A five year collaborative study of influenza in volunteer families from 1973–78 covered a period in which there were outbreaks every year but no major epidemics of influenza. Volunteers over the age of 15 years were bled before and after each of the five winters, and virus isolation was attempted from as many as possible when they reported episodes of illness. Children under 15 in the volunteer families were also swabbed when they were ill. Although most families experienced one or more attacks by influenza viruses, there was little transmission within families.

A study of stool Escherichia coli in 60 children with gastroenteritis and 18 control children was carried out in Auckland, New Zealand in 1977. Toxigenic strains, heat labile and heat stable, predominated in the stools of only three children, all of whom had concomitant rotavirus. Classical enteropathogenic E. coli (EPEC) were found in patients and controls. Only one patient had many EPEC in the stool (086. H2), they were variably toxigenic and rotavirus was also present. No toxigenic serotype was isolated. Two potential pathogens were sometimes found. Overall there was no evidence for a substantial causative role for disease producing E. coli in these children.

A group of 269 pupils of the Harbour and Transport Training Institute in Rotterdam (group A), aged 13–20 years, and of 109 patients of the Dr Mr Willem van den Bergh Foundation at Noordwijk (group B), aged 11–21 years, were immunized with a whole virus vaccine containing 10, 20, or 40 μg HA of A/USSR/92/77 (H1N1) influenza virus. A booster vaccination was administered 6 weeks later with 20 μg HA of the same virus. Many of the participants had been immunized during the two preceding years with a whole virus vaccine containing A/New Jersey/8/76 (H1N1) (A/NJ/76) virus. The side-effects, mostly of a moderate nature, increased with the dose of virus in the vaccine. In group A side effects were least frequent in the vaccinees who had never received A/NJ/76 vaccine. A single dose of A/USSR/77 vaccine did not produce satisfactory levels of homologous antibodies. After booster immunization with 20 μg HA of A/USSR/77 virus participants showed a higher homologous antibody response in all vaccine-dose groups if they had not been immunized with A/NJ/76 virus in previous years. After primary and especially after booster immunization with A/USSR/77 virus, a very high response against A/NJ/76 virus and adequate levels of A/NJ/76 antibody were found in participants who had been immunized previously with A/NJ/76 virus. Those who had not been immunized with this virus previously showed no or a very low antibody response to A/NJ/76 virus.

Of 22 strains of Salmonella gallinarum isolated from recent outbreaks of infection in poultry in Greece (15), Amman (3), Kenya (2), Lebanon (1) and Yemen (1), 20 were more resistant to furazolidone in vitro than 6 strains that had been isolated in the U.K. in the 1950s; the minimum inhibitory concentration of furazolidone was approximately 0·3 μg/ml for the sensitive strains and 1·3 or 2·5 μg/ml for the more resistant strains.

Furazolidone given continuously in the food did not control experimental infections in chickens caused by most of the strains that had been classed as more resistant by the in vitro tests. Chloramphenicol, trimethoprim and sulphadiazine or mixtures of the latter two were the best antibiotics for treating these infections, but they were less satisfactory than furazolidone for treating infections caused by the furazolidone-sensitive strains.

As a group, the furazolidone-resistant strains and furazolidone-resistant mutants of one of the sensitive strains were less virulent for chickens than the sensitive strains.

The technique of radial haemolysis (SRH) was used to assess the response to infection with different strains of influenza B virus, to determine the persistence of antibody following such infection and to examine sera from boys entering school at age 11 years. The technique detected 95 % of infections and in primary infection the antibody response was mainly to the infecting strain. Re-infections resulted in a broad response, both to the homotypic strain and to strains more distantly related. Antibody to the homotypic strain persisted for at least 3 years but in some individuals the reaction with heterotypic strains tended to become weaker – resulting in zones of incomplete lysis – or was lost. Examination of the sera collected on entry to the school showed that about 60 % of the boys bled before B/Hong Kong became widespread in the United Kingdom had antibody to strains representative of those isolated in the 1960s and few boys had antibody to B/Hong Kong. After 1974 antibody to B/Hong Kong and later strains became more common while antibody to earlier strains was less frequently detected. The significance of the results as an estimate of past experience is discussed.

Campylobacter jejuni was an almost regular finding in chickens and in minced meat from pigs and cattle sold in ordinary food stores. The bacteria survived on the food at 4 °C for one week and frozen at – 20 °C for three months. None of the stains tested survived heat treatment at 60 °C for longer than 15 min. C. jejuni is apparently a frequent guest in most kitchens. Correct food handling and heat treatment to at least 60 °C for 15 min should be enough to prevent infection.

