The mosquitoes Aedes aegypti, A. triseriatus, Culex pipiens, C. quinquefasciatus, and Anopheles quadrimaculatus were all found to be efficient experimental vectors of Shope's virus-induced fibromas of cottontail rabbits, transmitting the virus during interrupted feedings as well as after long intervals from an infective meal. The reduviid bugs, Triatoma infestans, T. phyllosoma pallidipennis and Rhodnius prolixus, and the bedbug, Cimex lectularius, were also capable of transmitting fibroma by interrupted or delayed feeding.

Evidence from various types of experiments indicated that arthropod transmission is mechanical, the virus being extremely stable in the insects. Some experiments did indicate the possibility of virus proliferation. Although mosquitoes did seem to serve as ‘flying pins’ when transmitting virus by interrupted feeding, they certainly were distinctive in that they maintained their ability to transmit for very long periods of time. To transmit fibromas, arthropods actually must draw virus up between the stylets of the mouthparts; mosquitoes were unable to transmit by feeding through skin moistened with a suspension of fibroma virus or by feeding subsequent to having their mouthparts painted with a virus suspension.

While cottontail tumours at peak virus titres are always infective for suitable insects, the fibromas of adult domestic rabbits generally are not infective, even though the virus titre is equivalent. However, the tumours of suckling domestic rabbits do become infective for insects.

1. An examination of eighty-nine samples of uncooked and thirty-eight samples of cooked food purchased by one particular hospital showed that the purchased food was bacteriologically clean.

2. A similar examination of 173 samples of food after it was cooked and prepared for serving in the hospital kitchens showed that, with the exception of cold chicken, the bacterial flora was greatly reduced by cooking. Ten of forty-six samples of cold chicken, however, were contaminated with fairly large numbers of Cl. welchii.

3. An investigation into the cooking and handling of the fowls indicated that contamination of the cooked fowls with kitchen dust was a probable explanation for the presence of Cl. welchii.

4. Immediate refrigeration of the fowls, well separated on shallow trays, was shown to be a satisfactory method of preventing the growth of contaminating Cl. welchii to any dangerous extent.

5. Six outbreaks of food poisoning, in which there was an association between cold chicken and the clinical symptoms of Cl. welchii food poisoning, are reported and discussed.

I have pleasure in thanking Dr Betty Hobbs of the Food Hygiene Laboratory of the Public Health Laboratory Service at Colindale for the serological typing of numerous strains of Cl. welchii; Mr D. B. Colquhoun for assistance with the phage-typing of the staphylococci; Mr G. Kerr for the photography; and the kitchen staff in the hospital concerned for making possible the numerous samplings of food and the other inquiries into the day-to-day affairs of the hospital catering department.

Skin lesions with histopathology similar to that seen in lesions in man have been produced in calves by the experimental inoculation of cultures of Myco. ulcerans. Sensitization of infected calves to mammalian tuberculin as well as to ulceranin has been demonstrated.

It is considered unlikely that cattle are a reservoir of infection for man.

The expenses of this investigation were met by a research grant from the Board of Management, Alfred Hospital.

We are indebted to Dr A. V. Jackson, Director of Pathology, Alfred Hospital, for the reports on histopathology.

1. A brief review of the literature on acid-fast bacilli found in skin lesions is given.

2. The characteristics are described of an acid-fast bacillus isolated from a skin lesion found in the South African Xenopus laevis.

3. Reasons are given to support the view that chromogenic acid-fast bacilli cultured from skin lesions belong to the group of ‘Saprophytic acid-fast bacilli’.

4. The possibility of using the Middlebrook-Dubos haemolysin test as a tool to differentiate atypical acid-fast bacilli is discussed.

Thanks are due to Dr Charles Pike for all the histological reports, to Mr T. R. West for the microphotographs, to Dr Piersma (Messrs Lederle) for the gift of special sensitive Old Tuberculin for the Middlebrook test, to Dr Nassau for patients' sera and the ‘Goss’ antigen and finally to Mr W. J. Fincham for the titrations of the haemolysin titres.

The virulence of nine strains of Klebsiella was tested in mice inoculated by peritoneal and oral routes, the latter being a convenient method of inducing pneumonic infections.

At similar doses, shorter survival was observed in young mice. Injected by the intraperitoneal route, organisms from 16 hr. old cultures proved more virulent than those from older cultures, but no such difference was obtained orally. Repeated subculture of a virulent strain failed to attenuate its oral virulence and killed suspensions of the same strain were without effect. With only two exceptions, all strains were more virulent when administered orally than intraperitoneally. Wherever possible the concept of relative virulence was employed in making statistical comparisons. It is, however, considered that virulence is an unsatisfactory taxonomic discriminant.

We would like to thank Dr I. Friedmann, Dr F. Fulton and Dr G. Meynell for their helpful criticism. We are also indebted to Dr Lynne Reid for her comments and to Mr G. B. Newman for checking the calculations. Thanks are also due to Mr G. D. Breach and Mr G. Latchford for technical assistance, to Mr D. Connolly for preparation of graphs and Mrs A. Gorvin for secretarial assistance.

