Socioeconomic impact on device-associated infections in limited-resource neonatal intensive care units: findings of the INICC.

PURPOSE: To evaluate the impact of country socioeconomic status and hospital type on device-associated healthcare-associated infections (DA-HAIs) in neonatal intensive care units (NICUs). METHODS: Data were collected on DA-HAIs from September 2003 to February 2010 on 13,251 patients in 30 NICUs in 15 countries. DA-HAIs were defined using criteria formulated by the Centers for Disease Control and Prevention. Country socioeconomic status was defined using World Bank criteria. RESULTS: Central-line-associated bloodstream infection (CLA-BSI) rates in NICU patients were significantly lower in private than academic hospitals (10.8 vs. 14.3 CLA-BSI per 1,000 catheter-days; p < 0.03), but not different in public and academic hospitals (14.6 vs. 14.3 CLA-BSI per 1,000 catheter-days; p = 0.86). NICU patient CLA-BSI rates were significantly higher in low-income countries than in lower-middle-income countries or upper-middle-income countries [37.0 vs. 11.9 (p < 0.02) vs. 17.6 (p < 0.05) CLA-BSIs per 1,000 catheter-days, respectively]. Ventilator-associated-pneumonia (VAP) rates in NICU patients were significantly higher in academic hospitals than in private or public hospitals [13.2 vs. 2.4 (p < 0.001) vs. 4.9 (p < 0.001) VAPs per 1,000 ventilator days, respectively]. Lower-middle-income countries had significantly higher VAP rates than low-income countries (11.8 vs. 3.8 per 1,000 ventilator-days; p < 0.001), but VAP rates were not different in low-income countries and upper-middle-income countries (3.8 vs. 6.7 per 1,000 ventilator-days; p = 0.57). When examined by hospital type, overall crude mortality for NICU patients without DA-HAIs was significantly higher in academic and public hospitals than in private hospitals (5.8 vs. 12.5%; p < 0.001). In contrast, NICU patient mortality among those with DA-HAIs was not different regardless of hospital type or country socioeconomic level. CONCLUSIONS: Hospital type and country socioeconomic level influence DA-HAI rates and overall mortality in developing countries.

TST reversion in a BCG-revaccinated population of nursing and medical students, São Paulo, Brazil, 1997-2000.

SETTING: A major university in São Paulo, Brazil, where vaccination against tuberculosis (TB) with bacille Calmette-Guerin (BCG) was routinely offered to first-year medical and nursing students. OBJECTIVES: To estimate the probability of negative tuberculin skin test (TST) results over a 4-year period following BCG revaccination, and to evaluate the effect of factors associated with reversion. DESIGN: Students were enrolled in 1997, initially given a two-step TST, and were retested annually or biannually for the duration of the study. Data on TB exposures and potential risk factors for TST negativity and reversion were collected through annual surveys. A linear mixture survival model was used to estimate the probability of negative TST results over time. RESULTS: Of 159 students, an estimated 20% had a negative TST result despite revaccination, and a further 31% reverted to negative over 4 years of follow-up. No cofactors significantly affected the probability of reversion. CONCLUSION: Overall, in the absence of reported exposure to Mycobacterium tuberculosis, 51% of students revaccinated upon entering nursing or medical school would have a negative TST result by the time they begin their internships. In this recently vaccinated population, reversion was common, suggesting that annual TST screening may remain a useful tool.

A multicenter evaluation of tuberculin skin test positivity and conversion among health care workers in Brazilian hospitals.

