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• W2025674013 abstract "A 16-year-old male was admitted with cough productive of blood-tinged sputum, vomiting, and urinary incontinence. During the prior 3 days, he had developed fatigue and epistaxis. He also complained of fever to 40°C, chills, myalgias, night sweats, worsening headache, abdominal pain, and a sore throat. The patient had been diagnosed with infectious mononucleosis 7 months earlier when he had had a sore throat, bilateral cervical lymphadenopathy, and subjective fever. These symptoms had resolved after 2 weeks. Then 4 months before admission, the patient had developed frontal headaches occurring twice weekly, a 40-pound weight loss, and progressively enlarging lymphadenopathy that initially involved the cervical region and progressed to multiple sites by the time of admission. The patient had not sought medical attention for these complaints. The patient was the product of a normal gestation and had no prior hospitalizations. His immunizations were complete for his age. He lived with his mother in an urban apartment and had traveled to a farm four months before admission where he had had limited contact with dogs, cats, cows, pigs, and chickens. He had been incarcerated for several hours one month before admission. He admitted to marijuana use and sexual activity. Upon admission the young man was alert, interactive and in no distress but had rigors. He had a temperature of 39.1°C, pulse of 110 beats/min, respiratory rate of 20 breaths/min, blood pressure of 129/67 mm Hg, and oxygen saturation of 97% in room air. His weight was 84 kg. Examination of his ears, eyes, nose and throat was normal. He had multiple palpable lymph nodes, ranging in size from 1 to 3 cm, located in the bilateral anterior cervical, submental, occipital, axillary, and inguinal regions. These were nonfluctuant, mobile, and had no associated warmth, erythema, or tenderness. Lung examination revealed tachypnea but clear breath sounds bilaterally and no retractions. The patient was tachycardic, but had good peripheral pulses and no cardiac murmur. Abdominal examination was significant for a liver edge that was palpable 4 cm below the right costal margin and a palpable splenic tip. The remainder of the physical examination, including complete neurologic assessment, was normal. The white blood cell (WBC) count was 20,700/mm3 with 59% neutrophils, 15% band forms, 17% lymphocytes, 7% monocytes, and 2% atypical lymphocytes. The hemoglobin was 12.3 g/dL, and platelet count was 192,000/mm3; peripheral smear showed no cellular atypia. Cerebrospinal fluid (CSF) analysis revealed 18 WBC/μL (97% lymphocytes, 3% monocytes), 1 red blood cell/μL, protein of 60 mg/dL, glucose of 61 mg/dL, and a negative Gram stained smear. A nasopharyngeal swab rapid assay for influenza was negative. Urine drug screen was positive for cannabinoids. Chest radiograph revealed an opacity in the retrocardiac space consistent with pneumonia. Computed tomography (CT) of the head showed no intracranial anomalies. CT of the chest, abdomen, and pelvis revealed mediastinal, hilar, and mesenteric adenopathy as well as hepatosplenomegaly without focal lesions. Vancomycin and cefotaxime therapy was initiated for pneumonia and the patient rapidly defervesced. Bacterial cultures of blood, urine, CSF, throat, and sputum, as well as viral cultures of the nasopharynx, CSF, and rectum, were negative. A tuberculin skin test had 0 mm of induration, and acid-fast stain of the sputum was negative. Bartonella, Brucella, Toxoplasma, Epstein-Barr virus (EBV), and cytomegalovirus (CMV) serologies were negative. Additional laboratory studies revealed the underlying diagnosis. Denouement The patient’s serum was positive for human immunodeficiency virus (HIV) antibody by enzyme-linked immunosorbent assay (ELISA) and Western blot. HIV viral load was 139,000 copies/mL, and CD4+ lymphocyte count was 289/mm3. The patient was diagnosed with underlying HIV infection and superimposed bacterial pneumonia. After initiation of antibiotic therapy for bacterial pneumonia, his respiratory symptoms rapidly improved and fever resolved. Because his CD4 count was <350/mm3 and his HIV viral load was high, HAART was initiated with a nucleoside analog, a protease inhibitor, and a non-nucleoside reverse transcription inhibitor. Further questioning of the patient revealed that he was bisexual, had 5 previous sexual partners, and had unprotected sex with males. At the time of his diagnosis with infectious mononucleosis 7 months prior to admission, he had been screened for HIV and had been seronegative at that time. That illness likely represented unrecognized acute HIV infection, defined as the presence of HIV RNA by polymerase chain reaction (PCR) in the setting of a negative or indeterminate HIV antibody test.1 Approximately 1.1 million persons in the United States currently are living with HIV infection. More than 150,000 persons were diagnosed between 2001 and 2004, and 2.8% of new infections occurred in adolescents 13–19 years old.2 High-risk groups include Hispanics, African-Americans, and women. Currently, the 15–44 year-old age demographic has the most rapidly accelerating rate of HIV seroconversion. Recent data on HIV prevalence among men who have sex with men demonstrated that approximately 25% were