Hypokalemia syndrome in dairy cows: 10 cases (1992-1996)

OBJECTIVE: To evaluate clinical findings in cows with recumbency associated with hypokalemia. DESIGN: Retrospective case series. ANIMALS: 10 adult dairy cows with weakness or recumbency and hypokalemia. PROCEDURE: Signalment, history, physical examination findings, results of diagnostic tests, and response to treatment were extracted from the medical record of each cow. RESULTS: 8 cows were recumbent on admission and 2 were profoundly weak. All cows had been given isoflupredone acetate as treatment for ketosis prior to admission. All were hypokalemic (serum potassium concentration, 1.4 to 2.3 mEq/L) with no other apparent cause for recumbency. Despite treatment with potassium, plasma potassium concentrations within the reference range were achieved in only 6 of the 9 cows treated. Two cows responded to treatment. Three cows died, 3 were euthanatized, 2 improved clinically and were discharged, 1 was discharged while still recumbent, and 1 was sent to slaughter prior to treatment. Histologic examination of muscle tissue from 2 cows revealed myonecrosis and vacuolation consistent with hypokalemic myopathy. CLINICAL IMPLICATIONS: Hypokalemia should be considered in the differential diagnosis for cows that are weak or recumbent, particularly after treatment for ketosis with isoflupredone acetate. Aggressive treatment with potassium salts administered orally is indicated.

A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin.

A sudden death syndrome was induced in chicks and poults fed diets containing Fusarium fujikuroi, formulated to contain 0-330 mg/kg moniliformin (M) with or without the maximum recommended therapeutic concentration of monensin. Lesions of monensin toxicosis were not observed. Clinical signs were referable to cardiac dysfunction (sudden death, dyspnea, cyanosis, depression). Poults and chicks dying early in the study had no gross lesions or had lesions of right ventricular dilation. Treated poults and chicks dying late in the study or euthanatized at termination of the study had lesions of bilateral myocardial hypertrophy, usually concentric. Absolute heart weights and relative heart weights, expressed as a percentage of body weight, were significantly greater in treated birds than controls (P < 0.05), whereas body weights were significantly less (P < 0.05). Microscopically, lesions progressed from acute myocardial degeneration to necrosis, fibrosis, and hypertrophy. Ultrastructural findings were consistent with the gross and microscopic lesions. Serum pyruvate concentrations were a useful indicator of M-induced cardiotoxicosis. Concentrations of serum pyruvate increased with increased concentration of dietary M, but were not affected by addition of monensin to the diet. In chicks ingesting 40-300 mg/kg M, serum pyruvate concentrations were significantly greater (P > 0.05) than those in controls (controls, 0.28 +/- 0.08 mmol/liter; exposed 0.38 +/- 0.11-0.55 +/- 0.13 mmol/liter). Poults ingesting 80-330 mg/kg M had significantly greater serum pyruvate concentrations than controls (controls 0.33 +/- 0.09 mmol/liter; exposed 0.43 +/- 0.13-1.00 +/- 0.006 mmol/liter). The Vetronics System was used to evaluate electrocardiographic alterations in a limited number of chicks and poults surviving to the end of the feeding trial. Electrocardiographic alterations in poults and chicks fed diets containing > or = 40 mg/kg and > or = 160 mg/kg M, respectively, were consistent with ventricular hypertrophy, myocardial injury, and hypoxia. Electrocardiographic alterations were more striking in poults than in chicks. Altered myocardial metabolism due to M toxicosis, in conjunction with the unusual susceptibility of domestic poultry to altered cardiac metabolism, is believed to be the cause of the organ-specific lesions in these birds. These findings suggest that cardiac injury with subsequent alterations in cardiac electrical conductance may be a cause of the sudden deaths observed in poultry chronically intoxicated with dietary M.

Purified moniliformin does not affect the force or rate of contraction of isolated guinea pig atria.

Chronic exposure to moniliformin results in the development of myocardial hypertrophy and degeneration. The cause of this hypertrophy is unknown. However, moniliformin-induced hypoxia or altered function of cardiac pyruvate dehydrogenase, rather than direct cardiostimulation have been proposed as potential mechanisms. Isolated guinea pig atria were used in a cumulative concentration-response model to evaluate the direct effect of moniliformin on the rate and force of atrial contraction. Moniliformin did not affect the rate or force of atrial contraction. These results are consistent with the hypothesis that moniliformin does not have a cardiostimulatory effect. Therefore cardiac stimulation. e.g. stimulation of beta-adrenergic receptors, is unlikely to be the cause of the myocardial hypertrophy observed in poultry chronically intoxicated with moniliformin.

