Multiple abortions associated with caprine herpesvirus infection in a goat herd.

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.

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.

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.

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)

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.

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)

Role of parathyroid hormone in the anemia of chronic terminal renal dysfunction in dogs.

Terminal renal dysfunction (TRD) was induced in 2 groups of dogs by partial surgical ablation of the kidney. Dogs of a control group and of 1 of the TRD groups were maintained on a diet containing normal phosphorus concentration, whereas dogs of the other TRD group were maintained on a low-phosphorus diet. Mild anemia developed in dogs of both TRD groups and could not be attributed to iron deficiency, increased erythrocyte concentration of 2,3-diphosphoglycerate, or absolute deficiency of erythropoietin (EP). Subsequently, all dogs were acutely depleted of approximately 25% of their blood volume. Erythropoietin concentration in dogs of the TRD groups was lower than that of controls, however, erythroid regenerative capacity was comparable with that of control dogs when plasma parathyroid hormone (PTH) concentration was lowered by reduced dietary intake of phosphorus. The PCV in dogs of the chronic TRD groups had a slight positive correlation with serum EP concentration, and a significant (P less than 0.05) negative correlation with plasma PTH and serum phosphorus and creatinine concentrations, using a correlation matrix. There was no longer a significant correlation between plasma PTH concentration and PCV after controlling for serum creatinine concentration by use of a multiple linear regression analysis. A significant (P less than 0.05) negative correlation also was observed between plasma PTH and serum EP concentrations, but not between serum EP and phosphorus or creatinine concentrations. Significance of the EP and PTH association was reduced when analyzed, using a multiple linear regression analysis that included serum creatinine values.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of incorporation of serum from dogs with renal impairment on canine erythroid bone marrow cultures.

Serum from dogs with surgically induced renal impairment was incorporated into the medium for erythroid bone marrow cultures. A significant correlation was found between serum activities of erythropoietin and numbers of erythroid colony-forming units grown in culture. Serum creatinine concentrations had no correlation, and serum parathyroid hormone activities had a negative correlation with numbers of erythroid colony-forming units that was below the level of significance. Purified 1-84 parathyroid hormone added to bone marrow cultures was found to be stimulatory to erythroid colony-forming unit growth in higher concentrations, but decreased the number of burst-forming units. Unmeasured substances in the canine serum appeared to have a greater effect on the canine erythroid bone marrow cultures than did creatinine or parathyroid hormone values.

Primary hyperparathyroidism in German shepherd dogs: a disorder of probable genetic origin.

Primary hyperparathyroidism was diagnosed in two German shepherd pups from a litter of four females. Clinical signs were apparent by two weeks of age and included stunted growth, muscular weakness, and polydipsia/polyuria. Radiography revealed diffuse reduction in bone density. Both pups had marked hypercalcemia, hypophosphatemia, increased plasma immunoreactive parathyroid hormone concentrations and increased fractional clearance of inorganic phosphate in the urine. Intravenous infusion of one affected pup with calcium gluconate failed to suppress the plasma concentration of immunoreactive parathyroid hormone, suggesting autonomous secretion of parathyroid hormone. Necropsy of the other pup at eight weeks of age revealed diffuse hyperplasia of parathyroid chief cells, nodular hyperplasia of thyroid C-cells, skeletal alterations consistent with fibrous osteodystrophy, hypercalcemic nephropathy, and extensive mineralization of the lungs and gastric mucosa. The dam and sire were half sibs. One male pup from a previous litter of six had developed similar clinical signs and radiographic lesions, suggesting autosomal recessive inheritance. This is the first report of hereditary primary hyperparathyroidism in domestic animals, a disease which may be analogous to hereditary neonatal primary hyperparathyroidism in children.