Changes in Streptococcus pneumoniae serotype 19A invasive infections in children from 1993 to 2011.

Among 594 Streptococcus pneumoniae serotype 19A invasive pneumococcal disease (IPD) isolates collected from 1993 to 2011, we identified 85 sequence types by multilocus sequence typing. CC320 was associated with multidrug resistance and reduced susceptibility to penicillin and ceftriaxone and still predominated among declining serotype 19A IPD isolates following PCV13 introduction.

Characterization of nontypeable and atypical Streptococcus pneumoniae pediatric isolates from 1994 to 2010.

Streptococcus pneumoniae is a major cause of bacteremia, meningitis, pneumonia, sinusitis, and acute otitis media in children. Although optochin susceptibility, bile solubility, and Quellung testing are the standards for identifying and differentiating pneumococci, there are several reports of nontypeable pneumococci that give inconsistent results with one or more of these tests. We characterized 52 isolates previously labeled as nontypeable pneumococci. Microbiological methods included repeating the Quellung reaction using a new and expanded group of antisera, optochin susceptibility and bile solubility tests, and automated Vitek 2 identification. Molecular methods included PCR detection of ply and psaA genes, multilocus sequence typing (MLST), 16S rRNA gene sequencing, and pyrosequencing. Of the 52 isolates, 38 (73%) were optochin susceptible, were psaA and ply positive, and could be serotyped by the Quellung reaction. The remaining 14 isolates, isolated from patients with otitis media (n = 6), bacteremia (n = 6), meningitis (n = 1), and pneumonia (n = 1), underwent further analysis. Three of these 14 isolates were nontypeable due to autoagglutination but were pneumococci by all tests and represented pneumococcal sequence types previously recognized by MLST. The 11 remaining isolates were optochin resistant, and 6 of these were bile soluble. Three of 11 were both psaA and ply positive and clustered with pneumococci by MLST (2 were bile soluble); 8 lacked psaA (5 ply positive, 4 bile soluble) and likely belonged to other Streptococcus species. In conclusion, few isolates were truly nontypeable by Quellung reaction, and MLST and the presence of psaA proved useful in distinguishing between atypical pneumococci and other streptococcal species.

Increase in prevalence of Streptococcus pneumoniae serotype 6C at Eight Children's Hospitals in the United States from 1993 to 2009.

Streptococcus pneumoniae serotype 6C, which was described in 2007, causes invasive disease in adults and children. We investigated the prevalence of 6C among pediatric isolates obtained from eight children's hospitals in the United States. S. pneumoniae isolates were identified from a prospective multicenter study (1993 to 2009). Fifty-seven serotype 6C isolates were identified by multiplex PCR and/or Quellung reaction. Five were isolated before 2000, and the prevalence increased over time (P < 0.000001). The median patient age was 2.1 years (range, 0.2 to 22.5 years). Clinical presentations included bacteremia (n = 24), meningitis (n = 7), pneumonia (n = 4), abscess/wound (n = 3), mastoiditis (n = 2), cellulitis (n = 2), peritonitis (n = 1), septic arthritis (n = 1), otitis media (n = 10), and sinusitis (n = 3). By broth microdilution, 43/44 invasive serotype 6C isolates were susceptible to penicillin (median MIC, 0.015 µg/ml; range, 0.008 to 2 µg/ml); all were susceptible to ceftriaxone (median MIC, 0.015 µg/ml; range, 0.008 to 1 µg/ml). By disk diffusion, 16/44 invasive isolates (36%) were nonsusceptible to erythromycin, 19 isolates (43%) were nonsusceptible to trimethoprim-sulfamethoxazole (TMP-SMX), and all isolates were clindamycin susceptible. Multilocus sequence typing (MLST) revealed 24 sequence types (STs); 9 were new to the MLST database. The two main clonal clusters (CCs) were ST473 and single-locus variants (SLVs) (n = 13) and ST1292 and SLVs (n = 23). ST1292 and SLVs had decreased antibiotic susceptibility. Serotype 6C causes disease in children in the United States. Emerging CC1292 expressed TMP-SMX resistance and decreased susceptibility to penicillin and ceftriaxone. Continued surveillance is needed to monitor changes in serotype prevalence and possible emergence of antibiotic resistance in pediatric pneumococcal disease.

