An 8-month-old previously healthy Hispanic female was in her usual state of health until 3 weeks before admission, when she presented to a community health clinic with irritability, dry cough, decreased oral intake, decreased urine output, and fever. She was diagnosed with acute otitis media and received 10 days of amoxicillin-clavulanic acid and 3 days of azithromycin. The fever persisted despite antibiotic therapy, ranging from 38°C to 39.4°C, and she developed a maculopapular rash on her head, face, trunk, and extremities 5 days before admission. One day before admission, she presented to a local hospital with persistent fever and morbilliform rash. She received ceftriaxone, prednisone, and diphenhydramine and was transferred to our hospital for suspected measles. The child's mother denied any vomiting, diarrhea, recent travel, or exposure to sick contacts. Immunizations were not up to date due to a brief febrile illness at the last scheduled 6-month checkup at the community health clinic. The child lived with 6 other persons, and there were no pets in the household. Her father had been deported to his country of origin, Honduras, 5 months earlier. On initial examination, the patient had a temperature of 39.1°C, pulse of 182 beats/min, respiratory rate of 20 breaths/min, and blood pressure of 120/84 mm Hg. Her weight was 7.7 kg (25th percentile); height, 66.6 cm (20th percentile); and head circumference, 41 cm (<5th percentile). She was awake but very irritable. The oropharynx was clear, with moist mucous membranes and crusting of the lips and nares. The conjunctivae were injected bilaterally. The neck was supple with bilateral anterior and posterior cervical lymphadenopathy. Lymph nodes were mobile, nontender, without overlying erythema, and measured approximately 1 cm in diameter. The abdominal examination was significant for massive hepatosplenomegaly with a liver edge palpable 6 cm below the right costal margin and spleen palpable 8 cm below the left costal margin. The skin showed an erythematous, nonblanching maculopapular rash on the face, neck, upper thorax, and upper and lower extremities, with sparing of the palms and soles. The white blood cell count was 12,000/mm3 with a differential of 8% neutrophils, 2% bands, 77% lymphocytes, 4% monocytes, 3% eosinophils, 3% metamyelocytes, and 3% atypical lymphocytes. The hemoglobin and hematocrit were 10.1 g/dL and 29.4%, respectively, and the platelet count was 204,000/mm3. Coagulation studies were normal. The C-reactive protein was 3.5 mg/dL. There was no laboratory evidence of renal or hepatic dysfunction. Cytomegalovirus serologies and Epstein-Barr virus (EBV) viral capsid antigen IgG were negative but the EBV viral capsid antigen IgM was positive, consistent with a probable acute EBV infection. The EBV early antigen and nuclear antibody assays were not performed, and no plasma EBV polymerase chain reaction was obtained. The measles IgG antibody was positive but the IgM was negative. A chest radiograph was normal without any evidence of mediastinal lymphadenopathy. Further maternal history and an additional laboratory test revealed the child's primary diagnosis. Denouement On further questioning, the mother revealed that she had been diagnosed with HIV infection and had an HIV viral load of 22,500 copies/mL during her third trimester of pregnancy. She had been treated with highly active antiretroviral therapy of zidovudine-lamivudine and lopinavir-ritonavir, but had not taken the medications consistently and had not revealed her diagnosis to her child's community clinic physicians. The child had born at full term via planned cesarean section, and the mother had received intrapartum prophylaxis with intravenous zidovudine (azidothymidine [AZT]). The baby was exclusively formula fed. The baby's initial HIV DNA PCR assay performed at 34 hours of life was indeterminate. AZT was prescribed, but the child did not complete the recommended 6-week course. She did not have a regular primary care physician and had received her primary immunizations at a local community health center where medical personnel were unaware of her perinatal HIV exposure. On admission to our institution, the child's HIV-1 DNA PCR was positive with