Infections due to Salmonella enteritidis are increasing worldwide. In the United States, between 1985 and 1989. 78% of the S. enteritidis outbreaks in which a food vehicle was identified implicated a food containing raw or lightly cooked shell eggs.

Under a US Department of Agriculture regulation published in 1990, eggs implicated in human food-borne S. enteritidis outbreaks were traced back to the source flock. The flock environment and the internal organs of a sample of hens were tested for S. enteritidis. We compared the S. enteritidis phage types of isolates from 18 human, egg-associated outbreaks and the 15 flocks implicated through traceback of these outbreaks. The predominant human outbreak phage type was recovered from the environment in 100% of implicated flocks and from the internal organs of hens in 88% of implicated flocks we tested. The results support the use of phage typing as a tool to identify flocks involved in human S. enteritidis outbreaks.

There are certain demonstrable changes that take place within the gastrointestinal tract during the process of adaptation to external stimuli. The body as a whole reacts in this adjustment to a changing environment. We have presented our evidence and indicated some instances where these gastrointestinal changes can be considered significant from an epidemiological and preventive medicine standpoint.

The loss of the self-disinfecting power, changes in acid-base equilibrium, and other demonstrable alterations within the lumen of the alimentary tract are only a part of the changes taking place in the organism during the process of adaptation to external environmental changes. If certain diseases are associated with a disturbance of the equilibrium between the parasites and the host, then it naturally follows that we must have more information upon the biological mechanism of the host in regard to its changes in susceptibility and resistance to the parasitic environment. Our present knowledge of bacteriology throws little light upon this epidemiological question. It has been the aim of the author to study the mechanism by which the organism adapts itself to certain environmental changes. We have avoided using pharmacological and other artificial agents that would produce body changes, but have restricted ourselves to simple alterations in diet, external temperature and similar mild or natural environmental factors, and followed the mechanism of adaptation to these physiological stimuli.

The loss of the power of a body-covering layer, to destroy bacteria in contact with it, must increase the hazards of invasion of this body surface by bacteria. We have shown that a sudden change in the intra-intestinal acid-base equilibrium leads to an inhibition of the mucosa to destroy bacteria within its lumen and is accompanied at times by the appearance of viable bacteria in the thoracic duct lymph stream.

If an organism does not adapt itself to its meteorological environment, it is more susceptible to its parasitic environment. The same is true of the nutritional environmental factors. Disturbances due to lack of adaptation to climatic changes can in part be offset by altering the diet. The weather and food factors cannot be separated and one can influence the other.

Changes in climate are beneficial to the well-being of the population living in the temperate zones where meteorological conditions are ever changing as compared to the steady cold in the arctic or constant heat as in the tropics. Changes in food are also beneficial. A high protein meal is stimulating. In the tropics where the skin is in a state of over-stimulation due to the high external temperature and humidity the ingestion of an alcoholic beverage to stimulate the splanchnic system before a meal is beneficial. Acidifying an infant's food in hot weather is a common practice. Many such instances could be cited. It seems to be of advantage to an organism to be in a changing environment. The tonus of our physiological systems is not static or fixed, but is ever changing. The more delicate the index used to measure functional changes, the more frequently are such changes observed. These alterations in environment must not exceed the power of the organism to adapt itself to these changes.

In a study comparing the responses of institutionnalized Down's syndrome (DS) and non-Down's (ND) inmates to enterovirus infections, the frequency of wild enteric viruses and the excreation patterns of oral polio vaccine (OPV) viruses were similar in both groups. Antibody titres developed to poliovirus types 2 nad 3 following vaccination were similar in DS and ND and ND vaccinees, but the responses to type I virus was signifcantly less in DS vaccinees. As judged by the development of poliovirus antibody in non-vaccinees, the spread of virus from OPV-immunized to unimmunized subjects in the institution was not noticeably different in DS and ND subjects.

An unexpected finding was that the excretion patterns of all three serotypes of poliovirus were strikingly similar for each individual to individual. The similarity of excreation occurred despite wide differences within an individual in the titres of neutralizing serum antibodies to the three serotypes. It is suggested that the rate at which a given individual eliminates enteroviruses may be largely determined by factors, the activities of which atre not reflected in serum antibody titres.