SETTING: Four general Brazilian hospitals. OBJECTIVE: To assess the occupational risk of Mycobacterium tuberculosis (TB) in participating hospitals. DESIGN: In phase one of this longitudinal study, a cross-sectional survey documented baseline tuberculin skin test (TST) positivity rates. In phase two, TST conversion rates were evaluated in participants with an initial negative two-step TST. TST conversion data were analyzed to determine risk factors for TB infection using an increase of > or = 10 mm compared to baseline TST. RESULTS: The initial TST positivity rate was 63.1%; the follow-up TST conversion rate was 10.7 per 1000 person-months (p-m). Hospital of employment, recent bacille Calmette-Guerin (BCG) vaccination, nosocomial TB exposure, and employment as a nurse were independent risk factors for TST conversion. Hospitals without TB infection control measures had higher conversion rates than those with control measures (16.0 vs. 7.8/ 1000 p-m, P < 0.001). CONCLUSIONS: This study indicates an important occupational risk of infection in health care settings with a high TB incidence. Longitudinal TST studies are a valuable tool to assess the occupational risk of TB, even in BCG-vaccinated populations, and should be used to direct limited resources for infection control.

Detection of bloodstream pathogens in a bacille Calmette-Guérin (BCG)-vaccinated pediatric population in Malawi: a pilot study.

Children in Malawi receive bacille Calmette-Guérin (BCG) vaccination within the first 3 days of life. Thus, we hypothesized that Malawian children infected with the human immunodeficiency type 1 virus (HIV-1) might be particularly vulnerable to dissemination of the BCG Mycobacterium bovis strain with which they were vaccinated. Following informed consent by parents, we studied children admitted to a Malawi general hospital during the 1998 wet and dry seasons. Blood from cohorts of acutely ill children was cultured for bacteria, including mycobacteria, and fungi, and tested for anti-HIV-1 antibodies. It was shown that non-typhi Salmonella and Escherichia coli were the predominant bloodstream pathogens during the wet and dry seasons, and that bloodstream dissemination of the BCG M. bovis strain is uncommon in HIV-1-infected children who receive the BCG vaccine.

Benchmarking for prevention: the Centers for Disease Control and Prevention's National Nosocomial Infections Surveillance (NNIS) system experience.

Healthcare-associated infections are a major cause of morbidity and mortality at hospitals in the United States. Surveillance of these infections identifies secular trends and provides data upon which prevention interventions can be based in order to improve patient safety. National surveillance of healthcare-associated infections was initiated in the United States in 1970. Since that time, the Centers for Disease Control and Prevention's (CDC) National Nosocomial Infections Surveillance (NNIS) system has provided standardized methods for collecting and comparing healthcare-associated infection rates and the national benchmark infection rate data for inter- and intra-hospital comparisons. The surveillance methods used and results of the implementation of these methods are reviewed. The number of hospitals participating in the CDC's national surveillance of healthcare-associated infections has grown from approximately ten to 20 hospitals in 1970 to over 300 hospitals in 2002. Over the years, NNIS system participants have used standardized definitions, standardized surveillance component protocols, risk stratification for calculation of infection rates and provided national benchmark infection rates for inter- and intra-hospital comparisons. These methods have resulted in a significant reduction in bloodstream infections, urinary tract infections and pneumonia in intensive care unit (ICU) patients and surgical site infections in surgical patients. The NNIS data show that national surveillance of healthcare-associated infections combined with an intervention prevention program can reduce infection rates, reduce morbidity and mortality and improve patient safety. Establishment of such healthcare-associated infection surveillance and prevention systems in countries throughout the world should be a priority.

Age-related differences in cell-specific cytokine production by acutely ill Malawian patients.

