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(See also Human Immunodeficiency Virus (HIV).)

Human immunodeficiency virus infection (HIV) is caused by the retrovirus HIV-1 (and less commonly by the related retrovirus HIV-2). Infection leads to progressive immunologic deterioration and opportunistic infections and malignancies; the end stage is acquired immunodeficiency syndrome (AIDS). Diagnosis is by viral antibodies in children > 18 mo and viral PCR assay in those < 18 mo. Treatment is with combinations of antiretroviral agents.

The general natural history and pathophysiology of pediatric HIV infection is similar to that in adults; however, the method of infection, clinical presentations, and treatments often differ. HIV-infected children also have unique social integration issues ( see Sidebar 1: Infections in Infants and Children: Integration of HIV-Infected Children).

Sidebar 1
Integration of HIV-Infected Children Infection in a child affects the entire family. Serologic testing of siblings and parents is recommended. The physician must provide education and ongoing counseling. The infected child should be taught good hygiene and behavior to reduce risk to others. How much he is told about the illness depends on age and maturity. Older children and adolescents should be made aware of their diagnosis and the possibility of sexual transmission and counseled appropriately. Families may be unwilling to share the diagnosis with people outside the immediate family because it can create social isolation. Feelings of guilt are common. Family members, including children, can become clinically depressed and require counseling. Because HIV infection is not acquired through the typical types of contact that occur among children, eg, through saliva or tears, most HIV-infected children should be allowed to attend school without restrictions. Similarly, there are no inherent reasons to restrict foster care, adoptive placement, or childcare of HIV-infected children. Conditions that may pose an increased risk to others (eg, aggressive biting or the presence of exudative, weeping skin lesions that cannot be covered) may require special precautions. The number of school personnel aware of the child's condition should be kept to the minimum needed to ensure proper care. The family has the right to inform the school, but people involved in the care and education of an infected child must respect the child's right to privacy. Disclosures of information should be only with the informed consent of the parents or legal guardians and age-appropriate assent of the child.

Epidemiology

In the US, HIV probably occurred in children almost as early as in adults but was not clinically recognized for several years. Thus far, > 9300 cases have been reported in children and adolescents, representing only 1% of total cases.

More than 90% of US children acquired the infection from their mother, either before or around the time of birth (vertical transmission). Most of the remainder (including patients with hemophilia or other coagulation disorders) received contaminated blood or blood products. A few cases have resulted from sexual abuse. Fewer than 5% of cases have no clear source. Vertical transmission now accounts for almost all new cases in US preadolescents.

Worldwide, about 2.5 million children are alive with HIV infection (8% of the total caseload worldwide), and about 700,000 more children are infected each year (16% of all new infections). In sub-Saharan Africa, where the epidemic has been present longest, some prenatal clinics report that 25 to 40% of all women of childbearing age are seropositive for HIV. HIV infection is rapidly increasing in India, China, Southeast Asia, and some areas of Eastern Europe and Russia. About 500,000 children die of HIV infection worldwide each year.

Transmission: Infection risk for an infant born to an HIV-positive mother who did not receive antiretroviral therapy during pregnancy is estimated at 13 to 39%. Risk is greatest for infants born to mothers who seroconvert during pregnancy and for those with advanced disease, low peripheral CD4⁺ T-lymphocyte counts, prolonged rupture of membranes, and high viral concentrations as evidenced by HIV p24 antigenemia, quantitative viral culture, or RNA concentration. In vaginal deliveries, a 1st-born twin is at greater risk than a 2nd-born twin, although this relationship may not hold true in developing countries.

Cesarean section may reduce the risk of transmission from mother to child. However, it is clear that mother-to-child transmission (MTCT) can be reduced significantly by giving antiretroviral therapy (including zidovudine Some Trade Names
RETROVIR
Click for Drug Monograph
[ZDV, AZT]) to the mother and neonate (see Infections in Infants and Children: Prevention). ZDV monotherapy reduces MTCT to about 8%; with current highly active antiretroviral therapy (HAART) regimens, the US MTCT rate is < 2%.

HIV has been detected in both the cellular and cell-free fractions of human breast milk. The incidence of transmission by breastfeeding is about 6/100 breastfed children/yr. Estimates of the overall risk of transmission through breastfeeding are 12 to 14%, reflecting varying durations of breastfeeding. Transmission by breastfeeding appears to be greatest in mothers with high plasma viral concentrations.