Increasing Numbers of Staphylococcal Scalded Skin Syndrome Cases Caused by ST121 in Houston, Texas.

BACKGROUND: The molecular epidemiology of Staphylococcus aureus strains causing staphylococcal scalded skin syndrome (SSSS) in the United States has not been described. We analyzed patient and S. aureus isolate characteristics associated with SSSS in children at Texas Children's Hospital. METHODS: Patients with SSSS were identified by ICD9/10 codes and available S. aureus isolates were identified from an ongoing S. aureus surveillance study. Medical records were reviewed for 58 patients with available S. aureus isolates. Isolate analyses included PCR for agr group, pvl (lukSF-PV), tst, eta and etb, pulsed-field gel electrophoresis, multi-locus sequence typing and antimicrobial susceptibilities. RESULTS: Cases of SSSS increased from 2.3/10,000 admissions in 2008 to 52.6/10,000 admissions in 2017 (P < 0.0001). The 58 study cases (57 methicillin-susceptible S. aureus, 1 MRSA) with isolates were from 2013 to 2017. The majority (88%) of isolates was of clonal cluster (CC) 121, agr group IV, pvl, tst and carried eta and/or etb and 26% were clindamycin resistant. Twelve ST121 isolates had high level resistance to mupirocin. Patients were treated with standard supportive care plus systemic antibiotics [clindamycin alone or in combination with another antibiotic (n = 44)]. One patient had a recurrent SSSS and one patient was transferred to a burn unit on day 3. CONCLUSIONS: Cases of SSSS are increasing at our hospital. Most S. aureus strains isolated were of one CC, CC121 and carried eta and etb. Supportive care plus clindamycin was effective treatment. We speculate that CC121 was recently introduced to our region and is responsible for the increasing numbers of SSSS cases observed at Texas Children's Hospital.

Adhesin genes and biofilm formation among pediatric Staphylococcus aureus isolates from implant-associated infections.

BACKGROUND: Microbial surface component recognizing adhesive matrix molecules (MSCRAMMs) facilitate Staphylococcus aureus adherence to host tissue. We hypothesized that S. aureus isolates from implant-associated infections (IAIs) would differ in MSCRAMM profile and biofilm formation in vitro compared to skin and soft tissue infection (SSTI) isolates. METHODS: Pediatric patients and their isolates were identified retrospectively. IAI and SSTI isolates were matched (1:4). Pulsed field gel electrophoresis was performed to group isolates as USA300 vs. non-USA300. Whole genome sequencing was performed and raw sequence data were interrogated for presence of MSCRAMMs (clfA, clfB, cna, ebh, efb, fnbpA, fnbpB, isdA, isdB, sdrC, sdrD, sdrE), biofilm-associated (icaA,D,B,C), and Panton-Valentine leukocidin (lukSF-PV) genes, accessory gene regulator group, and multilocus sequence types. In vitro biofilm formation was assessed for 47 IAI and 47 SSTI isolates using a microtiter plate assay. Conditional logistic regression was performed for analysis of matched data (STATA11, College Station, TX). RESULTS: Forty-seven IAI and 188 SSTI isolates were studied. IAI isolates were more often methicillin susceptible S. aureus and non-USA300 vs. SSTI isolates [34 (72%) vs. 79 (42%), p = 0.001 and 38 (81%) vs. 57 (30%) p <0.001, respectively]. Greater than 98% of isolates carried clfA, clfB, efb, isdA, isdB, and icaA,D,B,C while cna was more frequently found among IAI vs. SSTI isolates (p = 0.003). Most isolates were strong biofilm producers. CONCLUSIONS: S. aureus IAI isolates were significantly more likely to be MSSA and non-USA300 than SSTI isolates. Carriage of MSCRAMMs and biofilm formation did not differ significantly between isolates. Evaluation of genetic polymorphisms and gene expression profiles are needed to further delineate the role of adhesins in the pathogenesis of IAIs.

