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Biomedical subjects

T W Swerczek

Publications and source records attributed to T W Swerczek.

At least 55 records · Page 3Linked to original sources
PubMed1981

Prevalence of Strongylus vulgaris and Parascaris equorum in Kentucky thoroughbreds at necropsy.

At necropsy of 49 Thoroughbreds from farms with generally good parasite control programs in central Kentucky, examination was specifically made for presence of Strongylus vulgaris in all of the horses and of Parascaris equorum in 21 of them. None of the deaths of the horses was caused by infections of internal parasites. Visceral arteries were examined for specimens of S vulgaris and lesions related to migrating stages of this parasite. Contents of the small intestines were examined for P equorum. Specimens of S vulgaris were recovered from 19 (39%) horses, and arterial lesions were observed in 24 (49%) of them. Parascaris equorum was found in 9 (43%) horses. Both parasites were found to persist in generally low numbers on farms in spite of their parasite control programs applied in recent years.

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PubMed1980

Toxicoinfectious botulism in foals and adult horses.

Toxicoinfectious botulism was proved to be the cause of a neuromuscular paralytic syndrome in foals and adult horses. In eight successive cases, Clostridium botulinum type B was isolated at necropsy. Foals were either found dead without premonitory signs of illness or, most often, they had signs of progressive and symmetric motor paralysis. Stilted gait, muscular tremors, and the inability to stand longer than 4 to 5 minutes were the salient clinical signs. Other clinical manifestations included dysphagia, constipation, mydriasis, and frequent urination. As the disease progressed, dyspnea with extension of the head and neck, tachycardia, and respiratory arrest occurred. Death occurred most often 24 to 72 hours after the onset of clinical signs. The most consistent postmortem findings were congestion and edema of the lungs and excessive pericardial fluid, which contained free-floating strands of fibrin. Gastric ulcers, foci of necrosis in the liver, abscesses in the navel and lungs, and wounds of the skin and muscle were predisposing sites for development of toxicoinfectious botulism.

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PubMed1980

Experimentally induced toxicoinfectious botulism in horses and foals.

Four experiments were performed to elucidate the pathogenesis of toxicoinfectious botulism in horses and foals. Groups of horses and foals were inoculated with one of the following: (1) crude toxin of Clostridium botulinum, type B, given IV, (2) C botulinum spores, given IM, (3) C botulinum spores, given IM, in necrotic lesions, and (4) C botulinum spores, given orally with and without dexamethasone. Toxin of C botulinum in minute amounts is toxic to horses. Clostridium botulinum spores produced toxicosis only when necrotic lesions were present. When C botulinum spores were given orally, they were innocuous. Toxicosis occurred when dexamethasone and C botulinum spores were given orally to a foal with necrotic lesions. Corticosteroids appear to predispose foals to the disease. In the animals where C botulinum organisms infected necrotic lesions, the clinical signs and the lesions seen on necropsy were identical with those seen in spontaneously occurring toxicoinfectious botulism.

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PubMed1979

Contagious equine metritis--outbreak of the disease in Kentucky and laboratory methods for diagnosing the disease.

Contagious Equine Metritis (CEM) was initially reported during the 1977 breeding season in England (Crowhurst, 1977) and Ireland (Timoney, Ward & Kelly, 1977. The disease has also been diagnosed in France and Australia (Huges, Bryden & MacDonald, 1978). The first occurrence of CEM in the United States followed the importation or 2 stallions from France late in 1977 which resulted in an outbreak early in the 1978 breeding season (Swerczek, 1978). Mares usually develop clinical signs of CEM 8--10 days after being covered by an infected stallion, when a copious, greyish discharge is seen. Other mares may not show any outward signs of disease, but may have a shortened dioestrous period. Many mares recover spontaneously from the disease, but a small proportion become carriers of the CEM organism. The stallion does not show any clinical signs of disease, but remains a carrier. In this paper we recommend various laboratory procedures for the diagnosis of CEM in mares and stallions.

