Treatment of active disease is of special concern if there is antiretroviral naivete. In these circumstances, beginning concomitant therapy with antituberculosis and antiretroviral therapy can cause the immune reconstitution inlammatory syndrome IRIS) with toxic drug efects (Lai, 2016; Torok, 2011). hat said, recent studies support earlier administration of highly active antiretroviral therapy (HAART)-within 2 to 4 weeksafter beginning antituberculosis therapy (Blanc, 2011; Havlir, 2011; Karim, 2011). lso, for HIV-infected women, rifampin or rifabutin use may be contraindicated if certain protease inhibitors or nonnucleoside reverse transcriptase inhibitors are being administered. If there is resistance to rifabutin or rifampin, then pyrazinamide therapy is given. Of the secondline regimens, the aminoglycosides-streptomycin, kanamycin, amikacin, and capreomycin-are ototoxic to the fetus and are contraindicated (Briggs, 2015).
Neonatal Tuberculosis. Tubercular bacillemia can infect the placenta, but the fetus infrequently becomes infected-con genital tuberculosis. The term also applies to newborns who are infected by aspiration of infected secretions at delivery. Each route of infection constitutes approximately half of the cases.
manifests with hepatosplenomegaly, respiratory distress, fever, and lymphadenopathy (Dewan, 2014; Osowicki, 2016).
Cantwell and associates (1994) reviewed 29 cases of congenital tuberculosis reported since 1980. Only 12 of the mothers had active infection, and tuberculosis was frequently demonstrated by postpartum endometrial biopsy. Adhikari and colleagues (1997) described 11 South African postpartum women whose endometrial biopsy was culture-positive. Six of their neonates had congenital tuberculosis.
Neonatal infection is unlikely if the mother with active disease has been treated before delivery or if her sputum culture is negative. Because the newborn is susceptible to tuberculosis, most experts recommend isolation from the mother suspected of having active disease. If untreated, the risk of disease in the infant born to a woman with active infection is 50 percent in the irst year Qacobs, 1988).
his is a chronic, multisystem inflammatory disease of unknown etiology characterized by an accumulation of T-helper lymphocytes and phagocytes within noncaseating granulomas (Baughman, 2015; Celada, 2015). Predisposition to the disease is genetically determined and characterized by an exaggerated response of helper T lymphocytes to environmental triggers. Pulmonary involvement is most common, followed by skin, eyes, lymph nodes, and then all other organ systems. The prevalence of sarcoid in the United States is 20 to 60 per 100,000, with equal sex distribution. It is more than 10 times more common for blacks than for whites (Baughman, 2015). Most patients are between 20 and 40 years. Clinical presentation varies, but more than half of patients have dyspnea and a dry cough without constitutional symptoms that develop insidiously over months. Disease onset is abrupt in approximately 25 percent of patients, and 10 to 20 percent are asymptomatic at discovery.