Acquisition of HIV during adolescence significantly contributes to the large number of cases in young adults. Routes of transmission in adolescents are similar to those for adults (see Human Immunodeficiency Virus (HIV): Transmission), mostly unprotected sexual contact, and less commonly, injection drug use.

Classification: HIV infection causes a broad spectrum of disease, of which AIDS is the most severe. Epidemiologic classification schemes established by the Centers for Disease Control and Prevention (CDC) define the progression of clinical and immunologic decline. In children < 13 yr, clinical categories N, A, B, and C (defined by presence or absence of certain common opportunistic infections or malignancies) denote asymptomatic and mildly, moderately, and severely symptomatic HIV infection, respectively (see Table 1: Infections in Infants and Children: Clinical Categories for Children Aged < 13 Yr with HIV Infection* ). Similarly, mild, moderate, and severe immunocompromise is denoted as category 1, 2, or 3, respectively; these are defined by age-specific CD4⁺ T-lymphocyte counts (see Table 2: Infections in Infants and Children: Immunologic Categories for Children < 13 Yr with HIV Infection). Thus, a child classified in stage B3 would have moderately advanced clinical symptoms and severe immunocompromise.

Table 1
Clinical Categories for Children Aged < 13 Yr with HIV Infection*  This table is presented as a PDF and requires the free Adobe PDF reader. Get Adobe Reader

Table 2
Immunologic Categories for Children < 13 Yr with HIV Infection Immunologic Categories Age-Specific CD4+ T-Lymphocyte Counts and As Percentages of Total Lymphocyte Counts < 12 mo 1–5 yr 6–12 yr cells/μl % cells/μl % cells/μl % 1: No evidence of suppression ≥ 1500 ≥ 25 ≥ 1000 ≥ 25 ≥ 500 ≥ 25 2: Evidence of moderate suppression 750–1499 15–24 500–999 15–24 200–499 15–24 3: Severe suppression < 750 < 15 < 500 < 15 < 200 < 15 Adapted from Centers for Disease Control and Prevention. 1994 Revised classification system for HIV infection in children less than 13 years of age; official authorized addenda: HIV infection codes and official guidelines for coding and reporting ICD-9-CM. MMWR 1994: 43 (No. RR-12), pp. 1–19.

Symptoms and Signs

Infants infected perinatally usually are asymptomatic during the 1st few months of life. Although the median age at symptom onset is about 3 yr, some children remain asymptomatic for > 5 yr and, with appropriate antiretroviral (ARV) therapy, are expected to survive to adulthood. In the pre-ARV era, about 10 to 15% of children had rapid disease progression, with symptoms occurring in the 1st year of life and death occurring by 18 to 36 mo; these children were thought to have acquired HIV infection earlier in utero. Most children, however, probably acquire infection at or near birth and have slower disease progression (surviving beyond 5 yr even before ARV therapy was routinely used).

The most common manifestations of HIV infection in children include generalized lymphadenopathy, hepatomegaly, splenomegaly, failure to thrive, oral candidiasis, CNS disease (including developmental delay, which can be progressive), lymphoid interstitial pneumonitis, recurrent bacteremia, opportunistic infections, recurrent diarrhea, parotitis, cardiomyopathy, hepatitis, nephropathy, and malignancies.

Complications: Pneumocystis jiroveci (formerly P. carinii) pneumonia is the most common, serious, opportunistic infection in HIV-infected children and has high mortality. Pneumocystis pneumonia can occur as early as age 4 to 6 wk but occurs mostly in infants between age 3 and 6 mo who acquired infection before or at birth. Infants and children with Pneumocystis pneumonia characteristically develop a subacute, diffuse pneumonitis with dyspnea at rest, tachypnea, O₂ desaturation, nonproductive cough, and fever (in contrast to non–HIV-infected immunocompromised children and adults, in whom onset is often more acute and fulminant).

Other common opportunistic infections include Candida esophagitis, disseminated cytomegalovirus infection, and chronic or disseminated herpes simplex and varicella-zoster virus infections and, less commonly, Mycobacterium tuberculosis and Mycobacterium avium complex infections, chronic enteritis caused by Cryptosporidium or other organisms, and disseminated or CNS cryptococcal or Toxoplasma gondii infection.