Vancomycin MICs for Staphylococcus aureus vary by detection method and have subtly increased in a pediatric population since 2005.

Vancomycin MICs for Staphylococcus aureus isolates in a pediatric hospital with a high rate of staphylococcal infections were examined for any increase over a 7-year period. A broth microdilution scheme allowed direct comparison of the MICs generated by this method to MICs generated by Etest. MICs generated by both methods were determined with the same inoculum suspension. One hundred sixty-five S. aureus isolates were selected on the basis of the patients having been bacteremic or having received vancomycin as the definitive therapy for their infections. Of the 165 isolates, 117 were methicillin-resistant S. aureus and 48 were methicillin-susceptible S. aureus. Forty-seven were acquired in the hospital (nosocomial), 56 were community acquired, and 62 were community onset-health care associated. All but one isolate tested by broth microdilution had MICs of < 1.0 microg/ml, while 96% of these same isolates tested by Etest had MICs of > or = 1 microg/ml. A significant increase in MICs that occurred after study year 4 (2004 to 2005) was demonstrated by the Etest (P < 0.00007) but not by broth microdilution. MICs were not different for isolates of community or health care origin, regardless of methodology. The proportion of isolates with Etest MICs of < 1 and > or = 1 microg/ml between children with bacteremia for < or = 5 days and > 5 days (P = 0.3) was not different. We conclude that MICs for pediatric isolates have increased slightly since 2005 and therapeutic decisions based on vancomycin MICs need to be made by considering the methodology used.

Clinical Characteristics and Outcomes of Staphylococcus aureus Implant-associated Infections in Children.

BACKGROUND: Staphylococcus aureus is a significant cause of implant-associated infections (IAIs). Data detailing the optimal treatment of IAIs are lacking in children. We describe the clinical features and outcomes of pediatric patients with S. aureus IAIs seen at Texas Children's Hospital. METHODS: Patients and their isolates were identified from a S. aureus surveillance database from 2008 to 2016 in Houston, TX. Demographic and clinical data were collected retrospectively. Fisher's exact was used for statistical analysis. RESULTS: Forty-five patients with 47 IAIs were identified. Most patients had an infected orthopedic implant: 22 (47%) spinal rods and 19 (40%) with other orthopedic hardware. Thirty (64%) IAIs developed within 90 days of implant placement. Six patients had polymicrobial infections and 3 patients were bacteremic. Of the 47 IAI isolates, 34 (72%) were methicillin-susceptible S. aureus (MSSA) and 13 (28%) were methicillin-resistant S. aureus. All children underwent surgical irrigation, debridement and antibiotic therapy. Of the 47 IAI episodes, 22 of the implants were removed at time of initial presentation, 7 implants had delayed removal, and 18 implants remained in place. Successful treatment was achieved in all patients with immediate implant removal (22/22) and in 83% of patients with implant retention (15/18), including 10 patients with early postoperative infections (<3 months) and 5 patients with late postoperative infections (>3 months). Four patients had recurrence of infection. CONCLUSIONS: The majority of S. aureus IAIs were methicillin-susceptible S. aureus. All children with immediate implant removal and most children with retained implants were treated successfully with surgery and antibiotic therapy.

Analysis of Invasive Community-Acquired Methicillin-Susceptible Staphylococcus aureus Infections During a Period of Declining Community Acquired Methicillin-Resistant Staphylococcus aureus Infections at a Large Children's Hospital.

