Among 741 children under 5 years admitted to hospital with respiratory infections during two winters, infection with influenza A virus was diagnosed in 70 (9%), with influenza B virus in 8 (1%), and with respiratory syncytial virus (RSV) in 259 (35 %). Both influenza virus and RSV infections were diagnosed most frequently in children under the age of one year, and diagnosed more frequently in males than females. Influenza illnesses were more severe in boys than girls. Both infections occurred more often, but were not more severe, in children from a conurbation than in those from ‘rural’ areas. Convulsions were the cause of 36% of admissions with influenza A infections, but were rare in RSV infections. Bronchiolitis was the reason for 39% of admissions with RSV infections, but was rare in influenza infections. It is suggested that infants admitted to hospital are a good source of influenza virus strains for monitoring arttigenic variation.

A bacteriological survey on the distribution and occurrence of coliforms and pathogenic indicators of pollution within the surf-zone and near-shore waters along a section of the Natal coast before the use of submarine outfalls was reported previously. In that report more than half the beaches in the region were found to be of Class IV or III quality. After the submarine outfalls became operational, ten further sampling runs were made. A considerable improvement in the sea-water quality was apparent, most of the beaches being regraded to Class II or I, notably in the bathing areas.

Electron microscopic observation of negatively stained preparations of frozen and thawed suspensions of T4Bo phage clearly separated the morphological changes produced by low-temperature salt denaturation from those produced by eutectic phase changes. Salt denaturation caused contraction of tail sheaths. Eutectic phase changes appeared to cause two separate lesions. Firstly the tail sheath was disjointed 18–22 nm. below the collar and the tail core was disjointed at 40–60 nm. below the collar, giving rise to separated heads with a small tail remnant, and separated tails in which the sheath remarkably remained in its extended form. Secondly, tears were seen in the head membranes of particles with collapsed empty heads. In all the experiments the percentage of normal phage particles counted electron-microscopically was close to the percentage of viable phage as determined by plaque assay.

Escherichia coli O 27 H 7 was found in 16 stool samples submitted during a Caribbean cruise (Cruise Z) by 29 patients reporting with diarrhoea. A retrospective search revealed E. coli O 27 H 7 in 11 of 20 and 2 of 14 stool cultures from patients on two previous cruises (Y and X respectively) and in a culture from fresh cream (Cruise Y). The repeated occurrence of E. coli O 27 H 7 in the absence of any other apparent cause suggested that this serotype may have been responsible for the diarrhoea. The results of pathogenicity tests suggested that this strain elaborated heat-stable (ST) enterotoxin.

The possibility that food may have been the vector is discussed.

Disposable plastic two-piece suits were compared with conventional cotton suits, gowns, and plastic aprons by nurses in a burns unit. The plastic suits allowed fewer micro-organisms to be dispersed into the environment than the other garments but were less comfortable.

An account is given of K. pneumoniae capsule types occurring in horses, with particular reference to strains originating from the genital tract in the mare and the external genitalia of the stallion.

A survey of the prevalence of K. pneumoniae and E. aerogenes strains in the preputial flora of healthy stallions is described. The majority of horses were found to be carriers of these organisms. The cultural characteristics of these preputial strains are described and compared with those of K. pneumoniae strains associated with epidemic metritis in mares. The epidemiological significance of certain K. pneumoniae capsule types is discussed.

Escherichia coli was found in a similar proportion of stool specimens from infants who were breast-fed and from others fed on three different artificial-milk preparations. When E. coli was present its mean colony count in the stools of breast-fed infants was within the range of the mean counts for infants receiving the artificial-milk feeds.

There was no consistent relation between high counts of bifidobacteria (Lacto-bacillus bifidus) and low counts of E. coli. This suggests that measures aimed at implanting or stimulating the growth of bifidobacteria in the large intestine of artificially fed infants may not greatly influence the E. coli population therein.

The results are discussed in relation to the protection of artificially fed infants from E. coli enteritis.

A technique for estimating antibodies to the neuraminidase antigens of influenza A is described.

The antibody response to the haemagglutinin and neuraminidase antigens of influenza A (H3N2) was studied in a boys' public school over the four-year period 1970–4. During this time there were two outbreaks of influenza A and the effect of antibody on the result of natural challenge was investigated. No boy who had homotypic neuraminidase antibody had clinical influenza.

