Biomedical subjects
Publications and source records attributed to I G Mayhew.
Pigmented nevi have not been widely recognized in domesticated animals. We describe, for the first time, a giant congenital pigmented nevus in a horse. Because of a prominent neuroid component within the lesion, neurofibromatosis was the major differential diagnosis.
A fifth stage Strongylus vulgaris migrated through the spinal cord of a 2-year-old, male donkey resulting in progressive paraparesis and then tetraplegia. A profound neutrophilic pleocytosis was detected on analysis of cerebrospinal fluid. The parasite appeared to have entered the mid-lumbar spinal cord, migrated to the cranial thoracic segments, exited, then re-entered the spinal cord a few segments craniad. It then traveled further cranially and was found in the third cervical spinal cord segment. Some parts of the lesion were remarkably free from tissue necrosis, hemorrhage and inflammation. Severe granulomatous myelitis with hemorrhage and necrosis were seen at other sites. The latter were quite similar to lesions seen in equine protozoal myeloencephalitis.
Gastroesophageal candidiasis in association with ulceration was diagnosed in 5 foals in which signs of colic had been nonresponsive to medical treatment. The ulceration was found in the stomach of all foals and in the esophagus of 1 foal. Candida colonized hyperkeratotic mucosa surrounding the ulcers, and the associated inflammation resulted in splitting of the mucosal epithelium. Loss of the superficial mucosa may have allowed invasion by bacteria, leading to ulceration.
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Anhidrosis is loss of the ability to sweat. The problem is seen in horses kept in a hot humid climate, and it may cause severe impairment of thermoregulation in the equine athlete. British Thoroughbreds imported to her tropical colonies are the earliest recorded cases, and since then the syndrome has come to be described as one of Thoroughbreds, usually performance athletes, undergoing acclimatization to heat and humidity. A recent epidemiologic study of cases in Florida has shown, however, that many different breeds, and long time inhabitants of a hot climate, may be affected. Equine sweat glands are of the apocrine type, and sweating is stimulated by direct local release of epinephrine from adrenergic nerve endings and by circulating epinephrine. Lack of sweating could be due to a number of possible flaws in a sequence from central nervous stimulation through sweat stimulation and secretion to delivery of sweat to the skin surface. The most likely possibilities are inadequate sweat gland response due to habituation of receptors to a high circulating level of epinephrine and occlusion of the sweat ducts by keratin plugs. Hormonal or metabolic imbalance may play a role both in the onset and secondary signs associated with anhidrosis.
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The effects of large doses of phenylbutazone were evaluated in clinically normal horses. The drug was given to 4 groups of 2 horses each at the rate of 30 mg/kg of body weight, orally, or 30, 15, or 8 mg/kg IV daily for up to 2 weeks. All horses became anorectic and depressed after 2 to 4 phenylbutazone treatments, and the horses given 15 or 30 mg/kg died on or between days 4 and 7 of treatment. A decrease in total blood neutrophil count occurred in all horses, and was associated with toxic left shift in horses given the 2 larger dosage schedules. The horses also had progressive increases in serum urea nitrogen, creatinine, and phosphorus concentrations, accompanied by decreasing serum calcium concentrations. There was a progressive decrease in total serum protein in all 8 horses. Gastrointestinal ulcerations, renal papillary necrosis, and vascular thromboses were the predominant postmortem findings.
A pregnant 10-year-old Paint mare was examined because of an acute neurologic disturbance. Physical examination revealed signs consistent with extensive, asymmetric brain stem disease. The hemogram, serum chemical panel, and results of lumbosacral spinal fluid analysis were within normal limits. A primary diagnosis of equine protozoal myeloencephalitis was considered, and the mare was placed on treatment with trimethoprim-sulfadiazine. After 5 weeks of steady improvement, an acute exacerbation of neurologic signs necessitated euthanasia of the mare. At necropsy, large, malacic tracts were found extending through the brain stem and cerebral cortex. Cross sections of a nematode were observed microscopically and subsequently were identified as belonging to a single gravid female Draschia megastoma.
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The effect of iopamidol on the leptomeninges was tested and compared with that of metrizamide and normal saline solution in 18 dogs. Pathologic and clinical effects were evaluated at 24 hours and 14 days after cisternal injection of iopamidol, metrizamide, or normal saline solution. Pathologic changes were evaluated by microscopic examination of serial CSF samples and of sections of brain and spinal cord with the leptomeninges intact. Clinical changes were subjectively evaluated. Electromyograms and EEG were performed on each dog after physical and neurologic examination. There were no changes seen in neurologic status, electromyogram, or EEG in any of the dogs immediately after subarachnoid injection nor at 24 hours or 14 days later. Pathologic changes were limited to mild, moderate, or severe patchy hemorrhagic leptomeningitis seen at 24 hours after iopamidol or metrizamide was injected. The severity of changes were judged to be similar with both these agents. The CSF analysis and histologic evaluation of brain and spinal cord sections revealed a neutrophilic response to iopamidol and a mononuclear response to metrizamide. These findings indicate that iopamidol has minimal neurotoxicologic effect on the leptomeninges and therefore has merit as a myelographic agent.
