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Panton-Valentine leucocidin (PVL)-producing Staphylococcus aureus (PVL-SA) is typically associated with skin and soft tissue infections, such as abscesses (1). Transmission occurs between persons in close contact, often causing clusters of [...]

Staphylococcus simulans secretes lysostaphin, a bacteriolytic enzyme that specifically binds to the cell wall envelope of Staphylococcus aureus and cleaves the pentaglycine cross bridges of peptidoglycan, thereby killing staphylococci. The study of S. aureus mutants with resistance to lysostaphin-mediated killing has revealed biosynthetic pathways for cell wall assembly. To identify additional genes involved in cell wall envelope biosynthesis, we have screened a collection of S. aureus strain Newman transposon mutants for lysostaphin resistance. Bursa aurealis insertion in SAV2335, encoding a polytopic membrane protein with predicted protease domain, caused a high degree of lysostaphin resistance, similar to the case for a previously described femAB promoter mutant. In contrast to the case for this femAB mutant, transposon insertion in SAV2335, herein named lyrA (lysostaphin resistance A), did not cause gross alterations of cell wall cross bridges such as truncations of pentaglycine to tri- or monoglycine. Also, inactivation of LyrA in a methicillin-resistant S. aureus strain did not precipitate a decrease in [beta]-lactam resistance as observed for fem (factor essential for methicillin resistance) mutants. Lysostaphin bound to the cell wall envelopes of lyrA mutants in a manner similar to that for wild-type staphylococci. Lysostaphin resistance of lyrA mutants is attributable to altered cell wall envelope properties and may in part be due to increased abundance of altered cross bridges. Other lyr mutants with intermediate lysostaphin resistance carried bursa aurealis insertions in genes specifying GTP pyrophosphokinase or enzymes of the purine biosynthetic pathway.

BACKGROUND. Community-acquired, methicillin-resistant Staphylococcus aureus infections are increasing among children. OBJECTIVE. Our goal is to describe the clinical presentation of neonatal community-acquired S aureus disease and provide molecular analyses of the infecting isolates. PATIENTS AND METHODS. We retrospectively reviewed the demographics and hospital course of term and near-term previously healthy neonates, [less than or equal to] 30 days of age, with community-acquired S aureus infections presenting after nursery discharge between August 2001 and March 2005 at Texas Children's Hospital. Prospectively collected isolates were characterized by pulsed-field gel electrophoresis, staphylococcal cassette chromosome mec type, and the presence of PVL genes. RESULTS. Of 89 S aureus infections, 61 were methicillin-resistant S aureus; S aureus infections increased each year. Methicillin-resistant S aureus infections increased from 10 of 20 to 30 of 36 infections from 2002 to 2004. Most subjects, 65 of 89, were male. Symptoms began at 7 to 12 days of age for 26 of 45 male infants with methicillin-resistant S aureus. Most infections, 77 of 89, involved skin and soft tissue; 28 of 61 methicillin-resistant S aureus versus 7 of 28 methicillin-susceptible S aureus infections required drainage. Invasive manifestations included shock, musculoskeletal and urinary tract infection, perinephric abscess, bacteremia, empyema/lung abscess, and a death. Maternal S aureus or skin-infection history occurred with 13 of 61 methicillin-resistant S aureus versus 1 of 28 methicillin-susceptible S aureus infections. The predominant community clone, USA300 (PVL genes +), accounted for 55 of 57 methicillin-resistant S aureus and 3 of 25 methicillin-susceptible S aureus isolates. CONCLUSIONS. Community-acquired methicillin-resistant S aureus is a substantial and increasing proportion of S aureus infections in previously healthy neonates. Male infants 7 to 12 days of age are affected most often. Neonatal community-acquired S aureus infection may be associated with concurrent maternal infection. USA300 is the predominant clone among these neonatal isolates in our region. Key Words community-acquired Staphylococcus aureus, methicillin resistance, infant, newborn Abbreviations CA--community-acquired MRSA--methicillin-resistant S aureus SCCmec--staphylococcal cassette chromosome mec Tell--Texas Children's Hospital PVL--Panton-Valentine leukocidin PFGE--pulsed-field gel electrophomsis CSF--cerebrospinal fluid MSSA--methicillin-susceptible S aureus, Staphylococcus aureus frequently causes pediatric skin and soft tissue as well as invasive life-threatening infections. (1) The number of community-acquired (CA) methicillin-resistant S aureus (MRSA) infections at Texas Children's Hospital [...]

