Methicillin-resistant Staphylococcus aureus: a new zoonotic agent?

Staphylococcus aureus is a major cause of infection in hospitals and the community. One third of the general population is colonized by the bacterium, constituting a risk factor for acquisition of infection with this pathogen. Worldwide, the increasing antibiotic resistance of S. aureus complicates treatment of infection and control measures. Soon after the introduction of methicillin, the first isolates resistant to this antibiotic were reported and named methicillin-resistant S. aureus (MRSA). During the past decade a major change in MRSA epidemiology has been observed: whereas in the past MRSA was almost exclusively regarded a hospital pathogen, the advent of community-acquired MRSA has led to infections in people without hospital-related risk factors. Recent evidence has also identified a link between colonization of livestock and MRSA carriage and infections in people who work with animals. Screening of pigs and pig farmers in the Netherlands revealed high prevalence of MRSA sequence type (ST) 398 and it has become clear that the emergence of ST398 is not just a Dutch problem, as reports on livestock colonization and human infections are appearing worldwide. In Austria, the ST398 lineage has been detected in dust samples from pig breeding facilities and in food samples. Since the first Austrian detection of this emerging lineage in 2006, 21 human isolates, partially associated with infections, have been observed. MRSA has to be regarded as a new emerging zoonotic agent and livestock may constitute a growing reservoir of the ST398 lineage. More information is needed so that control measures to reduce the impact of the emerging MRSA ST398 lineage on public health can be developed and implemented.

Outbreak of staphylococcal food intoxication after consumption of pasteurized milk products, June 2007, Austria.

On June 13, 2007, the public health authority informed the Austrian Agency for Health and Food Safety about 40 children from two neighboring elementary schools who had fallen ill with abdominal cramps and vomiting on June 8. School milk products consumed on June 8 were suspected as the source of the outbreak. On June 8, the milk products provided by local dairy X to eight elementary schools and two nurseries. The short incubation period - all cases fell ill on the day on which the products were consumed - and the short duration of illness (1-2 days) strongly suggested intoxication. In order to identify the causative pathogen, its reservoir and the mode of transmission, a descriptive-epidemiological and microbiological investigation and a retrospective cohort study were conducted. Six of the 10 institutions served by dairy X completed questionnaires on demographics and food consumption. One school had a 79% response rate (203/258) and was chosen as the basis for our cohort study. A total of 166 of the 1025 children (16.2%) at the 10 institutions fulfilled the case definition. Consumption of milk, cacao milk or vanilla milk originating from dairy X was associated with a 37.8 times higher risk of becoming a case (95% CI: 2.3-116.5). Unopened milk products left over at the affected institutions yielded staphylococcal enterotoxins A and D. Six out of 64 quarter milk samples from three of 16 cows producing milk for dairy X tested positive for S. aureus. The isolates produced enterotoxins A and D, yielded genes encoding enterotoxins and D, and showed spa type t2953. S. aureus isolated from the nasal swab of the dairy owner harbored genes encoding enterotoxins C, G, H and I, and showed spa type t635. Our investigation revealed that the milk products produced in dairy X on June 7 were the source of the outbreak on June 8. The cows - not the dairy owner - the likely reservoir of the enterotoxin-producing S. aureus. From the risk assessment of the production process at the dairy, we hypothesize that staphylococcal toxin production took place during a 3-day period of storage of pasteurized milk prior to repasteurization for the production batch of 7.

A food-borne outbreak of Shigella sonnei gastroenteritis, Austria, 2008.

We report on the first foodborne outbreak of Shigella sonnei described in Austria. On July 14 2008, AGES was informed of a cluster of 22 laboratory-confirmed cases of infection with S. sonnei restricted to public health district X in the province of Salzburg. All cases had attended a youth-group trip to a small village in the province of Tyrol from July 7 to July 9. An outbreak case among the trip participants was a person who (1) attended the trip and (2) fell ill with diarrhea in the period between July 8 and July 12. Among the 61 trip participants, 42 fitted the outbreak case definition, including 31 culture-confirmed cases. A household outbreak case was a person who (1) did not participate in the trip, (2) fell ill with diarrhea not before July 10 and (3) had household contact with an outbreak case between one and three days before onset of illness. Of the 11 household outbreak cases, 10 were tested by stool culture and four of these had a laboratory-confirmed S. sonnei infection. In addition, one of the two hostel staff tested positive for S. sonnei. All 36 isolates were biotype gl, lysotype 12, and were indistinguishable from each other by PFGE. A cohort study among the trip participants revealed a risk ratio of 2.71 for consumption of salad (on at least 1 of the 3 days of the trip) (95% CI: 1.38-5.32, P = 0.004). Among the 42cases, 34 could be explained by consumption of salad. The landlady of the hostel, who prepared the salad with bare hands, was a carrier and was assumed to be the source of contamination of the salad. Without proper epidemiological analytical investigation of this shigellosis outbreak, its association with food consumption would not have been identified.