Age-related changes in human cell-specific cytokine responses to acute illness have not been well examined. We therefore evaluated age-related differences in T, B and natural killer (NK) peripheral blood lymphocyte cytokine responses of 309 acutely ill hospitalized people in Malawi, Africa, < 1 month-61 years of age. We used four-colour flow cytometry and performed Wilcoxon rank sum and Kruskal-Wallis tests, Pearson (rp) and Spearman (rs) correlations, and linear and logistic regression analyses to control for human immunodeficiency virus infection (HIV) status, the percentages of lymphocytes expressing CD4, and the nature of the acute infection. The percentages of CD8- and CD8+ T cells producing induced IL-8 decreased with age (rs = -0.44 and -0.53). The percentages of T cells producing TNF-alpha were higher, and the percentages producing IL-10 were lower, in those > or =13 than those < 13 years old (medians: 17.7 versus 10.5 and 1.4 versus 3.0, respectively). The percentages of CD8- T cells producing IFN-gamma were higher and stable in those > or =1 year old compared to infants (medians: 23.5 versus 10.4); the percentages of NK producing IFN-gamma were higher post-infancy and then declined to relatively low levels with increasing age. The percentages of T cells producing IL-2 were highest in those 5- <31 years old (median 5.6) and lowest in those > or =31 years old (median 1.9). The ratios of the percentages of T cells producing IL-4 to those producing IL-8 and to those producing IL-10 both increased with age. These data suggest that innate immunity, represented by NK IFN-gamma production, dominates in early life. A number of shifts occur after infancy and before adolescence, including a proinflammatory shift from IL-8 to TNF-gamma and a type 2 shift from IL-10 to IL-4 dominance. These findings suggest distinct age-related differences in the human response to acute illness and may be useful in directing future efforts at immunomodulatory therapies.

Prevalence of nosocomial infections in neonatal intensive care unit patients: Results from the first national point-prevalence survey.

OBJECTIVES: Patients admitted to neonatal intensive care units (NICUs) are at high risk of nosocomial infection. We conducted a national multicenter assessment of nosocomial infections in NICUs to determine the prevalence of infections, describe associated risk factors, and help focus prevention efforts. STUDY DESIGN: We conducted a point prevalence survey of nosocomial infections in 29 Pediatric Prevention Network NICUs. Patients present on the survey date were included. Data were collected on underlying diagnoses, therapeutic interventions/treatments, infections, and outcomes. RESULTS: Of the 827 patients surveyed, 94 (11.4%) had 116 NICU-acquired infections: bloodstream (52.6%), lower respiratory tract (12.9%), ear-nose-throat (8.6%), or urinary tract infections (8.6%). Infants with infections were of significantly lower birth weight (median 1006 g [range 441 to 4460 g] vs 1589 g [range 326 to 5480 g]; P <.001) and had longer median durations of stay than those without infections (88 days [range 8 to 279 days] vs 32 days [range 1 to 483 days]; P <.001). Most common pathogens were coagulase-negative staphylococci and enterococci. Patients with central intravascular catheters (relative risk = 3.81, CI 2.32-6.25; P <.001) or receiving total parenteral nutrition (relative risk = 5.72, CI 3.45-9.49; P <.001) were at greater risk of bloodstream infection. CONCLUSIONS: This study documents the high prevalence of nosocomial infections in patients in NICUs and the urgent need for more effective prevention interventions.

The effects of iron deficiency on lymphocyte cytokine production and activation: preservation of hepatic iron but not at all cost.

Worldwide, over 40% of children have iron deficiency anaemia, frequently associated with infections. Certain cytokines are involved in both immune activation/response to infection and iron transport/metabolism. We therefore assessed the relations among iron deficiency, cytokine production and lymphocyte activation markers in 142 hospitalized Malawian children. We examined peripheral blood lymphocyte antigens/cytokine production using four- colour flow cytometry and serum transferrin receptor (TfR) levels, an inverse measure of iron status unaffected by acute illness or infection, with an enzyme-linked immunosorbent assay. Wilcoxon rank sum tests and logistic regression analyses (LRA) were performed. Iron deficiency (TfR > or = 10 microg/ml) versus TfR < 10 microg/ml, was associated with higher percentages of lymphocytes producing: (a) induced or spontaneous IL-6 (medians: induced, 15.9% for iron-deficient children versus 8.8% for iron-replete children, P = 0.002; spontaneous, 24.4% versus 13.0%, P < 0.001) and (b) induced IFN-gamma (medians:18.4% versus 12.4%, P = 0.006). The percentages of CD8(+) T cells spontaneously producing IL-6 and of all lymphocytes producing induced TNF-alpha and IFN-gamma in the same cell had the strongest relationships to iron deficiency (b = + 0.0211, P = 0.005 and b = + 0.1158, P = 0.012, respectively, LRA) and were also positively related to the co-expression of the T cell activation markers HLA DR and CD38. Severe iron deficiency (TfR > or = 30 microg/ml) was associated with the percentage of lymphocytes producing induced IL-4 (medians: 0.5% versus 1.6%, P < 0.010). The cytokine patterns associated with iron deficiency in our study would preserve iron stores but also preferentially retain the activation capabilities of T cells, albeit not necessarily other immune cells, until a critical level of iron depletion is reached.

