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Children tuberculosis

Mendeleev was born in Tobolsk in western Siberia in 1834. His father was director of the local high school and the family lived comfortably. However, all that suddenly changed when Mendeleev was still a child. His father Ivan became blind from cataracts and had to resign his post. He went to Moscow to have them removed and had an operation that was a partial success. He could see again and recognize faces. However, he was still unable to read books and thus couldn t resume his career, and he did not live long after the operation. After his death, of tuberculosis, his widow got his pension, but the money was far from enough to support the family. [Pg.158]

Jouanguy, E., Lanhamedi-Cherradi, S., Altare, E, etal, Partial interferon-y receptor I deficiency in a child with tuberculoid bacillus Calmette-Guerin infection and a sibling with clinical tuberculosis. J. Clin. Invest. 100, 2658-2664 (1997). [Pg.265]

His parents, Ada and John H. Peat, lived at Bolden, County Durham, but Mrs. Peat was staying with her sister Alice in South Shields when their first child, Stanley, was born in 1902. John Peat was a mining engineer, but, despite his status, the family was rather poor and the care of the infant boy was handed over to his Aunt Alice and her husband, James Gibson, who were childless. Unfortunately, despite their care and attention, the child developed bovine tuberculosis when only a few months old, and had to receive hospital treatment for some time. Possibly as a result of this illness, the child was left with a permanent curvature of the spine. This disability was to have a profound effect on the development of Stanley Peat, since, denied an outlet for his energies in active sports and games, he was thrown back onto his mental resources for amusement and interest. [Pg.1]

Georg Friedrich Bernhard Riemann was the second of six children bom into the family of an impoverished Lutheran minister in lower Saxony, near modem Hannover, Germany. Riemann suffered from childhood malnutrition and was prone to excessive timidity, sickness, and nervous breakdowns throughout his difficult life, which ended in Italy while he was attempting recuperation from chronic tuberculosis (with a wife and young child at his side) at age 39. [Pg.428]

The tuberculous primary complex in the liver with caseation of the associated hepatic hilar lymph nodes may become the source of spread causing early systemic generalization. Given the clinical picture of a coarse-nodular or a miliary tuberculosis, this may result in the death of the newborn child. [Pg.476]

One girl in her third year, who had been immunized against tuberculosis at birth, developed an abscess of the associated lymph nodes (which were extirpated) and some weeks later developed intestinal BCG dissemination, which appeared to be cured by tuberculostatic treatment. Despite this, at the age of 22 years she developed a leftsided hemiplegia due to aneurysms and thrombosis of cerebral arteries, and 4 years later an oculomotor nerve paralysis was diagnosed. She died at 26 from recurrent intestinal BCG dissemination, which developed at the end of a pregnancy (a healthy premature child was bom). [Pg.402]

Another child who had been treated with valproate for several years was prescribed isoniazid for the treatment of tuberculosis. At the same time, seizures recurred, and the valproate was stopped and primidone 750 mg daily started. Seven months later seizures persisted, and she was admitted to hospital. Liver enzyme values were normal. Valproate 300 mg daily increased to 600 mg daily was added, and within 2 days she was vomiting and drowsy. After 5 days she had increased liver enzymes and her prothrombin time had fallen, so the valproate was stopped. Valproate levels were 81 micrograms/mL. It was speculated that the CNS effects and hepatic impairment were due to an interaction between the valproate and isoniazid. ... [Pg.578]

Liver In 1809 HIV-infected adults who took nevirapine-based antiretroviral drug therapy the cumulative proportion of early hepatotoxicity was 1.0-2.0%, an incidence rate of 3.6-7.6 per 100 person-years [94 ]. The median time to hepatotoxicity was 32 days. At 12 weeks, only 8% of patients had alanine aminotransferase monitoring at all the times recommended by national guidelines. There was no association between early hepatotoxicity and age, sex, baseline CD4 count, concurrent tuberculosis infection, prior participation in a prevention of mother-to-child-transmission program, or baseline weight. There was no association between early hepatotoxicity and mortality. [Pg.460]

Before vitamin D was discovered, a widely held concept was that rickets and infection were related. Children, with rickets as the manifestation of their vitamin D deficiency, suffered from the common infectious maladies of the late eighteenth, nineteenth, and early twentieth centuries, namely, tuberculosis, pneumonia, dysentery, and severe measles (Park 1923). The rachitic lung was listed as one of the clinical features of rickets (Khajavi and Amirhakimi 1977). In a severe form of rickets leading to inanition and death, children often succumbed to serious infections (Chesney 2010). Indeed, rickets was felt by many child health professionals to be the result of infection (Jenner 1895). [Pg.90]

Another area of infectious disease which has been virtually eliminated by first the sulphonamides then the antibiotics is child-bed fever which claimed many mothers. The death rate has dropped from about 600 a year in the late 1930s to only 2 in 1977. Similar salutary declines have been seen in the incidence of and death from respiratory tuberculosis, rheumatic fever, scarlet fever, syphilis and chronic rheumatic heart disease. [Pg.225]

In the most recent reauthorization of Public Law 94-142, the Individuals with Disabilities Education Act (idea), schools are mandated to provide children with chronic illness and other disabling conditions individualized educational and supportive services in the least restrictive educational setting. To qualify for special services under idea, a child must have a disability that is adversely affecting (his/her) educational performance. The disability category that usually applies to children with special health care needs is other health impaired. This classification is defined as having limited strength, vitality or alertness, due to chronic or acute health problems such as a heart condition, tuberculosis, rheumatic fever, nephritis, asthma, sickle cell anemia, hemophilia, epilepsy, lead poisoning, leukemia, or diabetes, which adversely affects a child s educational performance. ... [Pg.227]


See other pages where Children tuberculosis is mentioned: [Pg.61]    [Pg.157]    [Pg.6]    [Pg.4]    [Pg.731]    [Pg.1953]    [Pg.417]    [Pg.44]    [Pg.77]    [Pg.72]    [Pg.355]    [Pg.101]    [Pg.1181]    [Pg.225]    [Pg.121]   
See also in sourсe #XX -- [ Pg.2019 , Pg.2024 ]




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