Sepsis is aggravated by an inappropriate immune response to invading microorganisms, which occasionally leads to multiple organ failure. Several lines of evidence suggest that the ventricular myocardium is depressed during sepsis with features of diastolic dysfunction. Potential candidates responsible for septic cardiomyopathy include pathogen-associated molecular patterns (PAMPs), cytokines, and nitric oxide. Extracellular histones and high-mobility group box 1 that function as endogenous damage-associated molecular patterns (DAMPs) also contribute to the myocardial dysfunction associated with sepsis. If untreated, persistent shock causes cellular injury and the liberation of further DAMPs. Like PAMPs, DAMPs have the potential to activate inflammation, creating a vicious circle. Early infection control with adequate antibiotic care is important during septic shock to decrease PAMPs arising from invasive microorganisms. Early aggressive fluid resuscitation as well as the administration of vasopressors and inotropes is also important to reduce DAMPs generated by damaged cells although excessive volume loading, and prolonged administration of catecholamines might be harmful. This review delineates some features of septic myocardial dysfunction, assesses its most common underlying mechanisms, and briefly outlines current therapeutic strategies and potential future approaches.

Discriminating Escherichia albertii from other Enterobacteriaceae is difficult. Systematic analyses showed that E. albertii represents a substantial portion of strains currently identified as eae-positive Escherichia coli and includes Shiga toxin 2f–producing strains. Because E. albertii possesses the eae gene, many strains might have been misidentified as enterohemorrhagic or enteropathogenic E. coli.

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Escherichia albertii is a recently recognized close relative of Escherichia coli. This emerging enteropathogen possesses a type III secretion system (T3SS) encoded by the locus of enterocyte effacement, similar to enteropathogenic and enterohemorrhagic E. coli (EPEC and EHEC). Shiga toxin-producing strains have also been identified. The genomic features of E. albertii, particularly differences from other Escherichia species, have not yet been well clarified. Here, we sequenced the genome of 29 E. albertii strains (3 complete and 26 draft sequences) isolated from multiple sources and performed intraspecies and intragenus genomic comparisons. The sizes of the E. albertii genomes range from 4.5 to 5.1 Mb, smaller than those of E. coli strains. Intraspecies genomic comparisons identified five phylogroups of E. albertii. Intragenus genomic comparison revealed that the possible core genome of E. albertii comprises 3,250 genes, whereas that of the genus Escherichia comprises 1,345 genes. Our analysis further revealed several unique or notable genetic features of E. albertii, including those responsible for known biochemical features and virulence factors and a possibly active second T3SS known as ETT2 (E. coli T3SS 2) that is inactivated in E. coli. Although this organism has been observed to be nonmotile in vitro, genes for flagellar biosynthesis are fully conserved; chemotaxis-related genes have been selectively deleted. Based on these results, we have developed a nested polymerase chain reaction system to directly detect E. albertii. Our data define the genomic features of E. albertii and provide a valuable basis for future studies of this important emerging enteropathogen.

It was believed that food poisoning in Osaka in 2000 was due to small amounts of staphylococcal enterotoxin A (SEA) in reconstituted milk. Results of this study clearly indicate that SEH was also present in the raw material of reconstituted milk, indicating that the food poisoning was caused by multiple staphylococcal enterotoxins.Exotoxins produced by Staphylococcus aureus are enterotoxins and elicit an emetic response. Fourteen staphylococcal enterotoxins, designated staphylococcal enterotoxin A (SEA), SEB, SEC, SED, SEE, SEG, SEH, SEI, SEJ, SEK, SEL, SEM, SEN, and SEO, have been identified (2,4,7,9,10,11,13). However, only the first five (SEA through SEE) can be detected using a commercial kit. Moreover, as commercial kits are generally employed to detect the presence of staphylococcal enterotoxins in food poisoning, SEG, SEH, or SEI was rarely detected and implicated as the source of food poisoning.A mass outbreak of food poisoning caused by the consumption of reconstituted milk occurred in Osaka, Japan, in June 2000, and more than 10,000 cases were reported (6). A small amount of SEA and sea gene were detected in the reconstituted milk and the skim milk powder, which was the raw material for the reconstituted milk (6). In an outbreak of food poisoning in United States, caused by SEA present in chocolate milk, 200 ng or less SEA was presumed to be the cause (3). Although it was considered that the outbreak of food poisoning in Osaka could have been caused by SEA, the quantity of SEA detected, i.e., approximately 80 ng, was insufficient to cause food poisoning on such a large scale. Hence, we investigated the possibility of staphylococcal enterotoxins other than SEA as the cause of the outbreak.We got 11 batches of skim milk powder, which were the raw material of the food causing the outbreak. Ten of these batches were manufactured on 1 April 2000 and designated SM1, SM100, SM200, SM300, SM400, SM500, SM600, SM700, SM800, and SM830 in the order of manufacture, and the 11th batch, manufactured on 10 April 2000, was designated SM500 (10/April).Since the manufacturing process of skim milk required heat treatment for 3 s at 130°C, viable S. aureus strains were not isolated from the skim milk powder samples. However, Gram staining of these samples revealed the presence of gram-positive cocci in large numbers. The skim milk solution (10%, wt/vol) reconstituted in sterile water was centrifuged at 12,000 rpm for 3 min, and the DNA was extracted from the precipitate using a DNeasy tissue kit (QIAGEN GmbH, Hilden, Germany). PCR was performed to detect the sea, seb, sec, sed, see, seg, seh, and sei genes (5, 8). The seb, sec, sed, and see genes were not detected in any of the samples, the sea and seh genes were detected in 10 samples, and the seg and sei genes were detected in 7 samples ( Fig. 1 and Table 1).Since the skim milk samples that contained the sea gene also showed the presence of the seh gene and the seh gene showed stronger expression of enterotoxin compared to that shown by the seg or sei gene (8), there wa...