BACKGROUND: The epidemiology of community acquired (CA) Staphylococcus aureus infections is changing in the United States. We investigated the current epidemiology of S. aureus infections at Texas Children's Hospital. METHODS: Patients with CA-S. aureus skin and soft tissue and invasive infections were retrospectively identified from January 1, 2007 to December 31, 2014. Invasive CA-MSSA isolates were characterized by pulsed field gel electrophoresis, Spa typing, agr type and presence of lukSF-PV (pvl) genes. Medical records were reviewed. Statistical analyses included Fisher exact, χ for trend and Wilcoxon tests. RESULTS: CA-MRSA infections decreased by 60.4% (1461-578 infections) from 2007 to 2014 (P < 0.0001), while CA-MSSA infections averaged 550 infections annually. Invasive CA-MRSA infections decreased by 67.2% from 61 to 20 infections (P < 0.0001); invasive CA-MSSA averaged 44 infections annually. Among 296 invasive CA-MSSA isolates, 74 (25%) isolates were USA300 and 88 (30%) were pvl+. USA300 declined among invasive CA-MSSA over time (P < 0.008). Musculoskeletal infections were most common (242/296, 82%); 52/242 (21.5%) isolates were USA300 and 62/242 (25.6%) pvl+. All 18 isolates from musculoskeletal infections with deep venous thrombosis and/or septic shock were pvl+ and 16/18 (88.9%) were USA300. Pneumonia isolates were mainly USA300 (8, 66.7%) and pvl+ (11, 91.7%). CONCLUSIONS: MSSA now cause the majority of invasive CA-S. aureus infections at our institution. Molecular analysis of invasive CA-MSSA isolates suggests strain diversity with USA300 on the decline and that disease presentations are to some extent strain specific. Changes in the CA-S. aureus epidemiology may, in part, be related to changes in immunity to the USA300 clone in the general population.

Increase of the USA300 clone among community-acquired methicillin-susceptible Staphylococcus aureus causing invasive infections.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) USA300 is a predominant cause of community-acquired (CA) infection in the United States. We compared clinical characteristics of children with USA300 versus non-USA300 CA-methicillin-susceptible S. aureus (CA-MSSA) invasive infections at Texas Children's Hospital (TCH). METHODS: Medical records were reviewed from children with invasive CA-MSSA infections at TCH between August 1, 2001 and September 30, 2006. Isolates were characterized by pulsed-field gel electrophoresis and polymerase chain reaction for Panton-Valentine leukocidin genes (pvl). RESULTS: Invasive CA-MSSA infections increased from 14 in year 1 to 36 in year 5 (5-year total = 122 patients). Among the CA-MSSA isolates available for typing in the 5-year period, USA300 MSSA strains increased from 14% (2 of 14) to 35% (11 of 31) (P = 0.03). USA300 MSSA strains were more likely than non-USA300 MSSA strains to be nonsusceptible to erythromycin [66% (19 of 29) versus 28% (25 of 88); P < 0.01]. Osteomyelitis cases increased from 43% (6 of 14) in year 1 to 67% (24 of 36) in year 5. The majority of pvl(+) MSSA isolates were USA300 (71% (25 of 35); only 5% (4 of 82) of pvl(-) MSSA isolates were USA300. Patients with osteomyelitis caused by pvl isolates had significantly higher mean values for erythrocyte sedimentation rate at admission (P = 0.005) and erythrocyte sedimentation rate maximum value (P = 0.002), maximum C-reactive protein (P = 0.04), and absolute neutrophil count at presentation (P = 0.04) compared with patients whose isolates were pvl(-). CONCLUSIONS: USA300 accounted for a growing proportion of CA-MSSA isolates among children and was associated with increased numbers of invasive CA-MSSA infections at TCH, especially osteomyelitis. Associations were found in CA-MSSA osteomyelitis between pvl and increased concentrations of systemic inflammatory markers in patients.

Three-year surveillance of community onset health care-associated staphylococcus aureus infections in children.

