Hemosiderin deposits in the equine small intestine.
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Biomedical subjects
Publications and source records attributed to R Ochoa.
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These experiments systematically investigated ethanol preference in both the C57Bl/6N and C57Bl/6J mice utilizing three-choice 2-bottle preference test. In addition, these sublines were evaluated for whole brain methionine-enkephalin levels, which were significantly lower in C57Bl/6J mice (alcohol preferring) compared to C57Bl/6N mice (alcohol non-preferring). This finding supports the involvement of the peptidyl opiates in ethanol seeking behavior.
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Twenty seven adult horses positive to the agar gel immunodiffusion (AGID) test for equine infectious anemia (EIA), but with no history of clinical EIA, were used in transfusion studies to determine whether infectious EIA virus was present in 1 to 5 ml of their blood. Of 27 recipients, 21 (78%) became AGID test-positive at an average of 24 days after inoculation. Two horses that were initially negative when screened were retested and found to carry infectious virus in 5-300 ml of whole blood; the other 4 horses were not retested. Horse flies (Tabanus fuscicostatus Hine) were unable to transmit EIA virus from 10 AGID test-positive donors with no history of clinical EIA, but virus was transmitted from a pony with artificially induced acute EIA and from a horse that had recovered from a clinical attack of EIA 9 months earlier. Histopathologic changes indicative of EIA were noted in all test-positive recipients. The most consistent lesion was paracortical lymphoid hyperplasia in the splenic lymph node.
In 4 horses with equine infectious anemia (EIA), the predominant clinical sign was ataxia. Other clinical and laboratory findings often associated with EIA included weight loss, anemia, pyrexia, thrombocytopenia, hemorrhages, hypergammaglobulinemia, and high activity of biliary epithelial enzymes. Neuropathologic findings were nonsuppurative granulomatous ependymitis, meningitis, and encephalomyelitis and plasmacytic-lymphocytic infiltration of the brain and spinal cord. The onset of neurologic signs corresponded to the acute stage of infection in at least 2 horses, and the signs developed at least 18 months after infection in 1 case. Cerebrospinal fluid from 3 of the horses contained high concentration of protein and white cells, although changes in 1 horse may have been associated with a prior traumatic attempt to collect CSF. By comparison, CSF from 3 ponies inapparently infected with EIA was normal. Active production of anti-EIA antibody in the CSF was suspected on the basis of serologic findings.
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This study deals with the roles of T and B cells in Nocardia brasiliensis infection in mice. Nocardia injected into the animals' footpads caused inflammatory responses and mycetomas in situ, resulting in granulomatous lesions of subcutaneous tissues and eventual bone destruction. These clinical features resemble those of humans infected with Nocardia. The effect, if any, of antibody was studied by passively transferring anti-Nocardia serum into either immunologically normal or T-deficient infected mice. Such transfers had no protective function in either group. To the contrary, the antibody seemed to favor infection and worsen bone disease compared to that in mice not given antibody. Furthermore, passive transfer of the antibody along with injection of Nocardia coated with the antibody magnified the severity of subsequent symptoms. Although these experiments ruled out any role for antibody in protection from Nocardia, they did not directly prove T cell participation in such resistance. Therefore, the role of T cells during Nocardia infection was examined further by transferring spleen cells depleted of B lymphocytes bearing receptors for a Nocardia extract (NE). Lethally irradiated mice reconstituted with a population depleted of NE-specific B cells totally lacked the ability to form antibodies to NE; however, they mounted effective delayed-type hypersensitivity reactions and completely controlled their Nocardia infection, establishing the importance of cell-mediated immunity in halting this disease process.
Nonimmune pony foals 9 to 12 mo of age were vaccinated with third-stage Strongylus vulgaris larvae (L3) irradiated with 70, 100, or 130 Kr of gamma radiation. Ponies receiving per os inoculations of L3 irradiated with 70 or 100 Kr were protected from the clinical disease and lesions associated with challenge infections of 4,300 L3, when compared to nonvaccinated controls. Similarly, the numbers of worms from the challenging population recovered from successfully vaccinated animals were significantly lower than from nonvaccinated controls. The degree of resistance that develops in individuals can be semiquantitated based on clinical and pathological responses.
Bullous pemphigoid in a dog was diagnosed on the basis of clinical, histopathologic, and immunologic criteria. There were widespread ulcerative lesions of the skin. Numerous ulcerative lesions and occasional bullous lesions were on the oral mucous membranes. Histopathologic changes included dermal-epidermal separation, with subepidermal production of bullae. Direct immunofluorescent staining of the skin revealed depositions of immunoglobulin G and of the 3rd component of the complement system. Indirect immunofluorescent staining of donor skin sections pretreated with patient's serum revealed antibasement membrane antibody in the patient's serum. Most of the data in the serum immune profile were within normal ranges. Prednisolone therapy did not effect remission at the dosage of 4.4 mg/kg/day, but led to the beginning of remission within 7 days at a dosage of 6.6 mg/kg/day. The dosage was gradually reduced to 1.1 mg/kg, at 30 days, after which the drug was given on alternate days at that dosage. The healing was complete within 35 days, without any remissions when the dog was last examined (ie, over 6 months).
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Helminths similar to Strongyloides stercoralis were recovered from the jejunum and ileum of a 6-month-old Boston Terrier that was shedding unusually large eggs, both unembryonated and embryonated, as well as first-stage larvae in fresh feces. Clinical signs included stunting, mucoid and blood-flecked feces, radiographic evidence of diffuse interstitial pulmonary infiltrate, focal dermatitis, and anemia. Decreased intestinal absorption of carbohydrate was found by means of the oral glucose and oral lactose tolerance tests. Serum protein and calcium values were decreased. At necropsy, histopathologic findings included uneven crypt hyperplasia and mild inflammation in the ileum and jejunum, diffuse interstitial pulmonary inflammation, Kupffer's cell hyperplasia in the liver, and generalized lymph node hyperplasia.
Dermal and epidermal laminar lesions were correlated with acute intestinal, primary hepatic, septicemic, chronic laminar, and acute laminar diseases. Horses with acute intestinal disease had edema in the secondary dermal laminae. Those with hepatic disease had increased keratinization of the secondary epidermal laminae. Septicemia caused increased keratin formation in the primary and secondary epidermal laminae. Chronic laminitis caused architectural changes of the epidermal laminae characterized by hyperplasia and keratin formation of the basal epidermal layer. Horses with acute laminitis had epidermal necrosis, especially with peracute laminitis. Various insults to the epidermal laminae led to epithelial hyperplasia of the secondary epidermis with ventral deviation of the third phalanx.
Severe abdominal pain, classic colic signs and hemorrhagic gastro-entero-cecocolitis were induced in three conventional Shetland ponies by intravenous injection with Clostridium perfringens Type A enterotoxin. Histological examination showed marked congestion, edema and hemorrhage of the large and small intestine and sloughing of the tips of the intestinal villi. Marked vacuolar degeneration of hepatocytes with dilatation of the spaces of Disse also was found. Clinical changes consisted of severe hypoglycemia, markedly increased aspartate aminotransferase levels and leukopenia that occurred rapidly.
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