDonald S: Stress-induced mixed infection in Columbian black-tailed deer. In: The Comparative Pathology of Zoo Animals, ed. Montali RJ, Migaki G, pp. 415-420, 1980
2. Murie OJ: An epizootic disease of elk. J Mammal 11:214-222, 1930
3. Roberts DS, Graham NPH, Egerton JR, Parsonson IM: Infective bulbar necrosis (heel-abscess) of sheep, a mixed infection with Fusiformis necrophorus and Corynebacterium pyogenes. J Comp Path 78:1-10, 1968
4. Rosen MN: Necrobacillosis. In: Infectious Diseases of Wild Mammals, ed. Davis JW, Karstad LH, Trainer DO, pp. 286-292. Iowa State University Press, Ames, IA, 1970
5. Wobeser G, Runge W, Noble D: Necrobacillosis in deer and pronghorn antelope in Saskatchewan. Can Vet J 16(1):3-9, 1975
CASE IV – 97-601 (AFIP 2741022)
Signalment: Standardbred mare, unknown age.
History: The mare delivered a live, premature foal.
Gross Pathology: Portions of placenta and chorioallantois were submitted fixed in formalin. Nodules up to 1 cm in diameter were apparent on the allantois. The chorionic surface appeared irregular and multifocally thickened.
Laboratory Results: None.
Contributor’s Diagnosis and Comment: Subacute to chronic, suppurative and fibrinonecrotic placentitis with adenomatous hyperplasia of the allantoic epithelium.
Numerous Gram positive rods are present and presumed to be contaminants. The presence of Gram positive, acid-fast negative, filamentous bacteria is presumed to be the cause of the placentitis. The bacteria are likely Actinomyces spp. or Nocardia spp. Adenomatous hyperplasia of the equine allantoic epithelium (AHAE) is a proliferation of the allantoic epithelium at the region of the insertion of the umbilical vessels. In a series of 954 equine placentas, variations of this lesion were found in 63. Of these 63, 61 had other placental lesions, mostly chronic infectious placentitis. A relationship between the placentitis and the AHAE is uncertain. The lesions can result in formation of grossly visible nodules, but can begin as grossly inapparent hyperplasia and hypertrophy of the allantoic epithelium, with intra-epithelial cyst formation. This hyperplasia and hypertrophy can progress with formation of fibrous allantoic stroma, and eventually to fibroadenomatous proliferations producing grossly visible nodules.
AFIP Diagnoses: 1. Chorioallantois: Hyperplasia, adenomatous and cystic, allantoic, multifocal, moderate, with multifocal subacute inflammation, Standardbred mare, equine.
2. Chorioallantois: Allantochorionitis (placentitis), necrotizing, subacute, diffuse, moderate, with many filamentous bacteria.
Conference Comment: The etiology, pathogenesis, and association with abortion of cystic adenomatous hyperplasia in the equine allantois are uncertain. Because the allantoic endodermal epithelium is physiologically highly active, it is thought that the proliferative lesion might be secondary to chronic placental disorders, such as might be found with chronic bacterial placentitis. Since small cysts might be easily missed during placental examination, this lesion is possibly more common than what previous reports might indicate.
The allantois is normally nonglandular and nonsecretory. This lesion has been classified as neoplastic in some reports because of the invasive growth of glandular and apparently secretory epithelium arising from the allantoic epithelium. The epithelial proliferation is considered hyperplastic, however, based on the multifocal distribution of the lesions, lack of infiltration into the underlying chorionic stroma, the presence of many inflammatory cells within the glandular lumina rather than the stroma, and the frequent association with other placental lesions. Placental neoplasia is seen very rarely in domestic animals.
Contributor: The Ohio State University College of Veterinary Medicine, Department of Veterinary Biosciences, 1925 Coffey Road, Columbus, OH 43210
References: 1. McEntee M, Brown T, McEntee K: Adenomatous dysplasia of the equine allantois. Vet Pathol 25:387-389, 1988
2. Hong CB, Donahue JM, Giles RC, Jr, Petrites-Murphy MB, Poonacha KB, Tramontin RR, Tuttle PA, Swerczek TW: Adenomatous hyperplasia of equine allantoic epithelium. Vet Pathol 30:171-175, 1993
3. Poonacha KB, Donahue JM, Giles RC, Hong CB, Petrites-Murphy MB, Smith BJ, Swerczek TW, Tramontin RR, Tuttle PA: Leptospirosis in equine fetuses, stillborn foals, and placentas. Vet Pathol 30:362-369, 1993
4. Shivaprasad HL, Sundberg JP, McEntee K, Gordon L, Johnstone
AC, Lombardo de Barros CS, Hoffman RL: Cystic adenomatous hyperplasia
of the equine allantois: a report of eight cases. J Vet Diagn
Invest 6:107-110, 1994
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
 |
