Daniel D. Harrington

Streptococclcs 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 (R 2 = −0.19, P = 0.003), as were respiratory signs and gross lesions in the CNS (R 2 = −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. The distribution of clinical signs and the gross and microscopic lesions in pigs infected with S. suis varied among serotypes. However, these differences were not statistically significant and could not be used to distinguish between the various serotypes. These findings suggest that in pigs infected with S. suis, suppurative or fibrinopurulent inflammation in brain, heart, lungs, and serosae predominates and that bacterial culture is needed to confirm a diagnosis of streptococcosis in swine and to differentiate this disease from those caused by other pyogenic bacteria.

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.

Multiple serotypes and strains of Streptococcus suis in naturally infected swine herds.

We present a brief description of the epidemiology, clinical signs, and lesions in 21 accessions in which multiple serotypes of S. suis or multiple distinct isolates (strains) of the same capsular serotype of S. suis were identified. Isolates of the same capsular serotype that had different antibiogram profiles were considered to be distinct isolates or “strains” for the purposes of this study. Streptococcus suis isolates of the same capsular serotype and identical antibiogram profiles were considered to be identical organisms. These cases were selected to determine whether or not herds infected with multiple serotypes (or strains) of S. suis had unique features that might serve to distinguish these herds from those infected with a single serotype and strain of S. suis and to provide additional information on the development of this disease in swine. Selected cases were limited to those in which isolates were identified by capsular serotyping. Untypeable isolates of S. suis were not included in this study. Case selection criteria, data collection procedures, etc., were as previously described. 12 Of 277 accessions in which S. suis was identified, 21 accessions (7.6%) involving 37 pigs were cases in which 46 different isolates of S. suis were identified. The distribution of these isolates is shown in Tables 1 and 2. Because of the small sample size, statistical analyses were not performed. Although there was a slight increase in recovery of S. suis in the fall and winter months for all serotypes, S. suis was readily isolated throughout the year. In this study, there was a slight increase (approximately 5%) in the prevalence of serotypes 3, 7, and 8 and a decrease (approximately 10%) in the prevalence of serotype 2 from those reported previously. 12

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 (SAP) 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 (6 1.1%) 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. The results of this study indicated that the various serotypes of S. suis could not be readily separated based on antibiograms, epidemiologic factors (herd size, breed, etc.), or geographic location.

Association of magnesium deficiency with the blood pressure-lowering effects of calcium

The role of dietary calcium and magnesium in the development of hypertension was studied in nine groups, each consisting of nine spontaneously hypertensive rats aged 8-31 weeks. The animals were fed AIN 76A semi-purified diets varying in calcium (0.075, 0.5 and 2.5%) and magnesium (0.01, 0.05 and 0.75%) concentrations according to a 3 x 3 factorial design. Dietary calcium and systolic blood pressure were inversely related, significantly (P less than 0.05) after 12 weeks. Total and ultrafilterable serum calcium concentrations were also significantly negatively correlated with blood pressure (r = -0.46; P = 0.001 and r = -0.57; P = 0.001, respectively). Repeated measures analysis of variance indicated that dietary magnesium had no effect on systolic blood pressure, and no calcium x magnesium interaction on blood pressure was observed. Signs of magnesium deficiency, calcium deposits in the kidneys, and histological lesions were observed in groups on a high-calcium diet receiving normal and low levels of magnesium. Thus a lowering of blood pressure by calcium supplementation, without concomitant magnesium supplementation, was accompanied by biochemical and histological abnormalities in this animal model.

Development of an L6 myoblast in vitro model of moniliformin toxicosis

L6 myoblasts were used as an in vitro model to investigate the role of moniliformin and its interaction with monensin in turkey knockdown syndrome and sudden death syndromes in poultry. Cell viability and microscopic and ultrastructural alterations noted in L6 myoblasts cultured in the presence of moniliformin (0.0–0.3 μg/μl) were compared to those observed in parallel cultures also containing one of the following compounds: selenium (0–0.004 ng/μl), thiamine (0–0.3 μg/μl), or pyruvate (0–0.46 μg/μl). Marked dilation of the RER, membranous whorls, glycogen deposition, membrane-bound cytoplasmic inclusions and necrosis were observed in myoblasts exposed to 0.03/2-0.30 μg moniliformin/μl medium. Supplementation of medium with thiamine and pyruvate, or selenium, provided significant protection to cells exposed to 0.0–0.3 μg/μl or 0.0–0.15 μg moniliformin/μl, respectively. Dose-dependent differences in protein and ATP production were not detected. Myoblasts grown in medium containing 0–0.15 μg moniliformin/μl and 7.5–50.0 μM A23187, beauvericin or monensin had degrees of cytotoxicity similar to parallel cultures receiving only an ionophore. L6 myoblasts were a useful model of moniliformin toxicosis. The findings of this study suggest cytotoxicity due to moniliformin in L6 myoblasts may be due in part to oxidative damage and altered pyruvate metabolism, and that moniliformin does not predispose myoblasts to ionophore toxicosis. This study supports the results of in vivo investigations in poultry that moniliformin and monensin do not act synergistically to induce knockdown or monensin toxicosis.

Dietary Magnesium does not Affect Blood Pressure in Spontaneously Hypertensive Rats

To determine the therapeutic effectiveness of dietary magnesium in the treatment of established hypertension, 21 male spontaneously hypertensive rats were fed altered levels of magnesium oxide from 17 to 29 weeks of age. The rats were divided into three groups of approximately equal mean baseline systolic blood pressures and fed AIN 76A purified diets containing magnesium at 0.01% (low), 0.05% (normal), and 0.40% (high) levels. Mean systolic blood pressures in the conscious SHR during the 12 week period and terminal direct blood pressures under anesthesia were not significantly different among treatment groups. Total and ultrafilterable serum magnesium concentrations reflected dietary magnesium intake. Total and ultrafilterable serum calcium levels were significantly higher (p less than 0.05) in the low magnesium-fed SHR. Histopathologic alterations indicative of aging did not differ among treatment groups. Therefore, in spite of altered serum mineral status, blood pressure and histopathology were not affected by dietary magnesium.

Fibrinohemorrhagic Pneumonia in Pigs Naturally Infected with Streptococcus Suis

than currently known. The presence of this microorganism in a variety of animal species, including birds (L. E. Devriese, personal communication, 1994), could contribute to the increase of the number of capsular types and indicates that this bacterium should no longer be recognized solely as a swine pathogen. The large number of S. suis capsular types now identified results in more time and expense for diagnostic laboratories involved in serotyping. Based on data collected in recent years that indicate that most S. suis isolates from diseased pigs belong to 1 of the first 9 capsular types, we suggest that diagnostic laboratories routinely test for these serotypes only. When isolates are unreactive with antisera 1-8, they could be forwarded to a reference laboratory for further characterization.

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 hi poultry chronically intoxicated with moniliformin.