SUMMARYA summer outbreak of severe gastroenteritis followed by haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura in a nursery school and kindergarten is described. Sandwiches prepared with green butter made with contaminated parsley were the likely vehicle of infection. The parsley originated from an organic garden in which manure of pig origin was used instead of artificial fertilizers, Cornally identical VerotoxinogenicCitrobacter freundiiwere found as causative agents of HUS and gastroenteritis and were also detected on the parsley.

Salmonella enterica serotype O1,4,5,12:Hb:1,2, designated according to the current Kauffmann-White scheme as S. enterica serotype Paratyphi B, is a very diverse serotype with respect to its clinical and microbiological properties. PCR and blot techniques, which identify the presence, polymorphism, and expression of various effector protein genes, help to distinguish between strains with systemic and enteric outcomes of disease. All serotype Paratyphi B strains from systemic infections have been found to be somewhat genetically related with respect to the pattern of their virulence genes sopB, sopD, sopE1, avrA, and sptP as well as other molecular properties (multilocus enzyme electrophoresis type, pulsed-field gel electrophoresis [PFGE] type, ribotype, and IS200 type). They have been classified as members of the systemic pathovar (SPV). All these SPV strains possess a new sopE1-carrying bacteriophage (designated ⌽SopE309) with high SopE1 protein expression but lack the commonly occurring avrA determinant. They exhibit normal SopB protein expression but lack SopD protein production. In contrast, strains from enteric infections classified as belonging to the enteric pathovar possess various combinations of the respective virulence genes, PFGE pattern, and ribotypes. We propose that the PCR technique for testing for the presence of the virulence genes sopE1 and avrA be used as a diagnostic tool for identifying both pathovars of S. enterica serotype Paratyphi B. This will be of great public health importance, since strains of serotype Paratyphi B have recently reemerged worldwide.Salmonella enterica is one of the most diverse species in the bacterial kingdom. It is currently subdivided into six subspecies according to fermentative properties and into ca. 2,400 serotypes according to polymorphisms in the lipopolysaccharide (O antigen) and flagellar (H antigen) structures (20). Among S. enterica, two major pathogenic groups causing human infections have been identified: Salmonella strains restricted or adapted to humans (e.g., S. enterica serotype Typhi and S. enterica serotype Paratyphi A, B, and C) cause systemic clinical conditions such as septicemia and organ manifestation (typhoid fever), while the so-called enteritis salmonella strains (e.g., S. enterica serotype Enteritidis) cause local intestinal infections and originate epidemiologically from animal husbandry.However, human infections due to S. enterica serotype Paratyphi B with the O:H formula O1,4,5,12:Hb:1,2 are not restricted to systemic infections (paratyphoid fever) and humanto-human infection routes (15) but have been associated with gastroenteritis and food-borne infections as well (3,7,12). This clinical and epidemiological heterogeneity was regarded as a consequence of fermentative varieties among this serotype. Many such isolates do ferment d-tartrate and have been designated biovar S. enterica serotype Java, in contrast to non-dtartrate-fermenting strains, designated biovar S. enterica serotype Paratyphi B sensu stricto (3,12,13). Moreover, S. ent...

The presence and expression of sopB, sopD1, sopE1, and avrA genes encoding virulence associated effector proteins were studied comparatively in 405 Salmonella enterica strains. They belong to different serovars and clonal types (genotypes, phage types) and originated from different clinical (systemic infection, focal enteritis, enterocolitis) and epidemic sources (epidemics, sporadic cases). The sopB and sopD1 determinants were commonly prevalent, but sopE1 and avrA genes only in 55% and 80%, respectively. A correlation of this pattern of absence and presence of the respective genes to the epidemic and clinical origin could not be detected. In contrast, the expression of the respective genes appeared differently: SopB and SopE1 proteins are well produced, but SopD1 and AvrA proteins only rarely under the applied standard culture conditions. However, using a range of different environmental signals (temperature, pH, cations, etc.) some of the S. enterica nonproducer strains (e. g., S. Agona, S. Bovismorbificans, S. Virchow, etc.) begin to produce AvrA and SopD1. They turned now into an expression profile which was found typically for the epidemic strains of S. Typhimurium and S. Enteritidis. Also S. enterica strains from systemic infections could be characterized by their strong SopB and SopE1 expression while SopD1 and AvrA proteins were missing. Although it is premature to outline generally a correlation of these expression profiles and the clinical and epidemiological potency of Salmonellae, the reported results allow a first understanding how a fine tuning of their virulence will take place.

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