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Encephalitozoon cuniculi is a microsporidial parasite, which has rarely been reported to cause placentitis in animals. A late-term aborted fetus and placenta from a Quarterhorse were presented to the Livestock Disease Diagnostic Center, University of Kentucky, for diagnostic examination. There was a necrotizing placentitis, with distension of many chorionic epithelial cells by intracytoplasmic vacuoles containing 1-2-microm-diameter, elongated, gram-positive organisms. The organisms were identified as E. cuniculi by electron microscopy and by polymerase chain reaction using primers to microsporidial ribosomal DNA. Joints of the fetus were swollen, with gross and microscopic lesions of synovitis; however, E. cuniculi DNA was not detected.

A 14-year-old Thoroughbred gelding with a history of acute onset of hematuria was presented for necropsy. Transitional cell carcinoma of the urinary bladder with intra-abdominal dissemination was diagnosed. Tumor masses were observed on the splenic capsule and surrounding the distal abdominal aorta. Tumor cells showed diffuse cytoplasmic reactivity for cytokeratin but were negative for epithelial membrane antigen, carcinoembryonic antigen, tumor-associated glycoprotein 72, and vimentin.

Herpesvirus infection of pregnant goats may result in abortion of fetuses without other signs of infection in does. Fetuses aborted as a result of caprine herpesvirus infection have tissue necrosis and intranuclear inclusion bodies in multiple organs.

In late July of 1994 two 11-mo-old Holstein heifers were found dead inside a barn after a break-and-entry into it by several animals. The other animals showed no signs of sickness. The predominant postmortem findings were pulmonary edema and muscular hemorrhage. Chemical analysis found endosulfan, dieldrin, DDT and DDE in the rumen contents of both animals. The owner admitted that a very old bottle of pesticide had been knocked over and consumed by these animals; the lid consisted of plastic tape. The sale of DDT to the public was discontinued in the US on January 1, 1973, and the sale of dieldrin was halted in the US in 1987. This case demonstrates that poisoning by long obsolete farm chemicals still must be considered in differential diagnoses of acute deaths.

Sarcocystis neurona is a coccidial parasite that causes a neurologic disease of horses in North and South America. The natural host species are not known and classification is based on ultrastructural analysis. The small subunit ribosomal RNA (SSURNA) gene of S. neurona was amplified using polymerase chain reaction techniques and sequenced by Sanger sequencing reactions. The sequence was compared with partial sequences of S. muris, S. gigantea, S. tenella, S. cruzi, S. arieticanis, S. capracanis, Toxoplasma gondii, Eimeria tenella, and Cryptosporidium parvum. Alignments of available sites for all 10 species and alignments of the entire SSURNA sequence of S. neurona, S. muris, S. cruzi, T. gondii, and C. parvum were performed. Alignments were analyzed using maximum parsimony and maximum likelihood methods to determine relative phylogeny of these organisms. These analyses confirmed placement of S. neurona in the genus Sarcocystis and suggested a close relationship to S. muris, S. gigantea, and T. gondii. Molecular phylogeny suggests that Sarcocystis spp., which utilize the dog (Canis familiaris) as the definitive host, evolved from a common ancestor, whereas those species (including T. gondii) that utilize the cat (Felis domesticus) as the definitive host evolved from another common ancestor. This suggests a possible definitive host for S. neurona.

Pathology case records of 3,514 aborted fetuses, stillborn foals, or foals that died < 24 hours after birth and of 13 placentas from mares whose foals were weak or unthrifty at birth were reviewed to determine the cause of abortion, death, or illness. Fetoplacental infection caused by bacteria (n = 628), equine herpesvirus (143), fungi (61), or placentitis (351), in which an etiologic agent could not be defined, was the most common diagnosis. Complications of birth, including neonatal asphyxia, dystocia, or trauma, were the second most common cause of mortality and were diagnosed in 19% of the cases (679). Other common diagnoses were placental edema or premature separation of placenta (249), development of twins (221), contracted foal syndrome (188), other congenital anomalies (160), and umbilical cord abnormalities (121). Less common conditions were placental villous atrophy or body pregnancy (81), fetal diarrhea syndrome (34), and neoplasms or miscellaneous conditions (26). A diagnosis was not established in 16% of the cases seen (585). The study revealed that leptospirosis (78) was an important cause of bacterial abortion in mares, and that infection by a nocardioform actinomycete (45) was an important cause of chronic placentitis.