BACKGROUND: Staphylococcus aureus causes skin and soft tissue or invasive infections in children in the community, in the hospital or in other ways associated with the health care system (HCA). METHODS: Prospective community-acquired S. aureus infection surveillance at Texas Children's Hospital was initiated on August 1, 2001. Community onset HCA (CO HCA) infections were identified. Demographic and clinical data were collected. Antibiotic susceptibilities were determined. Data were analyzed by chi or Student's t test. CO HCO-isolates were characterized by pulsed field gel electrophoresis and staphylococcal chromosomal cassette carrying the mecA methicillin-resistant gene (SCCmec) typing. RESULTS: From August 1, 2001 to July 31, 2004, 61.5% of 322 in year 1, 62.9% of 259 in year 2 and 56.9% of 318 in year 3 of CO HCA isolates were methicillin-resistant S. aureus (MRSA). Among the CO HCA-MRSA isolates, 8.9% of 542 were from children with invasive infections compared with 24.1% of 357 CO HCA-methicillin-susceptible S. aureus (MSSA; P < 0.001). Sixty-six percent of children with CO HCA-S. aureus isolates were admitted to the hospital. Clindamycin resistance increased over the 3 years (CO HCA-MRSA, from 3.5% to 18.8%, P < 0.001; CO HCA-MSSA, from 3.2% to 10.2%, P = 0.053). Thirty-three of 35 (94.3%) CO HCA-MRSA carried SCCmecIV; 30 were USA300. Only 3 of 35 MSSA were related to USA300 by pulsed field gel electrophoresis. CONCLUSIONS: CO HCA-S. aureus infections remained steady over the 3-year study at Texas Children's Hospital. Clindamycin resistance increased >4-fold for CO HCA-S. aureus isolates over the 3 years and is no longer appropriate for empiric treatment of invasive infections suspected to be caused by CO HCA-MRSA at our hospital. In our setting, CO HCA-MRSA infections are steady in number despite substantial increases in community-acquired MRSA infections and both being related to the same clone.

Pulmonary manifestations in children with invasive community-acquired Staphylococcus aureus infection.

BACKGROUND: Primary pneumonia and metastatic pulmonary infection have become more common in patients with invasive community-acquired Staphylococcus aureus disease at Texas Children's Hospital (TCH; Houston). METHODS: In this study, we sought to describe pulmonary involvement in children with community-acquired S. aureus invasive infection and to determine whether the presence of genes encoding Panton-Valentine leukocidin (PVL) (luk-S-PV and luk-F-PV) and collagen adhesin (cna) is correlated with pulmonary manifestations. Patients with invasive staphylococcal infections admitted to TCH between 1 August 2001 and 30 June 2004 were studied. Chest imaging and postmortem examination reports were reviewed. Isolates were tested for the presence of genes encoding PVL and collagen adhesin by PCR. RESULTS: A total of 47 of 70 patients with community-acquired methicillin-resistant S. aureus (MRSA) infection had abnormal pulmonary imaging findings, compared with 12 of 43 patients with community-acquired methicillin-susceptible S. aureus (MSSA) infection (P < .001). Pneumonia and/or empyema, in addition to septic emboli, were the most common findings. Metastatic pulmonary disease occurred more frequently among patients with osteomyelitis. Severe necrotizing pneumonia was present in 3 children coinfected with influenza and parainfluenza virus. The presence of genes encoding PVL was investigated in 67 MRSA and 36 MSSA isolates. Abnormal chest imaging findings were observed for 51 of 80 patients with PVL-positive isolates, compared with 2 of 23 patients with PVL-negative isolates (P < .001). Only 2 isolates (both of which were MSSA) from patients with abnormal chest radiograph findings carried cna. PVL remained independently associated with abnormal chest imaging findings in patients with secondary pneumonia in a multivariate analysis (P = .03). CONCLUSIONS: Pulmonary involvement is commonly observed in patients with invasive community-acquired S. aureus infections. Community-acquired MRSA may cause primary community-acquired pneumonia, as well as metastatic pulmonary disease. The presence of genes encoding PVL is highly associated with pulmonary involvement by S. aureus.

Staphylococcus aureus infections in pediatric patients with diabetes mellitus.

OBJECTIVES: To describe Staphylococcus aureus infections in children with diabetes mellitus (DM). METHODS: Children with DM (cases) and S. aureus infections (2/02-6/10) were identified from a surveillance database. Patient charts were reviewed, and S. aureus isolates were characterized by molecular methods. Cases were compared to age-matched controls without DM but with CA-S. aureus skin and soft tissue infections (SSTI) using conditional logistic regression. RESULTS: Forty-seven cases were identified; 41 were matched with 123 controls. Four cases had osteomyelitis and 43 had SSTI. Mean age was 14.2 years and 63% of cases had hemoglobin (Hb) A1c levels above 10%. Cases and controls differed by gender (85% vs. 45% female, P < 0.001), BMI% (median 87% vs. 72%, P = 0.04), methicillin-resistant S. aureus (MRSA) infection (49% vs. 68%, P = 0.04), and recurrent infections (22% vs. 4%, P = 0.001). Among cases, 88% of recurrences were caused by MRSA. CONCLUSIONS: The majority of cases had poor glycemic control, more recurrences, fewer primary MRSA infections and were more likely to be female compared to a control group. Improved glycemic control may reduce the risk for infection, and decrease hospitalizations due to S. aureus infections.