Malignancies in immunocompromised children with HIV infection are relatively uncommon, but leiomyosarcomas and certain lymphomas, including CNS lymphomas and non-Hodgkin B-cell lymphomas (Burkitt's type), occur much more often than in immunocompetent children. Kaposi's sarcoma is very rare in HIV-infected children.

Diagnosis

HIV-specific tests: In children > 18 mo, diagnosis is made using serum antibody tests (enzyme immunoassay [EIA] and confirmatory Western blot) as in adults. Only very rarely will an older HIV-infected child lack HIV antibody because of significant hypogammaglobulinemia.

Children < 18 mo retain maternal antibody, causing false-positive results on EIA, so diagnosis is made by HIV DNA PCR, which can diagnose about 30% of cases at birth and nearly 100% by 4 to 6 mo of age. HIV viral culture has acceptable sensitivity and specificity but is technically more demanding and hazardous and has been replaced by DNA PCR in most laboratories. HIV RNA PCR (the “viral load” assay used for monitoring efficacy of treatment) is probably as sensitive as DNA PCR in infants not exposed to ARV therapy. However, because of possible insensitivity in the presence of ARV therapy and possible nonspecificity of lower RNA concentrations, HIV RNA PCR is not recommended for diagnosis in infants. The modified p24 antigen assay is less sensitive than HIV DNA PCR and culture and should be used only if the latter are unavailable.

An initial DNA PCR test should be performed within the 1st 2 wk of life, at about 1 mo of age, and between 4 and 6 mo. A positive test should be confirmed immediately using the same or another test (eg, culture). If the serial DNA PCR tests are all negative, the child is considered uninfected with > 95% accuracy (in the absence of any AIDS-defining illness). Follow-up antibody tests (one EIA at > 18 mo or, alternatively, 2 EIAs performed between 6 and 18 mo) are obtained to exclude HIV infection and confirm seroreversion (loss of passively acquired HIV antibodies). If an infant < 18 mo with a positive antibody test but negative virologic tests develops an AIDS-defining illness (category C—see Table 1: Infections in Infants and Children: Clinical Categories for Children Aged < 13 Yr with HIV Infection* ), HIV infection is diagnosed.

Newly available rapid tests for HIV antibody are derivatives of EIA assays that provide results within minutes to hours. They can be performed as point-of-care tests on oral secretions, whole blood, or serum. In the US, these tests are perhaps most useful in labor and delivery suites to test women of unknown HIV serostatus, thus allowing counseling, commencement of ARV therapy to prevent MTCT, and testing of the infant to be arranged during the birth visit. Similar advantages accrue in other episodic care settings (eg, emergency departments, sexually transmitted disease clinics) and in the developing world. Rapid assays require confirmatory tests, such as western blot testing. If expected HIV prevalence is low, even a specific rapid assay will yield mostly false positives (low positive predictive value by Bayes' theorem—(see Clinical Decision Making: Bayes' Theorem). However, if the expected probability of HIV (or seroprevalence) is high, the positive predictive value increases.

Before HIV testing of a child is performed, the mother or primary caregiver (and the child, if old enough) should be counseled about the possible psychosocial risks and benefits of testing. Written or oral consent should be obtained and recorded in the patient's chart, consistent with state, local, and hospital laws and regulations. Counseling and consent requirements should not deter testing if it is medically indicated; refusal of a patient or guardian to give consent does not relieve physicians of their professional and legal responsibilities, and sometimes authorization for testing must be obtained by other means (eg, court order). Test results should be discussed in person with the family, the primary caregiver, and, if old enough, the child; if the child is HIV-positive, appropriate counseling and subsequent follow-up care must be provided. In all cases, maintaining confidentiality is essential.

Children and adolescents meeting the criteria for AIDS must be reported to the appropriate public health department. In many states, HIV infection (before the development of AIDS) also must be reported.

