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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As the most common cause of sexually transmitted disease in women, chlamydial infections can lead to pelvic inflammatory disease, infertility, and ectopic pregnancy. To better understand the role played by sex hormones in modulating the immune response of the genital tract to microbial infections, we have developed a rat model to study Chlamydia trachomatis infection. Inbred female Lewis rats were primed with progesterone and inoculated by intrauterine instillation of C. trachomatis (mouse pneumonitis strain MoPn) into each uterine horn. When infected animals were examined for the presence of chlamydial antigens 14 days postinfection, both the uterus and vagina were found to be positive compared to those of saline-treated animals, which did not show specific staining. The involvement of local and systemic immune systems following chlamydial infection was determined by analyzing major histocompatibility complex (MHC) class II expression in the reproductive tract and lymphocyte proliferation in response to mitogenic and chlamydia-specific stimulation of cells from the spleen and lymph nodes (LN) draining the reproductive tract. Enhanced proliferation was observed in LN following mitogenic but not antigenic (MOMP [major outer membrane protein]) stimulation. In contrast, spleen cell proliferation was lower in chlamydia-infected rats than in saline-treated controls. MHC class II expression, an indicator of inflammatory responses, was upregulated in the uterus, on glandular epithelial cells, and adjacent to glands in response to chlamydial infection. In other experiments, when rats were infected at estrus and diestrus without prior progesterone priming, chlamydial inclusions were not detected in either the uterus or vagina. However, enhanced lymphocyte proliferation was observed in response to mitogenic and MOMP stimulation in the reproductive tract-draining LN from estrous and diestrous animals. These findings indicate that under appropriate endocrine conditions, the rat uterus is susceptible to C. trachomatis infection and that immune responses to this pathogen can be detected locally and systemically. Further, they suggest that clearance of the infection from the reproductive tract involves immune cells from the LN draining the reproductive tract.
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PMID:Chlamydia trachomatis infection in the female reproductive tract of the rat: influence of progesterone on infectivity and immune response. 948 72

Six gilts were inoculated intramuscularly with 2.5x10(6) tachyzoites of Neospora caninum on three different days of gestation to study the pathogenic effect of Neospora infection in pigs, including possible transplacental transmission. The gilts were euthanized 59, 30, and 9/10 days postinoculation (p.i.), corresponding to days 107, 102/106 and 110/111 of pregnancy. With the exception of one animal (euthanized day 9 p.i.) all gilts seroconverted as measured by the indirect, fluorescent antibody test (IFAT). Neosporosis with multifocal intralobular necrotizing hepatitis was seen in the two gilts inoculated 9/10 days before euthanasia. The uterus of one gilt inoculated 59 days before euthanasia revealed granulomatous and focal necrotizing endometritis with a corresponding multifocal necrosis of the trophoblasts of two fetuses. Transplacental neosporosis was indicated in the two fetuses by strongly elevated Neospora IFAT titres in pleural fluid and by the presence of multifocal necrotizing encephalitis and hepatitis together with non-suppurative myocarditis, pneumonitis, nephritis and hepatitis. Furthermore, N. caninum was re-isolated in cell culture from one of these fetuses. A third fetus from the same gilt revealed only disseminated, pinpoint necroses in the liver. Immunohistochemically, N. caninum tachyzoites were detected in association with histopathological changes in the liver and the endometrium of the gilts, and in the brain, liver, and allantochorion of the three fetuses.
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PMID:Experimental porcine neosporosis. 963 70

Pregnant BALB/c mice were inoculated intravaginally on day 5 of gestation with the Chlamydia trachomatis mouse pneumonitis biovar. Animals that received 10(5), 10(6), or 10(7) inclusion-forming units (IFU) of C. trachomatis delivered prematurely on days 15 to 16 of gestation. A focal inflammatory infiltrate was observed in the wall of the uterus on the day 14 of gestation in animals inoculated with 10(5) IFU. In this group of mice, immunohistochemical analysis showed chlamydial inclusions in the endometrium and fetal membranes.
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PMID:A murine model for the study of Chlamydia trachomatis genital infections during pregnancy. 1022 27

To study the abortifacient potential and fetoplacental tropism of Bacillus licheniformis bacteria, eight cows in the sixth to eighth month of gestation were inoculated intravenously either once (n = 4) or on four successive days (n = 4) with B. licheniformis at doses ranging from 10(9) to 10(12) colony-forming units. Cows were euthanatized and necropsied prior to abortion (n = 2), at the time of abortion (n = 2), or at calving (n = 4). Live-born calves (n = 5) were euthanatized immediately after delivery and necropsied. B. licheniformis was reisolated from placentomes/endometrium in six of eight (75%) cows and from one fetus aborted 43 days after inoculation. Lesions associated with B. licheniformis were restricted to the pregnant uterus, with the exception of one cow, which developed pneumonia. Necrosis in the fetal compartment of the placenta were present in three of four (75%) cows of both inoculation groups. Lesions were mainly restricted to fetal membranes and especially to the fetal side of the placentomes. Necrosis and diffuse neutrophil infiltrations of both villi and intervillous areas occurred in the fetal part of the placenta, and the placentomal interface was distended by bacteria, neutrophils, erythrocytes, and debris. Within trophoblasts, bacteria were located both free in the cytoplasm and in cytoplasmatic vesicles. Inflammation was present in three of eight (38%) calves. Placental and fetal lesions were similar to those found in cases of spontaneous abortions associated with B. licheniformis. The abortifacient potential of B. licheniformis and the tropism for the bovine placenta is demonstrated here for the first time.
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PMID:Experimental infection of pregnant cows with Bacillus licheniformis bacteria. 1033 27