An experimental model simulating infection of the urinary tract was used to investigate factors influencing the transfer of plasmid-mediated drug resistance in the human bladder in the absence of antibiotic therapy. When a small number of cells carrying plasmid-mediated drug resistance was added to an established population of sensitive cells, it was found that varying the physical conditions of the bladder model had no significant effect on the spread of the plasmid and, under all conditions used, exponential spread of the plasmid through the originally sensitive population occurred. When the initial donor cells were killed shortly after addition to the model, exponential transfer of resistance amongst the established sensitive population still occurred. Thus, even in the absence of antibiotic therapy, only a small number of initial transfer events was required for a fully resistant population to be developed. This was true of both actively multiplying and early stationary phase cultures. An initially greater proportion of resistant cells, or the use of an antimicrobial agent to which some of the cells are resistant, would ensure that this process occurred more rapidly.

Six hundred and eighty three samples of chicken giblets were examined for salmonellas. Three hundred and forty nine of these were neck and crop specimens and 334 were combined liver and heart samples. Two hundred and ten, in all, contained salmonellas.

The technique of examination included pre-enrichment in buffered peptone water at 37 °C for 18 h and subculture to three enrichment media: Muller-Kauffmann tetrathionate, selenite F and Rappaport's magnesium chloride malachite green broth. Inocula from buffered peptone water to 10 ml of tetrathionate and selenite were 1 ml in each case. The inoculum from the pre-enrichment medium to 10 ml of Rappaport was 0·005 ml. Tetrathionate and selenite were incubated at 43 °C for 48 h. Rappaport's medium was incubated at 37 °C for 48 h. Subcultures from all three enrichment broths were made at 24 h and 48 h to brilliant green MacConkey agar. Selective agars were incubated at 37 °C for 24 h.

The most successful technique for salmonella isolation used Rappaport's medium, which was significantly more efficient than either tetrathionate or selenite. This finding reinforces results obtained using sewage polluted natural water as test material and it is suggested that routine examination of environment samples for salmonellas could be based on Rappaport's medium alone.

If S. typhi, S. dublin or subgenus III salmonellas were likely to be present in the sample, the technique described here would require modification.

Two unidentified mycoplasmas, N3 and N11, isolated from the respiratory tract of horses, were found to cross-react with strains of M. mycoides subsp. mycoides in indirect immunofluorescence tests, growth-inhibition tests carried out by the running drop/agar-well method, and in complement-fixation and double immunodiffusion tests. Serologically, the equine mycoplasmas were not completely identical with any of the reference strains of M. mycoides with which they were compared. Their cultural characteristics, ability to digest coagulated serum and casein, and survival at 45 °C, however, suggested that they were more closely related to strains of M. mycoides subsp. mycoides, such as Y-goat, which are found in goats, than to strains of that subspecies which are pathogenic for cattle.

Epidemiological aspects of infection with leptospires of the Ballum serogroup in black rats (Rattus rattus) and brown rats (Rattus norvegicus) are described. Rats inhabiting a variety of habitats were investigated and isolates identified as belonging to the Ballum serogroup were obtained from 21 of 61 black rats (34%) and 63 of 243 brown rats (26%). The high level of endemic Ballum serogroup infection in these species reported here has not been described in other countries.

A statistical relationship was shown between the prevalence of infection in brown rat populations and population density but this was not evident for black rats. Epidemiological data indicates that the black rat is a maintenance host for leptospires of the Ballum serogroup in New Zealand. The brown rat does not appear to be an efficient maintenance host for these leptospires, however endemic infection can be maintained in high-density populations inhabiting synanthropic foci.

An hypothesis of ‘competitive exclusion’ (preferential maintenance of a particular serovar by a host species) is introduced with regard to leptospiral infection in brown rats. It is concluded that the establishment and maintenance of an endemic focus of leptospirosis is dependant on: introduction of a particular serovar; a suitable host; and a suitable host habitat. Within a maintenance population direct transmission appears to be more important than indirect transmission via the environment.

The distribution of salmonellas along the gastrointestinal tract and in associated lymph nodes were studied in 100 sheep and 100 cattle at slaughter. Animals were chosen from those slaughtered on the first day of the week, since this meant that they were likely to have been held at the abattoir for several days and thus to be at high risk of salmonella infection. The contents of the rumen, abomasum, ileum, caecum and rectum were sampled, together with the lymph nodes draining each of these sites.

Of the cattle, 77 were carrying salmonellas, including 61 with infected lymph nodes, whereas only 43 sheep were infected, 14 of them with infections in the nodes. The lower prevalence in sheep than in cattle might be explained by a shorter time between leaving the property and slaughter. In both species, within the gastrointestinal tract salmonellas were most frequently found in the caecum and rectum and least frequently in the abomasum. In cattle salmonellas were frequently present, usually in large numbers, in the lymph nodes draining the ileum, caecum and colon, but rarely in the ruminal and abomasal nodes; however this difference was not apparent in sheep. Over 70 % of infected animals yielded more than one serotype, the maximum number isolated from any one animal being ten.

