1/25. Progressive multifocal leukoencephalopathy (PML) and cerebral toxoplasmosis in an adult patient, with no symptoms of underlying immunosuppressing illness.We present a case of the coincidence of progressive multifocal leukoencephalopathy (PML) and central nervous system (CNS) toxoplasmosis in an adult patient, without a detectable cause of cell-mediated immunity impairment. The proper diagnosis was made postmortem on the basis of histological changes typical of both pathological processes. PML was characterized by the presence of subcortical focal demyelination, containing enlarged, densely basophilic oligodendrocyte nuclei, often with intranuclear inclusion, and bizarre astrocytes, mimicking neoplastic cells. PML was confirmed by detecting numerous papova virus particles in oligo- and astroglial nuclei by thin-section electron microscopy. Cerebral toxoplasmosis was characterized by the presence of multiple well-circumscribed necrotizing abscesses. Numerous toxoplasma gondii (T. gondii) cysts and free, non-encysted protozoan parasites were found among the inflammatory infiltrates. The diagnosis of cerebral toxoplasmosis was further confirmed by immunocytochemistry. In order to detect putative immunosuppressive background underlying both pathological processes, HIV infection was taken into consideration, however, no histopathological changes indicative of AIDS either in the CNS or in the peripheral organs were eventually found. Moreover no HIV provirus genome was identified in the formalin-fixed, paraffin embedded brain tissue by the polymerase chain reaction (PCR). Current view on the selected aspects of the pathogenesis of both disorders were discussed.- - - - - - - - - - ranking = 1keywords = toxoplasmosis, gondii (Clic here for more details about this article) |
2/25. sarcoidosis-related anterior uveitis in a patient with human immunodeficiency virus.BACKGROUND: This is the first ophthalmic report--to our knowledge--of an anterior uveitis secondary to sarcoidosis in a patient infected with human immunodeficiency virus (HIV). Other reported causes of uveitis in HIV-infected patients have included HIV, herpes zoster, tuberculosis, syphilis, toxoplasmosis, cryptococcus, rifabutin prophylaxis for mycobacterium, and protease inhibitors such as ritonavir and indinavir. uveitis secondary to sarcoidosis in the non-HIV population is classically seen in young, female, African-American patients. There are rare reports, found exclusively in the pulmonary literature, of sarcoidosis in HIV-infected patients. CASE REPORT: A 38-year-old African-American male infected with HIV was treated for chronic recurrent anterior uveitis secondary to sarcoidosis. His sarcoidosis was diagnosed 1 month earlier, along with the onset of his uveitis. During the previous 6 years he has been treated with anti-HIV antivirals as well as prophylaxis for opportunistic infections. To date, his infectious disease specialist continues to treat his HIV and systemic sarcoidosis. CONCLUSION: patients with HIV infection in whom sarcoidosis with secondary uveitis develops are very rare. Management of these patients requires careful use of topical and oral steroidal anti-inflammatories to control ocular and systemic sequelae of sarcoidosis. This case initiates some interesting questions about the immunology of sarcoidosis and its presence in immunocompromised patients. Use of steroids in an immunocompromised patient is clinically complex. Further clinical study is needed to elicit the full clinical significance of sarcoidosis and HIV infection.- - - - - - - - - - ranking = 0.1382193053053keywords = toxoplasmosis (Clic here for more details about this article) |
3/25. central nervous system toxoplasmosis in acquired immunodeficiency syndrome: An emerging disease in india.With the incidence of patients infected with human immuno-deficiency virus (HIV) increasing in india, the central nervous system (CNS) manifestations of the disease will be seen more frequently. The CNS may be primarily afflicted by the virus or by opportunistic infections and neoplasms secondary to the immune suppression caused by the virus. In india, although mycobacterium tuberculosis has been reported to be the most common opportunistic infection, toxoplasmosis may become as common owing to the ubiquitous nature of the protozoan. Since an empirical trial of medical therapy without histopathological diagnosis is recommended, the true incidence of this condition may remain under estimated. The role of ancillary tests such as radiology and serology in the initial diagnosis of this condition remain crucial. This report highlights two patients who were diagnosed to have acquired immuno-deficiency syndrome (AIDS) only after the biopsy of the intracranial lesion was reported as toxoplasmosis. Presently all patients for elective neurosurgery are tested for HIV antigen. The management protocol to be followed in a known patient with AIDS presenting with CNS symptoms is discussed in detail. The value of ancillary tests is also reviewed.- - - - - - - - - - ranking = 0.82931583183182keywords = toxoplasmosis (Clic here for more details about this article) |
