IN 1932 and 1934, Myers showed that lethal doses of certain bacterial toxins when mixed with emulsions of olive oil, in a fine state of division, and injected subcutaneously into animals failed to produce their lethal effects. Similar results were obtained by Walsh & Frazer (1934). Cataphoresis experiments have shown that oil globules in emulsions of oil in water type carry a negative charge. On this basis it was assumed that an adsorption phenomenon might be the explanation of the failure of the bacterial toxins to produce their lethal effects when mixed with emulsions of oil in water type and injected into animals.

During an epidemic of Sonne dysentery in Tooting Bec Hospital of which the epidemiological aspects have been described by one of us (Buckle, 1938), and during a recurrence of this epidemic, a number of strains were isolated of the causal organism (140) and various bacilli which were somewhat similar in their cultural and biochemical behaviour. It was thought that a close bacteriological and serological examination of these might be useful in giving information about the constancy of behaviour of the Sonne group, the question of possible biochemical subgroups of Sonne bacilli (Bojlén. 1934), and the relationship of the dysenteroid organisms isolated to the true dysentery bacilli, their classification, and significance.

Eleven cases of Weil's disease in miners from the west of Scotland have been encountered in the years 1937 and 1938. Only five showed jaundice.

Ten cases of infection previous to this period have been determined by serological means. Eight were jaundiced.

Information pointing to the occurrence of about eighteen more cases has been obtained from the Lanark public health authorities and from patients' statements.

The occurence of leptospiral infection appears limited at the moment but is quite serious in certain areas.

All available evidence points to the infectious being due to one specific strain of Leptospira.

I should like to thank the Physicians and Surgeons of the Royal Infirmary for permission to obtain sera from miners in their wards, and in particular Prof. A. W. Harrington, Dr J. C. Middleton and Dr J. N. Cruickshank for clinical details of cases. In addition, I would express my indebtedness to Dr J. M. Lang, Medical Officer of Health, Lanark, for the opportunity to investigate suspected cases, past and present.

1. The most common cause of bacillary food infection in this area is the aertrycke bacillus which has been responsible for most of the sporadic and familial outbreaks of so-called food poisoning. It was also responsible for one, the largest, outbreak of this condition in Dundee during the period under consideration.

2. The other sporadic cases were caused by different members of the group of Salmonella organisms—stanley, potsdam, senftenberg, while two cases were possibly due to a micro-organism having somatic relationship with the aberdeen bacillus although not possessed to the “i” flagellar antigen. It is probable, therefore, that these less frequently encountered Salmonellas are of wide distribution.

3. Two extensive outbreaks of milk-borne bacillary food infection due to the dublin type of the gaertner bacillus are described. In both, the source of infection was determined and proved to be a cow which had indubitably suffered from a septicaemic infection due to that micro-organism.

These two dublin outbreaks are of special interest in view of the findings of Conybeare & Thornton (1938) concerning the presence of antibodies to this bacillus in the blood of bovines and its presence in dejecta of a cow which, in view of the absence of evidence of illness, could only be regarded as a “carrier”.

If there be an appreciable number of carriers among bovines such observations as those of Montgomery (1938) concerning sporadic infantile meningitis due to the dublin bacillus are comprehensible though, of course, no explanation can be offered concerning the peculiar tendency to invade the meninges exhibited by this particular Salmonella.

1. A study of the literature of East Africa on the incidence of plague in field rodents shows that in no single instance has evidence been offered to prove they have any relation to the disease.

2. Recent epizootics in field rats in Kenya are described.

3. The health of house and field rats is discussed, with an account of the work carried out on a septicaemic condition present in field rats.

4. The results of bacteriological examination of 2750 field rats and attempted transmission experiments with 1285 field fleas, both investigations conducted during a period when there was heavy mortality among them, failed to establish the presence of B. pestis.

At the same time, mortality among the Rattus population, proved bacteriologically to have been caused by B. pestis, enabled successful transmissions to be accomplished with fleas from that species.

5. In the absence of any confirmatory bacteriological evidence to prove that epizootics among field rats are caused by B. pestis, and the failure to find natural infection among field fleas, together with the knowledge of their aversion to feed on man and lack of opportunity to develop such tastes, the theories that field rodents and their fleas “are definitely assisting in the perpetuation and spread of plague” or that they “ are possible factors in initial outbreaks of plague” (Thornton, 1930) appear to be fallacious.

6. Plague in Kenya is distinguished by its isolated and sporadic nature, even in endemic areas, and it is not dependent on types of housing or the general hygiene of inhabited areas, but on individual domestic habits. Any individual, neglectful in regard to food, particularly its storage and wastage, is the person responsible for the disease, by offering an unlimited supply of food to a dense rat population and encouraging its survival.