Racial disparities in invasive Streptococcus pneumoniae infections, 1998-2009.

BACKGROUND: Before the introduction of 7-valent pneumococcal conjugate vaccine (PCV7), invasive pneumococcal disease (IPD) rates among blacks were twice the rates in whites. We measured the effects of trends in PCV7-type and non-PCV7-type IPD rates on racial disparities in overall IPD and estimated the proportion of IPD caused by serotypes included in the 13-valent pneumococcal conjugate vaccine (PCV13). METHODS: We analyzed data from the Active Bacterial Core surveillance system, which performs active, laboratory- and population-based surveillance for IPD for 29.2 million people in the United States, for the period 1998-2009. For patients with unknown race, we multiplied imputed race to calculate age-, race-, and serotype-specific IPD incidence rates. RESULTS: During 1998-2009, 47 449 IPD cases were identified; race was unknown for 5419 (11%). After multiple imputation, 31 981 (67%) patients were considered white and 13 750 (29%) black. PCV7-type IPD rates in all ages in both races decreased to <1 case per 100 000, whereas there were no decreases in overall IPD rates after 2002. By 2009, PCV13 serotypes caused 71% of cases among whites aged <5 years compared with 58% among blacks (P < .01). PCV13 serotypes caused 50% of IPD cases in whites aged ≥5 years compared with 43% among blacks (P < .01). CONCLUSIONS: Despite near elimination of PCV7-type IPD in both races, overall disparities in IPD rates persisted because non-PCV7-type IPD rates are higher among blacks. Whereas PCV13 introduction may reduce racial disparities in IPD, higher valency conjugate vaccines and strategies to directly address underlying causes are needed to eliminate IPD disparities.

Lethal factor and anti-protective antigen IgG levels associated with inhalation anthrax, Minnesota, USA.

Bacillus anthracis was identified in a 61-year-old man hospitalized in Minnesota, USA. Cooperation between the hospital and the state health agency enhanced prompt identification of the pathogen. Treatment comprising antimicrobial drugs, anthrax immune globulin, and pleural drainage led to full recovery; however, the role of passive immunization in anthrax treatment requires further evaluation.

Emergence of ciprofloxacin-resistant Neisseria meningitidis in North America.

We report on three cases of meningococcal disease caused by ciprofloxacin-resistant Neisseria meningitidis, one in North Dakota and two in Minnesota. The cases were caused by the same serogroup B strain. To assess local carriage of resistant N. meningitidis, we conducted a pharyngeal-carriage survey and isolated the resistant strain from one asymptomatic carrier. Sequencing of the gene encoding subunit A of DNA gyrase (gyrA) revealed a mutation associated with fluoroquinolone resistance and suggests that the resistance was acquired by means of horizontal gene transfer with the commensal N. lactamica. In susceptibility testing of invasive N. meningitidis isolates from the Active Bacterial Core surveillance system between January 2007 and January 2008, an additional ciprofloxacin-resistant isolate was found, in this case from California. Ciprofloxacin-resistant N. meningitidis has emerged in North America.

Evaluation of new biomarker genes for differentiating Haemophilus influenzae from Haemophilus haemolyticus.

PCR detecting the protein D (hpd) and fuculose kinase (fucK) genes showed high sensitivity and specificity for identifying Haemophilus influenzae and differentiating it from H. haemolyticus. Phylogenetic analysis using the 16S rRNA gene demonstrated two distinct groups for H. influenzae and H. haemolyticus.

Increased penicillin nonsusceptibility of nonvaccine-serotype invasive pneumococci other than serotypes 19A and 6A in post-7-valent conjugate vaccine era.

According to population-based invasive pneumococcal surveillance in the United States during 2007, 898 (26%) of 3,511 isolates were penicillin nonsusceptible. Non-7-valent pneumococcal conjugate vaccine (PCV7) serotypes other than 19A accounted for 40% of these penicillin-nonsusceptible isolates; of these, serotypes 15A (11%), 23A (8%), 35B (8%), and 6C (5%) were most common (cumulatively 32% of penicillin-nonsusceptible isolates). Each except 6C represented a single serotype and clonal complex combination that predated the introduction of PCV7. We evaluated the genetic characteristics and nonsusceptibility to penicillin of non- PCV7 serotypes, and we found increased proportions of specific penicillin-nonsusceptible clones in serotypes 15A, 23A, 35B, and 6C, which potentially indicates a basic change of population structure within these individual serotypes.

Characteristics of O157 versus non-O157 Shiga toxin-producing Escherichia coli infections in Minnesota, 2000-2006.