The so-called SC (small colony) and LC (large colony) strains of Mycoplasma mycoides subsp. mycoides are said to be indistinguishable by the in vitro serological tests generally used in mycoplasmology. In mice the immunity given by a single dose of killed LC-strain vaccine against challenge with SC strains is – unlike that given by SC-strain vaccine – only partial.

When multiple doses of killed or living vaccines were given, the majority of 13 LC strains still failed to immunize completely against a SC strain. This suggests that, although some protective antigens are shared between both types of strain, at least one of importance is present in the SC strains but absent from the majority of LC strains. The difference between the protective-antigen content of SC and most LC strains is thus qualitative, and not merely quantitative.

Short laboratory feeding tests were carried out with the anticoagulants warfarin, difenacoum, and brodifacoum on a number of European rodent species: Clethrionomys glareolus, Microtus agrestis, M. arvalis, Apodemus flavicollis, A. sylvaticus, Mus musculus, Rattus rattus and R. norvegicus. It was found that the toxicity to all species was highest with brodifacoum and lowest with warfarin, and that only 0·005% brodifacoum would give a complete mortality in most species after one day's feeding. The potential of this compound for the control of microtine field rodents is suggested.

A general practice population of around 6700 was kept under clinical and laboratory surveillance from 1962 to 1975. Illnesses totalled 18703 in three morbidity classes: sore throat (Throats) 4451, acute febrile respiratory diseases (FRD) 4934, acute non-febrile respiratory diseases (Non-FRD) 9318. Specimens were examined for beta-haemolytic streptococci (BHS) from 37·1% of these illnesses: from Throats 33·3%, from FRD 67·8%, from Non-FRD 22·6%, and 515 specimens were collected from a miscellaneous (‘Other’) class consisting of healthy persons and ailments that could not have had a streptococcal component.

Strains of BHS were isolated from 7448 specimens as follows: group A (Streptococcus pyogenes) 353, group C 36, group G 15, other groups 274.

Group A strains were isolated from specimens at the following rates: Throats 16·7 %, FRD 2·4%, Non-FRD 0·9 %, Other 1·4 %. The last two classes reflect the carrier rate in the general community, which must be deducted to obtain the streptococcal morbidity in the other classes. Carriers thus accounted for 6% of the strains isolated from the Throats class and for 42 % of those from FRD illnesses.

No consistent seasonal trend of prevalence was detected. Long-term fluctuations in prevalence over several years affected all groups and most group A serotypes.

Serotyping was performed on 304 strains from 1963 to 1975. The commonest types found were T-types 4 and 12 and M-type 12.

Immunity against re-infection by identical strains appeared to be fairly strong and also against heterotypic strains that shared a T-antigen, but little protection was conferred against re-infection by group A strains with no shared M- or T-antigen. R-28 antigen is considered here as a marker epidemiologically equivalent to an M-antigen.

Epidemicity, as measured by a simple estimate of aggregation, appeared to be low and there were differences between and within serotypes.

The infecting organism appeared to linger in the pharynx, sometimes for several months, after a streptococcal illness.

A total of 19200 children, all contacts or relatives of known leprosy patients, and all free of visible leprosy lesions, were included in a controlled trial of BCG vaccination against leprosy in Uganda between 1960 and 1964. They were followed for an average of 8 years, during which time 261 developed early leprosy lesions. A less comprehensive follow-up was carried out for a further 5 years, when 8 more cases of leprosy were identified.

In the main intake, between 1960 and 1962, 16150 tuberculin-negative or weakly tuberculin-positive (Heaf Grades O-II) children were allocated by an effectively random process to either a BCG-vaccinated or an unvaccinated control group. Both groups were seen and examined in an identical fashion for leprosy at approximately 2-year intervals, and precautions were taken to ensure unbiased assessment of new cases of leprosy. After 8 years, 41 cases of leprosy had been identified in the BCG-vaccinated group, and 201 in the control group, a percentage reduction in the BCG-vaccinated group compared with the control group of 80%. The percentage reduction was similar for those initially tuberculin-negative, and for those initially weakly positive, and did not depend upon the age at vaccination. It was also similar for both sexes, for contacts of lepromatous and contacts of non-lepromatous leprosy, for children having contact with one or more than one patient, and for differing grades of physical contact and genetic relationship with a patient. The protective effect of BCG vaccination continued over the 8-year period, although it may have fallen off slightly at the end.