The literature dealing with the intradermal test in whooping cough has been reviewed, and the claims as to the specific value of the test have been investigated in 1300 cases.

A method for the extraction of endotoxin from Haemophilus pertussis has been described and the intradermal response to this preparation compared with that following whole vaccine.

The findings in this investigation do not support the claim that the intradermal response to Sauer's vaccine in the strength commonly employed (10,000 million organisms per c.c.) is of value either in demonstrating immunity to whooping cough or in the early diagnosis of this disease. The bacterial content of this vaccine appears to be too high for skin-testing purposes, giving rise to inflammatory lesions of a non-specific character rather than to allergic reactions of specific value. These reactions are less apparent when the vaccine is employed in a diluted form.

The intradermal response to pertussis endotoxin, on the other hand, though not invariably consisting of a clear-cut reaction (and in this respect falling short of the ideal as a reagent) is more consistent with the development of the allergic state towards H. pertussis, reactions presumably of this nature being present in the skin of approximately 85% of children with a past history of whooping cough. Similar reactions, however, can be elicited in the skin of about 30% of individuals with no history of the disease; but in view of the fact that, unlike the more invasive virus diseases, many individuals never develop whooping cough in spite of almost certain exposure when young, it is suggested that latent immunization or recent contact with the causative organism might account for this phenomenon. Whether these reactions indicate merely sensitization or a definite immunity to pertussis must remain, for the time being, sub judice.

The onset of bacterial hypersensitiveness, as judged by the pertussis endotoxin test, appears about the 10th day of whooping cough and becomes heightened during the subsequent course of the disease. Ultimately this cutaneous allergy undergoes a regression, which, however, is not always complete. For this reason the pertussis endotoxin test would appear to be of some value in assessing the immune state of the individual, and also as a diagnostic reaction in early, atypical or late cases of whooping cough where bacteriological findings by the cough plate method have proved disappointing.

A complex disease picture prevalent in this country has been traced (Spira, 1928) to the protracted ingestion of drinking water derived from the tap, and of food prepared in aluminium cooking utensils. No indication could at that time be given of the exact irritant, beyond stating that a mineral or metal seemed to be involved. Further observation revealed a frequent association with paraesthesiae affecting the hands and fingers, especially those supplied by the dorsal cutaneous branch of the ulnar nerve. The feet were affected to a lesser extent. Since there is, in the present state of our knowledge, only one poison which affects the ulnar nerve, namely, fluorine, Spira (1933) concluded that it may be this halogen which was one of the aetiological factors concerned. It was the wide-spread occurrence of mottled teeth in this country (Spira, 1942a, b), known to be produced by a drinking water with a content of not less than 1 part of fluorine per million parts of water (1 p.p.m.), equivalent to gr. 1/120 of fluorine to a pint of water, ingested during the period of calcification of the teeth, which helped to establish the fact that it is indeed fluorine which is the causative agent producing signs and symptoms of a hitherto obscure origin.

Escherichia coli O157.H7 was found in 10 of 3570 (0·28%) faecal samples from dairy cattle in 5 of 60 herds (8·3%). Several tentative associations with manure handling and feeding management practices on dairy farms were identified. Faecal/urine slurry samples, bulk milk samples, and milk filters from dairy herds were negative for E. coli 0157.H7. E. coli 0157.H7 was also isolated from 10 of 1412 (0·71 %) faecal samples from pastured beef cattle in 4 of 25 (16%) herds. The prevalence of E. coli 0157. H7 excretion in feedlot beef cattle was 2 of 600 (0·33 %). The identification of cattle management practices associated with colonization of cattle by E. coli 0157.H7 suggests the possibility that human E. coli O157.H7 exposure may be reduced by cattle management procedures.

(1) From a horse injected with sheep's red cells three months prior to the first bleeding and in a condition of constant haemolytic titre 122 litres of blood were taken in a period of 11 months. The horse's condition remained good throughout and has markedly improved during the year.