Other tests: Infected children require T-helper CD4⁺ and T-suppressor CD8⁺ lymphocyte counts and measurement of plasma viral RNA concentration (viral load) to help determine degree of illness and prognosis. CD4⁺ counts may be normal (eg, above the age-specific cutoffs of category 1 in Table 2: Infections in Infants and Children: Immunologic Categories for Children < 13 Yr with HIV Infection) initially but fall eventually. CD8⁺ counts usually increase initially and do not fall until late in the infection. These changes in cell populations result in a decrease in the CD4⁺:CD8⁺ cell ratio, a characteristic of HIV infection (although sometimes occurring in other infections). Plasma viral RNA concentrations in untreated children < 12 mo are typically very high (mean, about 200,000 RNA copies/mL). By 24 mo, viral concentrations in untreated children decrease (to a mean of about 40,000 RNA copies/mL). Although the wide range of HIV RNA concentrations in children make the data less predictive of morbidity and mortality than in adults, determining plasma viral concentrations in conjunction with CD4⁺ counts still yields more accurate prognostic information than does determining either marker alone. Less expensive alternative surrogate markers such as total lymphocyte counts and serum albumin levels may also predict AIDS mortality in children, which may be useful in developing nations.

Although not routinely measured, serum immunoglobulin concentrations, particularly IgG and IgA, often are markedly elevated, but occasional children develop panhypogammaglobulinemia. Patients may be anergic to skin test antigens.

Prognosis

With appropriate HAART regimens, most perinatally infected children survive well beyond 5 yr. About 10 to 15% of untreated children from industrialized countries die before 4 yr, most of these before 18 mo of age. In developing countries, pediatric AIDS mortality is much greater during the 1st few years of life.

Opportunistic infections, particularly Pneumocystis pneumonia, progressive neurologic disease, and severe wasting, are associated with a poor prognosis; with Pneumocystis pneumonia, mortality ranges from 5 to 40% if treated and is almost 100% if untreated. Prognosis is also poor for those in whom virus is detected early (ie, by 7 days of life) or symptoms develop in the 1st year of life. However, since the advent of HAART and P. jiroveci antimicrobial prophylaxis (see Infections in Infants and Children: Prevention of opportunistic infections), the incidence of opportunistic infections and malignancies has dramatically decreased in children with good treatment adherence. Adolescents who acquire HIV infection have a slower progression of disease, similar to that of adults.

Treatment

There are nearly 2 dozen ARV drugs (see Table 3: Infections in Infants and Children: Dosage and Administration of Antiretroviral Drugs for Children* ), including multidrug combination products, available in the US, each of which may have adverse effects and drug interactions with other ARV drugs or commonly used antibiotics, anticonvulsants, and sedatives. New ARV drugs, immunomodulators, and vaccines are under evaluation.

Table 3
Dosage and Administration of Antiretroviral Drugs for Children*  This table is presented as a PDF and requires the free Adobe PDF reader. Get Adobe Reader

Standard treatment is with HAART, which uses combinations of drugs to maximize viral suppression and minimize selection of drug-resistant strains. Most commonly, HAART consists of a “backbone” of 2 nucleoside analog reverse transcriptase inhibitors (ZDV plus didanosine Some Trade Names
VIDEX
Click for Drug Monograph
, ZDV plus lamivudine Some Trade Names
EPIVIR
Click for Drug Monograph
, or stavudine Some Trade Names
ZERIT
Click for Drug Monograph
plus lamivudine Some Trade Names
EPIVIR
Click for Drug Monograph
) given in combination with either a protease inhibitor ( nelfinavir Some Trade Names
VIRACEPT
Click for Drug Monograph
, lopinavir/ ritonavir Some Trade Names
NORVIR
Click for Drug Monograph
, or others) or a non-nucleoside reverse transcriptase inhibitor ( nevirapine Some Trade Names
VIRAMUNE
Click for Drug Monograph
or efavirenz Some Trade Names
SUSTIVA
Click for Drug Monograph
). Other combinations (eg, ZDV, lamivudine Some Trade Names
EPIVIR
Click for Drug Monograph
, and abacavir Some Trade Names
ZIAGEN
Click for Drug Monograph
; dual protease inhibitor regimens; tenofovir Some Trade Names
VIREAD
Click for Drug Monograph
-containing regimens) are used, but fewer data are available to support their use as 1st-line regimens. Monotherapy or dual nucleoside reverse transcriptase inhibitor therapy alone (except for ZDV chemoprophylaxis in HIV-exposed infants) is discouraged. Because expert opinions on therapeutic strategies change rapidly, consultation with specialists is strongly advised. Continually updated clinical practice guidelines are available at several web sites, the most useful among them being www.aidsinfo.nih.gov, www.hivguidelines.org, and www.unaids.org.

