Food poisoning from pasteurised milk

Food poisoning from pasteurised milk

1940 Food Poisoning from Pasteurised Milk The transmission of pathogenic bacteria or their toxins by pasteurised milk is so rare that every authentica...

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1940 Food Poisoning from Pasteurised Milk The transmission of pathogenic bacteria or their toxins by pasteurised milk is so rare that every authenticated instance deserves notice. On September 25th and 27th, 1937, 29 persons living in a town in Oklahoma sickened with the usual symptoms of food poisoning within one and a half to seven hours after a meal, usually within two or three hours.* The outbreak was, therefore, presumably toxic in origin. The common article of consumption was pasteurised milk; those who shared meals with the subsequent sufferers but eschewed milk escaped. The evidence suggested that all the milk incriminated had been pasteurised and bottled on September 24th. Samples of milk remaining in the bottles were found to contain potentially toxic staphylococci. Six producers supplied raw milk to the pasteuriser, and four of these supplies were found to be similarly infected. Samples, however, both of the pasteurised milk in general and of portions of the milk which actually caused illness were demonstrated hy the phosphatase test to have been efficiently treated and it is therefore assumed that this infection was destroyed and that re-infection subsequently occurred. Although the soluble toxin might not have been destroyed by heat, it has to be remembered that living staphylococci were isolated from the milk which had been pasteurised and bottled. The plant was found on inspection to be adequate as regards pasteurisation, but the cleaning and sterilising equipment was defective and bottling and capping were done by hand. Three out of five employees were found to have positive nose and throat cultures and one of these had pustules on his face and body. It is believed, therefore, that contamination occurred at the time of bottling and capping, either from hands or by coughing or sneezing across a group of still uncapped bottles. It is conceivable, however, that the bulk of the toxin causing illness might have been derived from the raw milk, have survived pasteurisation, and not have been elaborated by the later staphylococcal invasion. The complete elucidation of such epidemics, although it is facilitated by the brevity of the incubation period, is hampered by the difficulty of the laboratory technique involved in demonstrating that the strain of staphylococcus isolated is definitely toxic in this sense, and not just potentially so. In this connection recent work in the U.S. Department of Agriculturet affords some evidence that the differentiation of enterotoxic *Hackler, J. F. (1939) . Amer. J. Pub. Hlth., 29, 1247. +Slocum, G. G. and Linden, B. A. (1939). Amer. J. Pub. Hlth., 29, 1326.

PUBLIC HEALTH staphylococci may be simplified and expedited by other means than the feeding or intraperitoneal injection of sterile filtrates to kittens. A preliminary report indicates that enterotoxic strains incubated with horse serum at 37 ° C. for three hours and then stored overnight at 7 ° C. failed to agglutinate, whereas non-enterotoxic strains were completely agglutinated in 1 to 10 serum dilutions and almost completely in 1 to 20. If further work confirms the value of this mode of differentiation, epidemiological investigation will be greatly facilitated. This article also draws attention to the frequency of outbreaks of staphylococcal food poisoning from salt-cured ham and beef-tongue, this micro-organism apparently being able to withstand a higher salt concentration than salmonella.

Tuberculosis and,Social Conditions It has long been known that there is a close connection between poverty and tuberculosis, and that young adults are especially liable to become victims of this disease. The report* by Drs. D'Arcy Hart and Payling Wright, recently issued, presents the results of a statistical investigation into the changes in some of the more important factors in social conditions correlated with the rate of decline in the number of deaths from pulmonary tuberculosis, especially in the age group, 15 to 24, during the last 90 years. The social factors under consideration are standard of living as estimated by real earnings, sub-standard housing (percentage of population living more than two per room,) internal migration between different county boroughs, changes in the volume of industrial occupation, and nutrition. The authors have been very thorough in the compilation of their material, most careful in its analysis and modest in stating their conclusions, which provide ample food for thought for all public health authorities and social workers. In the first chapter, the rate of decline in deaths from respiratory tuberculosis is considered with reference to sex and age groups. It is shown that from 1850 to 1900 the decline was fairly steady for all groups, but that from 1900 the decline for the female age group, 15 to 24, has been retarded, as compared with the o t h e r groups, until 1933, since when it again approximated to the general rate of decline, but the mortality is naturally higher than it would have been had no retardation taken place. A similar but not so marked retardation is shown in the male age *Tuberculosis and Social Conditions in England with Special Reference to Young Adults. By P. D'Arcy Hart and G, Payling Wright. London. National Association for the Prevention of Tuberculosis, Pages vii-~- 165. Price 3s.

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