Thrombocytopenia is common in patients with invasive bacterial infections. Bacteria can activate platelets, but it is unclear if this affects platelet count. The aim of this study was to examine whether bacteraemia with Staphylococcus aureus, which readily activate human platelets, was more likely to be complicated by thrombocytopenia than bacteraemia with Escherichia coli or Streptococcus pneumoniae with different abilities to activate platelets.

We compared information from 600 adult patients with community-acquired bacteraemia with S. aureus (n = 140), E. coli (n = 420) and S. pneumoniae (n = 40) in Southern Sweden, 2012, linking information on positive blood cultures from microbiological databases and medical charts. The proportion of patients with thrombocytopenia (platelet count <150 × 109/ml) was calculated. Logistic regression was used to estimate the odds ratios (OR) for thrombocytopenia according to bacterial species adjusted for confounders.

The proportion of thrombocytopenia was 29% in S. aureus, 28% in E. coli and 20% in S. pneumonia bacteraemia (P = 0.50), corresponding to an OR of 1.2 (95% confidence interval 0.7–1.9) for thrombocytopenia for S. aureus as compared with E. coli or S. pneumoniae, adjusted for confounders.

This study indicates that platelet activation by bacteria is not a major causative mechanism in sepsis-associated thrombocytopenia.

The object of the Swedish Antarctic Expedition was to conduct researches relating to the geography and natural history of the Antarctic regions south of Cape Horn. The expedition was to start from Sweden during the autumn of 1901. On the approach of the Antarctic winter, in February or March 1902, some of the party were to be landed in a suitable place in the Antarctic regions, with the object of wintering there. The members remaining on board the ship “Antarctic,” were to carry on investigations in the regions around Cape Horn, the Falkland Islands and South Georgia. The next summer, i.e. in December 1902 or January 1903, the ship was to return in order to pick up the wintering party at their station; and, thus reunited, the whole expedition was to go back to Sweden, where, as we had calculated, we should arrive in the spring of 1903.

A prevalence survey of methicillin-resistant Staphylococcus aureus (MRSA) was performed in 2010 in 19 long-term care facilities in Luxembourg. Of the 954 participating residents, 69 (7·2%) were colonized by MRSA. Previous history of MRSA [odds ratio (OR) 7·20, 95% confidence interval (CI) 3·19–16·27], quinolone therapy in the previous year (OR 2·27, 95% CI 1·17–4·41) and ⩾24 h care administered per week (OR 4·29, 95% CI 1·18–15·56) were independent risk factors for MRSA colonization. More than 75% of strains were of clonal complex (CC)5, mainly spa-type t003 or sequence type (ST)225 and ST710, which is a rapidly emerging lineage prevalent in central Europe. Five residents were colonized by livestock-associated genotypes belonging to CC398. Previously dominant CC8 strains have recently been replaced by more resistant CC5 strains in Luxembourg.

Drinking water is a recognized mode of transmission of various parasitic and bacterial infections and high prevalence rates of water-borne infection have been found during past studies in rural areas of the Nile Delta (Farag et al. 1979; Khairy. Barakat & Omar, 1978).

The properties of 5-p-chlorophenyl silatrane as a rodenticide against Rattus norvegicus and Mus musculus were investigated in the laboratory. The high oral toxicity of the compound was confirmed. When the compound was given to laboratory rats and mice by stomach tube at lethal dosages, signs of poisoning were observed within a minute. When caged wild rats and mice were given a choice between plain and poisoned baits the optimum rodenticidal concentration in the bait was about 0.5% for both species, producing 50% mortality in wild rats and 95% mortality in wild mice. The results are discussed in relation to safety in use and the probable effectiveness of the compound as a rodenticide in field conditions.

1. Data on the maximum temperatures of growth of certain organisms, on the rate of toxin production by Cl. botulinum and the rate of multiplication of certain Salmonellas, is given, as a basis on which to define the time and temperature of dehydration in the preparation of dehydrated foods.

2. It is concluded that 50° C. is the minimum temperature below which dehydration should not be carried out. Where some heating below this temperature is unavoidable, the period of such heating should not exceed 4 hr.

3. Data on the microbial changes in dehydrated foods equilibrated at various humidities indicate that bacterial growth is not expected below about 15 % water content. Some experiments on the death of bacteria at water levels below this are discussed.

