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1.  Group B streptococcus endocarditis associated with multiple pulmonary septic emboli 
Clinics and Practice  2011;1(1):e7.
Endocarditis is a rare presentation of group B streptococcal infection. Its association with pulmonary septic embolism was only barely studied and limited data is available up to date. Multiple septic emboli is a common complication of bacterial endocarditis, but only a few cases have been documented in relation to group B streptococcus. We present the case of an 87 year old female patient with multiple underlying conditions that predisposed the development of bacterial endocarditis secondary to group B streptococcus and subsequently multiple pulmonary septic emboli. The patient was treated with ceftriaxone and azythromycin with good response and complete recovery without any further complications. In the event of a diagnosed case of group B streptococcus endocarditis, there should be a low threshold for the suspicion of septic pulmonary emboli especially in cases with right valves involvement.
PMCID: PMC3981222  PMID: 24765280
Group B streptococcus; endocarditis; septic emboli.
2.  Correlation of the expression of acrB and the regulatory genes marA, soxS and ramA with antimicrobial resistance in clinical isolates of Klebsiella pneumoniae endemic to New York City 
Nosocomial isolates of Klebsiella pneumoniae resistant to all commonly used antimicrobial agents have emerged in many regions of the world. It is unknown if efflux systems contribute to the multidrug resistance phenotype.
The expression of genes encoding the efflux pump AcrAB and the global regulators MarA, SoxS and RamA were examined and correlated with antimicrobial resistance.
Twenty isolates belonged to the two important clones representing KPC-possessing strains endemic to our region. Virtually all of these isolates had negligible or absent expression of the genes, and resistance to fluoroquinolones and aminoglycosides could be explained by alternative mechanisms. All of these isolates were susceptible to tigecycline. A group of 14 heterogeneous isolates was also examined. There was a correlation between expression of marA with expression of soxS. Only expression of soxS was significantly correlated with expression of acrB. With a background substitution in GyrA, increased expression of acrB and marA appeared to contribute to fluoroquinolone resistance in some isolates. A correlation was noted between expression of soxS and ramA (but not marA and acrB) and tigecycline MICs. Following in vitro exposure to tigecycline, resistance occurred in association with a marked increase in marA and acrB expression in isolates lacking expression of soxS and ramA.
While laboratory-derived tigecycline resistance was associated with increased acrB expression, the variation in tigecycline MICs in clinical isolates was associated only with selected regulator genes. It appears that other mechanisms beyond activation of the acrAB system mediate tigecycline resistance.
PMCID: PMC2707265  PMID: 19457933
efflux; tigecycline; multidrug-resistant

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