Sir, Esophageal candidiasis and immunodeficiency associated with acute HIV infection

Cilla, Gustavo; E, Pérez Trallero; Furundarena,; Cuadrado, Emilio; Ja, Iribarren; Neira, Fernando Córdova

doi:10.1097/00002030-198810000-00013

Cited by 20 publications

(7 citation statements)

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“…It was considered to be of fungal origin and resolved rapidly following appropriate therapy. Several case reports and one series report [30,[42][43][44][45][46][47][48][49] have described this condition in the setting of primary HIV infection and have suggested that severe transient immunosuppression could be a determinant factor [13,46,48]. Some patients with ulcerative esophagitis [49] could be secondarily colonized by Candida organisms after antibiotic therapy; in addition, the direct role of HIV and of other viruses in this condition cannot be excluded [47].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Symptomatic Primary Infection Due to Human Immunodeficiency Virus Type 1: Review of 31 Cases

Loés

Saussure

Saurat

et al. 1993

Clinical Infectious Diseases

141

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In this series of 31 patients with acute infection due to human immunodeficiency virus (HIV) type 1, the male-to-female ratio was 3.4:1 and the mean age was 31.3 years. Sexual transmission accounted for 83.9% of cases; 45.2% of the patients were homosexual and 38.7% were heterosexual. The mean duration of symptoms and signs was 21 days (range, 5-60 days). Fever (87.1%) and skin rash (67.7%) were most commonly reported. Physical examination findings were abnormal for 96% of the patients; the oral cavity (76.7%) and the skin (73.3%) were the most frequently involved sites. Thirteen of 25 patients with sexually acquired infection had genital or oral ulcers, whereas five intravenous drug users had none (P = .052). Thrombocytopenia was the most common hematologic abnormality and was detected in 17 of 23 patients tested. P24 antigenemia, an initially negative screening test for HIV antibody, and a low CD4+ lymphocyte count were noted in 23 of 29, 23 of 30, and 14 of 21 tested patients, respectively.

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Section: Discussionmentioning

confidence: 99%

“…The diagnostic value of such an analysis remains low, but its use at least once during the acute stage can explain some of the unusual clinical presentations associated with severe immunosuppression, such as candidal esophagitis [42][43][44][45][46][47][48][49].…”

Section: Discussionmentioning

confidence: 99%

Symptomatic Primary Infection Due to Human Immunodeficiency Virus Type 1: Review of 31 Cases

Loés

Saussure

Saurat

et al. 1993

Clinical Infectious Diseases

141

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“…OPC and esophageal candidiasis can occur at any time during the course of HIV infection, including primary HIV infection (82,330), the chronic asymptomatic phase and overt AIDS (1,80,152,177,237,277,285,329,366,389). During the chronic asymptomatic phase, both erythematous and pseudomembranous candidiases are predictive of progressive immunodeficiency and onset of AIDS, independently of the CD4 ϩ cell count (129,224,230,311).…”

Section: Correlation With Progression Of Hiv Infectionmentioning

confidence: 99%

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

2004

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Oropharyngeal and esophageal candidiases remain significant causes of morbidity in human immunodeficiency virus (HIV)-infected patients, despite the dramatic ability of antiretroviral therapy to reconstitute immunity. Notable advances have been achieved in understanding, at the molecular level, the relationships between the progression of HIV infection, the acquisition, maintenance, and clonality of oral candidal populations, and the emergence of antifungal resistance. However, the critical immunological defects which are responsible for the onset and maintenance of mucosal candidiasis in patients with HIV infection have not been elucidated. The devastating impact of HIV infection on mucosal Langerhans' cell and CD4+ cell populations is most probably central to the pathogenesis of mucosal candidiasis in HIV-infected patients. However, these defects may be partly compensated by preserved host defense mechanisms (calprotectin, keratinocytes, CD8+ T cells, and phagocytes) which, individually or together, may limit Candida albicans proliferation to the superficial mucosa. The availability of CD4C/HIV transgenic mice expressing HIV-1 in immune cells has provided the opportunity to devise a novel model of mucosal candidiasis that closely mimics the clinical and pathological features of candidal infection in human HIV infection. These transgenic mice allow, for the first time, a precise cause-and-effect analysis of the immunopathogenesis of mucosal candidiasis in HIV infection under controlled conditions in a small laboratory animal