(2) The net result was that the haemolytic titre during that time fell only to about 66% of its original value, the leucocytes to about 66%. haemoglobin scarcely at all, while the specific gravity of the blood and total protein have increased, the former by 10% the latter by 5%;.

(3) There was no relationship between the total number of leucocytes and the amount of antibody. The differential count showed an increase of 12% in the polymorphonuclear and a decrease of 12% in the mononuclear cells, these figures being not very far outside the experimental error. The eosinophile and mast cells showed no marked alteration in number, size or staining reactions.

The causes of death of the grouse are, of course, various. We ourselves have seen pleuropneumonia (in a bird long kept in captivity in Cambridge), pericarditis, necrotic patches in the liver, an obscure chronic disease of the peritoneum, and septic infection from a gangrenous fracture of the wing. On the other hand the great majority of birds, either picked up dead on the moor, or caught by keepers when weak and unable to fly, have been found to be all more or less in the same condition; they were wasted, badly infested with Trichostrongylus pergracilis, and often also with Davainea urogalli or Hymenolepis microps, or with both. More or less pathological change was seen in the caeca; the mucous membrane was often reddened, and under the binocular microscope considerable changes were seen, though we did not observe gross ulceration. Sections examined under the higher powers showed serious chronic inflammatory changes particularly in the immediate neighbourhood of the worms.

It is impossible to say with certainty that the outbreak of illness in Manchester was due to ergot, but the evidence available strongly supports the view that ergot was the cause. The train of symptoms and pathological changes, though not necessarily peculiar to ergot poisoning, are strongly suggestive of this origin and this conclusion is reinforced by the fact that all the sufferers consumed rye bread made from rye which contained a significant proportion of ergot. The ergot isolated from this rye, after being kept for many months under conditions which were unfavourable for the preservation of its toxic properties, was found at the expiration of this period to contain some toxin and the amount found was consistent with the ergot having been highly active when fresh and therefore quite capable of causing the outbreak of illness which developed at a period shortly after the harvest when the toxic properties of ergot are greatest.

As a result of my inquiry the following facts of interest have emerged:

1. A considerable quantity of rye is grown in England and Wales and more than half of it is allowed to ripen. The districts in which most of it is grown are Yorkshire, Lancashire, Cheshire, Monmouth and Essex. Rye in this country is seldom, if ever, free from ergot and the degree of infection varies from year to year in each district according to the season, weather, seed and other conditions.

2. Rye bread is eaten to a large extent (in Liverpool and Manchester at any rate) by Jews, and rye for these towns is obtained almost exclusively from Lancashire and Yorkshire.

3. The rye grain is usually not treated in any way before milling, that is to say, no attempt is made to remove any ergot which may be present; it is ground into meal in the condition in which it comes from the threshing machine.

4. On the assumption that some of the rye consumed in Manchester contained 1 per cent. of ergot, a half-pound loaf of bread of which this rye is a constituent would contain 4 to 5 grains of ergot. Although this is a relatively small dose, it is possible that if consumed over lengthy periods, especially if the ergot were in an actively toxic state, pathological conditions might ensue.

5. The samples of rye actually examined by the Public Analyst were not found to be toxic. This may possibly be accounted for on the ground that the method employed for extracting the toxin was not satisfactory, or to the fact that the ergot examined was at least six months old, by which time it would normally have lost most if not all of its toxicity.

6. Damp weather favours the growth of ergot and the climatic conditions of the summer of 1927 were just those most suited to the development of ergot. It is probable therefore that the rye crop was heavily infected and the ergot rich in toxins.

The clinical characters of the outbreak, so far as they have been recorded, strongly support the view that ergot was responsible; all the necessary factors and conditions for the production of illness were present and it is not surprising that it occurred.

In view of the potential danger the obvious preventive measures to which I have already referred should be put into operation. Rye crops should be grown with such precautions as to reduce the risk of ergot infection to a minimum. Millers of rye for human consumption should install the necessary machinery to remove, so far as possible, any small proportion of ergot which the rye may contain.

