Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The US guidelines for prevention and management of the difficult to diagnose symptomatic pelvic inflammatory disease (PID), which affects approximately 1 million every year, include microbial etiology and pathogenesis, the magnitude of the problem in terms of epidemiology and financial impact, risk assessment, prevention, diagnosis, treatment, and surveillance. The etiology of PID reveals multiple organisms, though mostly C. trachomatis and N. gonorrhoea. PID includes acute, silent, and atypical. C. trachomatis has been isolated in 20-40% of PID cases, while N. gonorrhoea in 27-80% of cervical cases. Other anaerobic bacteria isolated, which comprise 25-50% of acute cases, are Gardnerella vaginalis, Streptococcus species, Escherichia coli, and Hemophilus influenzae. PID results when organisms from the endocervix spread to the endometrium and fallopian tube mucosa. Contributing factors are IUD user's hormonal changes during menses (within 7 days of onset of menses), retrograde menses, and virulent characteristics of acute chlamydial and gonococcal PID. The estimated cost of PID for 1990 was $4.2 billion for 25 million in outpatient care and 275,000 hospitalized. Sexual practice related to the risk of PID are having sex with someone with STD, a young age at first intercourse, multiple sex partners, a high frequency of sexual intercourse and new partners within 30 days. Barrier methods (mechanical or chemical) decrease risk. Inconsistent risk is associated with oral contraceptive use and douching, but IUD's have an increased risk of adverse consequences and further transmission. Recommended action is community health promotion of education, as well as prompt and available clinical service, partner notification, training of health care providers, and routine screening. Individuals must self protect. Clinical diagnosis is difficult and imprecise. Minimum criteria for clinical diagnosis are lower abdominal pain, bilateral adnexal tenderness, cervical motion tenderness. Severe cases require oral temperature 38.3 Centigrade, abnormal cervical or vaginal discharge, elevated erythrocyte sedimentation rate and/or C-reactive protein, culture for N. gonorrhoea and non-cervical tests for C. trachomatis, and optionally endometrial biopsy, tubo-ovarian sonography, and laparoscopy. Failure to meet these criteria should not be withholding therapy. Sensitivity to the emotional needs and careful follow-up are necessary. Inpatient treatment recommendations are broad spectrum regimens such as: Cefoxitin plus doxycycline; for outpatients, cefoxitin plus doxycycline or tetracycline (erthyromycin may be substituted).
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PMID:Pelvic inflammatory disease: guidelines for prevention and management. 203 5

Following the attachment of gonococci to human fallopian tube mucosa in organ culture, the gonococci are endocytosed by specialized low columnar epithelial cells, are transported to the base of the epithelial cells, and are subsequently exocytosed into the subepithelial tissues. This transepithelial transport process by which "invasion" of the host occurs appears to be dependent on microbial factors is designated parasite-directed endocytosis to distinguish it from host-directed endocytosis by cells such as macrophages that eventually degrade the parasites. "Invasion" of the host by a number of human pathogens--bacteria (e.g., Neisseria meningitidis, Haemophilus influenzae, and Listeria monocytogenes), viruses, or protozoa--appears to be accomplished by parasite-directed endocytosis.
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PMID:Parasite-directed endocytosis. 314 16