Infecciones del tracto genital y urinario como factores de riesgo para parto pretérmino en adolescentes / Genitourinary infections as risk factors for preterm delivery in teenagers

Objetivo: Determinar las infecciones genitourinarias como factores de riesgo para parto pretérmino en adolescentes. Método: Estudio de casos y controles en las Unidades de Medicina Familiar del IMSS Querétaro, periodo octubre 2010 a octubre 2011. Se incluyeron 35 adolescentes con parto pretérmino y 148 con parto a término, mediante muestreo no aleatorio por cuota; se excluyeron aquellas con preeclampsia, eclampsia u otras enfermedades. Los datos se recolectaron del expediente clínico electrónico. Se estudiaron variables sociodemográficas; antecedentes gineco-obstétricos; tipo de parto (pretérmino y término); e infecciones urinarias y vaginales. La infección de vías urinarias fue diagnosticada mediante urocultivo y/o examen general de orina, con >105 UFC y >10 leucocitos por campo, respectivamente. La infección vaginal se diagnosticó por exudado vaginal con reporte de patógenos y/o por clínica. El análisis se realizó con porcentajes, promedios, chi2, razón de momios (Odds Ratio), prueba de t e intervalo de confianza. Resultados: De las adolescentes con parto pretérmino el 54,3 por ciento presentaron infección de vías urinarias, mientras que solo 33,8 por ciento de estas presentaron parto a término (p=0,02). El 57,1 por ciento de las adolescentes con parto pretérmino presentaron infección vaginal en comparación con 35,1 por ciento de las de parto a término (p=0,01). Conclusión: Las infecciones vaginales y urinarias incrementan dos veces el riesgo de presentar parto pretérmino en adolescentes.

Objective: To determine genitourinary infections as risk factors for preterm delivery in teenagers. Method: Case-control study in the Family Medicine Unit IMSS Querétaro, from October 2010 to October 2011. We included 35 teenagers with preterm delivery and 148 who delivered at term, using non-random sampling, we excluded those with preeclampsia, eclampsia or other diseases. Data were collected from electronic medical record. We studied socio-demographic variables, gyneco-obstetrics antecedents, mode of delivery (preterm and term), and genitourinary infections. Urinary tract infection was diagnosed by urine culture or urinalysis, with > 105 CFU and >10 leukocytes per field, respectively. Vaginal infection was diagnosed by vaginal culture with report of pathogens and / or by clinic. The analysis was performed using percentages, averages, chi-squared test, odds ratio, t-test and confidence intervals. Results: The 54.3 percentof the teenagers with preterm delivery had urinary tract infection, while only 33.8 percent of those with term delivery presented it (p = 0.02). Also 57.1 percent of adolescents with vaginal infection had preterm delivery compared with 35.1 percent of those giving birth at term (p=0.01). Conclusion: Vaginal and urinary infections increase twice the risk of preterm delivery in teenagers.

Progression of intravaginal infection by herpes simplex-2 in genetically athymic mice

The purpose of this paper was to study the pathogenesis of wild-type Herpes simplex-2 (HSV-2) primary intravaginal (IVAG) infection in genetically athymic (nude) mice. Nude (nu/nu) N: NIH(S) and Balb/c mice, as well as their euthymic counterparts were IVAG infected with 5 x 10(5) pfu of HSV-2. The progression of the infection was followed by HSV-2 immunolabeling using the peroxidase-antiperoxidase technique in tissue sections of the whole body, electron microscopy, and viremia titration at two different timepoints. 70 per cent of athymic NIH mice, 30 per cent of euthymic NIH mice, and 80 per cent of both athymic and euthymic Balb/c mice developed acute vulvovaginitis and died between 8-10 days post-infection (pi). Viremia was not detected in either athymic or euthymic mice. HSV-2 replicated in the vulvovaginal, vesical and perianal epithelia, then progressed towards the central nervous system mainly along autonomic nerves and ganglia. HSV-2 antigens were not detected in liver, spleen, kidney, skin, heart, lung or bone marrow. The conclusion is that the T-cell immune response seems to limit the IVAG infection of NIH mice at the inoculation site, but is not involved in preventing HSV-2 dissemination through the blood.