On Friday, 22 November 1996, the microbiologist at a hospital in Lanarkshire, Scotland, identified presumptive Escherichia coli O157 in faecal specimens submitted by three patients with bloody diarrhoea, and confirmed its presence in one. Over the next 6 h, 12 more potential cases were identified. Investigations first indicated then confirmed a single food premises as the source of infection. Effective control measures were applied promptly. The outbreak was declared over on 20 January 1997, by which time 512 cases had been identified, and infection with the outbreak strain confirmed in 279. Twenty deaths occurred in cases during the outbreak and there were two more in cases during 1997. Seventeen of these deaths resulted from the outbreak. This paper describes the outbreak's epidemiological investigation, referring to other investigations, and control measures, where appropriate.

This is the first study to provide a comprehensive insight into the molecular epidemiology of endemic Clostridium difficile and particularly that associated with a recently recognized epidemic strain. We DNA fingerprinted all C. difficile isolates from the stools of patients with symptomatic antibiotic-associated diarrhoea and from repeated samples of the inanimate ward environment on two elderly medicine hospital wards over a 22-month period. Notably, C. difficile was not recoverable from either ward immediately before opening, but was found on both wards within 1–3 weeks of opening, and the level of environmental contamination rose markedly during the first 6 months of the study period. C. difficile infection (CDI) incidence data correlated significantly with the prevalence of environmental C. difficile on ward B (r = 0·76, P < 0·05) but not on ward A (r = 0·26, P > 0·05). We found that RAPD and RS–PCR typing had similar discriminatory power, although, despite fingerprinting over 200 C. difficile isolates, we identified only six distinct types. Only two distinct C. difficile strains were identified as causing both patient infection and ward contamination. Attempts to determine whether infected patients or contaminated environments are the prime source for cross-infection by C. difficile had limited success, as over 90% of C. difficile isolates were the UK epidemic clone. However, a non-epidemic strain caused a cluster of six cases of CDI, but was only isolated from the environment after the sixth patient became symptomatic. The initial absence of this strain from the environment implies patient-to-patient and/or staff-to-patient spread. In general, routine cleaning with detergent was unsuccessful at removing C. difficile from the environment. Understanding the epidemiology and virulence of prevalent strains is important if CDI is to be successfully controlled.

A prevalence survey of nasal methicillin-resistant Staphylococcus aureus (MRSA) carriage was undertaken on a random sample of adults (aged over 16) resident in the community in Birmingham, UK during 1998. Microbiological samples were taken from the anterior nares at the subjects' general practice or in their home. Information about risk factors for the acquisition of MRSA was obtained via a self-completed questionnaire. A 58% response rate (280/483) was achieved. The prevalence of nasal MRSA colonization was 1.5% [4/274, 95% confidence interval (CI) 0.03–2.9%]. Twenty-three per cent (63/274) of subjects were nasal carriers of S. aureus. Six per cent (4/63) of S. aureus isolates were MRSA and 2 of the 4 MRSA carriers reported previous contact with health facilities. The prevalence of MRSA colonization in the general adult population in Birmingham appears to be low.

Ninety-three clinical isolates of vancomycin-resistant enterococci (VRE) collected from nine hospitals in Taiwan were examined for the presence of vanA, vanB, vanC1, or vanC2/vanC3 genes by a multiplex PCR. Forty-seven of these VRE isolates were vanA positive, 1 contained both vanC1 and vanA, 40 harboured vanB, 2 were vanC1, and 3 were identified to be vanC2/vanC3. Twenty-four vanA isolates were sensitive to teicoplanin and thus did not have a typical VanA phenotype. Five isolates with the VanC phenotype harboured vanB. None of the 40 clinically isolated vancomycin-susceptible E. faecium or E. faecalis and the vancomycin-resistant Leuconostoc and Pediococcus isolates were positive for any of the van genes. While performing nosocomial surveillance, VRE were isolated from 47 of 467 rectal swabs by culture. Compared with the conventional culture method, the sensitivity and specificity of the multiplex PCR for detecting and identifying vancomycin-resistance genes in enterococci directly from culture-positive broth were 97·9% and 100%, respectively. The results suggest that genotypic characterization of vancomycin-resistance is necessary for all clinical VRE isolates and that the multiplex PCR assay can be an alternative method for this purpose.

Acute poststreptococcal glomerulonephritis (APSGN) is an inflammatory kidney condition that can complicate Group A streptococcal infections. Two clusters of APSGN occurred recently in New South Wales (NSW), Australia; one in a rural town in December 1999 and the other in a Sydney suburb in January 2000. We interviewed carers of the affected children but found no common exposures except three of the Sydney cases were cousins in frequent contact. To assess the probability of these clusters occurring, we analysed hospital admissions for acute glomerulonephritis, as a proxy for APSGN in younger patients. The incidence of acute glomerulonephritis in NSW during 1989/90–1997/8 in residents aged under 20 years was 2·2/100000/year (95% CI 2·0–2·5). Incidence was highest in children aged 5–9 years, boys and Aboriginal children. We found no evidence for other clusters during that period. The recent clusters highlight the continued potential for unexpected future outbreaks of APSGN.

