Biomedical subjects
T J Divers
Publications and source records attributed to T J Divers.
Toxic hepatopathy in neonatal foals.
Six foals of three different breeds, born to healthy mares, appeared normal at birth, and died at two to five days of age with icterus, ataxia, head pressing, and terminal hepatic coma. Their livers were less than one-half normal weight. Most of the liver was dark red-brown and slightly rubbery. Histologically, these areas were characterized by severe bile ductule proliferation, mild portal tract fibrosis, and massive hepatocellular necrosis and lobular collapse. A small proportion of the liver, usually on the peripheral part of the lobes, was grossly light brown and slightly raised. Histologically, these areas had mild to severe bile stasis in canaliculi. In the thin marginal zone between the severely affected and mildly affected liver, there was mild bile ductule proliferation and periportal fatty change and necrosis. Alzheimer's type II cells, characteristic of hepatoencephalopathy, were numerous in the brains of all foals. Within two hours after birth, all the foals had been given an oral proprietary nutritional paste, the ingredients of which included a viable Aspergillus sp and an iron compound. Similar lesions were produced in an experimental foal.
Renal clearance and fractional excretion of electrolytes over a 24-hour period in horses.
Four consecutive 6-hour urine collections were obtained from 10 healthy adult horses given free access to a complete pelleted ration and water. Samples of blood were collected from the jugular vein at the start of the test period and then every 6 hours for 4 consecutive samples. Mean renal clearance of creatinine (CCr) varied significantly during the four, 6-hour collections, ranging from 1.474 in period II to 2.702 ml/min/kg of body weight during period III (P less than 0.05). The CCr in period III was significantly different from the 24-hour mean value of 1.877 ml/min/kg (P less than 0.05). The mean 6-hour clearances of potassium (CK), chloride (CCl), and calcium (CCa) also varied significantly during the 4 collections (P less than 0.05). The 24-hour mean CK and CCl were different from the mean during period III (P less than 0.05). There was significant correlation between mean 24-hour CCr and CK (P less than 0.01); CCr and CCl (P less than 0.05); CNa and CK (P less than 0.01); CNa and CCl (P less than 0.01); and CK and CCl (P less than 0.001). The 95% confidence interval for 6-hour mean values of fractional excretion of Na (FENa) was 0.032% to 0.522%; FEK was 23.345% to 48.074%; FECl was 0.588% to 1.861%; and FECa was -0.158% to 6.723%. Although FENa, FECl, and FECa were highly variable within and between individual horses, mean values for periods I to IV did not differ significantly over time or from 24-hour mean values. The FEK varied less throughout the 24-hour test period. Mean urine volume, urine concentrations of Cr and K, urine osmolality, urine-to-plasma osmolality, urine-to-plasma urea nitrogen, and plasma urea nitrogen varied significantly through time periods I to IV (P less than 0.05); however, means for time periods I to IV were not different from 24-hour means.
Toxic hepatic failure in newborn foals.
Eight foals, 2 to 5 days of age, with similar clinical signs and laboratory and pathologic findings, died from hepatic failure. The predominant clinical signs were depression and icterus. Abnormally high values were found for plasma ammonia content, aromatic-to-branch-chain amino acid ratio, total serum bilirubin content, gamma glutamyl transferase activity, alkaline phosphatase activity, and PCV; partial thromboplastin time and prothrombin time were prolonged. Some foals had high sorbitol dehydrogenase activity. These laboratory findings were suggestive of subacute hepatic disease and failure. Predominant pathologic findings were limited to the liver and brain. The livers were less than half the expected size for 2- to 5-day-old foals, had prominent bile ductule proliferation, hepatic cell necrosis, and mild periportal fibrosis. These findings suggested both prenatal and postnatal diseases caused by exposure to a hepatoxin. The predominant lesion in the brain was the presence of Alzheimer type II astrocytes, which are characteristic of hepatoencephalopathy. Although the periportal fibrosis was suggestive of in utero exposure to a toxin, epidemiologic information suggested that the hepatic failure more likely resulted from oral inoculation of a microorganism culture product at birth. The same disease was reproduced in 2 newborn foals by feeding this product.
Systemic granulomatous inflammation in a horse grazing hairy vetch.
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Ruptured urinary bladder in a post-parturient cow.
