Characterization of an outbreak of Clostridium perfringens food poisoning by quantitative fecal culture and fecal enterotoxin measurement.

Published criteria for implicating Clostridium perfringens as the cause of food-poisoning outbreaks include finding a median fecal C. perfringens spore count of greater than 10(6)/g among specimens from ill persons. We investigated a food-poisoning outbreak with the epidemiologic characteristics of C. perfringens-related disease in a nursing home in which the median fecal spore count for ill patients (2.5 X 10(7)/g) was similar to that for well patients (4.0 X 10(6)/g), making the etiology of the outbreak uncertain. All ill and well patients tested had eaten turkey, the implicated food item. C. perfringens enterotoxin was detected by reverse passive latex agglutination in fecal specimens from six of six ill and none of four well patients who had eaten turkey (P = 0.005), suggesting that this organism had caused the outbreak. This investigation suggests that detection of fecal C. perfringens enterotoxin is a specific way to identify this organism as the causative agent in food-poisoning outbreaks.

Risk factors for secondary transmission in households after a common-source outbreak of Norwalk gastroenteritis.

In November 1984, a foodborne outbreak of Norwalk gastroenteritis occurred in a K-12 public school in northern Vermont. The outbreak offered an opportunity to systematically study in detail secondary transmission rates in households. Eating salad at Tuesday's school-sponsored Thanksgiving Banquet was associated with illness among students and staff members (p less than 0.025). Seven of 11 serum pairs from ill persons showed a fourfold or greater rise in antibody titer to Norwalk virus compared with one of nine controls (p = 0.028). The study of secondary household transmission revealed that households with persons with primary illness were 5.5 times more likely to experience secondary illness than households with well school children or adults. As the number of individuals with primary illness in the household increased, the secondary illness rates increased. Pre-school children were twice as likely as adults to develop secondary illness.

Evidence for school transmission of Neisseria meningitidis during a Vermont outbreak.

A meningitis outbreak due to Neisseria meningitidis, serogroup C, serotype 2b, occurred in central Vermont in February, 1984. The highest incidence was in Northfield, where 7 cases occurred (129 per 100,000 population). Of these 7 cases 2 were students at Northfield High School and 5 were younger children; all had had close contact with Northfield High School students or staff in the week before illness. A case-control study demonstrated that these cases had significantly more exposure to Northfield High School students or staff in the 2 weeks before illness (112 hours) than did controls (8 hours) (P = 0.006). This finding was confirmed by a second case-control study designed to determine risk factors for the entire outbreak. School children in Northfield and their household contacts were given meningococcal A-C vaccine and sulfisoxazole prophylaxis. No further cases of meningococcal disease occurred in Northfield after the week that these control methods were initiated. Transmission of the outbreak strain of N. meningitidis appears to have occurred in a school setting with subsequent illness in household and close contacts of carriers of the outbreak strain.

[Differentiation of swine-Mycoplasma by latex-agglutination (author's transl)]. / Differenzierung von Schweine-Mycoplasmen mit Hilfe der Latex-Agglutination

UNLABELLED: The strains of Mycoplasma were grown in Shittlestone medium for 3-5 days. After centrifugation and washing, the mycoplasm were freeze-dried and stored at -20 degrees C. From this stock material immune sera and antigens were prepared. The immune sera were prepared by immunization of rabbits with a suspension of mycoplasma (2,2 mg dry weight per ml) and complete Freund's adjuvant. For the first immunication, 6.6 mg of antigen were injected into rabbits at different sites. 3 weeks later the second immunization followed by the intramuscular route (4.4 mg of antigen). The third and fourth immunizations were identical to the second one. Antiserum was obtained as usual. In order to avoid unspecific reactions in the latex agglutination, 1 ml of antiserum was added for absorption to 200 mg of freeze-dried sterile Whittlestone medium over 2 days at 4 degrees C. Antigen was prepared by ultrasonic disruption of mycoplasma (20 mg dry weight/ml physiological saline) and centrifugation 17300 X g, 30 min). The supernatant was used as antigen. The latex agglutination was performed in 0.1 M borate buffer pH 8,2. For preparation of the latex antigen compound 0.2 ml of a latex suspension (diluted 5 fold with water) were moxed with 0.5 ml of an antigen suspension (diluted 16 fold with buffer). After 10 min at room temperature, 4.3 ml of borate buffer were added. After 10 min, 0.3 ml of this solution were added again each to 0.3 ml of serial dilutions of anitserum. The suspensions were mixed and left for 20 h at 37 degrees C and after this time for 1 h at room temperature. Then the reactions were read. RESULTS: M. suipneumoniae and M. hyopneumoniae were found to be identical or very close related strains. Between M. hyorhinis and M. sp. E9 relationship was noted too. M. granularum was different to all other investigated strains of mycoplasma. All results of Latex agglutination are in agreement with investigations performed with the aid of other serological methods and of electrophoretic separations of cell proteins of these mycoplasma.