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.

More than 36000 individuals living in rural Malawi were skin tested with antigens derived from 12 different species of environmental mycobacteria. Most were simultaneously tested with RT23 tuberculin, and all were followed up for both tuberculosis and leprosy incidence. Skin test results indicated widespread sensitivity to the environmental antigens, in particular to Mycobacterium scrofulaceum, M. intracellulare and one strain of M. fortuitum. Individuals with evidence of exposure to ‘fast growers’ (i.e. with induration to antigens from fast growers which exceeded their sensitivity to tuberculin), but not those exposed to ‘slow growers’, were at reduced risk of contracting both tuberculosis and leprosy, compared to individuals whose indurations to the environmental antigen were less than that to tuberculin. This evidence for cross protection from natural exposure to certain environmental mycobacteria may explain geographic distributions of mycobacterial disease and has important implications for the mechanisms and measurement of protection by mycobacterial vaccines.

From December 1997 to April 1998, 1060 laboratory-confirmed cryptosporidiosis cases were reported in New South Wales, Australia. In a case-control study, compared with 200 controls, the 100 cases were younger (mean age 4·2 versus 7·1 years; P < 0·0001), more likely to report swimming at a public pool (59% versus 38%; adjusted OR and 95% CI = 2·7; 1·4–5·1) and swimming in a dam, river or lake (OR = 4·8; 1·1–20·3) but less likely to report drinking bottled water (OR = 0·4; 0·2–0·9). In subgroup analyses, in rural areas illness was associated mainly with contact with another person with diarrhoea, and in urban areas illness was associated with swimming in a public pool. Cryptosporidium oocysts were more commonly detected in pools to which at least two notified cases had swum (P = 0·04). Outbreaks of cryptosporidiosis can be prolonged, involve multiple pools and be difficult to control.

Invasive fungal infections are becoming an increasing public health problem owing to the growth in numbers of susceptible individuals. Despite this, the profile of mycoses remains low and there is no surveillance system specific to fungal infections currently existing in England and Wales. We analysed laboratory reports of deep-seated mycoses made to the Communicable Disease Surveillance Centre between 1990 and 1999 from England and Wales. A substantial rise in candidosis was seen during this period (6·76–13·70 reports per million population/year), particularly in the older age groups. Rates of cryptococcosis in males fluctuated over the decade but fell overall (1·05–0·66 per million population/year), whereas rates of female cases gradually rose up until 1998 (0·04–0·41 per million population/year). Reports of Pneumocystis carinii in men reduced substantially between 1990 and 1999 (2·77–0·42 per million population/year) but showed little change in women. Reports of aspergillosis fluctuated up until 1996, after which reports of male and female cases rose substantially (from 0·08 for both in 1996 to 1·92 and 1·69 per million population/year in 1999 for males and females respectively), largely accounted for by changes in reporting practice from one laboratory. Rates of invasive mycoses were generally higher in males than females, with overall male-to-female rate ratios of 1·32 (95% CI 1·25–1·40) for candidosis, 1·30 (95% CI 1·05–1·60) for aspergillosis, 3·99 (95% CI 2·93–5·53) for cryptococcosis and 4·36 (95% CI 3·47–5·53) for Pneumocystis carinii. The higher male than female rates of reports is likely to be a partial reflection of HIV epidemiology in England and Wales, although this does not fully explain the ratio in infants and older age groups. Lack of information on underlying predisposition prevents further identification of risk groups affected. Whilst substantial under-reporting of Pneumocystis carinii and Cryptococcus species was apparent, considerable numbers of superficial mycoses were mis-reported indicating a need for clarification of reporting guidelines. Efforts to enhance comprehensive laboratory reporting should be undertaken to maximize the utility of this approach for surveillance of deep-seated fungal infections.

Restriction fragment length polymorphism (RFLP) analysis and partial-genome DNA sequencing are commonly used to infer genetic relationships among pathogens. This study compares the application of both techniques to the analysis of 16 pseudorabies virus isolates collected during a 1989 outbreak. Genetic distances derived from RFLP and DNA sequence data were not significantly correlated with geographic distances between farms from which isolates were collected. RFLP-based genetic distance was, however, strongly correlated with temporal distance between isolates (days separating time of isolation). Sequence-based genetic distance was significantly correlated with temporal distance only when synonymous changes (nucleotide changes not leading to amino acid changes) were considered separately. Conversely, non-synonymous changes were correlated with the host species of origin of the viral isolate. These results indicate that selectively-neutral genetic changes most accurately reflect historical relationships, but that non-neutral changes most accurately reflect the biological environment of the viral isolate (e.g. host immune system).