Germ-free piglets were infected intranasally with porcine cytomegalovirus (PCMV) at 1 day (group A) or 3 weeks of age (group B). Viraemia and virus excretion by the nasal, pharyngeal and conjunctival routes was studied up to the time of death or to 12 weeks. Virus was also sought in tissues at death or at slaughter, as well as in a few urine samples.

Viraemia was detected in group A between days 5 and 19 after infection and in group B between days 14 and 16 inclusive. The chief route of virus excretion was the nasal mucosa, followed by the pharynx and conjunctiva; the maximal duration of excretion by these routes was 32, 25 and 14 days for pigs of group A and 9, 7 and 4 days for group B. The quantity of virus was also greater in the former group, of which 3 died of generalized PCMV infection.

A viruria was demonstrated in 2 animals.

Antibody detectable in indirect immunofluorescence (IIF) tests appeared towards the end of the third week, reaching maximal titres at 5 to 7 weeks after infection. The mean peak titre of antibody in group B was lower than in group A.

Corticosteroid treatment at days 56–62 after infection resulted in some recrudescence of virus excretion, accompanied in group B by about a twofold increase in IIF antibody. PCMV was isolated in cultures of lung macrophages from 4 of 7 animals killed at about 12 weeks after inoculation.

The effects of cigarette smoking on the incidence of epidemic influenza and on the serological response to influenza vaccination with killed subunit and live attenuated vaccines have been investigated during comparative vaccine trials in Western Australia. It was found that cigarette smokers with no pre-epidemic haemagglutination-inhibiting (HI) antibody (titres of ≤ 12) were significantly more susceptible to epidemic influenza than non-smokers. Smokers were no more susceptible however, if they had possessed detectable pre-epidemic HI antibody. A significantly higher proportion of smokers sero-converted after receiving the live virus vaccine than their non-smoking counterparts, but this could not be correlated with pre-vaccination HI antibody titres. The longevity of the immune response to the subunit vaccine was severely depressed 50 weeks post-vaccination in smokers who had possessed little or no immunity before vaccination (titres of ≤ 12). This antibody deficit was not observed in live virus vaccinees or subunit vaccinees with pre-vaccination HI antibody (titres of ≥ 24). Post-vaccinal symptoms were similar regardless of vaccine group or smoking history.

Feeding tests were carried out in the laboratory to evaluate WBA 8119 as a potential new rodenticide against wild common rats (Rattus norvegicus), ship rats (R. rattus) and house mice (Mus musculus). The results obtained are compared with data previously obtained for difenacoum, another member of the same series of 4-hydroxycoumarin anticoagulants.

With warfarin-resistant and non-resistant common rats, complete kills were obtained using a concentration of 0·0005% for 2 days, or 0·001 % for 1 day: a 1-day test at 0·0005% killed 6 out of 10 and 17 out of 20 of the two types respectively. At 0·005% complete kills of resistant ship rats were obtained after 2 days exposure and of resistant house mice after 1 day, but at 0·002% for 2 days there was some survival. Non-resistant ship rats and house mice were all killed after 2 days feeding on 0·002% bait.

In 2-day palatability tests, R. norvegicus showed no significant aversion to the poison at 0·002% and 100% mortality was obtained. The poison was significantly unpalatable to R. rattus at 0·005% and to M. musculus at 0·005% and 0·002 %, although with the last species these concentrations gave complete kills.

It is concluded that WBA 8119 has greater activity than other known anticoagulants against the three commensal species examined. The laboratory results suggest that concentrations between 0·0005% and 0·002% would be suitable for field use against common rats, and between 0·002% and 0·005% for ship rats and house mice.

The efficacy of the newly developed anticoagulant rodenticide WBA 8119 was evaluated against the house mouse (Mus musculus L.) using individual and family groups of warfarin-resistant animals. WBA 8119 at 0·002 %, O % and 0.01 % in pinhead oatmeal bait gave complete kills of mice in ‘no-choice’ feeding tests carried out in cages and small pens. In replicated 21-day treatments on families of mice confined in larger pens and conditioned to feeding on plain foods, the overall mortalities obtained using the three formulated poison baits were 71/72, 62/63 and 57/57 respectively.

The results of the WBA 8119 toxicity tests are considered in relation to previous findings on other anticoagulant rodenticides, particularly difenacoum. In equivalent tests, WBA 8119 performed better than difenacoum. The data thus support the laboratory findings that WBA 8119 is the most active anticoagulant so far tested for the control of warfarin-resistant house mice.