Correspondence analysis to evaluate the transmission of Staphylococcus aureus strains in two New York State maximum-security prisons.

Prisons/jails are thought to amplify the transmission of Staphylococcus aureus (SA) particularly methicillin-resistant SA infection and colonisation. Two independently pooled cross-sectional samples of detainees being admitted or discharged from two New York State maximum-security prisons were used to explore this concept. Private interviews of participants were conducted, during which the anterior nares and oropharynx were sampled and assessed for SA colonisation. Log-binomial regression and correspondence analysis (CA) were used to evaluate the prevalence of colonisation at entry as compared with discharge. Approximately 51% of admitted (N = 404) and 41% of discharged (N = 439) female detainees were colonised with SA. Among males, 59% of those admitted (N = 427) and 49% of those discharged (N = 393) were colonised. Females had a statistically significant higher prevalence (1·26: P = 0·003) whereas males showed no significant difference (1·06; P = 0·003) in SA prevalence between entry and discharge. CA demonstrated that some strains, such as spa types t571 and t002, might have an affinity for certain mucosal sites. Contrary to our hypothesis, the prison setting did not amplify SA transmission, and CA proved to be a useful tool in describing the population structure of strains according to time and/or mucosal site.

Community-associated methicillin-resistant Staphylococcus aureus transmission in households of infected cases: a pooled analysis of primary data from three studies across international settings.

Diverse strain types of methicillin-resistant Staphylococcus aureus (MRSA) cause infections in community settings worldwide. To examine heterogeneity of spread within households and to identify common risk factors for household transmission across settings, primary data from studies conducted in New York (USA), Breda (The Netherlands), and Melbourne (Australia) were pooled. Following MRSA infection of the index patient, household members completed questionnaires and provided nasal swabs. Swabs positive for S. aureus were genotyped by spa sequencing. Poisson regression with robust error variance was used to estimate prevalence odds ratios for transmission of the clinical isolate to non-index household members. Great diversity of strain types existed across studies. Despite differences between studies, the index patient being colonized with the clinical isolate at the home visit (P < 0·01) and the percent of household members aged <18 years (P < 0·01) were independently associated with transmission. Targeted decolonization strategies could be used across geographical settings to limit household MRSA transmission.

Prevalence and risk factors for Staphylococcus aureus colonization in individuals entering maximum-security prisons.

To assess the prevalence and risk factors for colonization with Staphylococcus aureus in inmates entering two maximum-security prisons in New York State, USA, inmates (N=830) were interviewed and anterior nares and oropharyngeal samples collected. Isolates were characterized using spa typing. Overall, 50·5% of women and 58·3% of men were colonized with S. aureus and 10·6% of women and 5·9% of men were colonized with MRSA at either or both body sites. Of MSSA isolates, the major subtypes were spa type 008 and 002. Overall, risk factors for S. aureus colonization varied by gender and were only found in women and included younger age, fair/poor self-reported general health, and longer length of prior incarceration. Prevalence of MRSA colonization was 8·2%, nearly 10 times greater than in the general population. Control of epidemic S. aureus in prisons should consider the constant introduction of strains by new inmates.

Molecular characterization of Staphylococcus aureus from outpatients in the Caribbean reveals the presence of pandemic clones.

Staphylococcus aureus infections continue to pose a global public health problem. Frequently, this epidemic is driven by the successful spread of single S. aureus clones within a geographic region, but international travel has been recognized as a potential risk factor for S. aureus infections. To study the molecular epidemiology of S. aureus infections in the Caribbean, a major international tourist destination, we collected methicillin-susceptible S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) isolates from community-onset infections in the Dominican Republic (n = 112) and Martinique (n = 143). Isolates were characterized by a combination of pulsed-field gel electrophoresis (PFGE), spa typing, and multilocus sequence typing (MLST) typing. In Martinique, MRSA infections (n = 56) were mainly caused by t304-ST8 strains (n = 44), whereas MSSA isolates were derived from genetically diverse backgrounds. Among MRSA strains (n = 22) from the Dominican Republic, ST5, ST30, and ST72 predominated, while ST30 t665-PVL+ (30/90) accounted for a substantial number of MSSA infections. Despite epidemiological differences in sample collections from both countries, a considerable number of MSSA infections (~10%) were caused by ST5 and ST398 isolates at each site. Further phylogenetic analysis suggests the presence of lineages shared by the two countries, followed by recent genetic diversification unique to each site. Our findings also imply the frequent import and exchange of international S. aureus strains in the Caribbean.

Effect of penicillin on the adherence of Streptococcus sanguis in vitro and in the rabbit model of endocarditis.

