1989 Volume 63 Issue 4 Pages 410-416
We had an outbreak of 14 cases of enterocolitis due to Clostridium perfringens (Cl. perfringens) in a hospital for the severe multiply-disabled, where the 100 disabled were admitted, in summer in 1985.
The signs and symptoms shown by this enterocolitis were primarily diarrhea without fever and loss of appetite.
The feces of 10 cases were examined bacteriologically. The test showed 103 to 106 cells of Cl. perfringens per one gram of their feces and all the strains isolated were untypable by the classification of Hobbs. Nine out of 10 cases were randomly selected and all of the 9 cases were proved to have enterotoxin producing strains.
All the strains were highly sensitive to many kinds of antibiotics except kanamycine and gentamicin.
Eleven out of the 14 cases were admitted in the same ward and the 7 out of the 11 cases were in the same room of this ward. Considering the spreading route of this infection, itis unlikely that this outbreak occurred due to food supplied from kitchen in this hospital, becauseall of the disabled, admitted in this hospital, had little chance by which some of the disabled only in a specific ward or room were supplied with bacteriologically contaminated meals from the point of view of cooking and supplying system of this hosptial. Adding to this fact, if this outbreak was due to food-born infection, the symptoms of most patients should occur within 1-2 days, because the incubation period of this disease is within a day, however, the patients increased day by day for more than a week. On the other hand, the 7 patients occurring in the same room were able to touch each otherby moving through walking, kneel walking and/or bottom shuffling. Furthermore, all of them inevitably wore diapers, some of them might touch and lick their own feces. Therefore there might be saveral chances by which the cells of Cl. perfringens in their feces were orally taken through their and/or care-takers' fingers, toys and clothes.
We discussed whether enterocolitis would be caused with such a small numbers of bacteria as these taken in this manner. It is said that cells of Cl. perfringens exist mainly as spores in feces and as cells during growth in foods propagated by the bacteria. Furthermore, the spores are known to resist against acid much more than the cells during growth. In order to ascertain whether the spores survived in gastric juice, we showed that most of the spores of Cl. perfringens from a case of this outbreak which had the ability to produce enterotoxin survived, when incubated in culture medium acidified (pH=1.6) with HC1 at 37°C for 30 minuites; on the other hand, it was shown that the cells during growth decreased in numbers to 1/104 of the initial counts.
From these facts, we suggested that this outbreak must not have been food-born, but due to orally taken bacteria in feces.
