Clostridium difficile strains from community-associated infections.

Clostridium difficile isolates from presumed community-associated infections (n = 92) were characterized by toxinotyping, pulsed-field gel electrophoresis, tcdC and cdtB PCR, and antimicrobial susceptibility. Nine toxinotypes (TOX) and 31 PFGE patterns were identified. TOX 0 (48, 52%), TOX III (18, 20%), and TOX V (9, 10%) were the most common; three isolates were nontoxigenic.

Clostridium difficile in retail meat products, USA, 2007.

To determine the presence of Clostridium difficile, we sampled cooked and uncooked meat products sold in Tucson, Arizona. Forty-two percent contained toxigenic C. difficile strains (either ribotype 078/toxinotype V [73%] or 027/toxinotype III [NAP1 or NAP1-related; 27%]). These findings indicate that food products may play a role in interspecies C. difficile transmission.

Toxinotype V Clostridium difficile in humans and food animals.

Clostridium difficile is a recognized pathogen in neonatal pigs and may contribute to enteritis in calves. Toxinotype V strains have been rare causes of human C. difficile-associated disease (CDAD). We examined toxinotype V in human disease, the genetic relationship of animal and human toxinotype V strains, and in vitro toxin production of these strains. From 2001 through 2006, 8 (1.3%) of 620 patient isolates were identified as toxinotype V; before 2001, 7 (<0.02%) of approximately 6,000 isolates were identified as toxinotype V. Six (46.2%) of 13 case-patients for whom information was available had community-associated CDAD. Molecular characterization showed a high degree of similarity between human and animal toxinotype V isolates; all contained a 39-bp tcdC deletion and most produced binary toxin. Further study is needed to understand the epidemiology of CDAD caused by toxinotype V C. difficile, including the potential of foodborne transmission to humans.

Impact of hydrogen peroxide vapor room decontamination on Clostridium difficile environmental contamination and transmission in a healthcare setting.

OBJECTIVE: To determine whether hydrogen peroxide vapor (HPV) decontamination can reduce environmental contamination with and nosocomial transmission of Clostridium difficile. DESIGN: A prospective before-after intervention study. SETTING: A hospital affected by an epidemic strain of C. difficile. INTERVENTION: Intensive HPV decontamination of 5 high-incidence wards followed by hospital-wide decontamination of rooms vacated by patients with C. difficile-associated disease (CDAD). The preintervention period was June 2004 through March 2005, and the intervention period was June 2005 through March 2006. RESULTS: Eleven (25.6%) of 43 cultures of samples collected by sponge from surfaces before HPV decontamination yielded C. difficile, compared with 0 of 37 cultures of samples obtained after HPV decontamination (P < .001). On 5 high-incidence wards, the incidence of nosocomial CDAD was significantly lower during the intervention period than during the preintervention period (1.28 vs 2.28 cases per 1,000 patient-days; P = .047). The hospital-wide CDAD incidence was lower during the intervention period than during the preintervention period (0.84 vs 1.36 cases per 1,000 patient-days; P = .26). In an analysis limited to months in which the epidemic strain was present during both the preintervention and the intervention periods, CDAD incidence was significantly lower during the intervention period than during the preintervention period (0.88 vs 1.89 cases per 1,000 patient-days; P = .047). CONCLUSIONS: HPV decontamination was efficacious in eradicating C. difficile from contaminated surfaces. Further studies of the impact of HPV decontamination on nosocomial transmission of C. difficile are warranted.

Clostridium difficile-associated diarrhea: an emerging threat to pregnant women.

OBJECTIVE: To estimate if Clostridium difficile-associated disease (CDAD) is increasing in peripartum women. STUDY DESIGN: Peripartum CDAD was assessed through 1) passive surveillance collecting clinical and pathology data on severe cases and 2) survey among infectious disease consultants (ICDs) in the Emerging Infections Network. RESULTS: Ten severe cases were collected; most had associated antibiotic use. Seven women were either admitted to the ICU or underwent colectomy. Three infants were stillborn, and 3 women died. The epidemic Clostridium difficile strain was found in 2 cases. Among 798 ICDs, 419 (52%) participated in the survey. Thirty-seven respondents (9%) recalled 55 cases, mostly in the postpartum period with 21 complications, mainly due to relapse. CONCLUSION: Severe CDAD may be increasing in peripartum women. Clinicians should have a low threshold for testing, be aware of the potential for severe outcomes, and take steps to reduce both the risk of disease and resultant complications.