4. Details are given of the general bacteriological examination of the process of dehydration on a commercial scale for dried soup, dried minced beef, dried carrot, cabbage and potato.

This work was carried out under the joint auspices of the Food Investigation Board of the Department of Scientific and Industrial Research, and the Ministry of Food, and is published by permission. The authors are indebted to Professor H. R. Dean for the provision of facilities, and to him, Professor G. S. Wilson, Dr A. W. Downie, and various other members of the Emergency Public Health Laboratory Service for help and advice.

Experiments were carried out in a test chamber of 16,500 cu.ft. capacity with air conditioned at 68° F. and 54% relative humidity. Ventilation was controlled at 3·0 changes/hr., air being recirculated with 0·5 air change/hr. of fresh air admitted. By spraying into the air ducting a concentrated suspension of Chr. prodigiosum a bacterial cloud was introduced into the chamber of over 5 × 106 organisms/cu.ft. of air as l μ particles. Viable organisms were still present in the atmosphere after 6 hr.

When a heat-generated vapour of hexylresorcinol was introduced in a concentration of between 6 and 7 μg/cu.ft. of air the bacterial count dropped from nearly one million organisms per cu.ft. to fewer than ten in 35 min.

When the bacterial suspension was sprayed into the chamber with hexylresorcinol vapour present, the peak concentration reached was about one-quarter and on stopping the spray, the bacterial count fell from one million per cu.ft. to fewer than ten in less than 25 min.

Hexylresorcinol is also effective when the bacterial aerosol is in particles of 6–7 μ in size (approx. 100 bacteria per particle).

Hexylresorcinol has no effect against a bacterial aerosol of B. subtilis spores in 1 μ particles.

No attempt has been made to analyse the mode of action of hexylresorcinol in diminishing the bacterial content of the air. The evidence collected clearly indicates the necessity for further study of this problem.

A family outbreak of Salmonella enteritidis PT4 infection is described in which home-made ice cream was identified as the vehicle of infection. The ice cream contained approximately 105S. enteritidis PT4 organisms per gm and was probably contaminated by an infected shell egg containing between 105−108 organisms. The continued relevance of the Chief Medical Officer's warning on the use of raw shell eggs is highlighted.

Home-made ice cream using the same recipe as ice cream that had been incriminated as the cause of the family outbreak of S. enteritidis PT4 infection was used to study the growth of the organism that might have occurred in the 3–4 h it took to prepare the product. When the inoculum was in the stationary phase, as it would be from shell or other cross contamination, there was a lag phase of 3 h before growth occurred at room temperature. Even when actively multiplying organisms were introduced, as may be found in an infected egg, there was less than 3 log10 increase in the salmonella count in 4 h at room temperature. It was, therefore, given the high S. enteritidis count, unlikely that the ice cream was cross-contaminated.

By contrast, raspberry sorbet at pH 3·73 proved to be lethal to a large inoculum of S. enteritidis and may be a relatively safe raw egg containing product.

Several epidemics of gonococcal conjunctivitis have occurred in Aboriginal populations in Central Australia. In 1997, the first outbreak in the Kimberley region of Western Australia occurred, spreading to Central Australia with a total of 447 cases. A genotyping method was applied directly to DNA extracted from patient samples to characterize the gonococcus causing the epidemic and to compare it with contemporaneous genital isolates. Those positive conjunctival specimens from Kimberley and Central Australia that could be genotyped were all indistinguishable, but were distinct from the genital gonococci, even when they shared the same auxotype and serotype. This suggested that the outbreak was due to a single genotype of Neisseria gonorrhoeae that had probably been carried between communities by infected individuals. We did not find evidence to support the existence of a genital reservoir of the types causing epidemic gonococcal conjunctivitis.

Experiments on immunity produced by vaccine were carried out in mice with two strains of salmonella.

Against intraperitoneal challenge protection was such that 40–80 % of vaccinated mice survived a dose that killed almost all controls. This level of immunity appeared to be maintained with little change for at least 5–7 months. An explanation for this stability is suggested.

Against infection by the natural route, either by direct feeding or by exposure to infected animals, protection from vaccine was of a comparatively low order.

