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Prevention and control of perinatal hepatitis B virus transmission in ...

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diagnosis. In the past, the <strong>in</strong>cidence <strong>of</strong> <strong>hepatitis</strong> B <strong>in</strong> Pol<strong>and</strong> was approx. 45 reported cases per100,000 population, but follow<strong>in</strong>g the <strong>in</strong>troduction <strong>of</strong> improved sterilization <strong>of</strong> medical equipment<strong>in</strong> 1986 <strong>and</strong> a selective programme <strong>of</strong> vacc<strong>in</strong>ation <strong>in</strong> 1991, the <strong>in</strong>cidence fell to about 35 per100,000 by 1993. In 1993, an <strong>in</strong>tensive vacc<strong>in</strong>ation campaign was launched, which has reducedthe <strong>in</strong>cidence to under 15 per 100,000. The <strong>in</strong>cidence <strong>of</strong> HBV <strong>in</strong>fection has decreased across allage groups <strong>and</strong> <strong>in</strong> both men <strong>and</strong> women, <strong>and</strong> <strong>in</strong> the under 3 years age group only 32 cases <strong>in</strong> totalwere reported <strong>in</strong> 1997. In 1996 <strong>and</strong> 1997, there was a slight relative <strong>in</strong>crease <strong>in</strong> the <strong>in</strong>cidence <strong>of</strong>HBV <strong>in</strong>fection <strong>in</strong> men aged 20-24 years. This group may be a target for future vacc<strong>in</strong>ationprogrammes <strong>and</strong> other activities <strong>of</strong> <strong>control</strong> for the <strong>in</strong>fection.Mast EE, Alter MJ, Margolis HS. Strategies to prevent <strong>and</strong> <strong>control</strong> <strong>hepatitis</strong> B <strong>and</strong> C <strong>virus</strong><strong>in</strong>fections: a global perspective. Vacc<strong>in</strong>e 1999; 17:1730-1733.Hepatitis Branch, Division <strong>of</strong> Viral <strong>and</strong> Rickettsial Diseases, National Center for InfectiousDiseases, Centers for Disease Control <strong>and</strong> <strong>Prevention</strong>, Atlanta, GA 30306, USA. eem1@cdc.govHepatitis B <strong>virus</strong> (HBV) <strong>and</strong> <strong>hepatitis</strong> C <strong>virus</strong> (HCV) are major causes <strong>of</strong> acute <strong>and</strong> chronic liverdisease worldwide. Chronic <strong>in</strong>fection with these <strong>virus</strong>es <strong>of</strong>ten leads to chronic liver disease,<strong>in</strong>clud<strong>in</strong>g cirrhosis or primary hepatocellular carc<strong>in</strong>oma. Both HBV <strong>and</strong> HCV are bloodborne<strong>virus</strong>es; however, HBV is transmitted efficiently by both percutaneous <strong>and</strong> mucosal exposures,<strong>and</strong> HCV is transmitted predom<strong>in</strong>antly by percutaneous exposures. Because the relativeimportance <strong>of</strong> various modes <strong>of</strong> <strong>transmission</strong> <strong>of</strong> these <strong>virus</strong>es differs by country, the choice <strong>of</strong>specific prevention <strong>and</strong> <strong>control</strong> strategies depends primarily on the epidemiology <strong>of</strong> <strong>in</strong>fection <strong>in</strong> aparticular country. Comprehensive <strong>hepatitis</strong> B prevention strategies should <strong>in</strong>clude (1) prevention<strong>of</strong> <strong>per<strong>in</strong>atal</strong> HBV <strong>transmission</strong>, (2) <strong>hepatitis</strong> B vacc<strong>in</strong>ation at critical ages to <strong>in</strong>terrupt <strong>transmission</strong><strong>and</strong> (3) prevention <strong>of</strong> nosocomial HBV <strong>transmission</strong>. The prevention <strong>of</strong> <strong>hepatitis</strong> C is problematicbecause a vacc<strong>in</strong>e to prevent HCV <strong>in</strong>fection is not expected to be developed <strong>in</strong> the foreseeablefuture. From a global perspective, the greatest impact on the disease burden associated with HCV<strong>in</strong>fection will most likely be achieved by focus<strong>in</strong>g efforts on primary prevention strategies toreduce or elim<strong>in</strong>ate the risk for <strong>transmission</strong> from nosocomial exposures (e.g., blood transfusion,unsafe <strong>in</strong>jection practices) <strong>and</strong> high-risk practices (e.g., <strong>in</strong>ject<strong>in</strong>g drug use).Mast EE, Hwang LY, Seto DS, Nolte FS, Na<strong>in</strong>an OV, Wurtzel H, Alter MJ. Risk factors for<strong>per<strong>in</strong>atal</strong> <strong>transmission</strong> <strong>of</strong> <strong>hepatitis</strong> C <strong>virus</strong> (HCV) <strong>and</strong> the natural history <strong>of</strong> HCV <strong>in</strong>fectionacquired <strong>in</strong> <strong>in</strong>fancy. J Infect Dis 2005; 192:1880-1889.Centers for Disease Control <strong>and</strong> <strong>Prevention</strong>, Atlanta, GA 30333, USA. emast@cdc.govThe goal <strong>of</strong> the present study was to assess risk factors for <strong>per<strong>in</strong>atal</strong> <strong>hepatitis</strong> C <strong>virus</strong> (HCV)<strong>transmission</strong> <strong>and</strong> the natural history <strong>of</strong> <strong>in</strong>fection among HCV-<strong>in</strong>fected <strong>in</strong>fants. In a cohort study,244 <strong>in</strong>fants born to HCV-positive mothers were followed from birth until age > or = 12 months.Maternal serum was collected at enrollment <strong>and</strong> delivery; <strong>in</strong>fant serum was collected at birth <strong>and</strong>at 8 well-child visits. Test<strong>in</strong>g <strong>in</strong>cluded detection <strong>of</strong> antibody to HCV, detection <strong>of</strong> HCV RNA(qualitative <strong>and</strong> quantitative), <strong>and</strong> genotyp<strong>in</strong>g. HCV-<strong>in</strong>fected <strong>in</strong>fants were followed annually untilage 5 years. Overall, 9 <strong>of</strong> 190 (4.7% [95% confidence <strong>in</strong>terval (CI), 2.3%-9.1%]) <strong>in</strong>fants born tomothers who were HCV RNA positive at delivery became <strong>in</strong>fected, compared with 0 <strong>of</strong> 54 <strong>in</strong>fantsborn to HCV RNA-negative mothers (P = 0.10). Among HCV RNA-positive mothers, the rate <strong>of</strong><strong>transmission</strong> was 3.8% (95% CI, 1.7%-8.1%) from the 182 who were human immunodeficiency<strong>virus</strong> (HIV) negative, compared with 25.0% (95% CI, 4.5%-64.4%) from the 8 who were HIVpositive (P < 0.05). Three <strong>in</strong>fected <strong>in</strong>fants resolved their <strong>in</strong>fection (i.e., became HCV RNAnegative). In multivariate analysis restricted to HCV RNA-positive mothers, membrane rupture >or = 6 h (odds ratio [OR], 9.3 [95% CI, 1.5-179.7]) <strong>and</strong> <strong>in</strong>ternal fetal monitor<strong>in</strong>g (OR, 6.7 [95%CI, 1.1-35.9]) were associated with <strong>transmission</strong> <strong>of</strong> HCV to <strong>in</strong>fants. If duration <strong>of</strong> membrane29

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