Changes in the prevalence of nasal colonization with Staphylococcus aureus in the United States, 2001-2004.

BACKGROUND: Staphylococcus aureus is a common cause of infection, particularly in persons colonized by this organism. Virulent strains of methicillin-resistant S. aureus (MRSA) have emerged in the general community. METHODS: A nationally representative survey of nasal colonization with S. aureus was conducted from 2001 through 2004 as part of the National Health and Nutrition Examination Survey. MRSA isolates were identified by the oxacillin disk-diffusion method. The pulsed-field gel electrophoresis (PFGE) type was determined for all MRSA isolates. A t statistic was used to compare the prevalence of colonization across biennia and across population subgroups. Cofactors independently associated with colonization were determined with backward stepwise logistic modeling. RESULTS: The prevalence of colonization with S. aureus decreased from 32.4% in 2001-2002 to 28.6% in 2003-2004 (P < .01), whereas the prevalence of colonization with MRSA increased from 0.8% to 1.5% (P < .05). Colonization with MRSA was independently associated with healthcare exposure in males and with having been born in the United States, age > or =60 years, diabetes, and poverty in females. In 2003-2004, a total of 19.7% (95% confidence interval, 12.4%-28.8%) of MRSA-colonized persons carried a PFGE type associated with community transmission. CONCLUSIONS: Nasal colonization with MRSA has increased in the United States, despite an overall decrease in nasal colonization with S. aureus. PFGE types associated with community transmission only partially account for the increase in MRSA colonization.

Comparison of seven techniques for typing international epidemic strains of Clostridium difficile: restriction endonuclease analysis, pulsed-field gel electrophoresis, PCR-ribotyping, multilocus sequence typing, multilocus variable-number tandem-repeat analysis, amplified fragment length polymorphism, and surface layer protein A gene sequence typing.

Using 42 isolates contributed by laboratories in Canada, The Netherlands, the United Kingdom, and the United States, we compared the results of analyses done with seven Clostridium difficile typing techniques: multilocus variable-number tandem-repeat analysis (MLVA), amplified fragment length polymorphism (AFLP), surface layer protein A gene sequence typing (slpAST), PCR-ribotyping, restriction endonuclease analysis (REA), multilocus sequence typing (MLST), and pulsed-field gel electrophoresis (PFGE). We assessed the discriminating ability and typeability of each technique as well as the agreement among techniques in grouping isolates by allele profile A (AP-A) through AP-F, which are defined by toxinotype, the presence of the binary toxin gene, and deletion in the tcdC gene. We found that all isolates were typeable by all techniques and that discrimination index scores for the techniques tested ranged from 0.964 to 0.631 in the following order: MLVA, REA, PFGE, slpAST, PCR-ribotyping, MLST, and AFLP. All the techniques were able to distinguish the current epidemic strain of C. difficile (BI/027/NAP1) from other strains. All of the techniques showed multiple types for AP-A (toxinotype 0, binary toxin negative, and no tcdC gene deletion). REA, slpAST, MLST, and PCR-ribotyping all included AP-B (toxinotype III, binary toxin positive, and an 18-bp deletion in tcdC) in a single group that excluded other APs. PFGE, AFLP, and MLVA grouped two, one, and two different non-AP-B isolates, respectively, with their AP-B isolates. All techniques appear to be capable of detecting outbreak strains, but only REA and MLVA showed sufficient discrimination to distinguish strains from different outbreaks.

Toxic shock associated with Clostridium sordellii and Clostridium perfringens after medical and spontaneous abortion.