4/25. carbamazepine--indinavir interaction causes antiretroviral therapy failure.OBJECTIVE: To report a case of antiretroviral therapy failure caused by an interaction between carbamazepine and indinavir. CASE SUMMARY: A 48-year-old HIV-positive white man was treated with antiretroviral triple therapy, consisting of indinavir, zidovudine, and lamivudine. His HIV-rna (viral load) became undetectable (<400 copies/mL) less than two months after this therapy was started; this was confirmed one month later. Shortly after the start of antiretroviral therapy, the patient developed herpes zoster, which was treated with famciclovir. tramadol was initially prescribed for postherpetic neuralgia; however, this was substituted with carbamazepine due to insufficient analgesic effect. indinavir plasma concentrations decreased substantially during carbamazepine therapy. carbamazepine was stopped after 2.5 months and, two weeks later, the HIV-rna was detectable (6 x 103 copies/mL). Resistance for lamivudine was observed in that blood sample; resistance for zidovudine might have been present, and resistance to indinavir was not detected. A few months later, a further increase of the HIV-rna occurred (300 x 103 copies/mL), after which the therapy was switched to a new antiretroviral regimen containing nevirapine, didanosine, and stavudine. DISCUSSION: physicians may prescribe carbamazepine for HIV-infected patients to treat seizures or postherpetic neuralgia, which are complications of opportunistic infections such as herpes zoster or toxoplasmosis. carbamazepine is a potent enzyme inducer, predominantly of the CYP3A enzyme system, while HIV-protease inhibitors such as indinavir are substrates for and inhibitors of CYP3A. Therefore, an interaction between these drugs could be expected. A low dose of carbamazepine (200 mg/d) and the usual dose of indinavir (800 mg q8h) in our patient resulted in carbamazepine concentrations within the therapeutic range for epilepsy treatment; indinavir concentrations dropped substantially. The virologic, resistance, and plasma drug concentration data, as well as the chronology of events, are highly indicative of antiretroviral treatment failure due to the interaction between carbamazepine and indinavir. CONCLUSIONS: Concomitant use of carbamazepine and indinavir may cause failure of antiretroviral therapy due to insufficient indinavir plasma concentrations. Drugs other than carbamazepine should be considered to prevent this interaction. amitriptyline or gabapentin are alternatives for postherpetic neuralgia; valproic acid or lamotrigine are alternatives for seizures. When alternate drug therapy is not possible, dosage adjustments, therapeutic drug monitoring, and careful clinical observation may help reduce adverse clinical consequences.- - - - - - - - - - ranking = 0.1382193053053keywords = toxoplasmosis (Clic here for more details about this article) |
5/25. A case of cerebral toxoplasmosis.A histopathologically proven case of cerebral toxoplasmosis in a young HIV positive patient has been presented. The clinical problems in management are highlighted.- - - - - - - - - - ranking = 0.69109652652651keywords = toxoplasmosis (Clic here for more details about this article) |
6/25. hiv-2 infection with cerebral toxoplasmosis and lymphomatoid granulomatosis.A Nigerian man had acute onset of headache and vertigo due to a cerebellar mass. A brain biopsy of the mass revealed toxoplasmosis despite repeated negative hiv-1 serology. The presence of an opportunistic infection and his country of origin raised the suspicion for hiv-2; this was confirmed by positive hiv-2 serology. Despite his preliminary pathological diagnosis, results of physiological magnetic resonance imaging (MRI) (perfusion MRI and proton magnetic resonance spectroscopy) were not typical for toxoplasmosis. The lesion showed a biochemical and perfusion pattern that was intermediate for infectious and neoplastic processes. Further neuropathology confirmed a secondary diagnosis of lymphomatoid granulomatosis.- - - - - - - - - - ranking = 0.82931583183182keywords = toxoplasmosis (Clic here for more details about this article) |