Rupture of the urinary bladder at the time of parturition occurred in a 2 year old Angus cow. Anamnesis included a dystocia followed by a gradual (16 days) onset of anorexia and abdominal distension. Prominent findings on the physical examination were marked dehydration, symmetrical distension of the lower abdomen with ascitic fluid, pneumoperitoneum, absence of rumen contractions, and constipation. Significant laboratory findings were elevations of plasma protein, serum urea nitrogen (SUN) and creatinine, hypochloremia, hyponatremia, hyperkalemia, and metabolic acidosis. The ascitic fluid was present in large quantities (50 liters) and had a markedly elevated urea nitrogen and creatinine concentration when compared to serum values for these substances. Parotid salivary secretion had a reversal of the normal sodium: potassium ratio which was attributed to an increase in aldosterone levels brought about by the hyponatremia. A ventral tear in the urinary bladder was successfully repaired by laparotomy.
Acute renal disorders in cattle: a retrospective study of 22 cases.
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Hemolytic anemia and fibrinoid change of renal vessels in a horse.
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Hemolytic anemia in horses after the ingestion of red maple leaves.
Signs of acute hemolytic anemia developed in 4 adult horses from 2 Georgia farms 3 to 4 days after the ingestion of wilted leaves from cut red maple trees (Acer rubrum). Clinical findings included weakness, polypnea, tachycardia, depression, icterus, cyanosis, and brownish discoloration of the blood and urine. Blood changes included methemoglobinemia, free plasma hemoglobin, decreased pcv, and Heinz bodies in erythrocytes. These findings plus hemoglobinuria suggested intravascular hemolysis. Three of the 4 horses diet 5 to 7 days after ingestion of the leaves. Gross pathologic changes included generalized icterus, splenomegaly and swollen, black kidneys. Microscopic changes including tubular nephrosis with hemoglobin casts, vacuolization of centrilobular hepatocytes, and sequestration of erythrocytes in splenic sinusoids. A disease indistinguishable from the field cases was induced in a pony by the oral administration of dried, ground red maple leaves at a dosage of 1.5 g/kg. The findings of methemoglobinemia, hemolysis, and Heinz bodies suggested that the toxic principle of the red maple leaf was an oxidant.
Heinz body anemia and methemoglobinemia in ponies given red maple (acer rubrum L.) leaves.
Ponies given dried red maple (Acer rubrum L.) leaves at a dose of 3.0 gm/kg body weight became ill and died one to five days after administration of the leaves. Two clinical patterns of disease were seen. Ponies given dried leaves collected after September 15 died by 18 hours, while ponies given dried leaves collected before September 15 became ill with a hemolytic syndrome and died by three to five days. Freshly harvested leaves administered immediately after collection did not produce disease in ponies, but when dried, they became toxic and remained so for at least 30 days. Overnight freezing did not alter the toxicity of the leaves. Leaves were toxic when administered at doses of 1.5 gm/kg of body weight. The clinical signs of ponies with the hemolytic syndrome included polypnea, tachycardia, icterus, cyanosis, scleral petechiation, and brownish discoloration of the urine and blood. Blood changes of ponies with the hemolytic syndrome included anemia, hemoglobinemia, Heinz bodies, depletion of erythrocyte reduced glutathione, increased erythrocyte fragility, and increased serum levels of aspartate amino transferase, sorbitol dehydrogenase, plasma protein, and bilirubin. Lesions of ponies that died from the hemolytic syndrome included icterus, centrilobular hepatic degeneration, hemoglobinemic nephrosis, and erythrophagocytosis by splenic, adrenal, and hepatic phagocytes. Only brownish discoloration of the blood and mild centrilobular hepatic degeneration were observed in the four ponies that died peracutely.
Neomycin toxicosis in calves.
Calves (n = 4) were given neomycin (2.25 or 4.5 mg/kg) twice daily IM and were compared with 2 calves given penicillin IM. The 2 hallmarks of aminoglycoside toxicosis, nephrotoxicosis and ototoxicosis, were seen with both dosages of parenterally administered neomycin. Nephrotoxicosis was confirmed by abnormal findings in urinalysis (granular casts, proteinuria, low specific gravity), renal biopsy results (tubular degeneration and necrosis), and increased 24-hour amounts of urinary enzymes (alanine aminopeptidase and gamma-glutamyltranspeptidase). Azotemia, decreased creatinine clearance, polyuria, and polydipsia also were documented in calves given neomycin. Clinically, deafness was suspected in 2 calves and was documented by electrical auditory-evoked response tests. Abnormalities in partial thromboplastin times and renal residues of neomycin were seen in all 4 calves that were given neomycin, but not in calves that were given penicillin.
Experimental induction of Proteus mirabilis cystitis in the pony and evaluation of therapy with trimethoprim-sulfadiazine.