OBJECTIVE: To better understand the risk of fatal toxic shock caused by Clostridium sordellii in women who had a recent medical abortion with mifepristone and misoprostol. METHODS: We performed active and passive surveillance for cases of toxic shock associated with medical or spontaneous abortion. To identify the cause of toxic shock, immunohistochemical assays for multiple bacteria were performed on formalin-fixed surgical and autopsy tissues. We extracted DNA from tissues, performed Clostridium species-specific polymerase chain reaction assays, and sequenced amplified products for confirmation of Clostridium species. RESULTS: We report four patients with toxic shock associated with Clostridium species infection after medical or spontaneous abortion. Two women had fatal Clostridium perfringens infections after medically induced abortions: one with laminaria and misoprostol and one with the regimen of mifepristone and misoprostol. One woman had a nonfatal Clostridium sordellii infection after spontaneous abortion. Another woman had a fatal C sordellii infection after abortion with mifepristone and misoprostol. All four patients had a rapidly progressive illness with necrotizing endomyometritis. CONCLUSION: Toxic shock after abortion can be caused by C perfringens as well as C sordellii, can be nonfatal, and can occur after spontaneous abortion and abortion induced by medical regimens other than mifepristone and misoprostol. LEVEL OF EVIDENCE: III.

Prevalence of Clostridium difficile environmental contamination and strain variability in multiple health care facilities.

BACKGROUND: Clostridium difficile spores can contaminate the hospital environment. Little is known about the prevalence and strain variability of C. difficile environmental contamination in health care facilities. The objective of this study was to assess C. difficile environmental contamination at various health care facilities in a metropolitan area and determine if the North American pulsed field gel electrophoresis type 1 (NAP1) strain was present. METHODS: A cross-sectional pilot survey was conducted. Forty-eight environmental samples were collected from six health care facilities. Samples were cultured for the presence of C. difficile, and positive samples underwent pulsed field gel electrophoresis, toxinotyping, and detection of binary toxin and/or tcdC deletion. RESULTS: C. difficile was cultured from 13 of 48 (27%) samples. Rooms housing a patient with C. difficile-associated disease (CDAD) were more likely to be culture positive than non-CDAD patient rooms (100% vs. 33%; P < 0.01); C. difficile was not isolated outside of patient rooms (0 of 12 samples). The NAP1 epidemic strain was found in 5 out of 6 facilities. CONCLUSION: C. difficile spores frequently contaminated the hospital environment. Rooms with a CDAD patient were more likely to be contaminated than rooms without a CDAD patient. The NAP1 strain was prevalent throughout the metropolitan area.

Moxifloxacin therapy as a risk factor for Clostridium difficile-associated disease during an outbreak: attempts to control a new epidemic strain.

An outbreak of Clostridium difficile-associated disease (CDAD) caused by the epidemic North American pulsed-field gel electrophoresis type 1 (NAP1) strain began after a formulary change from levofloxacin to moxifloxacin. Cases of CDAD were associated with moxifloxacin use, but a formulary change back to levofloxacin failed to reduce rates of disease. Substituting use of one fluoroquinolone with use of another without also controlling the overall use of drugs from this class is unlikely to control outbreaks caused by the NAP1 strain of C. difficile.

Emergence of community-associated methicillin resistant Staphylococcus aureus in Hawaii, 2001-2003.

OBJECTIVES: We conducted a retrospective study to determine trends and characteristics of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) in Hawaii. METHODS: We reviewed medical records of patients with MRSA infections during July 2001-June 2003 in four healthcare facilities. A case was defined as a patient with MRSA infection (colonization excluded), diagnosed in ambulatory settings or < or = 48 h after hospitalization, without previous MRSA or healthcare risk factors. Pulsed-field gel electrophoresis (PFGE) and typing of resistance and toxin genes was performed in 40 MRSA isolates. RESULTS: CA-MRSA infections increased from 28 (23% of MRSA infections) to 65 (32%) per quarter over the 2-year period (P<0.05). Pacific islanders accounted for 51% of 389 case-patients, but only 24% of the Hawaii population. In the pediatric hospital, Pacific Islanders represented 76% of 90 case-patients versus 35% of the hospital population. Hospital admission, required for 40% (154/389), was associated with prior antimicrobial treatment (P<0.01). The staphylococcal cassette chromosome mec type IV was detected in 38/40 isolates; 31 isolates carried Panton-Valentine leukocidin genes and 22 belonged to the same staphylococcal lineage. CONCLUSIONS: In Hawaii, prevention strategies for CA-MRSA infections should focus on Pacific Islanders. CA-MRSA infections in Hawaii appear to be related to strains causing disease throughout the United States.