Nasal Staphylococcus aureus colonization among mothers of term and late preterm previously healthy neonates with community-acquired Staphylococcus aureus infections.

We enrolled 35 case neonates with community-acquired Staphylococcus aureus infection and their mothers and 19 control mother-neonate pairs. We obtained neonatal and maternal anterior nasal cultures, and clinical isolates. S. aureus nasal colonization was greater in case than control pairs. Neonates were more often infected with their nasal strain than their mother's nasal strain.

Staphylococcus aureus sinus infections in children.

OBJECTIVE: Staphylococcus aureus can cause sinusitis in children. The predominant MRSA clone in the United States, USA300, has been associated with skin and soft tissue as well as invasive diseases. USA300 has increased among CA methicillin-susceptible S. aureus (CA-MSSA) isolates. We describe the clinical characteristics of pediatric patients with S. aureus cultured from sinus specimens, treated at Texas Children's Hospital (TCH), and characterized their isolates by molecular methods. METHODS: This was a retrospective study of children with endoscopic sinus surgery (ESS) cultures positive for S. aureus between 01/2005 and 12/2008 at TCH. Medical records were reviewed and associated S. aureus isolates were characterized by pulsed field gel electrophoresis (PFGE). Data were analyzed by Mann-Whitney U, Chi-square, Fisher's exact test, and Chi-square for trend. RESULTS: We identified 56 patients with S. aureus sinus infections; 12 (21%) were MRSA. Seven of 12 (58%) MRSA vs. 5/44 (11%) MSSA were USA300 (p<0.01). All MRSA isolates were non-susceptible to erythromycin compared to 30% of MSSA (p<0.01); 75% of the USA300 strains were non-susceptible to erythromycin compared to 36% of the non-USA300 strains (p<0.04). Co-pathogens were isolated from 77% (43/56) of the patient specimens. Both MRSA and USA300 isolates were associated with Haemophilus influenzae co-isolation (p<0.05). Patients with USA300 strains were significantly younger (p=0.02) and more likely to experience snoring as a symptom associated with their sinusitis (p=0.03) than those infected with non-USA300 strains. Children with MRSA (4/12) tended to have a greater recurrence rate than children with MSSA isolates (5/44) (p=0.09). No significant differences were observed between groups for fever or complications such as neck cellulitis, nasal abscess, meningitis, subdural empyema, and orbital cellulitis. CONCLUSION: MSSA was more commonly isolated than MRSA from sinus cultures of children who underwent ESS at TCH. The majority of ESS cultures positive for S. aureus, were mixed with other respiratory pathogens, principally H. influenzae. USA300 was the major clone among the MRSA sinusitis isolates, but was not associated with more complications than other S. aureus isolates.

Hospital-acquired Staphylococcus aureus infections at Texas Children's Hospital, 2001-2007.

