Three different types of bivalent influenza virus vaccine, a whole virus, an aqueous-surface-antigen vaccine and an adsorbed-surface-antigen vaccine were tested at three dosage levels in volunteers primed with respect to only one of the haemagglutinin antigens present in the vaccines.

The local and systemic reactions to all three vaccine types were mild in nature and, following first immunization, the aqueous-surface-antigen vaccine was the least reactogenic. The serum haemagglutination-inhibiting antibody response to the A/Victoria/75 component of the vaccines, to which the volunteer population was primed, was greatest following immunization with the aqueous-surface-antigen vaccine; the greatest antibody response to the A/New Jersey/76 component of the vaccines was observed following immunization with whole virus vaccine.

The specificity of serum anti-HA antibody from children immunized or infected with A/Victoria/75 (H3N2) or A/Texas/77 (H3N2) virus was examined using the single radial haemolysis test together with adsorption of antibody with three antigenic variants A/Hong Kong/68 (H3N2), A/Port Chalmers/73 (H3N2) and A/Victoria/75 (H3N2). The majority of young children reacted to vaccination or infection by producing strain-specific (SS) antibody to the homologous virus. A small proportion of children's sera contained cross-reacting (CR) antibodies capable of reacting with the haemagglutinins of all antigenic variants of the subtype including A/HK/1/68. In contrast, most adults reacted immunologically to either vaccination or infection by producing CR antibody, reacting with all variants of the antigenic subtype including the prototype virus A/HK/1/68 (H3N2).

It was observed that small children and pregnant women were affected to only a small extent by the H1N1 influenza outbreak of winter 1978–79. This supports earlier findings from the epidemic season of 1977–78 and demonstrates that the evolutionary changes in the epidemic virus were not reflected in any appreciable way in this curious phenomenon. The frequency of elderly subjects possessing antibodies against the epidemic H1N1 virus was low, and virtually equal in the pre-epidemic and post-epidemic sampling. This low attack rate contrasts with observations on young military servicemen, in whom the re-infection rate was high, thus indicating that the infection with the winter 1977–78 virus had conferred only modest protection against the closely related virus which caused the winter 1978–79 outbreak.

Four types of observations have been used to illustrate the seasonal characteristics of epidemic influenza: (1) The experience of a small population during 28 consecutive years, 1946–74, (2) world influenza outbreaks 1964–75 reported to the World Health Organization, (3) the experience of two widely separated localities at about the same latitude, 1969–74, and (4) the experience of two places at latitudes 30° + on opposite sides of the Equator, 1968–74.

The following tendencies are shown. (1) Outbreaks of influenza even in the small community came at approximately the same season almost every year. (2) Outbreaks are globally ubiquitous and epidemic loci move smoothly to and fro across the surface of the earth almost every year in a sinuous curve that runs parallel with the ‘midsummer’ curve of vertical solar radiation, but lags about six months behind it. Such findings exclude the mediation of seasonal control by any agencies of local distribution, and suggest a direct effect of variations in some component of solar radiation on virus or human host. (3) Antigenic variations in influenza A virus tended to have the same seasonal characteristics as epidemicity. This suggests that epidemicity and virus variation are two facets of one seasonally controlled process.

None of these seasonal characteristics can be explained by the current concept of influenzal epidemiology. A new hypothesis recently proposed and recapitulated in the Appendix offers a possible explanation. The primary agency mediating seasonal control remains unidentified.

Sources of information for monitoring infectious disease are routine data, special surveys and ad hoc investigations. In practice much use is necessarily made of routine notifications and laboratory records although this reporting is often incomplete and may therefore be biased.

In a retrospective study of a 16-year series (up to 1968) of routine records concerning the diagnosis of gastroenteritis at one Public Health Laboratory we found it possible to identify biases. During school outbreaks of dysentery, laboratory investigation of diarrhoea increased appreciably and such response to publicity affects the use of routine data in surveillance. Although the patients examined were probably representative diagnostically, their selection may not have reflected the age incidence of disease. Valid geographical comparisons within the urban area were not feasible because medical practitioners differed in their use of laboratory facilities and in their habits of notification. Nevertheless, as far as can be established retrospectively, these data did reflect time trends in disease incidence and so had value for monitoring purposes.

Several of the biases defined are likely to apply to other sets of routine data. A further communication will describe a statistical method of correcting for quantifiable bias.

Routine data used to study infectious diseases may contain biases which obscure trends. A 16-year series (up to 1968) of routine laboratory data was used to study patterns of incidence of infective gastroenteritis for which no laboratory diagnosis could be made. An artificial pattern was detected. This arose because GPs tended to refer a greater proportion of their patients during dysentery epidemics. Multiple regression analysis was used to separate out this effect so that the underlying trends could be observed.

The seasonal pattern of undiagnosed cases showed an autumn peak. There were also early-winter epidemics of disease with little or no excretion of red blood or pus cells in the diagnostic faeces specimen. Some of the winter communicable disease among older children and adults appeared to be associated with signs of a temporary fat malabsorption in pre-school age cases. Undiagnosed cases in older children and adults were not related to the E. coli serotypes causing disease in infants during this period.

The statistical method applied increased the usefulness of these routine data. Although this series of laboratory records is now more than a decade old the results of the analysis can be compared with new observations as more is learned about the epidemiology of previously unrecognized pathogens, especially rota-viruses.

