Dataset Information

Methicillin-Resistant Staphylococcus aureus Prostatic Abscess in a Liver Transplant Recipient.

ABSTRACT: Prostatic abscesses are usually related to gram-negative bacilli. However, methicillin-resistant Staphylococcus aureus (MRSA) has emerged as a substantial cause of prostatic abscesses in recent years. Herein, we report the case of a 31-year-old man with a history of orthotopic liver transplantation 10 years ago who presented with acute onset dysuria and abdominal pain and was diagnosed with a MRSA prostatic abscess. To our knowledge, this is the first case describing a prostatic abscess in a liver transplant recipient and the first reporting MRSA as the causative organism of a prostatic abscess in a solid organ transplant recipient.

SUBMITTER: Jana T

PROVIDER: S-EPMC4217349 | biostudies-other | 2014

REPOSITORIES: biostudies-other

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Methicillin-Resistant Staphylococcus aureus Prostatic Abscess in a Liver Transplant Recipient.

Jana Tanima T Machicado Jorge D JD Davogustto Giovanni E GE Pan Jen-Jung JJ

Case reports in transplantation 20141020

Prostatic abscesses are usually related to gram-negative bacilli. However, methicillin-resistant Staphylococcus aureus (MRSA) has emerged as a substantial cause of prostatic abscesses in recent years. Herein, we report the case of a 31-year-old man with a history of orthotopic liver transplantation 10 years ago who presented with acute onset dysuria and abdominal pain and was diagnosed with a MRSA prostatic abscess. To our knowledge, this is the first case describing a prostatic abscess in a liv ...[more]

PMID: 25389507

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Project description:Methicillin resistant Staphylococcus aureus (MRSA) infection is becoming refractory to existing antibiotic therapy owing to the inherent ability of S. aureus to develop rapid resistance and is considered a major threat to public health. We found that a natural isolate of Bacillus pumilus from the Columbia River Estuary produces a strong anti-MRSA compound, amicoumacin A. As amicoumacin A has been reported to exhibit anti-microbial, anti-inflammatory, and anti-ulcer activities, we sought to uncover its mechanism of action. Genome-wide transcriptome analysis of S. aureus COL in response to amicoumacin A showed alteration in the expression of genes involved in several cellular processes including cell envelope turnover, cross-membrane transport, virulence, metabolism, and general stress response. The most highly induced gene was lrgA, encoding an antiholin-like product, which has been shown to be induced in response to a collapse of membrane potential. In order to gain further insight into the mechanism of action of amicoumacin A, a whole genome comparison of wild-type COL and amicoumacin A-resistant mutants isolated by serial passage method was carried out. Single point mutations resulting in codon substitutions were uncovered in several distinct genes: ksgA, RNA dimethyltranferase; fusA, elongation factor G; dnaG, primase, ; lacD, tagatose 1,6-bisphosphate aldolase, ; and SACOL0611, encoding a putative glycosyl transferase gene. Based on these results, a candidate approach was undertaken to recreate the same amino acid substitution individually in FusA and KsgA, each of which resulted in two-fold resistance towards amicoumacin A. The fusA gene is known as the site for fusidic acid- resistant mutations; however the codon substitutions in EF-G that cause amicoumacin A resistance and fusidic acid resistance occur in separate domains and do not bring about cross resistance. Taken together, these results suggest that amicoumacin A might cause perturbation of the cell membrane and lead to energy dissipation. Decreased rates of cellular metabolism including protein synthesis and DNA replication in resistant strains might allow cells to compensate for membrane dysfunction and thus increase cell survivability.

Dataset Information

Methicillin-Resistant Staphylococcus aureus Prostatic Abscess in a Liver Transplant Recipient.

Publications

Methicillin-Resistant Staphylococcus aureus Prostatic Abscess in a Liver Transplant Recipient.

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