Therapy will be successful only if the family and child are able to adhere to a possibly complex medical regimen. Nonadherence not only leads to failure to control HIV, but also selects drug-resistant HIV strains, which reduces future therapeutic choices. Barriers to adherence should be addressed before initiation of therapy. These include availability and palatability of pills or suspensions; drug interactions with current therapy; pharmacokinetic factors such as need to administer some drugs with food or in the fasted state; the fact that children depend on others to administer drugs (and HIV-infected parents may have problems with remembering their own drugs); and for adolescents, denial or fear of their infection, distrust of the medical establishment, and lack of family support.

Indications: Initiation of ARV therapy depends on virologic, immunologic, and clinical criteria; authorities differ on these. The goal is to suppress HIV replication (as measured by plasma HIV RNA PCR viral load) and maintain or achieve age-normal CD4⁺ counts and percentages.

ARV therapy is recommended for all children > 12 mo of age with severe clinical or immunologic disease (clinical category C or immunologic category 3—see Table 1: Infections in Infants and Children: Clinical Categories for Children Aged < 13 Yr with HIV Infection*  and Table 2: Infections in Infants and Children: Immunologic Categories for Children < 13 Yr with HIV Infection), regardless of the plasma HIV RNA viral load. Therapy is considered for mildly to moderately symptomatic children > 12 mo of age (clinical categories A or B, or immunologic category 2) and those who have plasma HIV RNA viral loads of > 100,000 copies/mL. Some experts use lower thresholds (eg, > 50,000 HIV RNA viral copies/mL or CD4⁺ percentage of 15 to 20%). Children with no evidence of clinical disease or immunosuppression (category N1) may be followed closely without ARV therapy if their plasma HIV RNA is < 50,000 to 100,000 copies/mL.

Therapy should be given to all clinically symptomatic or immunosuppressed children < 12 mo of age (clinical categories A, B, C or immunologic categories 2 or 3) regardless of plasma HIV RNA viral load. Many experts treat asymptomatic infants < 12 mo (category N1) because HIV infection tends to progress rapidly in the 1st year of life.

Monitoring: Clinical and laboratory monitoring are important for identifying drug toxicity and therapeutic failure. Physical examination and monitoring of CBC, HIV RNA viral load, and lymphocyte subsets should be done q 3 to 4 mo; serum chemistry values, including liver enzymes, lipid profiles, and amylase and lipase levels, should be monitored once/yr to twice/yr at minimum.

Vaccination in symptomatic HIV infection: In general, live-virus (eg, oral poliovirus, varicella) vaccines and live-bacterial (eg, BCG) vaccines should not be given to children with AIDS or other manifestations of advanced HIV infection indicative of immunosuppression. An exception is measles-mumps-rubella vaccine in patients who are not severely immunocompromised (ie, not in category 3); this vaccine should be given at age 12 mo to enhance the likelihood of an immune response, ie, before the immune system deteriorates, if possible. The 2nd dose may be administered as soon as 4 wk later to attempt to induce seroconversion as early as possible. If the risk of exposure to measles is increased, such as during an outbreak, the vaccine should be given at an earlier age, such as at 6 to 9 mo.

Other childhood vaccines, eg, diphtheria and tetanus toxoids combined with acellular pertussis vaccine (DTaP), hepatitis B, Haemophilus influenzae type b and Streptococcus pneumoniae conjugates, and inactivated poliovirus (IPV), are given according to the usual immunization schedule (see Fig. 3: Approach to the Care of Normal Infants and Children: Recommended childhood and adolescence immunization schedule.). Pneumococcal polysaccharide vaccine at 2 yr and annual inactivated influenza vaccination beginning at age 6 mo also are recommended.

Because children with symptomatic HIV infection generally have poor immunologic responses to vaccines, when they are exposed to a vaccine-preventable disease such as measles or tetanus, they should be considered susceptible, regardless of the history of vaccination. Therefore, if indicated, they should receive passive immunization with immune globulin. Immune globulin also should be given to any nonimmunized household member who is exposed to measles.