A hospital outbreak of diarrhea due to an emerging epidemic strain of Clostridium difficile.

BACKGROUND: Increased Clostridium difficile-associated disease (CDAD) in a hospital and an affiliated long-term care facility continued despite infection control measures. We investigated this outbreak to determine risk factors and transmission settings. METHODS: The CDAD cases were compared according to where the disease was likely acquired based on health care exposure and characterization of isolates from case patients, asymptomatic carriers, and the environment. Antimicrobial susceptibility testing, strain typing using pulsed-field gel electrophoresis, and toxinotyping were performed, and toxins A and B, binary toxin, and deletions in the tcdC gene were detected using polymerase chain reaction. Risk factors were examined in a case-control study, and overall antimicrobial use was compared at the hospital before and during the outbreak. RESULTS: Significant increases were observed in hospital-acquired (0.19 vs 0.86; P < .001) and long-term care facility-acquired (0.04 vs 0.31; P = .004) CDAD cases per 100 admissions as a result of transmission of a toxinotype III strain at the hospital and a toxinotype 0 strain at the long-term care facility. The toxinotype III strain was positive for binary toxin, an 18-base pair deletion in tcdC, and increased resistance to fluoroquinolones. Independent risk factors for CDAD included use of fluoroquinolones (odds ratio [OR], 3.22; P = .04), cephalosporins (OR, 5.19; P = .006), and proton pump inhibitors (OR, 5.02; P = .02). A significant increase in fluoroquinolone use at the hospital took place during the outbreak (185.5 defined daily doses per 1000 patient-days vs 200.9 defined daily doses per 1000 patient-days; P < .001). CONCLUSIONS: The hospital outbreak of CDAD was caused by transmission of a more virulent, fluoroquinolone-resistant strain of C difficile. More selective fluoroquinolone and proton pump inhibitor use may be important in controlling and preventing such outbreaks.

Severe community-acquired pneumonia due to Staphylococcus aureus, 2003-04 influenza season.

During the 2003-04 influenza season, 17 cases of Staphylococcus aureus community-acquired pneumonia (CAP) were reported from 9 states; 15 (88%) were associated with methicillin-resistant S. aureus (MRSA). The median age of patients was 21 years; 5 (29%) had underlying diseases, and 4 (24%) had risk factors for MRSA. Twelve (71%) had laboratory evidence of influenza virus infection. All but 1 patient, who died on arrival, were hospitalized. Death occurred in 5 (4 with MRSA). S. aureus isolates were available from 13 (76%) patients (11 MRSA). Toxin genes were detected in all isolates; 11 (85%) had only genes for Panton-Valentine leukocidin. All isolates had community-associated pulsed-field gel electrophoresis patterns; all MRSA isolates had the staphylococcal cassette chromosome mec type IVa. In communities with a high prevalence of MRSA, empiric therapy of severe CAP during periods of high influenza activity should include consideration for MRSA.

Characterization of a strain of community-associated methicillin-resistant Staphylococcus aureus widely disseminated in the United States.