The redispersal factor for bacteria-carrying particles from a contaminated floor was determined after mopping, blowing and walking activity. Walking gave the highest redispersal factor, 3·5×10−3 m−1, which was three times higher than for blowing and 17 times higher than for mopping. The mean die-away rate for the bacteria-carrying particles used was 1·9/h without ventilation and 14·3/h with ventilation. It was calculated that in the operating rooms less than 15% of the bacteria found in the air were redispersed floor bacteria.

1. The tuberculin reactions of 259 Hong Kong Chinese, mostly adults, were determined by the Mantoux method. Each individual was tested with various dilutions of both old tuberculin and tuberculo-protein.

2. Of 215 subjects above the age of twenty, 93·1 per cent, yielded positive reactions to old tuberculin in dilutions of 1/1000 or higher.

3. Tuberculo-protein compared with old tuberculin of similar dilutions did not yield such a high percentage of positive reactions, seldom produced such vigorous reactions and never caused vesiculation. (This may have been due to deterioration.)

The present inquiry was undertaken to obtain some indication of the relative frequencies of deaths amongst infants from the various forms of diarrhoea and enteritis—‘neonatal’, ‘parenteral’ and ‘infectious’—in the Greater London area in the decade before the war. Since much of the material needed for such an analysis was not available in the published records, a sampling inquiry, making use of the more elaborate records maintained by the Medical Officer of Health, was undertaken for the Borough of Willesden. A comparison of the relevant epidemiological and social conditions in this borough with those in the Greater London area as a whole showed, that for such a purpose, it might properly be regarded as a representative sample.

There was little evidence for the occurrence of the neonatal form in Willesden during the period studied, nor did the seasonal distribution of the deaths suggest that many took place in consequence of preceding parenteral infections. On the other hand, there did seem to be some evidence that a significant proportion of these deaths were in some degree associated with one another, in time or place or both, and it is suggested that this distribution might have resulted from the widespread dissemination in the community of one or more strains of some common micro-organism of relatively low virulence for all but the infant population.

A less detailed study of data for other London boroughs, viz., Bermondsey, Croydon, East Ham, Tottenham and West Ham, supported the main conclusion reached from the Willesden records.

1. A new colicine type (type 15) of Shigella sonnei is described.

2. The epidemiological circumstances associated with its appearance in Edinburgh and Glasgow are summarized.

3. Our indices of reliability as an epidemiological marker are fulfilled by this new type.

1. In the period 1923–39, more than one-fifth of all deaths in the age group 0-2 years in the Administrative County of London are recorded as having been caused by bronchitis or broncho-pneumonia. It is very unlikely that the returns have been exaggerated by more than 10–15% through the inclusion of deaths from secondary broncho-pneumonia following measles, whooping cough or influenza. In the 8 years in which measles epidemics occurred, the peak of the measles mortality was from 2 to 17 weeks after, and never before, that of the mortality from broncho-pneumonia.

2. The winter rise in mortality from broncho-pneumonia is not associated with any comparable increase in the carrier rates for pneumococci and haemolytic streptococci.

3. The broncho-pneumonia mortality of infants in the Metropolitan Boroughs is strongly correlated with sub-standard housing incidence, social index and percentage below the poverty line. The relatively small value found for the coefficient of regression between broncho-pneumonia mortality and sub-standard housing may be due to the less rigorous winter temperatures occurring in the more overcrowded central areas.

4. Low external temperature appears to be the most important predisposing cause of fatal broncho-pneumonia in infants; their weekly death-rate from this disease in mid-winter is about seven times that in the late summer. This great seasonal fluctuation in mortality is also found for persons over 55 years in the Administrative County, and for persons of all ages in both the urban and rural districts of the Home Counties.

5. The weekly mortalities of infants from broncho-pneumonia in the Administrative County are most strongly correlated with low temperatures 2 weeks earlier. The two variables are so associated that the mortality rises sharply when the mean temperature of the coldest day of the week falls below 40° F. There is no indication that low temperatures in the spring are associated with higher death-rates from broncho-pneumonia than the same temperatures in the autumn, so that the data provide no support for the supposition that susceptibility increases during the winter in consequence of the progressive depletion in the body of protective nutrient substances.

6. Possible measures to reduce the mortality of infants from broncho-pneumonia are discussed.