OBJECTIVES. We conducted this study to assess the rate of methicillin-resistant Staphylococcus aureus colonization and its association with infection among infants hospitalized in methicillin-resistant S aureus-endemic NICUs. METHODS. Between March 2003 and February 2004, surveillance culture specimens from the nares, postauricular areas, axillae, and umbilicus of infants admitted to the NICUs at a children's hospital in Taiwan were obtained weekly for the detection of methicillin-resistant S aureus. All colonized and clinical isolates from each study infant with methicillin-resistant S aureus infection were genotyped with pulsed-field gel electrophoresis, with Sma1 digestion, and compared. RESULTS. A total of 783 infants were included in this study. Methicillin-resistant S aureus colonization was detected for 323 infants during their NICU stays, with detection with the first 2 samples for 89%. Nares and umbilicus were the 2 most common sites of initial colonization. Methicillin-resistant S aureus colonization was associated significantly with premature birth ([less than or equal to] 28 weeks) and low birth weight ([less than or equal to] 1500 g), and infants with colonization had a significantly higher rate of methicillin-resistant S aureus infection, compared with those without colonization (26% vs 2%). Methicillin-resistant S aureus colonization was noted for 84 of 92 infants with methicillin-resistant S aureus infections. Of the 68 episodes with previous colonization and isolates available for genotyping analysis, colonized and clinical isolates were indistinguishable in 63 episodes, highly related in 2 episodes, and distinct in 3 episodes. CONCLUSIONS. More than 40% of the hospitalized infants were colonized with methicillin-resistant S aureus during their stay in methicillin-resistant S aureus-endemic NICUs; this was associated significantly with methicillin-resistant S aureus infection. Most infants with methicillin-resistant S aureus infections had previous colonization with an indistinguishable strain. Key Words methicillin-resistant Staphylococcus aureus, colonization, infection, genotyping analysis, neonatal intensive care unit Abbreviations MRSA--methicillin-resistant Staphylococcus aureus HCW-- health care worker PFGE--pulsed-field gel electrophoresis MLST--multilocus sequence typing OR--odds ratio CI--confidence interval, METHICILLIN-RESISTANT Staphylococcus aureus (MRSA) is among the most important pathogens of bacteremia in the ICU. Colonized patients are the chief source of S aureus in hospitals. Colonizing strains may serve [...]

Adherence of Staphylococcus aureus to the host tissue is an important step in the initiation of pathogenesis. At least 10 adhesins produced by S. aureus have been described and it is becoming clear that the expression of these adhesins and their interactions with eukaryotic cells involve complex processes. Some of these, such as the fibronectin-binding proteins (FnBPs) and Clumping Factor A, are well characterized. However, in the last 10 years a number of novel S. aureus adhesins have been described. Functional analyses of these proteins, one of which is Eap (extracellular_adherence protein, also known as Map and p70), are revealing important information on the pathogenesis of staphylococcal disease. More than 10 years after the first report of Eap, we are beginning to understand that this protein, which has a broad spectrum of functions, may be a critical factor in the pathogenesis of S. aureus. This review will focus on the interactions of Eap with eukaryotic cells, plasma proteins and the extracellular matrix as well as on the recently recognized role of Eap as an important mediator in the immune response to staphylococcal infection.

In many cases of Staphylococcus aureus infection in the blood, the bacterium probably came from the patient's nose. This was documented by researchers who used molecular methods to show that over 80% of the patients they studied had the identical strain of bacterium in their blood as they did in their nose.

Some patients requiring dialysis can benefit by receiving continuous ambulatory peritoneal dialysis (CAPD). This technique, which frees the patient from bondage to a chair next to a large hemodialysis machine, requires the insertion of a catheter (a flexible tube) into the abdominal cavity. The largest single cause of catheter failure is infection around the catheter exit-site, and the organism responsible for the most infections is Staphylococcus aureus. S. aureus is a common organism, but can cause serious infection if given an appropriate foothold. Patients who develop infection around catheters often carry Staphylococcus aureus in their noses, and it is thought that constant shedding of bacteria from the nose may be the source of infection for the peritoneal catheter. To clarify the role that nasal carriage of the organism might play in the development of catheter infections, 140 patients due to begin CAPD were examined for S. aureus carriage. The external nasal passages were cultured, and 63 of the patients were found to carry S. aureus in the nares. Carriage of S. aureus was much more common among diabetic patients, occurring in 77 percent of the 30 patients with this disorder. The CAPD patients were followed for a median of 10.4 months. Analysis revealed that patients with no S. aureus colonization had a 92 percent chance of avoiding catheter exit-site infection, whereas those who carried S. aureus had only a 54 percent chance of remaining infection-free. The randomness of bacterial shedding from the nose may account for the fact that not all nasal carriers of S. aureus became infected, yet carriers are clearly a higher-risk group for infection during CAPD. The ease of performing a S. aureus culture recommends it as a routine screen to identify CAPD patients at high risk for infection. Further studies may determine whether prophylactic antibiotic suppression of nasal S. aureus will reduce the risk of catheter exit-site infection in high risk patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

The bacteria Staphylococcus lugdunensis has recently been identified as a unique strain of staphylococcus. It can cause endocarditis (inflammation of the lining of the heart chambers and the heart valves), an often fatal infection. The bacteria is resistant to penicillin, which is generally used to treat staphylococcal infections, but is sensitive to other antibiotics, including flucloxacillin, gentamicin, rifampicin, and erythromycin. A case report is presented of a 77-year-old man with fatal endocarditis caused by Staphylococcus lugdunensis. The man previously had rheumatic fever which caused damage to the infected heart valve. A large number of blood samples (978) known to contain staphylococcus were examined to see how often this strain was present; these samples were collected over a two-year-period and did not include a specimen from this patient. The strain is very rare, as it could not be isolated from any of the samples. Therefore, although Staphylococcus lugdunensis is rare, it can cause an aggressive endocarditis infection. Characteristics of Staphylococcus lugdunensis, which can be used in laboratory tests to identify the strain, have been established. These criteria should be included in laboratory testing so that S. lugdunensis can be identified and proper treatment can be administered. (Consumer Summary produced by Reliance Medical Information, Inc.)