In a group of 1074 strongly tuberculin-positive (Heaf Grades III-IV) children followed in parallel with the other two groups a total of 16 cases of leprosy were identified. When adjusted for age, this incidence is 58% lower than that in the unvaccinated control children who were initially tuberculin-negative, indicating a protective effect against leprosy of naturally-acquired strong tuberculin sensitivity.

Between 1970 and 1975, one new case of leprosy was identified in a child who had initially been strongly tuberculin-positive and had therefore not been vaccinated, one in a BCG-vaccinated child, and 6 in control children. Although the follow-up in this period was less comprehensive than that in the main part of the trial, the ascertainment of cases was unlikely to have been biased towards either vaccinated or control children. These results indicate a continuing protective effect of BCG up to 12–13 years after vaccination.

A prospective study of hepatitis that began in 1968 and continues to include more than half the dialysis units in the United Kingdom shows that type B infection has been completely controlled in such units since the last outbreak ended in 1973. Though occasionally a single patient has developed hepatitis B surface antigenaemia in the course of dialysis or after transplantation, the infection has not spread to other patients or staff in the survey units.

A detailed analysis of the results in 1974–75 shows clustering of patients with raised aminotransferase levels in about one-fifth of the units but, unlike past outbreaks of hepatitis B, these clusters are not accompanied by clinical hepatitis among staff. The possibility that some of the clusters are caused by hepatitis viruses other than type A or B is discussed. It is concluded that, when reliable tests for type non-A non-B infections become available, the continued existence of the survey will allow prompt assessment of any viral hepatitis problems that may still exist in UK units.

Inactivated vaccines prepared from influenza virus strains obtained by the recombination of A/PR/8/34 (H1N1) or A/FM/1/47 (H1N1) viruses with A/Victoria/3/75 (H3N2) virus, were tested for their antigenicity in hamsters. The parental origin of the genes of each cloned recombinant virus was determined by polyacrylamide gel electrophoresis, and vaccines prepared from each strain by concentration, purification on sucrose density gradients and inactivation with formalin. All the recombinant strains used in these studies possessed surface haemagglutinin and neuraminidase antigens derived from the A/Victoria/75 parent strain.

On inoculation into hamsters, at equivalent concentrations, these vaccines varied in their ability to induce haemagglutination-inhibiting (HI) antibodies in the serum. This variation was not dependent on concentration and was observed using neutralization and single radial haemolysis, as well as HI. The possible reasons for the findings are discussed.

Radioimmunoassay (RIA) for rubella-specific IgM antibodies was compared with haemagglutination-inhibition (HI) in conjunction with gel filtration for the diagnosis of rubella infection in pregnant women during a 1-year period. In total 476 women were investigated of whom 221 were tested for rubella IgM. Both techniques gave positive results with 64 sera, and RIA alone with one additional serum.

Difficulties associated with the removal of non-specific HI activity were encountered with four sera all of which were negative by RIA.

RIA was found to have practical advantages over the gel filtration method but is at present technically more difficult to perform.

Radial haemolysis (RH) was used to test sera for immunity to rubella from 1317 patients attending a general practice. One hundred and forty-one (10·7%) were treated as susceptible and offered an attenuated virus vaccine (RA 27/3). Pre-immunization sera from 43% of these patients were reactive at low levels in RH (< 15 international units rubella antibody per ml).

Pre- (S1) and post- (S2) immunization sera from 66 vaccinees were studied in detail. Antibody was detected by RH, haemagglutination inhibition (HI) and enzyme-linked immunosorbent assay (ELISA), and the specific IgM response was measured by a solid-phase M-antibody capture radioimmunoassay (MACRIA). The vaccine-induced IgM response was only detected if the S1 serum was non-reactive by all tests for rubella antibody. It was weaker than that seen following wild virus infection. It could be detected reliably for six weeks, and in most cases for nine weeks, after immunization. In contrast, patients with S1 specimens reactive by RH, HI or ELISA never showed an IgM response in the S2 specimen despite ‘significant’ antibody rises often being present.

It was considered that an IgM response to RA 27/3 was the best indicator of pre-immunization susceptibility to rubella. The failure of many vaccinees to make an IgM response implied that a significant proportion were already immune. It is suggested that the threshold for a report of immunity to rubella could be lowered from 15 i.u. antibody per ml and so fewer women immunized without vaccine being withheld from those who need it.

An outbreak of influenza caused by the A(H1N1) subtype in military recruits in February 1978 afforded an opportunity to study the association of ABO blood groups with influenza morbidity and serological response. Fifty-eight per cent of 336 recruits became clinically ill. There was no differential distribution of clinical influenza by blood group. However, seroconversion to a titre of ≥ 20 was significantly and appreciably higher in groups A and B than O and AB. Also, among those with serologically confirmed clinical influenza, the occurrence was significantly higher in groups A and B than groups O and AB.