Experimental transmission of Neisseria gonorrhoeae from pregnant rat to fetus.
ABSTRACT Sprague-Dawley rats were infected on day 20 of pregnancy by intraperitoneal inoculation with Neisseria gonorrhoeae. Disseminated gonococcal infection (DGI) and pelvic inflammatory disease (PID) strains in the presence of C1q but not in the presence of bovine serum albumin (BSA) were able to spread from the pregnant rat to the fetus and resulted in fetal mortality. Transmission of DGI and PID strains that are serum resistant (ser(r)) and sac-4 positive but not of a local infection strain that is ser(s) and sac-4 negative was facilitated by the C1q-dependent mechanism. This study provides the first experimental model that may mimic the transmission of gonococcal infection from mother to the fetus during pregnancy.
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Article: Experimental transmission of Neisseria gonorrhoeae from pregnant rat to fetus.
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ABSTRACT: The kinetics of infection and the pathogenic effects on the reproductive function of laboratory mice infected with Bartonella birtlesii recovered from an Apodemus species are described. B. birtlesii infection, as determined by bacteremia, occurred in BALB/c mice inoculated intravenously. Inoculation with a low-dose inoculum (1.5 x 10(3) CFU) induced bacteremia in only 75% of the mice compared to all of the mice inoculated with higher doses (> or =1.5 x 10(4)). Mice became bacteremic for at least 5 weeks (range, 5 to 8 weeks) with a peak ranging from 2 x 10(3) to 10(5) CFU/ml of blood. The bacteremia level was significantly higher in virgin females than in males but the duration of bacteremia was similar. In mice infected before pregnancy (n = 20), fetal loss was evaluated by enumerating resorption and fetal death on day 18 of gestation. The fetal death and resorption percentage of infected mice was 36.3% versus 14.5% for controls (P < 0.0001). Fetal suffering was evaluated by weighing viable fetuses. The weight of viable fetuses was significantly lower for infected mice than for uninfected mice (P < 0.0002). Transplacental transmission of Bartonella was demonstrated since 76% of the fetal resorptions tested was culture positive for B. birtlesii. The histopathological analysis of the placentas of infected mice showed vascular lesions in the maternal placenta, which could explain the reproductive disorders observed. BALB/c mice appeared to be a useful model for studying Bartonella infection. This study provides the first evidence of reproductive disorders in mice experimentally infected with a Bartonella strain originating from a wild rodent.Infection and Immunity 10/2001; 69(9):5313-7. DOI:10.1128/IAI.69.9.5313-5317.2001 · 4.16 Impact Factor
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ABSTRACT: A high index of suspicion is critical in the prevention of serious complications of gonorrheal infection. This article reviews published information regarding the pathophysiology, epidemiology, clinical characteristics, diagnosis, and treatment of gonorrhea. MEDLINE was used to search the literature for articles and studies that have a bearing on these issues. Keywords used were disseminated gonococcal infection; septic arthritis; gonorrhea and pregnancy; and gonorrhea and pathophysiology. We conclude that disseminated gonococcal infection (DGI) should be in the differential diagnosis of any sexually active patient who presents with arthritis, dermatitis, and/or tenosynovitis. Although the incidence of DGI has declined in recent years, it still is the most common cause of newly diagnosed arthritis requiring hospitalization. Careful culturing of every site that could be infected is imperative to aid in diagnosis and treatment. Prompt therapy with appropriate antibiotics such as ceftriaxone will prevent the more serious complications of DGI.Primary Care Update for OB/GYNS 07/2003; DOI:10.1016/S1068-607X(03)00025-8
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ABSTRACT: The mammalian uterus faces unique immunological challenges. It must nurture and protect the semiallogenic fetus from attack by the maternal immune system while guarding against infection by pathogens that compromise fetal and maternal health. Complement has recently been implicated in the etiology of pregnancy loss, but its regulation by steroid hormones and its role in host defense in the uterus are not clearly defined. Here we use biochemical, functional, and physiological assays to elucidate the regulation of complement proteins in the rat uterus. We demonstrate that estrogens (17 beta-estradiol) and glucocorticoids (dexamethasone) have major, but opposing, effects on the amount and latent activity of complement effectors in the uterus. Treatment with 17 beta-estradiol induced vasodilation and an increase in vascular permeability, which resulted in extravasation of plasma and complement into the uterus, rather than de novo complement biosynthesis. In vitro assays revealed that 17 beta-estradiol induced a potent bactericidal activity in uterine luminal fluid and that the antibacterial component was complement. These proinflammatory and immunomodulatory effects were evident within 4 h of treatment and were blocked by coadministration of dexamethasone. We also found that estrogen effects on the vasculature were mediated in part by activation of the contact system and bradykinin B1 receptors. These results indicate that complement plays a central role in innate immunity in the female reproductive tract and suggest that estrogens or glucocorticoids might be used therapeutically to enhance or inhibit complement-dependent processes in the uterus.Biology of Reproduction 03/2006; 74(2):265-74. DOI:10.1095/biolreprod.105.045336 · 3.45 Impact Factor