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1/17. coinfection of visceral leishmaniasis and Mycobacterium in a patient with acquired immunodeficiency syndrome.

    We report a case of coinfection of visceral leishmaniasis and mycobacterium avium-intracellulare in the same lesions in the small bowel and bone marrow of a 33-year-old man with acquired immunodeficiency syndrome who complained of abdominal pain and chronic diarrhea. The duodenal mucosa and bone marrow biopsy specimens showed numerous foamy macrophages packed with two forms of microorganisms that were identified histologically and ultrastructurally as Leishmania and Mycobacterium species. Visceral leishmaniasis is rarely suspected in patients residing in nonendemic countries including the united states. It should be included in the differential diagnosis for opportunistic infection in patients with acquired immunodeficiency syndrome. An appropriate travel history is important. To our knowledge, this is the first reported case showing coinfection of visceral leishmaniasis and mycobacterium avium-intracelluulare in the same lesion in a patient with acquired immunodeficiency syndrome.
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2/17. Penile intraepithelial neoplasia overlying Kaposi's sarcoma lesions: role of viral synergy?

    Several viral agents have been detected in the lesional tissue of Kaposi's sarcoma (KS). Their precise oncogenic role remains to be determined. A 32-year-old heterosexual man with acquired immunodeficiency syndrome (AIDS) who had penile lesions of KS with overlying epithelial changes characteristic of intraepithelial neoplasia associated with concurrent infection by human papillomavirus (HPV) and human herpesvirus 8 (HHV-8) is reported. The absence of viral dna from uninvolved skin suggests that this coinfection is more than coincidental and may involve synergy between these viruses, as has already been suggested for HPV and herpes simplex 2 virus.
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3/17. Long-term non-progression of hiv-1 in a patient coinfected with HTLV-II.

    A 37-year-old man coinfected with hiv-1 and human T-lymphotropic virus type II presumably through injection drug use had a high CD4 count and low HIV viral load without anti-retroviral therapy for over six years. As an HIV long-term non-progressor, his case supports the hypothesis that coinfection with HTLV-II does not adversely affect the course of HIV disease.
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4/17. Posterior segment manifestations of active ocular syphilis, their response to a neurosyphilis regimen of penicillin therapy, and the influence of human immunodeficiency virus status on response.

    OBJECTIVE: To determine the relative frequencies of signs in posterior segment ocular syphilis, the response to a neurosyphilis regimen of penicillin, and differences in findings between human immunodeficiency virus (HIV)-coinfected and -noncoinfected patients in a community setting. DESIGN: Retrospective, noncomparative, consecutive case series. PARTICIPANTS: Fourteen consecutive patients with posterior segment ocular syphilis over a 14-year period within or during the acquired immune deficiency syndrome era. INTERVENTION: neurosyphilis intravenous penicillin regimen. MAIN OUTCOME MEASURES: Initial and final visual acuity; treponemal and nontreponemal serologic analyses; cerebrospinal fluid cell count, protein, and Venereal disease research Laboratory analyses; posterior segment signs; and relapses and recurrences. RESULTS: Blacks and males were predominantly affected. Five (36%) of patients were HIV coinfected, and ocular syphilis led to the HIV infection diagnosis in three. Four (29%) patients had received previous antibiotic therapy for primary or secondary syphilis, raising the suspicion of relapse. Two patients had negative nontreponemal serologic results. All patients responded rapidly to neurosyphilis therapy. One patient subsequently relapsed after neurosyphilis therapy, and a second was reinfected with recurrence of ocular involvement. One previously undescribed retinal manifestation was discovered: a sectorial retinochoroiditis with delayed retinal circulation in the involved area. CONCLUSIONS: Ocular syphilis is a form of neurosyphilis and requires neurosyphilis therapy regardless of when it develops after primary infection. Conventional syphilis staging is of little use in understanding ocular syphilis. A high suspicion for this diagnosis is appropriate, especially in poorer black males with posterior segment inflammatory disease. Human immunodeficiency virus coinfection with ocular syphilis is common, but does not affect response to a neurosyphilis regimen of penicillin in the short term. awareness of the multiple presentations of posterior segment ocular syphilis will aid ophthalmologists in averting misdiagnosis or delayed diagnosis.
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5/17. Fatal pneumonia in an AIDS patient coinfected with adenovirus and pneumocystis carinii.