A technique for the subarachnoid perfusion-fixation of the central nervous system was developed to help identify various significant vascular accidents (SVAs) in the central nervous system (CNS) of 24 neonatal foals submitted for necropsy. SVAs, comprising subarachnoid, parenchymal and nerve root haemorrhages, and oedema and necrosis, occurred in 17 foals, more frequently in the spinal cord than the brain. They occurred as frequently in premature foals as in those born at full term, in foals born dead as in foals born alive, and in foals born following dystocia with an assisted delivery as in foals born unassisted. Eight of the live foals showed neurological signs. Those with syndromes of cerebral disease tended to have brain SVAs, whilst all 3 with signs of spinal cord disease had SVAs restricted to the spinal cord. No association between the SVAs and other specific disease processes was detected in these foals although 2 premature foals born dead with equine herpesvirus-1 infection did have spinal cord SVAs only. A similar distribution of brain and/or spinal cord SVAs was detected in the foals born dead as in the live foals, but the lesions were more severe. It is concluded that the birth process itself may be a major factor in the development of SVAs and that some affected foals may exhibit a syndrome referable to spinal cord involvement.
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Equine protozoal myeloencephalitis (EPM) was diagnosed in 10 horses. By electron microscopy, schizonts were found in intact host cells of the spinal cords or, more frequently, free in the extracellular spaces. Developmental stages of schizonts differed morphologically, and the late stage of schizogony was characterized by endopolygeny. These findings permitted tentative identification of the protozoon as a Sarcocystis sp. Free merozoites were present in the extracellular spaces or in cells of the spinal cord. Pericytes of capillaries were most frequently parasitized by merozoites were present in the extracellular spaces or in cells of te spinal cord. Pericytes of capillaries were most frequently parasitized by merozoites, but the cytoplasm of neurons, macrophages, intravascular and tissue neutrophils, and axons of myelinated nerve fibers also contained these organisms. The presence of parasites in the cytoplasm of tissue and circulating neutrophils suggest that this putative Sarcocystis sp. may have a hematogenous phase of infection.
Naturally occurring bovine sarcocystosis caused death and illness in eight dairy heifers. Clinical disease was characterized by cachexia, peripheral lymph node enlargement, and anemia. Increased amounts of serum enzymes and anti-Sarcocystis antibody titers were present in affected animal. Macroscopic findings in two heifers at necropsy included emaciation and serous atrophy. Necropsied heifers (No. 1 and 2) contained different developmental stages of Sarcocystis cruzi; each stage was characterized by specific histopathologic findings. Heifer 1 had vascular endothelial schizonts in various soft tissues, with mild mononuclear cell infiltration, alveolar capillary fibrinous thrombi, and multifocal splenic necrosis. Heifer 2 had developing young S cruzi cysts, in myofibrils of cardiac and skeletal muscles, with a concurrent multifocal degenerative myositis. Marked lymphoid hyperplasia occurred in both heifers.
From a clinical, radiological and morphological study of 9 horses with congenital malformations of the occiput, atlas and axis, and from a study of 2 reported cases, 3 diseases were defined: A. Familial occipitalisation of the atlas with atlantalisation of the axis in Arabian horses (7 cases in this report and the case reported by Leipold, et al., 1974). These horses had congenital atlantooccipital fusion, hypoplasia of the atlas and dens, malformation of the axis and modification of the atlantoaxial joint. B. Congenital asymmetrical occipitoatlantoaxial malformation (2 cases in this report). A Standardbred and a Morgan horse had atlantooccipital fusion, a wedge shaped vertebral piece attached to the caudal end of the axis and sigmoid scoliosis of the cervical vertebrae. C. Asymmetrical atlantooccipital fusion (the case reported by Schmaltz, 1915). This horse of an unknown breed had asymmetrical fusion between the atlas and occiput and cervical scoliosis. The clinical syndromes shown by horses with these malformations were variable but were broadly classified as: 1. Foal dead at birth, seen in one foal with A. 2. Tetraparesis at birth, seen in 5 foals with A. These foals were born with signs varying from tetraparesis to tetraplegia. 3. Progressive ataxia, seen in 2 foals with A. Clinical signs were due to a progressive focal cervical compressive myelopathy. 4. Congenital cervical scoliosis/deviated head, seen in the 2 horses with B and the horse with C. These horses had no signs of spinal cord or brain disease. The diagnoses were made clinically by palpation of the occipitoatlantoaxial region and were confirmed radiographically and/or by post mortem examination in all except one case. Pedigree analysis showed the familial nature of the particular occipitoatlantoaxial malformation seen in horses of only the Arabian breed.
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Immunotherapy was attempted in 2 Arabian foals with combined immunodeficiency. One foal was given a transplant of bone marrow from a selected full sibling, and 1 foal was given a fetal thymus transplant. Both foals died. Genetic evidence was obtained for survival of the transplanted tissues in both cases; however, a graft versus host reaction developed in the foal given the fetal thymus transplant.