Proteus mirabilis cystitis was induced in 9 ponies by chemically eroding the bladder mucosa before the organism was inoculated. Comparisons were made in the treatment of P mirabilis cystitis between ponies treated daily for 13 days with a trimethoprim-sulfadiazine (TMP-SDZ) paste and both positive and negative controls. Urine cultures from ponies treated with TMP-SDZ became negative for P mirabilis between days 3 and 9 after the start of the treatment, whereas positive controls remained infected until day 13. Urine cultures from all ponies were negative for P mirabilis on day 28. Urine concentrations of TMP and SDZ were relatively high after day 1 of therapy.
Serum concentrations of trimethoprim and sulfadiazine following oral paste administration to the horse.
Two fasted and 2 fed horses were dosed orally with a combined trimethoprim and sulfadiazine paste formulation at a dose of 35 mg (1:5 combined active ingredients)/kg. Serum concentrations of each drug were determined periodically for 3 consecutive days for the 4 horses. The extent and rate of absorption for trimethoprim were variable, but peak serum concentrations occurred generally within 3 hours; sulfadiazine absorption was slower, reaching peak concentrations by 6 hours. Fasting did not have a consistent effect on the serum concentration profiles for either drug. Both drugs achieved serum concentrations that equaled or exceeded the minimum inhibitory concentrations necessary to inhibit the growth of certain pathogens common to the horse. Thus, the paste formulation provides an effective means of dose administration of horses.
Diaphragmatic hernia in a cow.
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Neurologic disease induced by equine herpesvirus 1.
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The diagnosis and surgical correction of congenital portosystemic vascular anomalies in two calves and two foals.
Two calves and two foals presented with episodic clinical signs of diffuse central nervous system disease. Portosystemic anomalies were tentatively diagnosed based on the history, clinical signs and increased serum concentrations of blood ammonia and total serum bile acids with normal concentrations of liver derived enzymes. one calf died before intraoperative contrast portography, whereas the other calf and both foals had marked clinical improvement after intensive medical therapy. Surgical correction was attempted in these three animals and was successful in one foal. A right paracostal celiotomy was superior to a ventral median approach for exposure to the portal vascular system and shunt access.
Hepatic failure in dairy cattle following mastitis or metritis.
Hepatic failure developed following mastitis or metritis in five adult cows. In all five cases, cows initially showed clinical signs compatible with endotoxemia, which resolved with appropriate therapy for the mastitis or metritis. Subsequently, signs of liver failure developed including profound anorexia, weight loss, cessation of milk production, and in one case, photosensitization. Four cows had laboratory evidence of liver disease and failure (abnormally prolonged sulfobromophthalein [BSP] clearance half-life and abnormally high serum liver enzyme activity). Hepatocellular necrosis or vacuolization was seen on histopathologic examination of liver specimens from all five cows. The hepatocellular necrosis, in some cases, was thought to be due to the direct or indirect effects of endotoxin on the liver. Three of the cows responded to symptomatic therapy. One cow failed to respond and one was not treated.
Ulcerative dermatitis, thrombocytopenia, and neutropenia in neonatal foals.
This report describes transient ulcerative dermatitis, severe thrombocytopenia, and mild neutropenia in 6 foals from 4 mares from geographically diverse regions of the United States. The foals presented at <4 days of age with oral and lingual ulcers, and crusting and erythema around the eyes, muzzle, and perineal, inguinal, axillary, trunk, and neck regions. There was a severe thrombocytopenia (0-30,000 platelets/microL), leukopenia (1900-3200 white blood cells/microL), and mild neutropenia (500-1800 neutrophils/microL). Four of the 6 foals had petechiae and ecchymotic hemorrhages and 3 had bleeding tendencies. Results of examination of a bone marrow biopsy from 1 foal were normal and results of a platelet surface immunoglobulin test in another were negative. Histopathology of the skin in all foals showed subepidermal clefting with subjacent vascular dilation, dermal hemorrhage, and superficial papillary necrosis. The foals were treated supportively with broad-spectrum antibiotics (5/6), corticosteroids (3/6), gastric ulcer prophylaxis (6/6), whole-blood transfusion (4/6), and platelet-rich plasma (1/6). The skin lesions and thrombocytopenia (>50,000 platelets/microL) improved in 2 weeks (4/6). Two foals had a decline in their platelet counts when the steroids were decreased and needed protracted treatment. All foals survived and were healthy as yearlings. Two mares that had 2 affected foals each, upon subsequent pregnancies to different stallions, had healthy foals when an alternate source of colostrum was given. The findings in the cases in this report suggest a possible relationship between colostral antibodies or some other factor in the colostrum and the thrombocytopenia and skin lesions, although further investigation is warranted to confirm or refute this hypothesis.