The effect of penicillin treatment of Streptococcus sanguis in vitro, on subsequent bacterial density in the bloodstream and on cardiac valves in the rabbit model of endocarditis was studied. As experimental tools for this study, isogenic pairs of S. sanguis differing in resistance to streptomycin or rifampin were prepared by genetic transformation. Rabbits with traumatized heart valves received an intravenous inoculation of penicillin treated (1 mug/ml) and untreated S. sanguis, each marked by resistance to either streptomycin or rifampin. The number of penicillin-treated and untreated bacteria attached to the valvular surfaces was determined by differential counting on streptomycin or rifampin containing media. Penicillin pretreatment reduced cardiac valve colonization 5 min after inoculation ("adherence ratio" x 10(8) was 4.11 for the control and 3.66 for the penicillin-treated bacteria, P < 0.001). The results were not due to differences in serum killing or bacterial densities in the bloodstream. There was no difference in valvular bacterial densities 24 h after bacterial inoculation (adherence ratio x 10(8), 7.26 untreated vs. 6.34 penicillin-pretreated, P > 0.10). In vitro experiments were performed using platelet-fibrin surfaces to test the possibility that penicillin-induced loss of lipoteichoic acid was responsible for decreased streptococcal adherence. Pretreatment of S. sanguis cultures with inhibitory concentrations of penicillin or with antiserum against lipoteichoic acid and precoating of the platelet-fibrin surfaces with lipoteichoic acid, all caused reduction in bacterial adherence. The findings are interpreted as support for the role of lipoteichoic acid as an adhesin in S. sanguis interactions with particular host tissue surfaces.

A human endothelial cell membrane protein that binds Staphylococcus aureus in vitro.

We have investigated S. aureus adherence to human endothelial cells utilizing an in vitro model. Staphylococcus binding to confluent endothelial cell monolayers was saturable in both dose and time response studies suggesting that the binding interaction was specific. We have developed a technique, based on the pH dependent affinity of iminobiotin for streptavidin, for the isolation of an endothelial cell membrane component that binds S. aureus, in vitro. A 50-kD membrane component was isolated and purified using this approach. This component was trypsin sensitive, periodate insensitive, and did not label with [3H]glucosamine. [35S]Methionine and [125I]iodine labeling confirmed that the protein was synthesized by and expressed on the endothelial cell surface. Functional binding studies demonstrated that staphylococci, but not endothelial cells, bound to the protein when immobilized on microtiter wells. Preincubation of staphylococci with the purified protein significantly (P less than 0.001) reduced staphylococcal binding to cultured endothelial cells. The capacity of S. aureus to colonize and invade endovascular surfaces may in part be a consequence of staphylococcal interaction with this endothelial cell membrane protein.

What determines nasal carriage of Staphylococcus aureus?

Nasal carriage of Staphylococcus aureus is an important risk factor for infection by this organism in both community and hospital settings; this article reviews the role of host and bacterial factors in carriage. A host genetic influence appears likely but the phenotypic determinants are unknown. Possibilities include variability in host adhesins, immune response or secretion of antimicrobial molecules. Colonization resistance by S. aureus, together with the observation that persistent carriers often carry a single strain whereas intermittent carriers can be colonized with unrelated strains over time, suggests that bacterial factors could also be involved.

'Culture-negative' prosthetic valve endocarditis. Hazards of postoperative steroid therapy for unexplained fever.

Two patients had prolonged unexplained fever along with multiple negative blood cultures after cardiac valve replacement surgery. Following the administration of corticosteroids for presumed postpericardiotomy syndrome, both patients improved symptomatically and defervesced, only to have positive blood cultures for Staphylococcus epidermidis shortly thereafter. The theoretical and practical risks of the empiric use of anti-inflammatory agents for unexplained post-operative fever are reviewed. "Culture-negative" prosthetic valvular infection due to prior antibiotic prophylaxis or therapy must be strongly considered in the evaluation of such unexplained fever.

Tuberculous meningitis in an urban medical center.

Forty-five cases of tuberculous meningitis at a large urban medical center were reviewed. Reasons for the continued incidence, prognostic factors, and current therapy of this life-threatening form of tuberculosis were examined. Thirty-nine of 45 patients were black, Hispanic, and/or 65 years of age or older (87%). Underlying conditions included alcohol abuse in 12, intravenous drug abuse in 7, recent steroid therapy in 4, head trauma in 4, recent pregnancy in 4, and the acquired immunodeficiency syndrome in 1. Thirty-four patients (76%) presented with altered mental status and/or focal neurologic findings. Significant mortality (31%) occurred despite the administration of antituberculous therapy to all but 1 patient. Six of 14 deaths (43%) occurred in the first week of hospitalization. One-third of survivors had neurologic sequelae at the time of follow-up. Neurologic deficits on admission, advanced age, and alcohol abuse were frequent among those who succumbed. Early recognition and treatment in hospital failed to improve outcome in advanced cases. From these findings we conclude that both aggressive treatment of primary tuberculous infections as well as prevention of secondary cases are necessary to effect any further reduction in the incidence, morbidity, and mortality of tuberculous meningitis.