Somatic cell nuclei of giant pandas can dedifferentiate in enucleated rabbit ooplasm, and the reconstructed eggs can develop to blastocysts. In order to observe whether these interspecies cloned embryos can implant in the uterus of an animal other than the panda, we transferred approximately 2300 panda-rabbit cloned embryos into 100 synchronized rabbit recipients, and none became pregnant. In another approach, we cotransferred both panda-rabbit and cat-rabbit interspecies cloned embryos into the oviducts of 21 cat recipients. Fourteen recipients exhibited estrus within 35 days; five recipients exhibited estrus 43-48 days after embryo transfer; and the other two recipients died of pneumonia, one of which was found to be pregnant with six early fetuses when an autopsy was performed. Microsatellite DNA analysis of these early fetuses confirmed that two were from giant panda-rabbit cloned embryos. The results demonstrated that panda-rabbit cloned embryos can implant in the uterus of a third species, the domestic cat. By using mitochondrial-specific probes of panda and rabbit, we found that mitochondria from both panda somatic cells and rabbit ooplasm coexisted in early blastocysts, but mitochondria from rabbit ooplasm decreased, and those from panda donor cells dominated in early fetuses after implantation. Our results reveal that mitochondria from donor cells may substitute those from recipient oocytes in postimplanted, interspecies cloned embryos.
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PMID:Interspecies implantation and mitochondria fate of panda-rabbit cloned embryos. 1213 8

The unexpected occurrence of a fever higher than 38 degrees Celsius at least twice in 48 hours after childbirth is a common problem. A well-executed clinical examination of a patient with a high fever is necessary to determine the origin of the infection. It is necessary to remain vigilant because it could be a sign of severe infection threatening a mother's life. The fever can sometimes remain moderate while the infection progresses at lightning speed. This is especially the case in weak patients (e.g., those with tuberculosis, AIDS, or malnutrition); thus it will be necessary to keep an attentive eye on them. Major causes to be familiar with and to recognize include malaria (always to be considered), uterine infection (the most common postpartum infection), kidney infection, tender breasts, pneumonia, meningitis, or appendicitis. Things health workers should consider if they suspect uterine infection are birth history, endometritis, and the fact that, in the absence of treatment, the infection can spread to the Fallopian tubes and eventually to the general circulation (septicemia). Special cases include uterine infections accompanied by retention of placental debris or membranes, fever after abortion, and fever after cesarean section. Health workers must consider all cases of retention, even those without a fever, as a potential infection. They must administer antibiotic treatment within 5 days after emptying the uterus. The treatment of choice for fever following an abortion is 3 g ampicillin for 7 days. In cases of infection after an abortion, health workers should consider uterine perforation and retention. Fever usually occurs 4-5 days after a cesarean section. Antibiotic treatment is usually necessary.
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PMID:[Postpartum infections]. 1234 37

Group B streptococci (GBS) are an important cause of neonatal sepsis, pneumonia and meningitis. In some newborns, GBS sepsis may have a severe course, including septic shock with high mortality rate, whereas other newborns are colonized with GBS on their surfaces without any clinical signs of bacterial infections. Interferon (IFN)-gamma is produced in neonatal GBS sepsis, and transforming growth factor (TGF)-beta is also found in the uterus. The involvement of IFN-gamma and TGF-beta in the earliest phase of infection might be a determinant of susceptibility and/or progression of infection in vivo. The aim of this study was to assess the effect of IFN-gamma and TGF-beta on adherence and intracellular viability in ECV304 cells of GBS serotype III isolated from cerebrospinal fluid (CSF) and vagina (strains 90356 and 80340, respectively). Interaction of GBS-ECV304 cells showed that the CSF isolate exhibited a more efficient adherence mechanism than the vagina isolate (P<0.001). Intracellular viability was observed for the CSF 90356 isolate within 2 h incubation. Results suggest the expression of additional bacterial virulence factors that favor some GBS type III strains to cause invasive disease. Detection of genotypic virulence marker (162-kb) in the CSF 90356 isolate by PFGE emphasizes the high risk of invasive infection by some GBS-III strains. Treatment of ECV304 cells with IFN-gamma and/or TGF-beta increased adherence of both GBS strains (P<0.001). Intracellular survival of the CSF 90356 isolate was observed after 24 h incubation following treatment of ECV304 cells with IFN-gamma and TGF-beta. Our data suggest that both IFN-gamma and TGF-beta may favor virulence of GBS strains. Variation of IFN-gamma and TGF-beta producing capacity of host cells of different individuals may influence development of invasive disease by GBS-III.
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PMID:The effects of interferon-gamma and transforming growth factor-beta on adherence and survival of group B Streptococcus type III strains in ECV304 cells. 1257 48