BACKGROUND: Escherichia coli O157:H7 (O157) is the Shiga toxin-producing E. coli (STEC) serotype most frequently isolated and most often associated with hemolytic uremic syndrome (HUS) in the United States. Non-O157 STEC serotypes can also cause serious illness, but their impact as pathogens remains undefined. We compared characteristics of non-O157 and O157 STEC infections identified through sentinel surveillance. METHODS: Sentinel sites included a metropolitan health maintenance organization laboratory and a hospital laboratory serving a small city and rural area. We received sorbitol-MacConkey agar plates from every stool culture performed at both sites during 2000-2006. Colony sweeps were screened for stx1 and stx2 by polymerase chain reaction. E. coli identity, serotype, and presence of stx1 and/or stx2 were confirmed on individual isolates. RESULTS: Two hundred six STEC isolates were identified: 108 (52%) were non-O157 serotypes, and 98 (48%) were O157. Of non-O157 cases, 54% involved bloody diarrhea, and 8% involved hospitalization. Non-O157 isolates with at least stx2 were not more likely to cause severe illness (bloody diarrhea, hospitalization, or HUS) than were non-O157 isolates with only stx1. O157 cases were more likely than non-O157 cases to involve bloody diarrhea (78% vs 54%; P < .001), hospitalization (34% vs 8%; P < .001 and HUS (7% vs 0%; P = .005). When including only isolates with at least stx2, O157 cases were still more likely to involve bloody diarrhea (78% vs 56%; P = .02) and hospitalization (33% vs 12%; P = .01) than non-O157 cases. CONCLUSIONS: Differences in severity among STEC infections could not be explained by stx2, suggesting that additional factors are important in STEC virulence.

Antibiotic resistance patterns in invasive group B streptococcal isolates.

Antibiotics are used for both group B streptococcal (GBS) prevention and treatment. Active population-based surveillance for invasive GBS disease was conducted in four states during 1996-2003. Of 3813 case-isolates, 91.0% (3471) were serotyped, 77.1% (2937) had susceptibility testing, and 46.6% (3471) had both. All were sensitive to penicillin, ampicillin, cefazolin, cefotaxime, and vancomycin. Clindamycin and erythromycin resistance was 12.7% and 25.6%, respectively, and associated with serotype V (P < .001). Clindamycin resistance increased from 10.5% to 15.0% (X(2) for trend 12.70; P < .001); inducible clindamycin resistance was associated with the erm genotype. Erythromycin resistance increased from 15.8% to 32.8% (X(2) for trend 55.46; P < .001). While GBS remains susceptible to beta-lactams, resistance to alternative agents such as erythromycin and clindamycin is an increasing concern.

Long-Term Sentinel Surveillance for Enterotoxigenic Escherichia coli and Non-O157 Shiga Toxin-Producing E. coli in Minnesota.

Background. Enterotoxigenic Escherichia coli (ETEC) and non-O157 Shiga toxin-producing E. coli (STEC) are not detected by conventional culture methods. The prevalence of ETEC infections in the United States is unknown, and recognized cases are primarily associated with foreign travel. Gaps remain in our understanding of STEC epidemiology. Methods. Two sentinel surveillance sites were enrolled: an urban health maintenance organization laboratory (Laboratory A) and a rural hospital laboratory (Laboratory B). Residual sorbitol MacConkey (SMAC) plates from stool cultures performed at Laboratory A (1996-2006) and Laboratory B (2000-2008) were collected. Colony sweeps from SMAC plates were tested for genes encoding STEC toxins stx1 and stx2 (1996-2008) and ETEC heat-labile and heat-stable toxins eltB, estA 1, 2 and 3 (2000-2008) by polymerase chain reaction (PCR)-based assays. Results. In Laboratory A, a bacterial pathogen was identified in 7.0% of 21 970 specimens. During 1996-2006, Campylobacter was the most common bacterial pathogen (2.7% of cultures), followed by Salmonella (1.2%), Shigella (1.0%), and STEC (0.9%). Among STEC (n = 196), O157 was the most common serogroup (31%). During 2000-2006, ETEC (1.9%) was the second most common bacterial pathogen after Campylobacter (2.6%). In Laboratory B, of 19 293 specimens tested, a bacterial pathogen was identified for 5.5%, including Campylobacter (2.1%), STEC (1.3%), Salmonella (1.0%), and ETEC (0.8%). Among STEC (n = 253), O157 was the leading serogroup (35%). Among ETEC cases, 61% traveled internationally. Conclusions. Enterotoxigenic E. coli and STEC infections were as common as most other enteric bacterial pathogens, and ETEC may be detected more frequently by culture-independent multiplex PCR diagnostic methods. A high proportion of ETEC cases were domestically acquired.