Group B streptococcal arthritis in adults.

Group B streptococcal arthritis in adults is uncommon. This report describes seven cases seen at these institutions over the past five years and reviews the previous 17 documented cases. Of seven adults, three were diabetics, three had prosthetic hips, and one had undergone splenectomy. Six had undergone no prior dental, genitourinary, or gastrointestinal procedures. The most common clinical presentation was fever and acute joint pain. Five patients had monoarticular arthritis; two had multiple joint involvement. Underlying joint abnormalities included osteoarthritis (two), prosthetic hip (three), and neuropathic joint (one). Bacteremia was documented in three and suspected in the remaining four patients, often without a primary source. Therapy included parenteral antibiotics, usually penicillin G, and drainage of the involved joint. Two of three patients with prosthetic implants required Girdlestone procedures; the third was apparently cured. The three diabetic patients died, one with resolution of group B streptococcal arthritis. The seventh patient was cured. Group B streptococcal arthritis is a serious infection in adults with diabetes and late prosthetic hip infections.

Prevention of endothelial cell cytokine induction by a Staphylococcus aureus lipoprotein.

Staphylococcal strain 8325-4, unlike other staphylococcal strains, fails to induce cytokine IL-1 and IL-6 gene expression in human endothelial cells. In the present investigation, this strain was shown to release a product that inhibited cytokine gene expression in endothelial cells infected with another staphylococcal strain. This inhibition was due to prevention of internalization, but not adherence, of bacteria by endothelial cells. Induction of endothelial cell cytokine gene expression by lipopolysaccharide was not affected by the staphylococcal supernatant. In contrast to endothelial cells, 8325-4 did not inhibit Wb-induced cytokine gene expression in monocytes. Further characterization of the inhibitory factor suggests that it is a lipoprotein and that both protein and lipid components play a role in its inhibitory function.

Multiple antibiotic changes during the first 72 hours of hospitalization.

BACKGROUND: Increasing concern about inappropriate antibiotic use prompted us to examine whether our patients were receiving frequent and perhaps unwarranted changes of antibiotic therapy. METHODS: We evaluated antibiotic prescribing by the physicians in the Emergency Department and by those on the inpatient medical service during the first 72 hours of hospitalization in 119 patients admitted with suspected serious infections to an acute care, university-affiliated, municipal teaching hospital. The appropriateness of antibiotic prescriptions was assessed independently and retrospectively by 2 infectious disease specialists (each based at a different hospital) using a 4-grade scale (from 1 = wrong choice to 4 = appropriate). Of their evaluations of the 427 antibiotic regimens given to the 119 patients during 4 defined intervals during their first 72 hours of hospitalization, 90% agreed with each other within 1 grade. Their evaluations were then compared with the selections that had been made at each interval by the prescribing physicians. RESULTS: Successive prescribing physicians changed the antibiotic regimens in 77% of cases during the first 24 hours and in 56% during the next 48, often without apparent clinical or microbiologic indications. By 72 hours, the 119 patients had received a mean of 3.1 +/- 1.3 (+/-SD) different antibiotics, and 40 received between 4 and 7. Only 7% of the patients had no change in the regimen prescribed originally. CONCLUSIONS: Many patients had multiple changes of antibiotics, often unnecessarily, resulting in exposure to too many agents.

Use of colony morphology to characterize carriage profiles of coagulase negative staphylococci.

The absence of a reliable method to distinguish among coagulase negative staphylococcal strains in mixed culture hinders elucidation of colonization traits and precise tracking of colonization. This study examined whether colonial morphology could be used to correctly identify coagulase negative staphylococcal strains in mixed cultures. Staphylococci were isolated from nasal and hand cultures of ten subjects at 0 and 3 months. Samples were initially screened for the predominant coagulase negative staphylococcal strain by colonial morphology. The strains were subsequently identified by phenotypic and biochemical testing. Pulsed field gel electrophoresis demonstrated that the morphologic criteria correctly grouped the strains in 91.1% (41/45) of samples. This study suggests that colonial morphology is a reliable method for the initial characterization of coagulase negative staphylococcal strains. This approach has potential value for epidemiological studies that involve establishing links between commensal flora and their potential role as pathogens in subsequent clinical infections.