A highly stable strain of Staphylococcus aureus with a pulsed-field gel electrophoresis type of USA300 and multilocus sequence type 8 has been isolated from patients residing in diverse geographic regions of the United States. This strain, designated USA300-0114, is a major cause of skin and soft tissue infections among persons in community settings, including day care centers and correctional facilities, and among sports teams, Native Americans, men who have sex with men, and military recruits. The organism is typically resistant to penicillin, oxacillin, and erythromycin (the latter mediated by msrA) and carries SCCmec type IVa. This strain is variably resistant to tetracycline [mediated by tet(K)]; several recent isolates have decreased susceptibility to fluoroquinolones. S. aureus USA300-0114 harbors the genes encoding the Panton-Valentine leucocidin toxin. DNA sequence analysis of the direct repeat units within the mec determinant of 30 USA300-0114 isolates revealed differences in only a single isolate. Plasmid analysis identified a common 30-kb plasmid that hybridized with blaZ and msrA probes and a 3.1-kb cryptic plasmid. A 4.3-kb plasmid encoding tet(K) and a 2.6-kb plasmid encoding ermC were observed in a few isolates. DNA microarray analysis was used to determine the genetic loci for a series of virulence factors and genes associated with antimicrobial resistance. Comparative genomics between USA300-0114 and three other S. aureus lineages (USA100, USA400, and USA500) defined a set of USA300-0114-specific genes, which may facilitate the strain's pathogenesis within diverse environments.

Prevalence of Staphylococcus aureus nasal colonization in the United States, 2001-2002.

BACKGROUND: Staphylococcus aureus is a common cause of disease, particularly in colonized persons. Although methicillin-resistant S. aureus (MRSA) infection has become increasingly reported, population-based S. aureus and MRSA colonization estimates are lacking. METHODS: Nasal samples for S. aureus culture and sociodemographic data were obtained from 9622 persons > or = 1 year old as part of the National Health and Nutrition Examination Survey, 2001-2002. After screening for oxacillin susceptibility, MRSA and selected methicillin-susceptible S. aureus isolates were tested for antimicrobial susceptibility, pulsed-field gel electrophoresis clonal type, toxin genes (e.g., for Panton-Valentine leukocidin [PVL]), and staphylococcal cassette chromosome mec (SCCmec) type I-IV genes. RESULTS: For 2001-2002, national S. aureus and MRSA colonization prevalence estimates were 32.4% (95% confidence interval [CI], 30.7%-34.1%) and 0.8% (95% CI, 0.4%-1.4%), respectively, and population estimates were 89.4 million persons (95% CI, 84.8-94.1 million persons) and 2.3 million persons (95% CI, 1.2-3.8 million persons), respectively. S. aureus colonization prevalence was highest in participants 6-11 years old. MRSA colonization was associated with age > or = 60 years and being female but not with recent health-care exposure. In unweighted analyses, the SCCmec type IV gene was more frequent in isolates from participants of younger age and of non-Hispanic black race/ethnicity; the PVL gene was present in 9 (2.4%) of 372 of isolates tested. CONCLUSIONS: Many persons in the United States are colonized with S. aureus; prevalence rates differ demographically. MRSA colonization prevalence, although low nationally in 2001-2002, may vary with demographic and organism characteristics.

An epidemic, toxin gene-variant strain of Clostridium difficile.

BACKGROUND: Recent reports suggest that the rate and severity of Clostridium difficile-associated disease in the United States are increasing and that the increase may be associated with the emergence of a new strain of C. difficile with increased virulence, resistance, or both. METHODS: A total of 187 C. difficile isolates were collected from eight health care facilities in six states (Georgia, Illinois, Maine, New Jersey, Oregon, and Pennsylvania) in which outbreaks of C. difficile-associated disease had occurred between 2000 and 2003. The isolates were characterized by restriction-endonuclease analysis (REA), pulsed-field gel electrophoresis (PFGE), and toxinotyping, and the results were compared with those from a database of more than 6000 isolates obtained before 2001. The polymerase chain reaction was used to detect the recently described binary toxin CDT and a deletion in the pathogenicity locus gene, tcdC, that might result in increased production of toxins A and B. RESULTS: Isolates that belonged to one REA group (BI) and had the same PFGE type (NAP1) were identified in specimens collected from patients at all eight facilities and accounted for at least half of the isolates from five facilities. REA group BI, which was first identified in 1984, was uncommon among isolates from the historic database (14 cases). Both historic and current (obtained since 2001) BI/NAP1 isolates were of toxinotype III, were positive for the binary toxin CDT, and contained an 18-bp tcdC deletion. Resistance to gatifloxacin and moxifloxacin was more common in current BI/NAP1 isolates than in non-BI/NAP1 isolates (100 percent vs. 42 percent, P<0.001), whereas the rate of resistance to clindamycin was the same in the two groups (79 percent). All of the current but none of the historic BI/NAP1 isolates were resistant to gatifloxacin and moxifloxacin (P<0.001). CONCLUSIONS: A previously uncommon strain of C. difficile with variations in toxin genes has become more resistant to fluoroquinolones and has emerged as a cause of geographically dispersed outbreaks of C. difficile-associated disease.