Pathologic and microbiologic examinations were performed on 1,211 aborted equine fetuses, stillborn foals, and placentas from premature foals in central Kentucky during the 1988 and 1989 foaling seasons to determine the causes of reproductive loss in the mare. Placentitis (19.4%) and dystocia-perinatal asphyxia (19.5%) were the 2 most important causes of equine reproductive loss. The other causes (in decreasing order) were contracted foal syndrome and other congenital anomalies (8.5%), twinning (6.1%), improper separation of placenta (4.7%), torsion of umbilical cord (4.5%), placental edema (4.3%), equine herpesvirus abortion (3.3%), bacteremia (3.2%), fetal diarrhea (2.7%), other placental disorders (total of 6.0%), and miscellaneous causes (1.6%). A definitive diagnosis was not established in 16.9% of the cases submitted. Streptococcus zooepidemicus, Escherichia coli, Leptospira spp., and a nocardioform actinomycete were organisms most frequently associated with bacterial placentitis, and Aspergillus spp. was the fungus most often noted in mycotic placentitis. No viral placentitis was noticed in this series. Dystocia-perinatal asphyxia was mostly associated with large foals, maiden mares, unattended deliveries, and malpresentations. The results of this study indicate that in central Kentucky, the noninfectious causes of equine reproductive loss outnumber the infectious causes by an approximate ratio of 2:1, placental disorders are slightly more prevalent than nonplacental disorders, Leptospira spp. and a nocardioform actinomycete are 2 new important abortifacient bacteria in the mare, the occurrence of contracted foal syndrome is unusually frequent, the incidence of twin abortion has sharply declined, and torsion of the umbilical cord is an important cause of abortion in the mare.

Leptospirosis was diagnosed in 51 equine fetuses and 16 stillborn foals with gestational ages from 3 1/2 to 11 months. Diagnosis was based on one or more of the following: positive fetal antibody titer, positive fluorescent antibody test, demonstration of spirochetes in kidney and/or placental sections stained by the Warthin-Starry technique, high leptospiral titers in aborting mares, or isolation of Leptospira spp. from fetal organs. Gross lesions were observed in 80.3% of the fetuses, stillborn foals, and placentas. Gross placental lesions included nodular cystic allantoic masses, edema, areas of necrosis of the chorion, and necrotic mucoid exudate coating the chorion. The liver (23 cases) was enlarged, mottled, and pale to yellow. The kidneys (seven cases) were swollen and edematous with pale white radiating streaks in cortex and medulla. Microscopic lesions were observed in 96% of fetuses, stillborn foals, and placentas. Placental lesions consisted of thrombosis, vasculitis, mixed inflammatory cell infiltration of the stroma and villi, cystic adenomatous hyperplasia of allantoic epithelium, and villous necrosis and calcification. Fetal lesions included hepatocellular dissociation, mixed leukocytic infiltration of the portal triads, giant cell hepatopathy, suppurative and nonsuppurative nephritis, pulmonary hemorrhages, pneumonia, and myocarditis. Spirochetes were demonstrated with the Warthin-Starry stain in the allantochorion and/or kidney of 69 of the 71 cases. Using the direct fluorescent antibody technique, 56/60 cases tested positively for leptospires. Leptospires were isolated from fetal tissues in 20/42 cases. Sixteen of the isolates were identified by restriction enzyme analysis as Leptospira interrogans serogroup Pomona serovar kennewicki; case Nos. 36 and 41 were serovar grippotyphosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Histoplasmosis was diagnosed in nine horses during 1986-1990. The infection with Histoplasma capsulatum caused granulomatous placentitis and abortion in one mare in the 7th month of gestation and three mares in the 10th month. Four newborn foals died from severe granulomatous pneumonia within a few days of birth; and a weanling thoroughbred developed granulomatous pneumonia and lymphadenitis at 5 months of age.

Leptospirosis was documented as the cause of abortion in a 5-year-old mare. Leptospires were detected in tissue specimens from fetal kidneys and from placenta by histologic evaluation of silver-stained sections. Antibodies against Leptospira interrogans serovar pomona were detected in fetal serum at a titer of 1,600 by use of a microscopic agglutination test. The mare had serum titers of 6,400; 0; 400; 800; 3,200; and 6,400 to L interrogans serovars bratislava, canicola, grippotyphosa, hardjo, icterohaemorrhagiae, and pomona, respectively. A serologic survey identified titers of at least 6,400 against serovars bratislava and pomona in 5 other horses on the farm. Titers of at least 100 against serovar bratislava were detected in 53% of the horses on the farm. Leptospires were detected by direct fluorescent-antibody testing in urine samples from the mare that aborted and from 2 of the other 5 horses.