Comparison of serum and cell-specific cytokines in humans.

Cytokines function at the cellular, microenvironmental level, but human cytokine assessment is most commonly done at the macro level, by measuring serum cytokines. The relationships between serum and cellular cytokines, if there are any, are undefined. In a study of hospitalized patients in Malawi, we compared cytometrically assessed, cell-specific cytokine data to serum interleukin 2 (IL-2), IL-4, IL-6, IL-8, IL-10, gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) levels in 16 children and 71 (IL-2, -4, -6, -10) or 159 (IL-8, IFN-gamma, and TNF-alpha) adults, using Wilcoxon rank sum tests and Pearson's (r(p)) and Spearman's (r(s)) rank correlations. For the entire study group, correlations between identical serum and cellular cytokines mainly involved IL-8 and IFN-gamma, were few, and were weakly positive (r < 0.40). Blood culture-positive persons had the most and strongest correlations, including those between serum IL-2 levels and the percentages of lymphocytes spontaneously making IL-2 (r(s) = +0.74), serum IL-8 levels and the percentages of lymphocytes spontaneously making IL-8 (r(p) = +0.66), and serum IL-10 levels and the percentages of CD8(+) T cells making TNF-alpha (r(p) = +0.89). Human immunodeficiency virus (HIV)-positive persons had the next largest number of correlations, including several serum IL-8 level correlations, correlation of serum IL-10 levels with the percentages of lymphocytes producing induced IL-10 (r(s) = +0.36), and correlation of serum IFN-gamma levels and the percentages of lymphocytes spontaneously making both IL-6 and IFN-gamma in the same cell (r(p) = +0.59). HIV-negative, malaria smear-positive, and pediatric patients had few significant correlations; for the second and third of these subgroups, serum IL-8 level was correlated with the percentage of CD8(-) T cells producing induced IL-8 (r(s) = +0.40 and r(s) = +0.56, respectively). Thus, the strength of associations between serum and cellular cytokines varied with the presence or absence of bloodstream infection, HIV status, and perhaps other factors we did not assess. These results strongly suggest that serum cytokines at best only weakly reflect peripheral blood cell cytokine production and balances.

Costs and savings associated with infection control measures that reduced transmission of vancomycin-resistant enterococci in an endemic setting.

OBJECTIVE: To determine the costs and savings of a 15-component infection control program that reduced transmission of vancomycin-resistant enterococci (VRE) in an endemic setting. DESIGN: Evaluation of costs and savings, using historical control data. SETTING: Adult oncology unit of a 650-bed hospital. PARTICIPANTS: Patients with leukemia, lymphoma, and solid tumors, excluding bone marrow transplant recipients. METHODS: Costs and savings with estimated ranges were calculated. Excess length of stay (LOS) associated with VRE bloodstream infection (BSI) was determined by matching VRE BSI patients with VRE-negative patients by oncology diagnosis. Differences in LOS between the matched groups were evaluated using a mixed-effect analysis of variance linear-regression model. RESULTS: The cost of enhanced infection control strategies for 1 year was $116,515. VRE BSI was associated with an increased LOS of 13.7 days. The savings associated with fewer VRE BSI ($123,081), fewer patients with VRE colonization ($2,755), and reductions in antimicrobial use ($179,997) totaled $305,833. Estimated ranges of costs and savings for enhanced infection control strategies were $97,939 to $148,883 for costs and $271,531 to $421,461 for savings. CONCLUSION: The net savings due to enhanced infection control strategies for 1 year was $189,318. Estimates suggest that these strategies would be cost-beneficial for hospital units where the number of patients with VRE BSI is at least six to nine patients per year or if the savings from fewer VRE BSI patients in combination with decreased antimicrobial use equalled $100,000 to $150,000 per year.