Radioimmunoassay (RIA) tests for anti-hepatitis A virus (HAV) IgM were carried out on 728 sera: 382 were tested by both a method using an anti-μ serum bound to a solid phase and a method involving preliminary separation of IgM by sucrose density gradient (SDG) centrifugation, 354 by the anti-μ method alone and two by the SDG method alone. Similar proportions of sera were found to be positive by each method (42·5%, 41·7%), but equivocal results were commoner by the SDG method (4·7% compared with 1·5%). There were 21 (5·5%) discrepant results from the sera tested by both methods, 20 of which could have been due to the higher sensitivity of the anti-μ method.

The SDG method generally gave unequivocal results on sera collected within six weeks of the onset of jaundice. Separation of the IgM fraction by re-orientation centrifugation was quick, but otherwise offered no special advantage over separation on a swing-out rotor. The use of 2 mercaptoethanol (2 ME) reduction to assess the purity of the IgM fraction increased confidence in the specificity of the test. It led, however, to the exclusion of 16 reactive sera (4·2%), all of which were found to be positive in the anti-μ test.

The anti-μ method gave better discrimination between positive and negative sera than the SDG method and detected IgM both earlier and later in infection. The results of tests designed to check the specificity of the anti-μ procedure were satisfactory. As it is potentially cheaper and easier to perform, the anti-μ method seems, in all respects, to be superior to the SDG method.

A simple solid-phase enzyme immunoassay is described for the detection of antibody classes showing activity against foot-and-mouth disease (FMD) virus in bovine sera. The assay achieves a preliminary separation of the specific class of antibody from other serum proteins through immuno-adsorption to class-specific immunoglobulin-coated wells of micro-titre plates. The specific antibody is reacted with FMD virus, which is then detected by an enzyme-labelled anti virus IgG.

A group of 240 urban and 200 rural dwellers in Western Samoa over the age of 20 years was studied for serological evidence of current or past infection with heptatitis B virus (HBV). Overall, 5·5% of subjects were found to be currently infected with HBV and a further 74·5% showed detectable levels of antibody. Antibody to the hepatitis B core antigen was found to be a better marker of past infection than antibody to the surface antigen of the virus. Both the infection rate and carrier rate were higher in males than females and subjects living in rural areas were more likely to be infected than those living in urban areas.

A number of adenovirus serotypes have been associated with both sporadic cases and outbreaks of conjunctivitis and pharyngoconjunctival fever but only adenovirus type 8 and adenovirus type 19 have been responsible for wide-spread epidemic kerato-conjunctivitis. In Melbourne, Australia, in the past eight years these two serotypes have been prevalent, resulting in an outbreak of adenovirus type 8 kerato-conjunctivitis in 1976–7 followed by adenovirus type 19 keratoconjunctivitis in 1978–9. During these two periods of peak incidence, 53 cases of adenovirus type 8 and 43 cases of adenovirus type 19 kerato-conjunctivitis were confirmed by isolation.

Sera of 1000 persons in Voyvodina were tested with radioimmunoassay for antibodies against hepatitis A virus (HAV).

The morbidity and age incidence of positive findings have been analysed and compared with relevant findings in other countries. Below the age of 19 years the morbidity rates are higher (0·138 to 0·595 per mill) and the prevalences of seropositives are lower (17·1–64·0%) than the respective frequencies above that age (0·011 to 0·052 per mill and 85·7–98·7 % respectively). Below the first year of life seropositivity is more frequent than in 1- to 14-year old children. After the first year until the age of 30–39 years the frequency of seropositives increases with increasing age up to a maximum of about 90%.

An antigenic scheme for Citrobacter koseri was described previously and consisted of 14 ‘O’ antigens. Three additional antigens are now added to the scheme and type strains for these antigens are designated. Their origins and their biochemical and serological reactions are described.

The antibody titres in 250 subjects, aged 5 to 22 years, who were vaccinated with a mannitol-lyophilized antimeningococcal A + C vaccine, stable only when stored at − 20°C, were followed for two years. As measured by indirect haemagglutination (IHA) and indirect immunofluorescence (IF) techniques, titres for both A and C Neisseria meningitidis antibodies remained high. Two years after vaccination titres of antibodies against type A showed fourfold increase over the initial titres in from 46 % to 100 % of groups of subjects and against type C in from 42 % to 80%.

For 130 subjects vaccinated with a new lactose–lyophilized antimeningcoccal A + C vaccine (presumed stable at 4°C) antibody titres were measured up to 16 months after inoculation with this vaccine stored at −20°C and also after storage for several periods at 4°C. Antibody titres in all these subjects had fallen to their initial titres by 16 months.

The importance of evaluating the results on subjects showing low initial titres (≤1/8 as measured by IHA) is discussed, as inclusion of high initial titres influences the extent of the response.

Samples of sewage, sewage sludge and sewage effluent from one or more of four sewage treatment plants were examined for the presence of Leptospira, Mycobacterium, Escherichia coli, Brucella abortus and Bacillus anthracis. Brucella abortus and Bacillus anthracis were not isolated. Eleven strains of E. coli potentially enteropathogenic for calves or piglets, eight pathogenic strains of Mycobacterium and one pathogenic Leptospira strain were isolated from 101, 189 and 189 samples respectively.

Sewage sludge is not considered to play a major part in the epidemiology of disease caused by these organisms.