Resistance to infection by an artificial route was, therefore, not a measure of resistance to infection by the natural route.

1. A quantitative comparison has been made of the observed mortalities from respiratory tuberculosis with those expected from a simple scheme of generation mortality.

2. This scheme gives a good account of the observed rates until about 1930, but is unsatisfactory thereafter.

3. It is concluded that these discrepancies cannot be due to chance, and that the generation effect has become obscured by other factors.

4. In particular the shift of maximum mortality into later life is not directly explained by the hypothesis, nor is such a shift a necessary consequence of the generation hypothesis of mortality.

I am greatly indebted to Dr J. C. McDonald for advice and constructive criticism during the writing of this paper; my thanks are also due to Dr G. S. Wilson for his comments.

Two incidents of toxin-type food poisoning in N.E. Scotland associated with the consumption of red whelks (Neptunea antiqua) are described. Four patients developed symptoms within 1 h of consuming whole whelks. These included visual distrubances—double vision and difficulty in focusing-ingling of the fingers, prostration and in one subject nausea, vomiting, diarrhoea and ataxia. In all cases recovery was complete in 24 h. Using a newly developed analytical technique the concentration of the causative toxin, tetramine, in the salivary glands of the whelks consumed was estimated at 0.07%, equivalent to a content of 3.75mg/100g of the shellfish.

Bacteriological diagnosis of the Enterica is only established with certainty on recovery of the infecting organism by recognised laboratory methods. In default, recourse must be made to a serological investigation into the agglutinating power of the patient's serum, when, theoretically, little difficulty ought to be experienced. In enterica suspects, unvaccinated or uninfluenced by previous enterica disease, demonstration of agglutinins reacting with the Bact. typhosum, paratyphosum A, B, or C in relatively high dilutions of their sera should be considered adequate evidence. In the vaccinated, elevation of agglutination titre—as determined by repeated examinations during the course of the disease—has been generally accepted as criterion for existence and type of infection. The principle of ascending dilutions, on which such “quantitative serum analysis” is based, is explained by the fact that in an infection with one organism a specific agglutinin is formed for that particular organism and group agglutinin is for other organisms closely related biologically; the specificity, therefore, of the agglutination reaction must be wholly dependent on the basis of dilution, the specific agglutinin being present in greatest quantity and operative in a range much exceeding that of the secondary group agglutinins. Reasonable as this view may seem in principle, it is far from easy of application in practice. Lack of accurate information as to the day of disease on which serum was taken, unreliable case histories in regard to vaccination or previous enterica infections, and inability of private practitioners to induce patients to submit to repeated blood collection constituted here primary difficulties.

A 2-year case-control study was conducted to describe the epidemiology of Haemophilus influenzae type b (Hib) and investigate Hib disease risk factors in the Republic of Ireland. Between October 1991 and September 1993, 149 laboratory confirmed incident cases were matched with community controls. Annual Hib disease incidence was 25·4 per 100000 children under 5 years, with peak incidence (65·8 per 100000) in the 6–11 months age-group. Meningitis was the predominant clinical condition. Twenty-four (16·1%) isolates were resistant to ampicillin. Crèche or day-care attendance and the presence of chronic illness emerged as risk factors for Hib disease. Empirical first line treatment for suspected Hib infection warrants alternatives to ampicillin such as cefotaxime. Completed immunization with Hib conjugate vaccine by 6 months of age is required for maximum disease prevention. Until all children are receiving Hib vaccine on schedule, those who are crèche or day-care attendees and those with chronic illness should be prioritized for timely immunization.

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) has rapidly emerged in the USA as a cause of severe infections in previously healthy persons without traditional risk factors. We describe the epidemiology of severe CA-MRSA disease in the state of Georgia, USA and analyse the risk of death associated with three different clinical syndromes of CA-MRSA disease – pneumonia, invasive disease, and skin and soft-tissue infections (SSTIs). A total of 1670 cases of severe CA-MRSA disease were reported during 2005–2007. The case-fatality rate was 3·4%; sex and race of fatal and non-fatal cases did not differ significantly. While CA-MRSA pneumonia and invasive disease were less common than SSTIs, they were about 15 times more likely to result in death [risk ratio 16·69, 95% confidence interval (CI) 10·28–27·07 and 13·98, 95% CI 7·74–25·27, respectively]. When controlling for age and the presence of other clinical syndromes the odds of death in patients manifesting specific severe CA-MRSA syndromes was highest in those with pneumonia (odds ratio 11·34). Possible risk factors for severe CA-MRSA SSTI and pneumonia included the draining of lesions without medical assistance and an antecedent influenza-like illness.