Vaccination in asymptomatic HIV infection: Such children should receive DTaP, IPV, H. influenzae type b and S. pneumoniae conjugates, hepatitis B, and measles-mumps-rubella vaccines, according to the usual immunization schedules. Although oral poliovirus vaccine (OPV) has been given to these patients without adverse effects, the live polioviruses in OPV can be excreted and transmitted to immunosuppressed contacts, creating an increased risk for paralytic poliomyelitis caused by vaccine virus infection (this is no longer a consideration in areas such as the US in which only IPV is used).

Varicella vaccine is safe and recommended in patients with early HIV infection (categories N1 or A1). Because HIV-infected children ≥ 2 yr are at increased risk of invasive pneumococcal infection, they should receive pneumococcal polysaccharide vaccination at age 2 yr (in addition to the infant series of pneumococcal conjugate vaccination). Revaccination once after 3 to 5 yr is recommended. Inactivated influenza vaccination should be administered annually for HIV-infected children ≥ 6 mo of age.

In the US and in areas of low TB prevalence, BCG vaccine is not recommended. However, in developing countries where TB prevalence is high, the WHO recommends that BCG be given to all infants at birth if they are asymptomatic, regardless of maternal HIV infection. Some cases of disseminated BCG infection in severely immunocompromised AIDS patients have been reported.

Passive immunization after exposure to measles, tetanus, and varicella is advisable.

Vaccination for seronegative children living with a patient with symptomatic HIV infection: Such children, as well as seropositive ones, should receive IPV vaccine rather than OPV. Measles-mumps-rubella vaccine may be given because these vaccine viruses are not transmitted. To reduce the risk of transmission of influenza to patients with symptomatic HIV infection, annual influenza vaccination (inactivated or live) is indicated for household contacts.

Varicella vaccination of seronegative siblings and susceptible adult caregivers of HIV-infected children is strongly encouraged to prevent acquisition of the wild-type varicella-zoster infection, which can cause severe disease in immunocompromised hosts; however, person-to-person transmission of the varicella vaccine virus does occur rarely.

Prevention

For postexposure prevention, see Human Immunodeficiency Virus (HIV): Postexposure prophylaxis (PEP).

Prevention of perinatal transmission: Appropriate prenatal ARV therapy attempts to optimize maternal health, interrupt MTCT, and minimize in utero drug toxicity. In the US and countries where ARV agents are available and the infrastructure for HIV diagnostic testing exists, treatment with ARV drugs is standard for all HIV-infected pregnant women (see also Human Immunodeficiency Virus (HIV): Prevention of transmission). In HIV-infected women not previously receiving ARV agents who do not meet adult criteria for HAART, ZDV is administered orally 300 mg bid beginning at 14 to 34 wk gestation and is continued throughout pregnancy and is given IV during labor 2 mg/kg for the 1st hour and then 1 mg/kg/h until delivery. ZDV 2 mg/kg po qid is administered to the neonate for the 1st 6 wk of life. Women whose clinical or immunologic status does not meet treatment criteria for HAART are nevertheless recommended to initiate HAART if the viral load is > 1000 copies/mL. In the immediate postpartum period, a decision can be made whether to continue maternal therapy. Women whose clinical or immunologic status meets treatment criteria (see Human Immunodeficiency Virus (HIV): Prognosis) are given a multiple-drug regimen, preferably including ZDV.

Pregnancy is not a contraindication to HAART regimens, although the pregnant woman and her health care provider should discuss the possible benefits and risks of such therapy and the absence of definitive safety data. ZDV monotherapy reduces MTCT from 25% to 8%; many ARV combinations are also effective. With current HAART regimens, the US MTCT rate is < 2%. Thus, although the final decision to accept ARV therapy remains with the pregnant woman, it should be stressed that the proven benefits of therapy appear to outweigh the theoretical risks of fetal toxicity.

Most experts believe that HIV-infected women already receiving combination ARV therapy who become pregnant should continue that therapy, even during the 1st trimester; an alternative is to stop all therapy until the beginning of the 2nd trimester and resume at that time.

To reduce MTCT from HIV-infected pregnant women who are in labor but have had no prior therapy (or even for neonates delivered to untreated HIV-infected women), clinicians have used both ARV combinations and cesarean delivery. Rapid HIV testing of pregnant women who present in labor without documentation of their HIV serostatus may allow immediate institution of such measures. An expert in pediatric or maternal HIV infection should be immediately consulted in this situation.