    BACKGROUND: Adenovirus infections are common in immunocompromised hosts. However, pulmonary adenovirus infections rarely cause significant morbidity in HIV-infected patients. PATIENT: Here we describe a 27-year-old man with AIDS who presented with tachypnea, hypoxemia and an infiltrate in the upper left lobe on chest X-ray. bronchoscopy was performed and pneumocystis carinii was detected in bronchoalveolar lavage (BAL) fluid. Treatment with cotrimoxazole and prednisone initially resulted in improvement, but after 10 days the patient's clinical condition deteriorated rapidly and he died after 23 days due to respiratory failure. RESULTS: On autopsy histopathologic examination showed abundant "smudge cells," suggestive of adenoviral infection. Electron microscopy revealed adenovirus-like particles arrayed in a paracrystalline manner. Subsequent immunohistochemistry confirmed the extensive presence of adenovirus in addition to P. carinii. CONCLUSION: This case demonstrates a pathogenetic role for adenovirus coinfection in P. carinii pneumonia (PCP). Earlier diagnosis, e.g. by PCR analysis of the BAL fluid or transbronchial biopsy, might have led to the consideration of ribavirin treatment.
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6/17. AIDS-related body cavity-based lymphoma. A case report.

    BACKGROUND: Body cavity-based lymphomas are rare malignancies in human immunodeficiency virus (HIV)-infected patients, but because of their unusual clinical, morphologic and immunophenotypic features, they are recognized as a distinct subgroup of lymphomas connected to human herpesvirus 8 (HHV-8) infection. CASE: A 39-year-old, HIV-positive, homosexual man was admitted to the hospital because of a left-sided pleural effusion that contained malignant lymphoid cells. He responded partially to a low-dose cyclophosphamide/doxorubycin/vincristine/prednisone regimen and died five months after the diagnosis of lymphoma. On cytology, the sediments contained exclusively large, round, neoplastic, lymphoid cells with abundant basophilic cytoplasm and large, round nuclei with prominent nucleoli. Many cells had immunoblastic features, and some had plasmocytoid differentiation. Mitotic figures were numerous. On flow cytometry, the homogeneous population of large cells expressed CD45, CD38, HLA-DR and CD7 positivity. Other specific T-, B- and NK-cell markers tested negative. polymerase chain reaction demonstrated Epstein-Barr virus (EBV) and HHV-8 in the malignant effusion. CONCLUSION: Primary effusion from lymphoma with molecular evidence of HHV-8 and EBV coinfection represents a distinct clinical and morphologic entity in AIDS patients. However, immunophenotypic markers of malignant clones can be diverse in different cases.
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7/17. Pulmonary coinfection by trichomonas vaginalis and Pneumocystis sp. as a novel manifestation of AIDS.

    A 41-year-old man was hospitalized, presenting increasing dyspnea and extensive ground-glass opacities on chest X-ray. Infection by human immunodeficiency virus was confirmed. Cytologic examination of bronchoalveolar lavage fluid revealed numerous trichomonads and aggregates of Pneumocystis sp. Treatment was followed by rapid improvement of respiratory symptoms and chest X-ray. The trichomonad species found in the lungs was identified as trichomonas vaginalis by small-subunit rRNA gene amplification and sequencing. With the exception of rare cases of contamination of newborn babies during delivery, T. vaginalis has never been found in lungs in healthy or immunocompromised adults. In the present case, T. vaginalis is found as coinfecting agent. Our data, like those found in the literature, suggest that trichomonads are overlooked parasites that may be regularly implicated in diverse human pathologies.
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8/17. Rapid progression of hiv-1 infection to AIDS.

    Homosexually acquired human immunodeficiency virus type 1 infection is usually slowly progressive, and reports of its rapid progression to acquired immunodeficiency syndrome are rare. We present a case of acute human immunodeficiency virus type 1 and cytomegalovirus coinfection that progressed to acquired immunodeficiency syndrome and death in 7 months. The factors that determine the clinical outcome of human immunodeficiency virus type 1 infection are poorly defined; however, coinfection with other agents, such as cytomegalovirus, may influence its natural history.
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9/17. Clinical vignette in antiretroviral therapy: jaundice.