Three cases of continued fever are described in which the Salmonella type “Dublin” was isolated from the blood. The cultural and serological behaviour of the three strains so obtained are compared with those of 34 strains of typical S. enteritidis (Gärtner) (including strains from commercial rat virus) and with those of 12 other strains of S. dublin (including six from calf-dysentery in Denmark). The suggestion is made that the “Dublin” type is of bovine habitat and that cows' milk is the vehicle of human infection.

We evaluated the association between typhoid fever and Helicobacter pylori infection, as the latter microorganism may influence gastric acid secretion and consequently increase susceptibility to Salmonella typhi infection. Anti-H. pylori IgG and IgA antibody titres (ELISA) and gastrin concentration (RIA) were determined in the plasma of 87 blood culture-confirmed typhoid fever cases (collected after clinical recovery) and 232 random healthy controls without a history of typhoid fever, in the Jatinegara district, Jakarta. Patients with typhoid fever more often than controls were seropositive for H. pylori IgG (67% vs. 50%, P<0·008), when antibody titres were dichotomized around median titres observed in controls. H. pylori IgA seropositivity was not associated with typhoid fever. Plasma gastrin concentrations indicative of hypochlorhydria (i.e. gastrin ⩾25 or ⩾100 ng/l) were not significantly elevated in typhoid fever cases compared to controls (P=0·54 and P=0·27 respectively). In a multivariate analysis, typhoid fever was independently associated with young age (<33 years, median age of the controls) [odds ratio (OR) 7·93, 95% confidence interval (CI) 3·90–16·10], and H. pylori IgG seropositivity (OR 1·93, 95% CI 1·10–3·40). Typhoid fever was independently associated with H. pylori IgG seropositivity, but not with elevated gastrin concentration. Therefore, the association suggests a common risk of environmental exposure to both bacteria, e.g. poor hygiene, rather than a causal relationship via reduced gastric acid production.

Rabbits were immunized by multiple intradermal injections followed by six intravenous doses of vaccinia virus inactivated by heating to 65° C. Particular attention was paid to confirming that the virus used was fully inactivated and incapable of reactivation. The immunized rabbits developed neutralizing and other antibodies to a titre comparable with those developed in response to live virus, but multiple intravenous injections were required to elicit a maximum titre. A qualitatively different response was seen only in immunodiffusion tests in agar gel where two or three fewer lines developed with antisera to heated virus than with those to live virus. The rabbits were subsequently challenged intradermally either with vaccinia and cowpox or with rabbitpox. They showed some immunity to vaccinia and cowpox, compared with normal controls, but less than that elicited by live virus. Their resistance to lethal doses of rabbitpox was life-saving though some rabbits did develop lesions. Later rechallenge of the rabbits showed that they had not developed further immunity, in distinction from the normal controls. The implications of these findings are discussed.

I wish to thank the National Fund for Research into Poliomyelitis and Other Crippling Diseases for their generous support in providing a Research Fellowship during which this work was done. I wish to thank also Professor A. W. Downie F.R.S. and the Staff of the Department of Bacteriology, University of Liverpool, for their encouragement and assistance respectively.

Rinderpest neutralizing antibody was found to be transferred from the immune dam to the calf via the colostrum. No antibodies were detected in the sera of calves before suckling. The colostrum of immune cows contained rinderpest antibodies to a higher titre than that of the serum; 30–48 hr. after the ingestion of such colostra, newborn calves possessed high antibody levels in their sera, levels greater than those of their dams' sera but less than those of the colostrum ingested.

After the neonatal period the serum titres of calves declined linearly. The mean half-life of maternally derived rinderpest antibody in calves was 36.7 days and the extinction point 10.9 months.

Two young calves, from susceptible dams, which each ingested daily for 5 weeks 1 gallon of milk containing rinderpest antibodies failed to show evidence of their absorption from the intestinal tract.