The Need for Specific Prevention and Treatment Guidelines for Children
Mother-to-child transmission is an important mode of acquisition of HIV infection and of OIs in children. HIV-infected women coinfected with opportunistic pathogens may be more likely than HIV-uninfected women to vertically transmit these infections to their infants. For example, higher rates of perinatal transmission of hepatitis C and cytomegalovirus have been reported from HIV-infected than from HIV-uninfected women.[7,8] In addition, HIV-infected women or HIV-infected family members coinfected with certain opportunistic pathogens may be more likely to transmit these infections horizontally to their children, increasing the likelihood of primary acquisition of such infections in young children. For example, Mycobacterium tuberculosis infection in children primarily reflects acquisition from family members who have active tuberculosis (TB) disease, and increased incidence and prevalence of TB among HIV-infected individuals are well documented. HIV-exposed or -infected children in the United States may have a higher risk of exposure to M. tuberculosis than would comparably aged children in the general US population because of residence in households with HIV-infected adults. Furthermore, HIV-infected women may have reduced transplacental transfer of antibodies that protect their infants against serious bacterial infections than women without HIV infection. Therefore, these guidelines for treatment and prevention of OIs consider both HIV-infected and HIV-uninfected children born to HIV-infected women.
The natural history of OIs in children may differ from that in HIV-infected adults. Many OIs in adults are secondary to reactivation of opportunistic pathogens, which often were acquired before HIV infection when host immunity was intact. However, OIs in HIV-infected children more often reflect primary infection with the pathogen. In addition, among children with perinatal HIV infection, the primary infection with the opportunistic pathogen occurs after HIV infection is established, at a time when the child's immune system may be compromised already. This can lead to different manifestations of specific OIs in children than in adults. For example, young children with TB are more likely than adults to have extrapulmonary and disseminated infection, even without concurrent HIV infection.
Data related to the efficacy of various therapies for OIs in adults are often extrapolated to children, but issues related to drug pharmacokinetics, formulation, ease of administration and dosing and toxicity require special considerations for children. Young children, in particular, metabolize drugs differently from adults and older children, and the volume of distribution differs. Unfortunately, data often are lacking on appropriate drug dosing recommendations for children aged <2 years.
Pediatr Infect Dis J. 2013;32(12):1303-1307. © 2013 Lippincott Williams & Wilkins