Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subfecundity is caused by disease and nutrition as well as by genetic, environmental, and psychological components. Sexually transmitted diseases (STDs) are caused by 21 different pathogens of which syphilis, gonorrhea, and chlamydia are the most important. Syphilis is caused by the bacterium Treponema pallidum with incidence of 10% in Thailand. 20% in Papua New Guinea, and 40% in Ethiopia. Stillbirths in infected mothers range from 66% to 80%. Gonorrhea is caused by the bacterium Neisseria gonorrhoea and its incidence was 18% in female patients in Ugandan clinic. 20% of women in Africa with cervical gonorrhea develop salpingitis. The risk of pelvic inflammatory disease is several times higher in IUD users. The bacterium Chlamydia trachomatis caused infertility in 15.4% of men in a 1991 study. Herpes simplex virus 2 infects 15-30% of sexually active adults, and the chance of fetal transmission is 40% when maternal lesions are present. Diseases other than STDs include tuberculosis (TB) whose development is aided by conditions such as malnutrition, malaria, leprosy, syphilis, and African sleeping sickness. Genital TB causes a 5-50% rate of menstrual disorders including amenorrhea and a 55-85% rate of sterility in women. Malaria is caused by Plasmodium protozoa, and the feverish state included by it can lead to oligospermia. Severe malarial anemia can lead to fetal and maternal mortality. The protozoa Trypanosoma causes African sleeping sickness that produces azoospermia and impairs the pituitary gland and ovaries. Schistosomiasis (bilharzia) and filariasis have less direct effect on fecundity but they negatively impact nutritional status. Maternal nutrition substantially impacts fetal and infant survival. During the Dutch famine of 1944-45 there was a 50% decrease in births 9 months subsequently. A 10-15% weight loss results in amenorrhea.
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PMID:Endemic disease, nutrition and fertility in developing countries. 163 64

Different proposals have been offered to explain the polymorphism of the sickle cell hemoglobin gene. One of these proposals (Eaton and Mucha 1971) suggested that differential fertility of male subjects with the sickle cell trait contributes to the persistence and stability of the sickle cell gene frequency. Eaton and Mucha claimed that oligospermia, induced by hyperpyrexia, is a less common problem in these subjects because they probably have milder and shorter episodes of fever from malaria infection than subjects with a normal genotype. We have looked for evidence to support this hypothesis by comparing the testicular function, testicular size, and serum concentrations of the reproductive hormones in adult male subjects with the sickle cell trait and in an age-matched group of subjects with normal hemoglobin genotype. The mean serum concentration of testosterone, luteinizing hormone, follicle-stimulating hormone, and prolactin of both groups, measured by radio-immunoassay, were not statistically different from each other. Also, there was no detectable difference in any of the common indexes of semen quality between the two groups. The testicular volume index and several anthropometric indexes of subjects with the sickle cell trait and subjects with the normal hemoglobin genotype were also statistically similar. The results suggest that gonadal function is similar in adult males with the normal genotype and those with the sickle cell trait. Any increase in fertility observed in the latter group is probably due to extragonadal factors.
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PMID:Is there increased fertility in adult males with the sickle cell trait? 875 61