Toxin production by an emerging strain of Clostridium difficile associated with outbreaks of severe disease in North America and Europe.

BACKGROUND: Toxins A and B are the primary virulence factors of Clostridium difficile. Since 2002, an epidemic of C difficile-associated disease with increased morbidity and mortality has been present in Quebec province, Canada. We characterised the dominant strain of this epidemic to determine whether it produces higher amounts of toxins A and B than those produced by non-epidemic strains. METHODS: We obtained isolates from 124 patients from Centre Hospitalier Universitaire de Sherbrooke in Quebec. Additional isolates from the USA, Canada, and the UK were included to increase the genetic diversity of the toxinotypes tested. Isolate characterisation included toxinotyping, pulsed-field gel electrophoresis (PFGE), PCR ribotyping, detection of a binary toxin gene, and detection of deletions in a putative negative regulator for toxins A and B (tcdC). By use of an enzyme-linked immunoassay, we measured the in-vitro production of toxins A and B by epidemic strain and non-dominant strain isolates. FINDINGS: The epidemic strain was characterised as toxinotype III, North American PFGE type 1, and PCR-ribotype 027 (NAP1/027). This strain carried the binary toxin gene cdtB and an 18-bp deletion in tcdC. We isolated this strain from 72 patients with C difficile-associated disease (58 [67%] of 86 with health-care-associated disease; 14 [37%] of 38 with community-acquired disease). Peak median (IQR) toxin A and toxin B concentrations produced in vitro by NAP1/027 were 16 and 23 times higher, respectively, than those measured in isolates representing 12 different PFGE types, known as toxinotype 0 (toxin A, median 848 microg/L [IQR 504-1022] vs 54 microg/L [23-203]; toxin B, 180 microg/L [137-210] vs 8 microg/L [5-25]; p<0.0001 for both toxins). INTERPRETATION: The severity of C difficile-associated disease caused by NAP1/027 could result from hyperproduction of toxins A and B. Dissemination of this strain in North America and Europe could lead to important changes in the epidemiology of C difficile-associated disease.

Necrotizing enterocolitis associated with clostridium perfringens type A in previously healthy north american adults.

BACKGROUND: Necrotizing enteritis associated with Clostridium perfringens type C ("pigbel") is a well-known syndrome in severely protein-deprived populations in the Pacific. It is exceedingly rare in the developed world. C perfringens type A is a common cause of acute gastroenteritis and, in a handful of infections, has been reported in association with a syndrome resembling necrotizing enteritis. STUDY DESIGN: This study includes a case series and literature review. Charts and autopsy reports from four patients with adult necrotizing enterocolitis (ANEC) were reviewed. C perfringens isolates were subtyped by mouse bioassay and pulsed-field gel electrophoresis. Fixed tissue specimens were tested with an anticlostridial antibody using an immunohistochemical assay. RESULTS: Between 2000 and 2003, ANEC developed in four previously healthy men; three died. The small bowel was affected in three patients and the colon in two patients. Portal or mesenteric vein thrombosis occurred in three patients. C perfringens type A was isolated from three patients and immunohistochemical assay demonstrated clostridial antigens limited to affected areas of the intestine of all four. The nonculture positive patient had a strong epidemiologic link to one of the others, and a compatible clinical course. C perfringens of the same pulsed-field gel electrophoresis-defined molecular subtyped was isolated from stool samples of one patient, his wife, and food from a restaurant they patronized. CONCLUSIONS: ANEC associated with C perfringens type A infection occurred in four North American adults. Culture for C perfringens type A should be performed in cases of ANEC. Alternative tests such as immunohistochemical assay were diagnostically useful. Additional research might uncover virulence factors, host factors, and the burden of disease in the population.