an HIV RNA viral load of 2,389,087 copies/mL. The HIV-2 DNA PCR was negative. The initial CD4 count was 1800/mm3 and CD4% was 20%. The child was treated with a highly active antiretroviral therapy regimen of lamivudine, AZT, and, lopinavir-ritonavir along with trimethoprim-sulfamethoxazole for Pneumocystis jiroveci (carinii) prophylaxis. However, she did not tolerate lopinavir-ritonavir, and this was replaced with nevirapine. HIV genotyping displayed no resistance to the nucleoside analog reverse transcriptase inhibitor, nonnucleoside reverse transcriptase inhibitor, or protease inhibitor classes of antiretroviral agents. Three months after presentation, the child's HIV viral load was 76 copies/mL and CD4 count was 1871/mm3 (CD4% of 45%). She is presently followed at the Children and Youth Ambulatory Services Clinic and the infectious diseases clinic at Georgetown University Hospital. Growth and development are normal for age, her viral load is presently undetectable, and her last CD4 count was 2183/mm3 (CD4% of 32.1%). This case of perinatally acquired HIV infection in a child born to a Hispanic woman raises several interesting clinical points and serves to highlight troubling issues about the ongoing HIV epidemic in Washington, DC. The initial clinical presentation upon referral to our institution was consistent with acute Epstein-Barr virus (EBV) infection, although the extent of the splenomegaly and lymphadenopathy was likely better explained by the child's underlying HIV infection. In addition, the morbilliform rash could have been due to HIV infection, acute EBV infection, or EBV infection combined with the use of amoxicillin. The most frequent findings of perinatally acquired HIV infection include diffuse lymphadenopathy, hepatoplenomegaly, failure to thrive, chronic diarrhea, and a history of recurrent bacterial infections (eg, skin/soft-tissue infections and pneumonias). Laboratory findings may include an absolute lymphopenia, anemia, thrombocytopenia, and an elevation of liver transaminases. An important factor in this case was the indeterminate initial HIV test result and the lack of appropriate follow-up evaluations, considering that this infant was known at the time of birth to be at high risk for perinatally acquired HIV. Infants born to HIV-positive mothers have positive enzyme-linked immunosorbent assay and Western Blot results due to passive transfer of maternal antibodies, which can persist up to 18 months of age. Therefore, confirmation of perinatally acquired HIV infection requires virus-specific testing. Our patient's indeterminate HIV DNA PCR should have triggered more frequent clinic visits and prompt follow-up testing by an HIV DNA or RNA PCR. HIV virologic testing by HIV DNA or RNA PCR assays are recommended in infants born to HIV-positive mothers at 14 to 21 days, 1 to 2 months, and 4 to 6 months. HIV infection in the newborn can be ruled out definitively if there are ≥2 negative virologic tests, with one test at >1 month of age and the other at ≥4 months of age, or if there are 2 negative antibody tests, both performed at >6 months of age.1 The World Health Organization estimated that in 2006 between 410,000 and 660,000 infants were newly infected with HIV worldwide, whereas in 2007 between 2.2 and 2.6 million children younger than 15 years were living with HIV/AIDS, with greater than 90% living in sub-Saharan Africa.2 In the United States, the decrease in maternal-to-child transmission is a significant achievement in the fight against HIV. The number of perinatal HIV infections peaked in the United States at 1650 in 1991 and declined to a range of 144 to 236 by 2002.3 In 1994, the Pediatric AIDS Clinical Trials Group published recommendations for the use of AZT prophylaxis to reduce maternal-to-child transmission of HIV4 and in 2001, the Centers for Disease Control and Prevention (CDC) recommended routine HIV screening early in pregnancy for all pregnant women. These interventions led to a decline in the rate of vertical transmission from 1995 to 2005, with 142 children (<13 years) diagnosed with perinatal HIV/AIDS in the United States in 2005.3 The CDC has estimated that greater than 1 million adolescents and adults were living with HIV in