    HIV caregivers face many challenges following initiation of art. The development of jaundice is uncommon but worrisome. In this case, two distinct and contrasting episodes of jaundice were observed. In the first instance, isolated elevation of the indirect bilirubin without elevation of the alkaline phosphatase was noted. The normal PT and serum aminotransferase levels indicate the absence of intrinsic liver dysfunction. Elevations in the indirect bilirubin may result from either impaired uptake/conjugation or excess production. The latter, usually from acquired hemolysis, may be a complication of an occult NHL. A work-up for this AIDS-related malignancy was not initiated since the caregivers recognized jaundice as a complication of IDV, which inhibits UDP-glucuronyl transferase and produces a Gilbert's-like syndrome. physicians can expect to encounter this syndrome even more frequently with ATV. Experienced patients given RTV-boosted ATV have experienced elevations of unconjugated hyper-bilirubinemia in up to 45 percent of cases in clinical trials. However, such elevations do not reflect liver dysfunction and symptomatic jaundice requiring dosage reduction that occurred infrequently (7 to 8 percent of study patients). counseling patients about this syndrome may promote adherence and prevent self-directed interruptions of ATV that compromise efficacy. The second case of jaundice provides a more formidable diagnostic challenge. The triad of LFT abnormalities (mild elevation of aminotransferases, normal PT, and marked cholestatic jaundice) implies an acute process that is mildly toxic to hepatocytes without affecting their synthetic function. The subacute nature of the patient's cholestatic jaundice suggests either intrahepatic infiltrative disease of the liver or extrahepatic obstruction of the biliary tree, most likely due to the patient's relatively modest level of pain and lack of fever. Despite LFT abnormalities occurring 17 months after a switch in his art, cumulative drug-related toxicities must still be considered. ritonavir can produce significant elevations in the AST/ALT, especially with pre-existing chronic liver disease as with hepatitis c virus coinfection. The NRTIs can produce hepatic steatosis, a result of mitochondrial toxicity and impaired fatty acid oxidation. However, jaundice and cholestasis are not typical of the latter syndrome. With a negative contrast CT that excludes parenchymal liver disease, investigation of the biliary tree to assess the presence of AIDS-related cholangitis was the next step. Performing a sphincterotomy or stent placement, and obtaining brushings or biopsy specimens to determine the extent of extrahepatic obstruction may help define a pathogen and be life-saving. The negative results of the ERCP justify the final diagnostic step, a liver biopsy to evaluate microscopic infiltrative disease that might not have been detected on contrast abdominal CT. Examples might include granulomatous disease (MAC), fungal etiologies (histoplasmosis), carcinomatosis (lymphoma, hepatoma, cholangiocarcinoma), and microvascular disease (bacillary angiomatosis). The failure to observe granulomatous inflammation in the liver does not exclude MAC infection, as MAC may involve other peri-aortic or mesenteric lymph nodes. This form of iris is unlikely given the abdominal CT findings, lack of systemic complaints, and extended persistence of liver aminotransferases. The nonspecific results of the liver biopsy are a common outcome in advanced AIDS patients with elevated alkaline phosphatase levels. Despite not having identified a pathogen, the biopsy establishes chronic liver disease and prompts re-evaluation and change of treatment to NFV. The subsequent normalization of the patient's aminotransferase levels suggests a prior adverse effect of LPV/r in the setting of unexplained, chronic liver disease. Most importantly, this case highlights the importance of HIV caregivers to review art for safety when noting chronic liver dysfunction. patients need to be counseled to minimize acetaminophen use, to consume alcohol in moderation, and to avoid behavior with risk for hepatitis c. Finally, all HIV patients should receive appropriate vaccination against hepatitis a and B if serology shows lack of protective immunity.
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10/17. Disseminated cutaneous leishmaniasis after visceral disease in a patient with AIDS.

    leishmaniasis is emerging as a common and serious opportunistic disease for patients with HIV infection. Almost all cases of HIV-Leishmania coinfection have been described in Mediterranean countries and they occur with various clinical presentations, ranging from typical visceral forms to asymptomatic or atypical cases, including cutaneous and mucocutaneous leishmaniasis. Pentavalent antimony compounds have been the mainstays of antileishmanial therapy for half a century and new lipid formulations of amphotericin b seem reliable, but the most effective treatment remains unknown. We describe a patient who was HIV infected and an intravenous drug user, with an unusual disseminated cutaneous leishmaniasis, after an initial visceral disease and after a 13-month maintenance treatment with liposomal amphotericin. The severe concurrent immunosuppression probably played an essential role in leading to this atypical cutaneous form, characterized by diffuse, nonulcerated, nonscabby maculopapular lesions.
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