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PubMed1978

Malignant medulloepithelioma of the optic nerve in a horse.

An 18-month-old Standardbred filly had a large intraocular tumor involving the optic nerve. The tumor was a malignant medulloepithelioma, a rare intraocular neoplasm derived from the primitive medullary epithelium. By light microscopy the tumor had cords and lobules of primitive neuroepithelial cells that formed clefts and true rosettes. Electron microscopy of the rosettes showed a girdle of zonulae adherentes joining the apices of the cells as well as several basal bodies. This is the sixth report of equine intraocular medulloepithelioma, and, to the best of our knowledge, the first intraocular medulloepithelioma arising from the optic nerve head in a horse. Massive involvement of the optic nerve should be suspected when an eye containing an intraocular mass in the posterior segment lacks light perception. In such cases a long segment of opitc nerve should be resected.

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PubMed1978

Pathologic changes and pathogenesis of Parascaris equorum infection in parasite-free pony foals.

Parasite-free pony foals (n = 10) were infected orally with 1000,000 Parascaris equorum embryonated eggs. One pony foal each was euthanatized on days 1, 3, 5, 7, 11, 16, 23, 27, 42, or 80 after infection. Foals infected for more than 7 days showed signs of coughing, anorexia, rough coat, and weight loss. Cellular changes in the blood were mild anemia, marked eosinophilia, and leukopenia. Gross postmortem lesions included hemorrhage, edema, and white-to-yellow necrotic foci (0.5 to 1.00 mm) in lungs, liver, and bronchial and hepatic lymph nodes. Microscopically, the liver was hemorrhagic and had focal necrosis and eosinophilic granulomas. Eosinophilic lymphadenitis with edema was in the hepatic and bronchial lymph nodes. The lungs had focal areas of necrosis with hemorrhage and interstitial pneumonia with hyalinization of the alveolar walls. Larvae were first seen in the liver at postinfection hour 24 and in the lungs on postinfection day (PID) 11. Average length of larvae in the liver was 1 mm and 2.5 mm in the lungs. Larvae were not found in the liver after PID 11 or in the lungs after PID 42. The migratory pathway of P equorum was similar to that of Ascaris lumbricoides because the larvae migrated via lymph and blood vessels to the liver and then to the lungs. After migrating through the lungs, the larvae were coughed up and swallowed and then developed in the small intestine.

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PubMed1976

Pine oil toxicity in the horse: drug detection, residues and pathological changes.

This report concerns the detection and acute toxicity of pine oil (a commercially available disinfectant) after intravenous administration in horses. alpha Terpineol was identified as a major constituent of pine oil. alpha Terpineol was recovered from equine tissues by extraction into heptane and detected by gas chromatography, using either flame ionization detection or pentafluoropropionic anhydride derivatization and electron capture detection. After intravenous injection of 0.1 ml/kg, death due to massive pulmonary edema occurred within minutes. In this animal blood and tissue levels of alpha-terpineol of between 150 and 300 ppm were observed. After smaller doses of pine oil (0.033 ml/kg), horses survived until euthanized up to 48 hours later. Blood levels of alpha-terpineol became undetectable in one of these animals after 2 hours, and no tissue levels were detected at postmortem. Marked histopathological changes were seen in the lungs of animals which survived the initial injection period. It appears that after intravenous injection of pine oil in horses lesions are largely related to the respiratory tract, and the mechanism of death is acute pulmonary edema.

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PubMed1975

Immature germ cells in the semen of thoroughbred stallions.

Small but significant numbers of primary and secondary spermatocytes and spermatids have been observed in the semen of some Thoroughbred stallions. Extensive histological examination of the testes of affected animals has not been undertaken but in one young stallion which died as the result of a leg injury, the premature dehiscence of these cells seemed to be related to segmental defects within the seminiferous tubules. The causes of lesions leading to premature shedding of germ cells are discussed.

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