This paper consists of an epidemiological study of 52 cases of Q fever occurring in metropolitan Adelaide in 1957 and also a description of the results of a survey of 516 sera obtained from abattoir workers.The only case occurring outside the abattoirs was a dairy farmer who probably became infected while visiting the abattoirs. If this were so the incubation period (35 days) of his disease would have been exceptionally long.The general features of the outbreak, which lasted several months, differed from those on the North American continent in that the latter occurred explosively within a few days with very high attack rates. The situation in the Adelaide abattoirs is similar to that in Brisbane, where the disease appears to be endemic. However, unlike in Adelaide, cases are commonly recognized outside the abattoirs in Brisbane.In the abattoirs the disease affected mainly inspectors, those working on killing beef, and those working on offal. Mutton workers were not so severely affected. However, all these groups had similar incidences of low titre antibodies suggesting that in the past Q fever spread equally in all killing departments. In departments not directly associated with slaughtering the incidence both of cases in 1957 and low titre antibodies was relatively small.It was suggested that the epidemiological features of Q fever in Adelaide could be explained by the irregular appearance of animals from infected herds situated perhaps in Queensland—a known endemic area. Perhaps the appearance of such animals in the Adelaide abattoirs might be governed by meteorological conditions such that they were prevented from going to the ordinarily most convenient slaughterhouse.
JOURNAL
SummaryThe clinical presentation of acute dilatation of the colon as a complication of ulcerative colitis is described. Four representative case histories from a series of 14 patients who presented in this way are reported.It is suggested that neither hypokalaemia nor destruction of the myenteric plexus is an important aetiological factor in the development of this condition. A more likely explanation would appear to be that this condition is due to structural damage to smooth muscle by ulceration and inflammation advancing through the thickness of the intestinal wall.The misleading clinical manifestations of smallintestinal obstruction and the significance of diminution of diarrhoea are discussed, emphasizing the pitfall of interpreting the latter as a favourable response to therapy.The value of simple radiological examination of the abdomen, without recourse to barium studies, which would be dangerous in such circumstances, is also emphasized.The policy of including colectomy in addition to faecal deflection in the treatment of acute dilatation of the colon in ulcerative colitis is jUstified by the results in this series.We wish to thank Mr. Bryan Brooke, who operated on all 14 patients, for permission to publish details of cases under his care, and to acknowledge his guidance, encouragement, and advice in the publication of this paper. Our thanks are also due to the Department of Pathology and Mr. Dee of the Department of Clinical Photography, Queen Elizabeth Hospital, Birmingham, for the histological sections and photomicrographs.
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