Infants can acquire HIV infection via the transplacental route or, more commonly, during delivery; high maternal viral load is the most important risk factor in transmission.
Infants have high baseline levels of CD4 cells due to amplified thymic activity in the months after birth. Therefore, they frequently develop immunocompromise from HIV at relatively high CD4 counts (eg, 1,000-1,200/mm3); in contrast, in adults, PJP is most common with CD4 counts <200/mm3.
| Risk factors | • High maternal viral load (eg, insufficient prenatal care, lack of antiretroviral therapy) • Breastfeeding by infected mother | | --- | --- | | Clinical features | • Failure to thrive • Chronic diarrhea • Lymphadenopathy, hepatosplenomegaly • Pneumocystis pneumonia • Prolonged/refractory candidiasis | | Diagnosis | • HIV DNA or RNA PCR | | Treatment | • Combination antiretroviral therapy |
Prenatal screening and maternal antiretroviral therapy markedly reduce infection rates, but infant HIV infection can still occur (eg, mothers infected late in pregnancy or with insufficient prenatal care) and is typically confirmed by DNA or RNA PCR testing (antibody testing is not performed at age <18 months as maternal antibodies may cause false positives).
Ddx includes→ Suspected conditions include combined T- and B-cell syndromes (eg, severe combined immunodeficiency disorder [SCID]) or T-cell–specific disorders, such as HIV infection. In the setting of generalized lymphadenopathy, this patient's findings are most consistent with HIV infection. HIV replication occurs mostly in CD4+ T cells, resulting in decreased CD4+ T cells; however, because B cell and CD8+ T cell production persists, total absolute lymphocyte count is often normal. Therefore, lymph node enlargement commonly occurs as the immune system responds to high viral loads. In contrast, patients with SCID (eg, adenosine deaminase deficiency) typically have profound lymphopenia and the absence of lymphoid tissue
In children with HIV, PJP is often the initial AIDS-defining illness, and it usually presents at age 3-6 months. Common manifestations include low-grade fever, tachypnea, poor feeding, and progressive dyspnea. Generalized adenopathy and hepatomegaly are often present. Patients often have severe hypoxia, and chest x-ray classically shows bilateral perihilar reticulonodular infiltrates that become more diffuse as the illness progresses. Because the pathogen cannot be cultured, the diagnosis is established when the yeast-like organism is identified in pulmonary fluid (eg, induced sputum, bronchiolar lavage).
First-line treatment is trimethoprim-sulfamethoxazole; to reduce the risk for respiratory decompensation, a short course of corticosteroids is concurrently administered in those with a PaO2 <70 mm Hg or an alveolar-arterial gradient of >35 mm Hg. Following resolution, PJP prophylaxis is required until CD4 counts improve past age-related risk levels (eg, >1,500/mm3for patients age 1-11 months vs ≥200/mm3 [for ≥3 months] in adults). Antiretroviral therapy should be initiated within a few weeks.