An outbreak of Pontiac fever with respiratory distress among workers performing high-pressure cleaning at a sugar-beet processing plant.

BACKGROUND: In August 2000, the Minnesota Department of Health was notified of and investigated an outbreak of febrile respiratory illness among workers at a sugar-beet processing plant. METHODS: A case was defined as fever and respiratory symptoms occurring in a worker at the sugar-beet plant on or after 31 July 2000. Case patients were interviewed, medical and work records were reviewed, and clinical samples were obtained. The plant was inspected, and environmental samples were collected. RESULTS: Fourteen of 15 case patients performed high-pressure water cleaning in the confined space of an evaporator vessel. Symptoms included fever and chills (100%), chest tightness (93%), cough (80%), and shortness of breath (73%). In case patients, median temperature was 39.4 degrees C, median oxygen saturation was 93%, and median white blood cell count was 12x10(3) cells/ mu L. Four (29%) of 14 case patients showed evidence of Legionella pneumophila exposure, according to serologic testing. Water sources contained up to 10(5) cfu/mL of L. pneumophila and 22,200 endotoxin units/mL. CONCLUSIONS: Outbreak features were consistent with Pontiac fever. Respiratory symptoms, which are atypical for Pontiac fever, could be attributed to a high exposure dose of L. pneumophila from confined-space aerosolization or to endotoxin exposure. This outbreak demonstrates the potential occupational hazards for those performing high-pressure cleaning in confined spaces.

Outbreak of osteomyelitis/septic arthritis caused by Kingella kingae among child care center attendees.

OBJECTIVE: Kingella kingae often colonizes the oropharyngeal and respiratory tracts of children but infrequently causes invasive disease. In mid-October 2003, 2 confirmed and 1 probable case of K kingae osteomyelitis/septic arthritis occurred among children in the same 16- to 24-month-old toddler classroom of a child care center. The objective of this study was to investigate the epidemiology of K kingae colonization and invasive disease among child care attendees. METHODS: Staff at the center were interviewed, and a site visit was performed. Oropharyngeal cultures were obtained from the staff and children aged 0 to 5 years to assess the prevalence of Kingella colonization. Bacterial isolates were subtyped by pulsed-field gel electrophoresis (PFGE), and DNA sequencing of the 16S rRNA gene was performed. A telephone survey inquiring about potential risk factors and the general health of each child was also conducted. All children and staff in the affected toddler classroom were given rifampin prophylaxis and recultured 10 to 14 days later. For epidemiologic and microbiologic comparison, oropharyngeal cultures were obtained from a cohort of children at a control child care center with similar demographics and were analyzed using the same laboratory methods. The main outcome measures were prevalence and risk factors for colonization and invasive disease and comparison of bacterial isolates by molecular subtyping and DNA sequencing. RESULTS: The 2 confirmed case patients required hospitalization, surgical debridement, and intravenous antibiotic therapy. The probable case patient was initially misdiagnosed; MRI 16 days later revealed evidence of ankle osteomyelitis. The site visit revealed no obvious outbreak source. Of 122 children in the center, 115 (94%) were cultured. Fifteen (13%) were colonized with K kingae, with the highest prevalence in the affected toddler classroom (9 [45%] of 20 children; all case patients tested negative but had received antibiotics). Six colonized children were distributed among the older classrooms; 2 were siblings of colonized toddlers. No staff (n = 28) or children aged <16 months were colonized. Isolates from the 2 confirmed case patients and from the colonized children had an indistinguishable PFGE pattern. No risk factors for invasive disease or colonization were identified from the telephone survey. Of the 9 colonized toddlers who took rifampin, 3 (33%) remained positive on reculture; an additional toddler, initially negative, was positive on reculture. The children of the control child care center demonstrated a similar degree and distribution of K kingae colonization; of 118 potential subjects, 45 (38%) underwent oropharyngeal culture, and 7 (16%) were colonized with K kingae. The highest prevalence again occurred in the toddler classrooms. All 7 isolates from the control facility had an indistinguishable PFGE pattern; this pattern differed from the PFGE pattern observed from the outbreak center isolates. 16S rRNA gene sequencing demonstrated that the outbreak K kingae strain exhibited >98% homology to the ATCC-type strain, although several sequence deviations were present. Sequencing of the control center strain demonstrated more homology to the outbreak center strain than to the ATCC-type strain. CONCLUSIONS: This is the first reported outbreak of invasive K kingae disease. The high prevalence in the affected toddler class and the matching PFGE pattern are consistent with child-to-child transmission within the child care center. Rifampin was modestly effective in eliminating carriage. DNA sequence analysis suggests that there may be considerable variability within the species K kingae and that different K kingae strains may demonstrate varying degrees of pathogenicity.