the United States in 2006, with men who have sex with men, blacks/African Americans, and Hispanics/Latinos disproportionately affected.3,5,6 HIV has remained a primarily urban disease, and Washington, DC has one of the highest rates of HIV/AIDS in the United States, with 164 new cases per 100,000 reported in 2004.6 Through December 31, 2008, the District of Columbia Department of Health (DCDOH) reported 16,513 DC residents were living with HIV/AIDS, or 3.2% of the population over the age of 12 years.6 Black/African Americans accounted for 52.2% of DC residents over 12 years but constituted 75.6% of DC residents living with HIV/AIDS, with 4.7% of the district's black population infected.6 Blacks/African Americans make up 12% of the US population yet account for nearly half of new HIV infections, whereas Hispanics/Latinos account for 15% of the US population and 17% of new infections.5 From 1983 to 2008, DCDOH received reports of 349 pediatric cases of HIV/AIDS (<13 years), with 331 (94.8%) cases in Blacks/African Americans and 9 (2.6%) in Hispanics/Latinos. Perinatal transmission accounted for 90.8% of these infections, with all cases from 2006 to 2008 occurring in mother-child pairs who had not received appropriate antiretroviral prophylaxis. In 2006, DCDOH engaged in multiple efforts to implement the new CDC HIV testing recommendations, including routine voluntary opt-out HIV testing for all persons 12 to 64 years of age and new education and social marketing efforts with local health care providers.6 DCDOH also changed its system of reporting HIV and AIDS cases from code-based reporting in 2001 to a confidential integrated name-based reporting system in 2006. After instituting these changes, the rate of newly diagnosed HIV/AIDS cases decreased from 164 cases per 100,000 in 2004 to 137 per 100,000 in 2007, to 102.8 per 100,000 in 2008.6,7 Washington, DC still suffers from a higher incidence of HIV infection than several African countries, including Ethiopia, Nigeria, and Rwanda.8 DCDOH reported in 2009 an HIV case rate nearly 10 times the US rate and higher than comparable cities such as Baltimore, Chicago, Detroit, New York City, and Philadelphia.6,7 A retrospective, observational cohort analysis from the Children's National Medical Center of new pediatric HIV cases (<13 years) diagnosed from 2000 to 2005 reported that 28 (33.3%) of 84 cases were children born to immigrant mothers.9 Children born to mothers of African origin constituted the largest proportion of new HIV cases in DC. In all, 25 mothers (29.7%) were from African countries, with only 3 (3.6%) from Latin-American countries. The age of diagnosis was significantly later for infants born to immigrant mothers despite similarly low rates of antiretroviral prophylaxis among immigrant mothers and mothers of US origin. At Georgetown University Hospital, 37 HIV-positive patients are currently followed by the pediatric infectious diseases service through a multidisciplinary team approach including an HIV medical social worker and adolescent medicine specialists. Of the 37 patients, 34 were perinatally infected and 3 acquired HIV by sexual behavior. Their ages range from 22 months to 24 years, 4 months (average, 12.8 years). Of 37 patients, 23 (62.2%) are females, 23 (62.2%) are African Americans, 11 (29.7%) are of African descent, and 3 (8.1%) are Hispanic/Latino. African countries represented include Ethiopia, Uganda, Kenya, Zambia, and Malawi. The patient described in this report is the first newborn with newly diagnosed perinatal HIV followed at Georgetown in more than 5 years and highlights the continued importance of HIV screening in pregnant women and appropriate follow-up of HIV-exposed neonates. We believe pediatricians play a vital role in the prevention of perinatal HIV transmission by identifying newborns born to infected mothers, by verifying receipt of maternal antiretroviral prophylaxis, by ensuring at-risk infants receive prophylactic AZT, and by scheduling appropriate follow-up to confirm or exclude the diagnosis of HIV infection in early infancy. ACKNOWLEDGMENTS The authors thank Charlotte Barbey-Morel, MD, and Janet Osherow, MSW, for their care of this patient and for their review of this manuscript.