Dermatophilus congolensis-associated placentitis, funisitis and abortion in a horse.

Placentitis, funisitis and fetal bronchopneumonia were diagnosed in an aborted full-term Thoroughbred fetus and its placenta by histopathological examination. Dermatophilus congolensis organisms were isolated from placenta, lung and stomach content. The genotypic identification of aerobic culture was confirmed by sequential analysis of the entire 16S rDNA gene. This is the first report of Dermatophilus congolensis-associated abortion in any species.

Prevalence of latent, neuropathogenic equine herpesvirus-1 in the Thoroughbred broodmare population of central Kentucky.

REASON FOR PERFORMING STUDY: An emerging problem of equine herpesvirus-1 (EHV-1) infection in horses in the USA is a high-mortality myeloencephalopathy that commonly occurs where large numbers of horses are stabled. EHV-1 isolates recovered from recent neurological outbreaks represent a mutant virus strain that possesses enhanced neuropathogenicity. A central question of EHV-1 myeloencephalopathy is the latency carriage rate for these mutants of EHV-1 in USA horse populations. OBJECTIVE: To estimate the prevalence of neuropathogenic strains of EHV-1 as latent infections in the Thoroughbred broodmare population of central Kentucky. METHODS: Submandibular lymph nodes (SMLN) were collected during post mortem examination of 132 Thoroughbred broodmares. Total DNA purified from SMLN tissue was tested for the presence of latent EHV-1 DNA by an ultrasensitive magnetic bead-based, sequence-capture, nested PCR method. Differentiation of active from latent infections by EHV-1 was achieved by detection of transcripts of EHV-1 glycoprotein B by reverse transcription PCR. RESULTS: Latent EHV-1 DNA was detected in the SMLN tissues of 71 (54%) of the 132 mares submitted for necropsy. Thirteen (18%) of the 71 latently infected horses harboured the neuropathogenic biovar of EHV-1. Of the 13 horses latently infected with an ORF30 mutant strain of EHV-1, 11 also carried a latent, wild-type strain of the virus in their SMLN tissues. CONCLUSIONS: Neuropathogenic strains of EHV-1 have established a significant presence in the Thoroughbred broodmare population of central Kentucky as latently infected carrier horses. The data also indicate that a highly sensitive DNA detection method is required to identify many instances of EHV-1 latency. POTENTIAL RELEVANCE: The presence of a relatively large biological reservoir of latent, neuropathogenic EHV-1 has the potential for posing emerging equine health and economic threats to the future prosperity of the USA horse industry.

Fibrocartilaginous embolic myelopathy in a horse.

Fibrocartilaginous embolic myelopathy was diagnosed in a 11-year-old, male, Tennessee Walking Horse by histopathological examination of the spinal cord after the horse was killed because of severe neurological dysfunction. Both ventral funiculi of C6 and C7 cervical spinal cord had extensive necrosis with blood vessels containing fibrocartilaginous emboli. A similar fibrocartilaginous embolus was observed in a single large spinal artery adjoining the vertebral leptomeninges.

Transitional cell carcinoma of the urinary bladder in a Thoroughbred, with intra-abdominal dissemination.

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.

Survey for internal parasites in cattle in Kentucky (1993).

Fecal samples were examined between 17 September and 1 November 1993 from 1765 cattle (one bull, 533 cows, 474 heifers, 22 steers, and 735 calves) on pasture on 15 farms in 11 counties in Kentucky for eggs or larvae of internal parasites. All of the cattle were beef-type except for 22 which were dairy-type. In fecal samples from the bull, cows, heifers, steers, and calves, the types of helminth eggs present were trichostrongyles (excluding Nematodirus) in 0%, 25%, 31%, 86%, and 93%, Nematodirus in 0%, 0%, < 1%, 0%, and 34%, Strongyloides in 0%, 0%, < 1%, 0%, and 7%, Trichuris in 0%, 0%, 0%, 0%, and 2%, Capillaria in 0%, 0%, 0%, 0%, and < 1%, and Moniezia in 0%, 1%, 8%, 5%, and 21%, respectively. Dictyocaulus viviparus larvae were present in feces of calves (7%) on one farm and heifers (< 1%) on another farm.

Pathological changes associated with equine arteritis virus infection of the reproductive tract in prepubertal and peripubertal colts.