infected with HIV, and 48% were unaware of their status. Both infection and unrecognized infection were highest among non-Hispanic blacks.3 Approximately 40–90% of new HIV infections are associated with systemic symptoms classified as acute HIV infection. This entity was first described in 1985 as an infectious mononucleosis-like illness seen in association with inversion of CD4:CD8 ratios.4 Symptoms of acute HIV infection usually occur 7 to 14 days after infection.1 The most common signs and symptoms are summarized in the table and include fever, malaise, and rash. Duration of acute illness usually is less than 2 weeks; however, symptoms lasting up to 10 weeks have been described in the literature.1 Laboratory anomalies may include lymphopenia or thrombocytopenia, but no laboratory findings are pathognomonic for acute HIV infection.TABLE 1: Frequency of Signs and Symptoms Associated With Acute HIV InfectionThe differential diagnosis of acute HIV infection includes a number of infectious diseases, including EBV, CMV, roseola, and various viral forms of hepatitis. Brucella, Bartonella, and Mycobacteria species can cause nonspecific febrile illnesses and lymphadenopathy similar to HIV. Parasitic pathogens to consider in the differential diagnosis include toxoplasmosis and malaria; spirochetes, particularly syphilis, also can mimic the protean manifestations of acute HIV infection. Noninfectious etiologies such as lymphoma, leukemia, and systemic lupus erythematosus also should be considered. Since any influenza-like illness can present like acute HIV infection, the diagnosis requires a high degree of clinical suspicion. During acute HIV infection, viral loads greater than 1,000,000 copies/ml are not uncommon, and HIV antibody testing by ELISA is generally negative. ELISAs and other serologic assays typically become positive 3–4 weeks after infection; however, seroconversion can take months to occur. In this window period after infection but before seroconversion, the diagnosis of acute HIV infection requires HIV RNA PCR or p24 antigen detection testing, both of which can be positive one to 2 weeks after infection.1 Some states have begun to screen for HIV with nucleic acid amplification assays in addition to standard ELISAs in an attempt to diagnose persons who present during acute HIV infection. Investigators from North Carolina demonstrated that of 109,000 patients screened over a 1-year period, 583 were HIV-positive by ELISA and subsequent Western blot, but another 23 (3.8% of all HIV-positive patients) were positive by PCR assay and seronegative.6 Because these patients with acute HIV are highly viremic, they are at much greater risk of transmitting the virus. Thus their unrecognized infection represents a missed opportunity to prevent horizontal and vertical transmission. Current guidelines on the use of antiretroviral therapy in HIV-infected adults and adolescents recommend initiation of HAART in any patient with an AIDS-defining illness and asymptomatic patients with CD4 counts <200/mm3. Treatment should be offered to patients with CD4 between 200 and 350/ mm3 regardless of viral load. In patients with a CD4 counts >350/mm3 and viral load >100,000 copies/ml, many clinicians would defer therapy but some would initiate treatment.7,8 Unfortunately, data on the long-term benefit of initiation of HAART during acute HIV infection are limited. A recent study9 compared patients treated with HAART within 2 weeks (acute) and 2 weeks to 6 months after seroconversion (early) with those who had declined therapy. The treatment groups received HAART for at least 12 weeks, but then stopped treatment of at least 4 weeks. In the “acute” treatment group, viral load and CD4 count benefits were seen up to 6 months after termination of therapy with a trend towards longer-term benefit. Among patients with “early” treatment, CD4 counts remained improved up to 18 months post-therapy but viral load benefit was lost by this point. Until more definitive information is available, treatment of acute HIV infection is considered optional, and the decision must balance the theoretical benefits against the potential risks.8 It has now been a quarter century since HIV/AIDS was first described in the United States and one decade since the advent of HAART. Over this period, significant strides have been made in the diagnosis and management of HIV infection. Prognosis now is excellent for patients who remain compliant with HAART. While new diagnoses of HIV infection have decreased in the United States during the last decade, incidence rates continue to increase in certain demographics, including adolescents and men who have sex with men.2,3 As such, acute HIV infection should remain on the differential diagnosis of fever and lymphadenopathy, especially in those patients with high-risk social histories. Timely diagnosis can have profound ramifications not only in terms of that individual’s health but also in terms of limiting further transmission of the virus." @default.
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• W2025674013 title "An Adolescent with Fever, Cough, & Diffuse Lymphadenopathy" @default.
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• W2025674013 doi "https://doi.org/10.1097/01.inf.0000256756.70575.4d" @default.
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