Use and efficacy of tuberculosis infection control practices at hospitals with previous outbreaks of multidrug-resistant tuberculosis.

OBJECTIVE: To evaluate the implementation and efficacy of selected Centers for Disease Control and Prevention guidelines for preventing spread of Mycobacterium tuberculosis. DESIGN: Analysis of prospective observational data. SETTING: Two medical centers where outbreaks of multidrug-resistant tuberculosis (TB) had occurred. PARTICIPANTS: All hospital inpatients who had active TB or who were placed in TB isolation and healthcare workers who were assigned to selected wards on which TB patients were treated. METHODS: During 1995 to 1997, study personnel prospectively recorded information on patients who had TB or were in TB isolation, performed observations of TB isolation rooms, and recorded tuberculin skin-test results of healthcare workers. Genetic typing of M tuberculosis isolates was performed by restriction fragment-length polymorphism analysis. RESULTS: We found that only 8.6% of patients placed in TB isolation proved to have TB; yet, 19% of patients with pulmonary TB were not isolated on the first day of hospital admission. Specimens were ordered for acid-fast bacillus smear and results received promptly, and most TB isolation rooms were under negative pressure. Among persons entering TB isolation rooms, 44.2% to 97.1% used an appropriate (particulate, high-efficiency particulate air or N95) respirator, depending on the hospital and year; others entering the rooms used a surgical mask or nothing. We did not find evidence of transmission of TB among healthcare workers (based on tuberculin skin-test results) or patients (based on epidemiological investigation and genetic typing). CONCLUSIONS: We found problems in implementation of some TB infection control measures, but no evidence of healthcare-associated transmission, possibly in part because of limitations in the number of patients and workers studied. Similar evaluations should be performed at hospitals treating TB patients to find inadequacies and guide improvements in infection control.

Vancomycin-resistant enterococci colonization in patients at seven hemodialysis centers.

BACKGROUND: Vancomycin-resistant enterococci (VRE) are increasing in prevalence at many institutions, and are often reported in dialysis patients. We studied the prevalence of and risk factors for VRE at seven outpatient hemodialysis centers (three in Baltimore, MD, USA, and four in Richmond, VA, USA). METHODS: Rectal or stool cultures were performed on consenting hemodialysis patients during December 1997 to April 1998. Consenting patients were recultured during May to July 1998 (median 120 days later). Clinical and laboratory data and functional status (1 to 10 scale: 1, normal function; 9, home attendant, not totally disabled; 10, disabled, living at home) were recorded. RESULTS: Of 478 cultures performed, 20 (4.2%) were positive for VRE. Among the seven centers, the prevalence of VRE-positive cultures varied from 1.0 to 7.9%. Independently significant risk factors for a VRE-positive culture were a functional score of 9 to 10 (odds ratio 6.9, P < 0.001), antimicrobial receipt within 90 days before culture (odds ratio 6.1, P < 0.001), and a history of injection drug use (odds ratio 5.4, P = 0.004). CONCLUSIONS: VRE-colonized patients were present at all seven participating centers, suggesting that careful infection-control precautions should be used at all centers to limit transmission. In agreement with previous studies, VRE colonization was more frequent in patients who had received antimicrobial agents recently, underscoring the importance of judicious antimicrobial use in limiting selection for this potential pathogen.