Chlamydia trachomatis is a pathogen of the genital tract and ocular epithelium. Infection is established by the binding of the metabolically inert elementary body (EB) to epithelial cells. These are taken up by endocytosis into a membrane-bound vesicle termed an inclusion. The inclusion avoids fusion with host lysosomes, and the EBs differentiate into the metabolically active reticulate body (RB), which replicates by binary fission within the protected environment of the inclusion. During the extracellular EB stage of the C. trachomatis life cycle, antibody present in genital tract or ocular secretions can inhibit infection both in vivo and in tissue culture. The RB, residing within the intracellular inclusion, is not accessible to antibody, and resolution of infection at this stage requires a cell-mediated immune response mediated by gamma interferon-secreting Th1 cells. Thus, an ideal vaccine to protect against C. trachomatis genital tract infection should induce both antibody (immunoglobulin A [IgA] and IgG) responses in mucosal secretions to prevent infection by chlamydial EB and a strong Th1 response to limit ascending infection to the uterus and fallopian tubes. In the present study we show that transcutaneous immunization with major outer membrane protein (MOMP) in combination with both cholera toxin and CpG oligodeoxynucleotides elicits MOMP-specific IgG and IgA in vaginal and uterine lavage fluid, MOMP-specific IgG in serum, and gamma interferon-secreting T cells in reproductive tract-draining caudal and lumbar lymph nodes. This immunization protocol resulted in enhanced clearance of C. muridarum (C. trachomatis, mouse pneumonitis strain) following intravaginal challenge of BALB/c mice.
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PMID:Transcutaneous immunization with combined cholera toxin and CpG adjuvant protects against Chlamydia muridarum genital tract infection. 1474 49

A Chlamydophila abortus-induced abortion model was carried out on the basis of the experimental infection of ewes at day 75 of gestation. The infection induced abortions and the birth of weak lambs during the last 3 weeks of pregnancy. To study the kinetics of the infection in the placenta and in other organs, infected ewes were killed at 105, 120, and 130 days of gestation and also several days after abortion or parturition. Infected ewes developed a systemic infection that caused a mild and transient pneumonia and focal hepatitis. Pathologic changes were observed in placentas at 120 day of gestation, although the lesions varied between animals and even between placentomes of the same placenta. The first placental area infected was the maternal stroma and epithelium next to the intercaruncular areas, where neutrophilic response seemed to control the infection. A substantial degree of multiplication of C. abortus was then observed in the trophoblast cells of the placentome, periplacentomal choriallantoic membranes, and hilius, with an inflammatory exudate composed mainly of neutrophils, some macrophages, and very scarce lymphocytes. After abortion, the lesions affected the intercotyledonary areas of the aborted placentas, whereas in the uterus significant lymphocyte infiltration was observed, together with a rapid decrease of the C. abortus antigen in the degenerated caruncular tissues.
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PMID:Kinetics of infection and effects on the placenta of Chlamydophila abortus in experimentally infected pregnant ewes. 1534 22

Numerous bacteria, including Chlamydophila pecorum and Chlamydophila pneumoniae, are known to occur in diseased sites in koalas. In the present study the significance of such organisms was investigated by demonstrating their distribution in situ, in tissues collected opportunistically from wild koalas. Chlamydiaceae were demonstrated in epithelial cells and macrophages in association with pyogranulomatous pyelonephritis (8/11 kidneys), focal interstitial nephritis (3/21), and active inflammation and fibrosis of the entire upper female reproductive tract (10/10). In one case of pyelonephritis, Gram-positive cocci were also demonstrated in association with Chlamydiaceae and, in another, haematogenous filamentous bacteria appeared to be the sole aetiological agent. Three cases of chlamydial metritis were also superficially co-infected by a mixture of other bacteria. Chlamydiaceae were also demonstrated in pulmonary alveolar macrophages and epithelial cells in association with pneumonitis, and in hepatic and splenic macrophages in one koala. The study illustrated the prominent role of Chlamydiaceae in renal disease and disease of the uterus, uterine tube and ovarian bursa, with implications for pathogenesis and therapy. In addition, macrophages appeared to be a potential site of latent persistence from which systemic spread of infection might occur.
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PMID:Immuno-histochemical demonstration of the role of chlamydiaceae in renal, uterine and Salpingeal disease of the koala, and demonstration of chlamydiaceae in novel sites. 1604 22


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