In 1998, an outbreak of gastroenteritis affected at least 448 persons including 122 staff at a resort hotel in Bermuda. A survey among staff indicated that gastroenteritis was associated with eating or drinking at the hotel (OR = 6·0, 95% CI = 2·4–15·1). Multiple specimens of drinking water had elevated faecal coliform levels and Escherichia coli present, suggestive of faecal contamination. Stools from 18 of the 19 persons with gastroenteritis that were tested were positive for genogroup-II Norwalk-like viruses (NLVs). RT–PCR analysis of a 3 l specimen of water produced a genogroup-II NLV genome with a sequence identical to that of NLVs in the stools of three ill persons. This outbreak shows the value of new molecular diagnostics to link illness with a contaminated source through the use of sequence analysis. The risk of outbreaks such as these could be reduced in tourism dependent regions like Bermuda and the Caribbean by regular evaluation of data from the inspection and monitoring of drinking water supplies and waste water systems, by ensuring the chlorination of supplemental drinking water supplies and by establishing food-safety initiatives.

We conducted a seroepidemiological study to evaluate the potential impact of mass varicella vaccination on the transmission of varicella-zoster virus (VZV) in Italy, where vaccination is not mandatory. We tested 3179 serum samples, collected from September 1996 to October 1997, for specific anti-VZV antibodies using a commercially available ELISA. The results confirmed that varicella typically involves children (82·1% seroprevalence among 10- to 14-year-olds) and that the mean age of acquiring the infection seems to be increasing. The results also revealed that southern Italy, compared to the rest of the country, has a greater circulation of VZV and an earlier age of acquisition. The potential impact of mass vaccination among 12- to 18-month-old children on the epidemiological trend of the infection must be carefully considered, in that failure to reach high levels of coverage could lead to an increase in the mean age of acquisition, which is already occurring in Italy.

An outbreak of echovirus 11 infection was observed in a children's home that housed 16 children. Nine children younger than 1 year shared a large room on the first floor, which contained a large basin. Three of them presented with aseptic meningitis with CSF and stool samples positive for echovirus 11. The other six infants who shared the room were asymptomatic but their stools were positive for echovirus 11. Seven infants aged 1–2 years stayed on the second floor and were asymptomatic. One of them had positive stool culture for echovirus 11. No virus was isolated from stool samples taken from the 26 staff members. However, serology was suggestive for recent echovirus 11 infection in seven asymptomatic staff members. All seven worked either exclusively on the first floor or alternately on both floors. Our survey demonstrated that echovirus 11 may spread very efficiently in children's homes. The rate of meningitis in the infected infants was 30% while all the recently infected adults were asymptomatic.

Staphylococcus aureus is the most prevalent pathogen causing mastitis of dairy ruminants. This study was developed to ascertain the genotypes and genealogical relationship among strains isolated from milk of bovines with mastitis in Argentina. Molecular epidemiological analysis of S. aureus was performed on 112 isolates from 21 districts. Clonality was assessed by SmaI pulsed-field gel electrophoresis (PFGE) typing, automated EcoRI ribotyping and restriction enzyme analysis of plasmid (REAP) DNA profiles. A total of 22 band patterns distributed in four clusters were found by SmaI PFGE analysis. The similarity of clusters 2, 3 and 4 with cluster 1 was 0·73, 0·69 and 0·33, respectively, and 101 of 112 isolates belonged in cluster 1. PFGE band patterns from 42 isolates within cluster 1 were indistinguishable from each other (type A). The second largest group of isolates with indistinguishable PFGE band patterns was subtype A11, which was composed of 19 isolates. Automated ribotyping assigned the 112 isolates into 13 ribotypes. Among these, the most prevalent ribotypes I and VI were composed of 49 and 35 isolates respectively. Although there was certain correspondence between PFGE genotypes and ribotypes, further discrimination was achieved by combining both methods. REAP DNA profile analysis was useful to provide even further discrimination between isolates with identical PFGE genotype and ribotype. The most prevalent S. aureus strains A/I and A11/VI were widely distributed in the country and were not restricted to individual nearby locations. Prevalence of these two strains varied consecutively within a period of 8 years. Whether the shift in type prevalence was due to selection of a phenotypic trait remains undisclosed.

African swine fever (ASF) suspected clinically in Madagascar (1998–9) was confirmed by polymerase chain reaction (PCR) and nucleotide sequencing, following virus isolation. No haemadsorption or cytopathic effect could be detected following leukocyte inoculation, but viral growth in cells was confirmed by PCR. Detection of ASF virus genome was carried out by amplification of a highly conserved region coding for the p72 protein. Nucleotide sequencing of the amplicon revealed 99·2% nucleotide identity between the recent Malagasy strains and a virus recovered from the 1994 outbreak in Mozambique (SPEC265). A serological survey performed on 449 sera, revealed that only 5·3% of the sera taken from pigs between 1998 and 1999 were positive.