Nosocomial outbreak of Microbacterium species bacteremia among cancer patients.

To date, only 6 sporadic Microbacterium species (formerly coryneform Centers for Disease Control and Prevention [CDC] groups A-4 and A-5) infections have been reported. The source, mode of transmission, morbidity, mortality, and potential for nosocomial transmission of Microbacterium species remain unknown. From 26 July through 14 August 1997, 8 episodes of coryneform CDC group A-5 symptomatic bacteremia occurred in 6 patients on the oncology ward at the Maine Medical Center. One patient died. All isolates were identified at CDC as Microbacterium species and had identical DNA banding patterns by pulsed-field gel electrophoresis. To assess risk factors for Microbacterium species infection, a retrospective cohort study was conducted. The presence of a central venous catheter was the strongest risk factor (6/6 vs. 22/48; relative risk, 3.2; P<.0001). This outbreak demonstrates significant Microbacterium species-associated morbidity and mortality in immunocompromised populations and confirms the potential for epidemic nosocomial transmission.

Anesthesia-associated carbon monoxide exposures among surgical patients.

OBJECTIVE: To estimate the extent of, and evaluate risk factors for, elevated carboxyhemoglobin levels among patients undergoing general anesthesia and to identify the source of carbon monoxide. DESIGN: Matched case-control study to measure carboxyhemoglobin levels. SETTING: Large academic medical center. PARTICIPANTS: 45 surgical patients who underwent general anesthesia RESULTS: Case-patients were more likely than controls to undergo surgery on Monday or Tuesday (10/15 vs 7/30; matched odds ratio [mOR], 7.7; 95% confidence interval [CI95], 1.8-34; P=.01), in one particular room (7/15 vs 4/30; mOR, 8.5; CI95, 1.5-48; P=.03) or in a room that was idle for > or =24 hours (11/15 vs 1/30; mOR, 95.5; CI95, 8.0-1,138; P< or =.001). In a multivariate model, only rooms, and hence the anesthesia equipment, that were idle for > or =24 hours were independently associated with elevated intraoperative carboxyhemoglobin levels (OR, 22.4; CI95, 1.5-338; P=.025). Moreover, peak carboxyhemoglobin levels were correlated with the length of time that the room was idle (r=0.7; CI95, 0.3-0.9). Carbon monoxide was detected in the anesthesia machine outflow during one case-procedure. No contamination of anesthesia gas supplies or CO2 absorbents was found. CONCLUSIONS: Carbon monoxide may accumulate in anesthesia circuits left idle for > or =24 hours as a result of a chemical interaction between CO2-absorbent granules and anesthetic gases. Patients administered anesthesia through such circuits may be at increased risk for elevated carboxyhemoglobin levels during surgery or the early postoperative period.

Seasonal variation in the etiology of bloodstream infections in a febrile inpatient population in a developing country.

OBJECTIVES: Published data suggest that Streptococcus pneumoniae, non-typhi Salmonella species, and Mycobacterium tuberculosis are the predominant causes of bloodstream infection (BSI) in hospitalized populations in sub-Saharan Africa. This study was conducted during the wet season to ascertain the etiology and prevalence of BSI among febrile inpatients in a hospital where the dry season BSI profile in a similar study population had already been documented. METHODS: In the period from March to May 1998, consecutive febrile (> or = 37.5 degrees C) adult (> or = 14 y) patients presenting to a Malawi hospital were enrolled after providing informed consent. Following clinical evaluation, blood was drawn for culture (bacteria, mycobacteria, and fungi), human immunodeficiency virus (HIV) testing, and malaria smears. RESULTS: Of 238 enrolled patients, 173 (73%) were HIV-positive and 67 (28%) had BSI. The predominant wet season BSI pathogens were non-typhi Salmonella species (41%), M. tuberculosis (19%), and Cryptococcus neoformans (9%) (cf. the predominant dry season pathogen was S. pneumoniae). Mycobacteremia was more likely in HIV-positive than in HIV-negative patients (13/173 vs. 0/65; P < 0.05). A logistic regression model yielded clinical predictors of BSI that included chronic fever, oral candidiasis, or acute diarrhea. CONCLUSION: Pathogens causing BSI in febrile inpatients in a Malawi teaching hospital vary by season. Season- and country-specific studies, such as this one, provide data that may facilitate empirical therapy of febrile illnesses whose etiologies vary by season.