OBJECTIVE: To document the introduction of the methicillin-resistant Staphylococcus aureus (MRSA) USA300 clone into a children's hospital. Current molecular epidemiology of infections due to the USA300 strain of MRSA in the pediatric healthcare setting remains obscure. DESIGN: Retrospective study of patients with hospital-acquired S. aureus infection during the period from August 1, 2001, through July 31, 2007, at Texas Children's Hospital in Houston. METHODS: Patients with hospital-acquired S. aureus infection from whom an isolate was available for molecular analysis were included. Clinical information was obtained from patient medical records and the electronic hospital information system. S. aureus isolates underwent antimicrobial susceptibility testing, pulsed-field gel electrophoresis, and polymerase chain reaction testing for staphylococcal cassette chromosome (SCC) mec, agr, the diamine N-acetyltransferase gene, and the Panton-Valentine leukocidin genes (pvl). RESULTS: Of 242 patients with hospital-acquired S. aureus infection, 147 (61%) had methicillin-susceptible S. aureus infection. Of the 95 MRSA isolates causing hospital-acquired infection, 69 (73%) were USA300 isolates, and that rate did not increase over time. Skin and soft tissue infection (P < .001), onset of infection less than 10 days after admission (P = .007), and lack of comorbidities (P < .001) were associated with hospital-acquired MRSA infection caused by the USA300 strain, compared with other isolates (hereafter referred to as non-USA300 isolates). Nine of 10 patients with a S. aureus infection at the time of death were infected with a non-USA300 strain. USA300 carried SCCmec IV, agr I, the diamine N-acetyl transferase gene, and pvl. USA300 isolates were more susceptible to clindamycin, gentamicin, and trimethoprim-sulfamethoxazole than were other non-USA300 isolates (P < .01). CONCLUSIONS: In our patient population, the annual numbers of observed cases of hospital-acquired S. aureus infection have remained constant. USA300 was the most common clone and, compared with other non-USA300 MRSA isolates, was associated with skin and soft tissue infection, early onset of infection after admission, and greater susceptibility to antimicrobial agents.

Venous thrombosis associated with staphylococcal osteomyelitis in children.

BACKGROUND: Venous thrombosis (VT) in children with Staphylococcus aureus osteomyelitis occurs rarely. We describe clinical features of infections and molecular characterization of isolates of children at Texas Children's Hospital with S aureus osteomyelitis and VT. METHODS: We reviewed records and imaging studies (chest radiographs, ultrasound, computed tomography, and MRI) of 9 patients at Texas Children's Hospital with acute S aureus osteomyelitis and new onset VT between August 1999 and December 2004. Isolates were fingerprinted by pulsed-field gel electrophoresis and tested for the presence of genes encoding selective virulence factors. RESULTS: The mean age of the patients was 10.6 years. All 9 of the patients had osteomyelitis with sites of infection adjacent to the VT. The femoral and popliteal veins were most commonly affected. Two patients had VTs develop on the same side in which a central line had been in place. Four patients had chest radiographs consistent with septic emboli; inferior vena cava filters were placed in 3. Evaluation for hypercoagulable state revealed 3 patients with lupus anticoagulant, 1 with anticardiolipin IgG antibody, and 5 with no defect. Most laboratory abnormalities had resolved at follow-up. Seven patients had infections caused by methicillin-resistant S aureus belonging to the same clonal group (USA300); all were community acquired. Seven isolates carried the Panton-Valentine leukocidin (luk-S-PV and luk-F-PV) genes. CONCLUSIONS: The predominant community-acquired, methicillin-resistant S aureus clone in Houston, Texas, (USA300) may have a unique propensity to cause VT in association with osteomyelitis. Management of the venous thrombosis in this setting may be complicated by the rapid evolution of septic emboli.

In vitro activities of cethromycin (ABT-773), a new ketolide, against Streptococcus pneumoniae strains that are not susceptible to penicillin or macrolides.

Pneumococcal resistance to antimicrobials presents problems to physicians for empirical treatment of acute otitis media (AOM). Three hundred thirty-three isolates of Streptococcus pneumoniae selected for nonsusceptibility to penicillin (MIC >0.1 microg/ml) from the middle ear (n = 325) or mastoid (n = 8) of children seen between 1994 and 2000 at four children's hospitals in the United States were tested by broth microdilution for susceptibility to nine antibiotics. Using NCCLS 2002 breakpoints, resistance to the following drugs was as indicated: amoxicillin, 1%; azithromycin, 71%; cefprozil, 71%; ceftriaxone, 2%; cefdinir, 98%; erythromycin, 70%; levofloxacin, 0%; and trimethoprim-sulfamethoxazole, 93%. Of the penicillin- and erythromycin-nonsusceptible isolates, 97% were inhibited by cethromycin (ABT-773) and 83% were inhibited by telithromycin at a concentration of