Adenomatous hyperplasia with or without cystic formation of allantoic epithelium was observed in 63/954 equine placentas examined from 1 February 1988 to 31 January 1990. In 61/63 placentas, the adenomatous hyperplasia was associated with other placental lesions: 49 with chronic or chronic-active placentitis, six with placental edema, three with fetal diarrhea, one with placentitis and fetal diarrhea, one with fetal diarrhea and placental edema, and one with hyperplasia of chorionic epithelium. When lesions were less severe, the hyperplastic lesions were not grossly visible, but when lesions were severe, nodular, tumorous, cystic masses were observed at or near the insertion site of umbilical blood vessels. Histologically, lesions classified as stage 1 were characterized by hypertrophy and hyperplasia of epithelial cells and formation of intraepithelial glands (lumina). Lesions classified as stage 2 were characterized by the presence of fibro-adenomatous changes in the allantoic stroma. Lesions classified as stage 3 were characterized by the formation of the nodular masses, which were composed of glandular or cystic structures of various sizes lined by cuboidal or low to medium columnar epithelium. These glands or cysts were empty or contained amphophilic secretion, a mixture of neutrophils and secretion material, or neutrophils. The cause of adenomatous hyperplasia of the equine allantois is not certain; however, there is a close connection between chronic placental disorders and this hyperplastic lesion.

Placentas from aborted, stillborn, and premature foals were examined during the 1988 and 1989 foaling seasons, and 236 of 954 (24.7%) had placentitis. Microorganisms associated with placentitis were isolated or demonstrated from 162 of 236 (68.6%) placentitis cases. Leptospira spp. and a nocardioform actinomycete were 2 important, newly emerging bacteria associated with equine placentitis. Major pathogens identified in decreasing order were Streptococcus zooepidemicus, Leptospira spp., Escherichia coli, a nocardioform actinomycete, fungi, Pseudomonas aeruginosa, Streptococcus equisimilis, Enterobacter agglomerans, Klebsiella pneumoniae, and alpha-hemolytic Streptococcus. Pathogens were not recovered in 64 cases (27.1%) and overgrowth by saprophytic bacteria was recorded in 10 cases (4.2%). Twenty-seven cases (16.6%) had mixed bacterial growth and 93 cases (57.4%) had bacteria cultured from both placenta and fetal organs. The majority of the placentitis cases caused by bacteria, with the exception of Leptospira spp. and the nocardioform actinomycete, occurred in 2 forms. One was acute, focal or diffuse; had an infiltration of neutrophils in the intervillous spaces or necrosis of chorionic villi; was associated with bacteremia; and frequently occurred in the placenta from fetuses expelled before or at midgestation. The other was observed from foals expelled at late gestation, was mostly chronic and focal or focally extensive, and occurred mostly at the cervical star area. Chronic placentitis was characterized by the presence of 1 or a combination of the following lesions: necrosis of chorionic villi, presence of eosinophilic amorphous material on the chorion, and infiltration of mononuclear inflammatory cells in the intervillous spaces, villous stroma, chorionic stroma, vascular layer, and allantois.(ABSTRACT TRUNCATED AT 250 WORDS)

A study to determine the prevalence of leptospira-induced abortions in the central Kentucky equine population during the 1990 foaling season and to determine the leptospira serovars responsible was conducted. From July 1, 1989 through June 30, 1990, 32 (4.4%) of 726 submissions (fetuses, stillborn foals, and/or placentas) were diagnosed as leptospirosis by the fluorescent antibody test and/or microscopic agglutination test. Attempts were made to isolate leptospires from the fetal tissues and/or the dam's urine in 31 of these cases. Leptospira interrogans serovar kennewicki was isolated from 11 (35.5%) and serovar grippotyphosa from 2 (6.5%) of the 31 cases. Of 12 cases that were culture negative with serologically positive fetal fluids, 8 had titers against serovar pomona, 1 against bratislava, 1 against grippotyphosa, 1 against hardjo, and 1 against both bratislava and pomona.

Skeletal or cardiac myodegeneration, or both, was observed in 4 free-ranging female white-tailed deer that were found dead or recumbent and unable to rise. Gross pathologic findings included white or chalky streaks in heart or skeletal musculature. Degeneration, necrosis, and mineralization were observed microscopically in affected striated muscles. Although the precise cause of myodegeneration was not determined, changes were considered compatible with nutritional or exertional myopathy.