Emerging infections with community-associated methicillin-resistant Staphylococcus aureus in outpatients at an Army Community Hospital.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) infection typically occurs in chronically ill patients requiring long-term antimicrobial therapy or hospitalization. However, community-associated MRSA (CA-MRSA) necrotizing soft tissue infections seem to be increasing in incidence. Our aim was to describe the incidence and microbiologic characteristics of CA-MRSA isolates collected at an army community hospital. METHODS: We report a retrospective review of MRSA isolates identified during 1998-2003 at the microbiology laboratory of Moncrief Army Community Hospital that serves a community of approximately 40,000 transient residents yearly in Fort Jackson, South Carolina. We evaluated the incidence of MRSA in our laboratory during 1998-2003. For MRSA isolates from 2003, we evaluated antimicrobial susceptibility patterns. Six selected isolates were evaluated by molecular typing, resistance gene analysis, and toxin analysis. RESULTS: During 1998-2003, 241 (23%) of 1041 S. aureus isolates identified at the hospital microbiology laboratory were resistant to methicillin. Of these 241 MRSA isolates, 223 were cultured from outpatients. The incidence of MRSA in our population increased from 12% of S. aureus isolates in 1998 to 43% in 2003. In 2003, MRSA was cultured from 76 different patients. Isolates of MRSA were often resistant to erythromycin (91%), although resistance to other agents was less common: Ciprofloxacin (14%), levofloxacin (14%), clindamycin (3%), tetracycline (3%), and trimethoprim sulfamethoxazole (1%). No isolates were resistant to vancomycin, gentamicin, nitrofurantoin, or rifampin. Six CA-MRSA isolates were compared by pulsed-field gel electrophoresis (PFGE). Five were PFGE type USA300, and one was PFGE type USA100, based on the U.S. Centers for Disease Control and Prevention (CDC) classification scheme. The five USA300 isolates carried SCCmec type IV, and the USA100 carried SCCmec II. None of the isolates were positive by PCR for genes encoding enterotoxins A-E and H, or toxic shock syndrome toxin (TSST-1), but the five USA300 isolates carried the gene coding for Panton-Valentine leukocidin toxin. CONCLUSIONS: The incidence of MRSA at our institution is increasing. Isolates of MRSA show resistance patterns and microbiologic characteristics consistent with CA-MRSA isolates from the United States. Clinicians should consider the possibility of CA-MRSA in patients with soft-tissue infections who do not respond to initial therapy with beta-lactam antimicrobial agents.

A clone of methicillin-resistant Staphylococcus aureus among professional football players.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) is an emerging cause of infections outside of health care settings. We investigated an outbreak of abscesses due to MRSA among members of a professional football team and examined the transmission and microbiologic characteristics of the outbreak strain. METHODS: We conducted a retrospective cohort study and nasal-swab survey of 84 St. Louis Rams football players and staff members. S. aureus recovered from wound, nasal, and environmental cultures was analyzed by means of pulsed-field gel electrophoresis (PFGE) and typing for resistance and toxin genes. MRSA from the team was compared with other community isolates and hospital isolates. RESULTS: During the 2003 football season, eight MRSA infections occurred among 5 of the 58 Rams players (9 percent); all of the infections developed at turf-abrasion sites. MRSA infection was significantly associated with the lineman or linebacker position and a higher body-mass index. No MRSA was found in nasal or environmental samples; however, methicillin-susceptible S. aureus was recovered from whirlpools and taping gel and from 35 of the 84 nasal swabs from players and staff members (42 percent). MRSA from a competing football team and from other community clusters and sporadic cases had PFGE patterns that were indistinguishable from those of the Rams' MRSA; all carried the gene for Panton-Valentine leukocidin and the gene complex for staphylococcal-cassette-chromosome mec type IVa resistance (clone USA300-0114). CONCLUSIONS: We describe a highly conserved, community-associated MRSA clone that caused abscesses among professional football players and that was indistinguishable from isolates from various other regions of the United States.