Staphylococcal infections in the intensive care unit.

Staphylococcus aureus and coagulase-negative staphylococci are among the most common causes of nosocomial infections in the intensive care unit (ICU). The clinical presentation of staphylococcal device-related infections, pneumonias, or surgical wound infections is not unique. However, treatment of these infections is increasingly problematic because of the resistance of clinical isolates to a widening number of antimicrobial agents. The confluence of critically ill patients and the need for multiple invasive procedures, as well as the use of broad-spectrum antimicrobial agents in the ICU, set the stage for the emergence of these multidrug-resistant staphylococci. In the past 10 years, there has been a progressive increase in the overall resistance of staphylococci to antimicrobial agents. Conventional infection control measures, such as handwashing and isolation precautions, to prevent the spread of staphylococcal infections in the ICU setting remain of critical importance. New approaches, including the prophylactic use of topical antistaphylococcal agents to eliminate nasal colonization in high-risk ICU patients and the development of antistaphylococcal vaccines, are currently being investigated.

Staphylococcus epidermidis infections.

Staphylococcus epidermidis, an organism routinely found on the skin and in the hospital environment, has become a primary pathogen in infections associated with prosthetic devices. Because these infections are indolent and often clinically silent, diagnosis and therapy are often difficult. Pathogens are often misidentified as contaminants. Their variable, often resistant antibiotic susceptibility pattern and the uncertain correlation of in-vitro beta-lactam sensitivity testing with therapeutic efficacy make selection of an effective antibiotic regimen difficult. Vancomycin combined with rifampin, gentamicin, or both, is recommended for empiric therapy of these infections. Usually, removal of the prosthetic device is also necessary and may contribute equally to a successful therapeutic outcome.

Staphylococcus aureus binding to human nasal mucin.

Colonization of human nasal mucosa with Staphylococcus aureus sets the stage for subsequent systemic infection. This study characterizes S. aureus adhesion to nasal mucosa in vitro and investigates the interaction of S. aureus with human nasal mucin. S. aureus binding to cell-associated and cell-free mucus was greater than to nonmucin-coated epithelial cells. Scanning electron microscopy of S. aureus incubated with human nasal mucosal tissue showed minimal binding to ciliated respiratory epithelium. In a solid-phase assay, S. aureus bound to purified human nasal mucin-coated wells significantly more than to bovine serum albumin-coated microtiter wells. Binding to mucin was saturable in a dose- and time-dependent fashion. Staphylococcal adherence to human nasal mucin was inhibited by bovine submaxillary mucin but not by fibrinogen. Pretreatment of mucin with periodate but not with pronase reduced adherence. Trypsin treatment of the bacteria significantly reduced adherence to mucin. 125I-labelled nasal mucin bound to two surface proteins (138 and 127 kDa) of lysostaphin-solubilized S. aureus. Binding to human nasal mucin occurs in part via specific adhesin-receptor interactions involving bacterial proteins and the carbohydrate moiety in mucin. These experiments suggest that S. aureus binding to mucin may be critical for colonization of the nasopharyngeal mucosa.

A 220-kilodalton glycoprotein in yeast extract inhibits Staphylococcus aureus adherence to human endothelial cells.

A 220-kDa glycoprotein from yeast extract causes a twofold decrease in S. aureus adherence to human endothelial cells in vitro. Medium constituents can have a significant effect on bacterial adherence interactions.

Acidic fibroblast growth factor modulates Staphylococcus aureus adherence to human endothelial cells.

Alteration of human endothelial cells may increase their susceptibility to staphylococcal invasion and thus may contribute to the development of intravascular staphylococcal disease. Acidic fibroblast growth factor, a potent regulator of endothelial cell function, had a significant effect on Staphylococcus aureus infection of cultured human endothelial cells. Three of four S. aureus strains had diminished adherence to endothelial cells when the latter were grown in the presence of acidic fibroblast growth factor (P less than 0.05). The diminished adherence was time dependent, maximal at 72 h, and independent of the initial bacterial inoculum. A twofold enhancement of S. aureus adherence was observed when endothelial cells were pretreated with heparitinase. Adherence was unaffected by endothelial cell activation by interleukin-1 or endotoxin. Thus, acidic fibroblast growth factor exerted a protective effect, deterring S. aureus adherence to cultured endothelial cells. Endothelial cell heparan sulfate was also directly involved in the adherence process. Subtle modulations of endothelial cells can significantly affect the ability of S. aureus to adhere to and then infect these cells. Similar alterations may contribute to the ability of S. aureus to infect endovascular tissue in vivo.