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“…Opportunistic infections traditionally attributed to advanced immunosuppression in late-stage HIV such as Pneumocystis jirovicii pneumonia and esophageal candidiasis can be seen during acute HIV infection, as with our patient, although this is less common. 8,9 The presence of any such opportunistic infection in the absence of a clear reason for immunosuppression warrants consideration for HIV testing. 10 Standard enzyme-linked immunoassays to detect the presence of anti-HIV antibodies are the most commonly used screening tests, with high sensitivity (> 99.5%) but a substantial rate of false-positive results.…”

Section: Acute Hiv Infectionmentioning

confidence: 99%

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confidence: 99%

Severe transient neutropenia with fever and abdominal pain in a 30-year-old man

Hudgins

Wong

2013

CMAJ

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A 30-year-old man presented to the emergency department with a 3-day history of fever, chills, nausea, vomiting, diarrhea and abdominal pain. The patient's symptoms had progressed rapidly until he had a productive cough with yellow sputum, which led him to visit the emergency department.The patient's medical history included hepatitis C, asthma and cholecystectomy. Results of serologic testing for HIV 4 months earlier had been negative. The patient was taking ipratropium and salbutamol. In addition, he stated that he regularly used both cocaine and morphine intravenously.On physical examination, the patient appeared unwell. Although he was drowsy, he was easily arousable. His temperature was 38.7°C, with a blood pressure of 70/44 mm Hg and a pulse of 93 beats/min. He did not have any rashes, and his oropharynx was unremarkable. He had no cervical, axillary or inguinal lymphadenopathy. His chest examination was unremarkable, except for a mild inspiratory wheeze. The patient's heart sounds were normal, with no additional sounds or murmurs. His abdomen was diffusely tender to palpation, but there was no rebound tenderness or guarding, nor was there evidence of hep at o splen o megaly or palpable masses. His right knee showed signs of recent trauma.The results of initial laboratory investigations showed a leukocyte count of 0.7 (normal 4.0-11.0) × 10 9 /µL and a neutrophil count of 0.4 (normal 2.0-7.5) × 10 9 /µL. Liver enzyme testing showed an alanine aminotransferase concentration of 48 (normal 4-55) U/L and an aspartate aminotransferase concentration of 179 (normal 5-35) U/L. We admitted the patient to hospital, where he received piperacillin-tazobactam for febrile neutropenia; however, his neutropenia spontane ously remitted the following day. His condition responded quickly to aggressive supportive measures, including fluids delivered intravenously. After 1 day, the patient's leukocyte count had risen to 20.7 × 10 9 /µL, and his neutrophil count was 19.1 × 10 9 /µL. Cultures of blood drawn before antibiotics were administered grew Bacillus cereus in 1 of 2 vials after 16 hours, prompting us to add vancomycin to the drug regimen, pending susceptibility testing. Chest radiography showed patchy airspace disease in the lower lobe of the patient's left lung. A computed tomography scan of the abdomen and pelvis showed a normal liver and biliary tree, diverticulosis without diverticulitis, a trace right pleural effusion and a trace amount of free pelvic fluid. What is your differential diagnosis?a. Mononucleosis secondary to Epstein-Barr virus (EBV) or cytomegalovirus (CMV) b. Acute hepatitis A infection c. Acute HIV infection d. Levamisole toxicity secondary to adulterated cocaine e. Endocarditis secondary to B. cereusWe thought that an infectious agent was the most likely explanation for our patient's unusual symptoms, specifically (c) HIV or (d) B. cereus. Given the unusual presentation of his condition, however, we ordered serologic tests for EBV and CMV, which were negative. Although the results of serologic test...

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Sir, Esophageal candidiasis and immunodeficiency associated with acute HIV infection

Cited by 20 publications

References 0 publications

Symptomatic Primary Infection Due to Human Immunodeficiency Virus Type 1: Review of 31 Cases

Symptomatic Primary Infection Due to Human Immunodeficiency Virus Type 1: Review of 31 Cases

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

Severe transient neutropenia with fever and abdominal pain in a 30-year-old man

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