The nature and extent of changes associated with equine arteritis virus (EAV) infection of the reproductive tract was documented in 21 prepubertal and 15 peripubertal colts. This study was part of an investigation into the relationship between stage of reproductive tract maturity and susceptibility to the experimental establishment of persistent infection with EAV. After intranasal challenge with a field isolate of EAV, all colts developed clinical signs of equine viral arteritis (EVA) from which they recovered rapidly. Clinical signs during the acute phase consisted of fever, serous to mucopurulent ocular and nasal discharge, oedema of the limbs, scrotum or prepuce, scleral injection, conjunctivitis, icterus, cough, diarrhoea, stiff gait, lethargy, inappetence and depression. At necropsy, the most significant macroscopic lesions included excessive accumulation of fluid within the thoracic and abdominal cavities, lymph node enlargement and oedema of the reproductive tract. Colts killed 7 to 14 days after challenge had acute necrotizing vasculitis involving the testes, epididymides, vasa deferentia, ampullae, prostatic lobes, vesicular glands and bulbourethral glands. Vasculitis was characterized by striking fibrinoid necrosis of small muscular arteries with extravasation of erythrocytes and proteinaceous material into the media, adventitia and perivascular tissues. Colts examined on days 28-180 had lymphocytic and plasmacytic inflammatory cell infiltrates in the lamina propria and muscularis of the epididymides and accessory sex glands. The vascular lesions found during the acute phase of EAV infection contrasted with the multifocal lympho-plasmacytic infiltrates found within the parenchyma of the reproductive tract during the chronic phase. One peripubertal colt was found to be persistently infected with EAV 15 months after challenge. This colt had marked lympho-plasmacytic infiltrates in the ampullae at necropsy.

Causes of abortion, stillbirth, and perinatal death in horses: 3,527 cases (1986-1991).

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.

Equine abortion and stillbirth in central Kentucky during 1988 and 1989 foaling seasons.

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.

Histoplasmosis in horses.

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 in equine fetuses, stillborn foals, and placentas.

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)

Adenomatous hyperplasia of equine allantoic epithelium.

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.

Etiology and pathology of equine placentitis.

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)

Equine protozoal myeloencephalitis: antigen analysis of cultured Sarcocystis neurona merozoites.

Antigens of cultured Sarcocystis neurona merozoites were examined using immunoblot analysis. Blotted proteins were probed with S. cruzi, S. muris, and S. neurona antisera produced in rabbits, S. fayeri (pre- and post-infection) and S. neurona (pre- and post-inoculation) sera produced in horses, immune sera from 7 histologically confirmed cases of equine protozoal myeloencephalitis (EPM), and pre-suckle serum from a newborn foal. Eight proteins, 70, 24, 23.5, 22.5, 13, 11, 10.5, and 10 Kd, were detected only by S. neurona antiserum and/or immune serum from EPM-affected horses. Equine sera were titered by the indirect immunofluorescent antibody (IFA) method using air-dried, cultured S. neurona merozoites. Anti-Sarcocystis IFA titers were found in horses with or without EPM. Serum titers did not correspond to the number of specific bands recognized on immunoblots.

Brucella abortus-associated meningitis in aborted bovine fetuses.

Granulomatous meningitis was present in 6/33 bovine fetuses from which Brucella abortus (B. abortus) had been isolated. Meningitis was severe in three fetuses, moderate in one fetus, and mild in the remaining two fetuses. The meningitis was characterized by the infiltration of a mixed population of lymphocytes, plasma cells, and macrophages in the leptomeninges. Vasculitis characterized by the infiltration of lymphocytes and plasma cells in the vascular wall was observed in the vessels of the cerebral cortices of 4/6 fetuses. Gram negative coccobacilli were present in the cytoplasm of the leptomeningeal macrophages and extracellularly. Brucellar antigens labeled by the avidin-biotin-peroxidase complex method were present in massive amounts in leptomeningeal macrophages and in small foci of stained cells in the choroid plexus and ependyma. The findings indicate that B. abortus is one of pathogens capable of inducing meningitis in bovine fetuses.

Allelic polymorphism and transassociation of molecules encoded by the HLA-DQ subregion.

A monoclonal antibody, CC11.23, with monomorphic specificity predominantly for products of the HLA-DQ subregion, has been used to demonstrate primary structural variation among DQ molecules. Two cell lines of each haplotype (DR1-7) were radiolabeled with [3H]tyrosine. alpha and beta chains were isolated from CC11.23-reactive preparations, and their amino-terminal tyrosine sequences were determined. Each DR haplotype (with the exception of DRw6) was found to express a distinct DQ molecule with a minimum of three allelic forms of the DQ alpha chain and five allelic forms of the DQ beta chain. At the primary structural level, the locus for the DQ beta chain appears to be as polymorphic as the locus for the DR beta chain. Unlike the locus for the DR alpha chain (which is essentially nonpolymorphic), the locus for the DQ alpha chain was found to be polymorphic. Comparison of DQ molecules from two different heterozygous cell lines with those from homozygous cell lines revealed that in heterozygotes, DQ alpha chains from either allele can associate with DQ beta chains from one allele. The formation of hybrid HLA-DQ molecules by both cis and trans gene complementation, coupled with several polymorphic forms of each of the DQ subunits, considerably increases the repertoire of DQ alloantigens in heterozygotes.