Streptococcus suis infection in swine: a retrospective study of 256 cases. Part II. Clinical signs, gross and microscopic lesions, and coexisting microorganisms.

A retrospective study of 256 cases of naturally acquired Streptococcus suis infections in swine submitted to the Indiana Animal Disease Diagnostic Laboratory from 1985 to 1989 was undertaken to describe the clinical signs, lesions, and coexisting organisms associated with S. suis serotypes 1-8 and 1/2. Infected pigs generally had clinical signs and gross lesions referable to either the respiratory system or to the central nervous system (CNS), but not both. Neurologic signs were inversely related to gross lesions in the respiratory tract (R2 = -0.19, P = 0.003), as were respiratory signs and gross lesions in the CNS (R2 = -0.19, P = 0.003). Suppurative bronchopneumonia was the most common gross lesion observed (55.2%, overall). Fibrinous and/or suppurative pleuritis, epicarditis, pericarditis, arthritis, peritonitis, and polyserositis were also reported. In 68% of the pigs, other bacteria in addition to S. suis were isolated. Escherichia coli (35.0%) and Pasteurella multocida (30.0%) were the most commonly recovered bacterial agents. Mycoplasma and viral agents were identified less often, and their role in the development of streptococcosis was difficult to assess. In pigs infected with serotypes 2-5, 7, 8, and 1/2, suppurative meningitis with suppurative or nonsuppurative encephalitis, suppurative bronchopneumonia, fibrinopurulent epicarditis, multifocal myocarditis, and cardiac vasculitis were the most common microscopic lesions observed, whereas pigs infected with serotype 1 generally presented with suppurative meningitis and interstitial pneumonia. Microscopic lesions were morphologically similar among serotypes and were also similar to those reported with other pyogenic bacteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Confirmation of a pulmonary component of multicentric lymphosarcoma with bronchoalveolar lavage in two dogs.

Histologic examination of lung tissue has been the only definitive diagnostic procedure used to confirm pulmonary involvement with lymphosarcoma (LSA) in dogs. Lung involvement with LSA was diagnosed by cytologic examination of bronchoalveolar lavage fluid in 2 dogs with multicentric LSA. Both dogs had cough or dyspnea, in addition to peripheral lymphadenopathy or visceral organomegaly. Both dogs had nonspecific, abnormal thoracic radiographic findings, including diffuse pulmonary interstitial pattern, hydrothorax, and mediastinal and retrosternal lymphadenopathy. In these 2 dogs, postmortem lung histologic examination, performed immediately after bronchoalveolar lavage, confirmed the cytologic diagnosis of pulmonary infiltration with LSA.

Streptococcus suis infection in swine: a retrospective study of 256 cases. Part I. Epidemiologic factors and antibiotic susceptibility patterns.

A retrospective study of 256 cases of naturally acquired Streptococcus suis infections in swine submitted to the Indiana Animal Disease Diagnostic Laboratory from 1985 to 1989 was performed to determine the epidemiologic factors and antibiotic susceptibility patterns associated with S. suis serotypes 1-8 and 1/2. A standardized computer form was used to record the history, signalment, and clinical signs obtained from the records of selected cases and the microscopic lesions identified after review of the histopathology slides for each case. A computer statistics package (SAS) was used to evaluate the data. Although the number of recovered S. suis isolates increased in the fall and winter months, most serotypes were readily isolated throughout the year; only serotypes 1, 4, 7, and 1/2 increased in frequency of isolation in the fall, winter, and spring months. The majority (61.1%) of infected pigs in this study were < 12 weeks of age. More than 75% of pigs infected with serotypes 1, 6, 7, and 1/2 were < 12 weeks of age. There was extensive overlap in the age distributions for pigs with each serotype, and statistically significant differences for most serotypes were not observed. Fifty percent of pigs infected with S. suis serotypes 1 and 1/2 were 3-10 weeks of age, 50% of pigs infected with serotype 2 were 6-14 weeks of age, and 50% of pigs infected with serotypes 3, 4, 5, 7, and 8 were 2-16 weeks of age. Isolates of S. suis were not uniformly susceptible to penicillin, and a large percentage of isolates were resistant to many antibiotics in common usage.(ABSTRACT TRUNCATED AT 250 WORDS)