Despite the limited statistical power, the results of our study show an association between HIV infection and clinical malaria; if confirmed, this finding could be important for public health in sub-Saharan Africa.
This study describes the dissemination of a carbapenem-resistant Acinetobacter baumannii (CRAB) strain in a university hospital in Northeast Italy. Characterization of the outbreak strain was combined with a retrospective analysis of all CRAB isolates collected in the same hospital during the 5 years preceding the outbreak, with the aim of elucidating the origin of the epidemic spread. The outbreak strain was shown to belong to the International Clone II and carry the bla gene, flanked by two ISAba1 sequences in opposite orientation (Tn2006 arrangement). The epidemic clone harbored also the bla allele of the carbapenemase intrinsic to A. baumannii, the determinant of ArmA 16S rRNA methylase and a class 1 integron, with the aacA4, catB8, and aadA1 cassette array. Genotype analysis, performed by macrorestriction analysis and VRBA, revealed that isolates related to outbreak strain had been sporadically collected from inpatients in the 2 years preceding outbreak start. Carriage of bla, armA, and the integron further supported relatedness of these isolates to the outbreak clone. Outbreak initially involved three medical wards, typically hosting elderly patients with a history of prolonged hospitalization. The study highlights the need to adopt strict infection control measures also when CRAB isolation appears to be a sporadic event.
The interaction of Escherichia coli 0111:B4 with polymorphonuclear leukocytes in the presence of specific antibodies and complement was studied. This strain, which is resistant to phagocytosis by polymorphonuclear leukocytes, may be ingested and killed by the phagocytes in the presence of both antibodies and fresh serum. The ineffectiveness of fresh serum to promote ingestion of E. coli 0111:B4 by the phagocytes in the absence of antibodies reflects the inability of this strain to activate the complement system through the alternative pathway. Investigation of the mechanisms of the bacterial killing by polymorphonuclear leukocytes showed that both antibodies and complement were required for the oxygen-independent bactericidal system, whereas they were not needed for the oxygen-dependent system.
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