Breastfeeding (or donating to milk banks) should be strongly discouraged in HIV-infected women in countries where safe and affordable alternative sources of feeding are readily available. However, in countries where infectious diseases and malnutrition are important causes of early childhood mortality and safe, affordable infant formula is not available, the protection from mortality risks of respiratory and GI infections afforded by breastfeeding may counterbalance the risk of HIV transmission. In these developing countries, the WHO recommends that mothers continue to breastfeed.

Prevention of adolescent transmission: Because adolescents are at special risk for HIV infection, they should receive education, have access to HIV testing, and know their serostatus. Education should include information about transmission, implications of infection, and strategies for prevention, including abstaining from high-risk behaviors and engaging in safe sex practices (correct and consistent use of condoms) for those who are sexually active.

Efforts should be targeted at adolescents at high risk of HIV infection. Informed consent is necessary for testing and the release of information regarding serostatus. Decisions regarding disclosure of HIV status to a sex partner without the patient's consent should be based on the likelihood that the partner is at risk, whether the partner has reasonable cause to suspect the risk and to take precautions, whether there is a legal requirement to withhold or disclose such information, and the possible effects of such disclosure on future relationships.

Prevention of opportunistic infections: Prophylaxis against Pneumocystis pneumonia is indicated for HIV-infected children with significant immunocompromise (ie, immunologic category 3). Generally, chemoprophylaxis is continued for life, although older adolescents and children on HAART with immune reconstitution (ie, immune category 1 or 2 for several months) may be able to stop prophylaxis as long as they remain in category 1 or 2. At present, lifelong chemoprophylaxis, regardless of the CD4⁺ count, is recommended for those surviving an episode of Pneumocystis pneumonia. Pneumocystis prophylaxis also is recommended for all HIV-exposed infants born to HIV-infected women beginning at 4 to 6 wk of age. Prophylaxis may be stopped when HIV has been reasonably excluded by serial HIV PCR or culture. The drug of choice is trimethoprim-sulfamethoxazole Some Trade Names

(TMP-SMX) 75 mg TMP/375 mg SMX/m² po bid on 3 consecutive days/wk (eg, Monday-Tuesday-Wednesday); alternative schedules include the same total dose once/day for 3 days/wk, or bid every day of the week or on alternate days. For patients ≥ 5 yr who cannot tolerate TMP-SMX, aerosolized pentamidine Some Trade Names
NEBUPENT
PENTAM 300
Click for Drug Monograph
(300 mg via specially designed inhaler) may be given once/mo. IV pentamidine Some Trade Names
NEBUPENT
PENTAM 300
Click for Drug Monograph
has also been used but appears to be less effective and potentially more toxic. Another alternative, especially for those < 5 yr, is daily oral dapsone Some Trade Names
ACZONE
Click for Drug Monograph
(2 mg/kg, not to exceed 100 mg). Other drugs that may be useful include pyrimethamine Some Trade Names
DARAPRIM
Click for Drug Monograph
with dapsone Some Trade Names
ACZONE
Click for Drug Monograph
, pyrimethamine Some Trade Names
DARAPRIM
Click for Drug Monograph
-sulfadoxine, and oral atovaquone Some Trade Names
MEPRON
Click for Drug Monograph
. However, experience with these drugs is very limited, and they should be considered only when the recommended regimens are not tolerated or cannot be used.

For prophylaxis against Mycobacterium avium complex infections in children ≥ 6 yr with CD4⁺ counts < 50/μL (or children 2 to 6 yr with CD4⁺ counts < 75/μL, 1 to 2 yr < 500/μL, or < 1 yr < 750/μL), weekly azithromycin Some Trade Names
ZITHROMAX
Click for Drug Monograph
or daily clarithromycin Some Trade Names
BIAXIN
Click for Drug Monograph
is the drug of choice, and daily rifabutin Some Trade Names
MYCOBUTIN
Click for Drug Monograph
is an alternative. Data are limited on the use of prophylaxis for other opportunistic infections, such as cytomegalovirus, fungal disease, and toxoplasmic encephalitis.

Last full review/revision November 2005

Content last modified November 2005