Cytokines and malaria parasitemia.

The balance between pro- and antiinflammatory cytokines may be important in malaria presentation and outcome. Malaria tends to be more severe in children than in adults, presumably because partial immunity develops with age. However, the full nature of, and age-related differences in, anti-malarial immunity are unknown. We compared: (1) serum and cell-specific cytokines of patients with acute malaria to those of patients with other acute illnesses and to those of healthy adults and (2) the cytokine responses of parasitemic children and parasitemic adults. Flow cytometry was done on the peripheral blood mononuclear cells of 148 hospitalized children, 161 febrile hospitalized adults, and 20 healthy adults in Malawi, Africa, a malaria-endemic country. Serum cytokines were also assessed for 80 of these patients. Thirty-eight participants were parasitemic with Plasmodium falciparum. Serum interleukin (IL)-10 (an antiinflammatory, immunoregulatory, and type 2 cytokine) levels were higher in malaria patients than in other patients (medians 502 pg/mL vs 16 pg/mL, P = 0.002), and the percentages of various lymphocyte populations making IL-6 (a proinflammatory, type 2 cytokine regulating iron distribution) were lower in malaria patients than in other patients (e.g., for spontaneous production by children's CD8(+) T cells: medians 1.4% vs 33.1%, P = 0.004). For adult patients, the percentages of lymphocytes spontaneously making IL-4 (a type 2 cytokine) were significantly lower in those with malaria than in those without malaria (medians 0.9% vs 2.1%, P = 0.005). The percentages of monocytes spontaneously making IL-8 (a chemotactic, proinflammatory chemokine) were higher in parasitemic children than in parasitemic adults (medians 5.8% vs 1.7%, P = 0.003). A number of cellular proinflammatory, type 1 parameters were significantly higher in all children (with or without malaria) than in all adults; these included the percentages of various lymphocyte populations making IL-6, both IL-6 and interferon-gamma, or IL-8. These data support the importance of IL-10 in malaria parasitemia. Given the lack of an IL-4 (type 2) response, IL-10's primary role may be immunoregulatory rather than type 2 in nature. In this study, the immune response to malaria was more proinflammatory in children than in adults. This difference, if corroborated by other studies, could be related to malaria's greater severity in children.

Occupational transmission of Mycobacterium tuberculosis to health care workers in a university hospital in Lima, Peru.

From November 1996 through March 1997, presumptive active pulmonary tuberculosis (TB) was detected in 44 health care workers (HCWs) at a university hospital in Lima, Peru. To further assess the magnitude of the outbreak and determine risk factors for occupational Mycobacterium tuberculosis transmission, we identified HCWs in whom active pulmonary TB was diagnosed from January 1994 through January 1998, calculated rates by year and hospital work area, and conducted a tuberculin skin test (TST) survey. Thirty-six HCWs had confirmed active pulmonary TB. The rate of TB was significantly higher among the 171 HCWs employed in the laboratory than among HCWs employed in all other areas. In multivariate analysis, the only independent risk factor for HCW M. tuberculosis infection in HWCs employed in the laboratory was the use of common staff areas. Very high rates of active pulmonary TB were detected among HCWs at this hospital, and occupational acquisition in the laboratory was associated with HCW-to-HCW transmission.