1. Whole cultures of Clostridium welchii, Type C (organisms plus toxin), produced enterotoxaemia and death when fed to new-born piglets.

2. The disease could rarely be produced by suspensions of washed organisms given in the same way but was readily initiated by feeding bacteria-free toxin from Type C cultures.

3. Piglets dying from enterotoxaemia induced by bacteria-free toxin showed all the extensive pathological changes of the natural disease; their intestines contained Type C organisms and far greater quantities of toxin than had been given by mouth.

4. Type C organisms could not be demonstrated in the intestines of piglets from healthy litters of the same age, although such animals were carriers of the Type A strain.

5. The clinical signs, with particular reference to the development of hypo-glycaemia, and the pathology of both natural and experimentally induced cases of enterotoxaemia are described.

6. In the light of these findings the pathogenesis and epidemiology of enterotoxaemia in the piglet are discussed.

We wish to thank Mrs B. L. Wardale and Mr P. J. D. V. Brett for general assistance. This study was aided financially by a general grant to one of us (R.F.W.G.) from the Agricultural Research Council.

1. Salmonella incidents in Northern Ireland from 1951–58 are compared with the published findings in England and Wales.

2. Caecal swabs from 489 pigs killed in two bacon factories showed a salmonella isolation rate of 2%.

3. Salmonella organisms were isolated from twenty-three out of 100 samples of caecal faeces and from only six of 100 caecal swabs taken from the same animals. Three per cent of meat samples from these pigs and 70% of sausage samples from this meat contained Salmonellae.

4. Rectal swabs from 162 pigs on five farms producing infected pigs showed Salmonellae in 9% of those examined.

5. Twenty-four per cent of pig-meal samples taken on these farms contained Salmonellae, and the same salmonella types were found in the meal at the mill and in fish meal and bone meal before mixing.

6. It is probable that some salmonella types pass from feedingstuffs through pigs to human food and cause human infections.

We should like to express our thanks to Dr Joan Taylor of the Salmonella Reference Laboratory, Colindale, for typing many of the Salmonellae; to Mr J. Stuart of the Veterinary Division, Ministry of Agriculture, Northern Ireland, for help in sampling at an abattoir and on the farms; to the staff of the Northern Ireland Hospitals Authority, Central Laboratory, for technical assistance; to Mr J. Patton and Dr D. Luke for much help and advice at many stages of this inquiry; to Miss A. McCann for the secretarial work; to the Northern Ireland Hospitals Authority for a grant towards the expenses in 1958; and to our colleagues in the Local Authorities, General Practice, on the farms and in the factories who were always most helpful and co-operative.

1. The susceptibility of mice of different ages to intramuscular, intraperitoneal, and oral administration of EMC virus, and to intracerebral and intramuscular injection of both the Texas and the Connecticut-5 strains of Coxsackie virus have been studied. In all cases susceptibility decreases with age. The development of resistance to a given virus may vary in rate and extent according to the route by which the virus is given.

2. The multiplication of small amounts of EMC virus in muscle, and of the Texas and Connecticut-5 strains of Coxsackie virus in both muscle and brain, has been studied in mice of different ages. A very high degree of multiplication of all three viruses was observed in both muscle and brain of young mice, but no significant multiplication of the EMC virus in older muscle could be detected with these small inocula, nor of either of the Coxsackie strains in older muscle or brain.

3. Multiplication of EMC virus in young mice was shown to take place within the muscle itself. Haemagglutination tests showed that less haemagglutinin, as well as less infective virus, was produced in the muscles of older mice following the injection of small amounts of virus.

4. Multiplication of EMC and GDVII viruses could be demonstrated even in older mice if a sufficiently large amount of virus was inoculated initially.

5. The rapid initial disappearance of infectivity from the site of inoculation was shown to be mainly due to dispersal of inoculated virus around the body.

6. The simplest hypothesis which will accommodate the observed data on virus multiplication and on the development of resistance with age appears to be that the accessibility of the host cell to virus decreases with age. We found no evidence that the ability of the host cell to support virus multiplication declines with age.

This work was done in the Department of Zoology, Oxford University. One of us was in receipt of a Medical Research Council training grant. The expenses of the research were met by a grant from the Nuffield Foundation, to whom we should like to express our gratitude.

1. Methods are described for altering the susceptibility of the surviving allantois to infection by influenza viruses.

2. Under natural conditions susceptibility is a linear function of age between 10 and 18 days of incubation. The drop is 0·11 log10 unit per day for all strains of influenza tested.

3. In whole eggs this decline is masked by the effect of acid allantoic fluid which prevents infection when the pH falls below 6. The effect is not directed against the virus particle, nor does it do permanent damage to the cell, as surviving tissues are equally susceptible whatever the pH of the allantoic fluid that bathed them in ovo.

4. Surviving membranes can be made less susceptible by incubating the eggs at 35° rather than 38° C.; by maintenance for 24 hr. in vitro; by use of deficient or inappropriate medium. These methods lower susceptibility more for some strains than for others.

5. All treatments which lower susceptibility also increase its variation from egg to egg.