7/25. Disseminated histoplasmosis presenting as pyoderma gangrenosum-like lesions in a patient with acquired immunodeficiency syndrome.A 33-year-old Hispanic woman with newly diagnosed human immunodeficiency virus (HIV) infection, a CD4 T-lymphocyte count of 2, viral load of 730,000 copies/mL, candidal esophagitis, seizure disorder, a history of bacterial pneumonia, and recent weight loss was admitted with tonic clonic seizure. On admission, her vital signs were: pulse of 88, respiration rate of 18, temperature of 37.7 degrees C, and blood pressure of 126/76. Her only medication was phenytoin. On examination, the patient was found to have multiple umbilicated papules on her face, as well as painful, erythematous, large, punched-out ulcers on the nose, face, trunk, and extremities of 3 months' duration (Fig. 1). The borders of the ulcers were irregular, raised, boggy, and undermined, while the base contained hemorrhagic exudate partially covered with necrotic eschar. The largest ulcer on the left mandible was 4 cm in diameter. The oral cavity was clear. Because of her subtherapeutic phenytoin level, the medication dose was adjusted, and she was empirically treated with Unasyn for presumptive bacterial infection. Chest radiograph and head computed tomography (CT) scan were within normal limits. sputum for acid-fast bacilli (AFB) smear was negative. Serologic studies, including histoplasma antibodies, toxoplasmosis immunoglobulin m (IgM), rapid plasma reagin (RPR), hepatitis c virus (HCV), and hepatitis b virus (HBV) antibodies were all negative. Examination of the cerebrospinal fluid was within normal limits without the presence of cryptococcal antigen. Blood and cerebrospinal cultures for bacteria, mycobacteria, and fungi were all negative. Viral culture from one of the lesions was also negative. The analysis of her complete blood count showed: white blood count, 2300/microl; hemoglobin, 8.5 g/dL; hematocrit, 25.7%; and platelets, 114,000/microl. Two days after admission, the dermatology service was asked to evaluate the patient. Although the umbilicated papules on the patient's face resembled lesions of molluscum contagiosum, other infectious processes considered in the differential diagnosis included histoplasmosis, cryptococcosis, and penicillium marnefei. In addition, the morphology of the ulcers, particularly that on the left mandible, resembled lesions of pyoderma gangrenosum. A skin biopsy was performed on an ulcer on the chest. Histopathologic examination revealed granulomatous dermatitis with multiple budding yeast forms, predominantly within histiocytes, with few organisms residing extracellularly. methenamine silver stain confirmed the presence of 2-4 microm fungal spores suggestive of histoplasma capsulatum (Fig. 2). Because of the patient's deteriorating condition, intravenous amphotericin b was initiated after tissue culture was obtained. Within the first week of treatment, the skin lesions started to resolve. histoplasma capsulatum was later isolated by culture, confirming the diagnosis. The patient was continued on amphotericin b for a total of 10 weeks, and was started on lamivudine, stavudine, and nelfinavir for her HIV infection during hospitalization. After amphotericin b therapy, the patient was placed on life-long suppressive therapy with itraconazole. Follow-up at 9 months after the initial presentation revealed no evidence of relapse of histoplasmosis.- - - - - - - - - - ranking = 0.1382193053053keywords = toxoplasmosis (Clic here for more details about this article) |
8/25. Bilateral peripheral facial palsy secondary to lymphoma in a patient with HIV/AIDS: a case report and literature review.Neurological complications represent one of the most important causes of morbidity and mortality in patients with HIV/AIDS. However, peripheral neuropathy comprises only 5% to 20% of the total neurological complications and facial nerve palsy, especially when it is bilateral, is a less common manifestation. Peripheral facial palsy has been considered as a possible neurological complication of the early stage of HIV infection but the number of reported cases in the literature is limited. Histological findings of nervous tissue in peripheral facial palsy at an early stage of HIV infection include a degenerative and not suppurative inflammatory process, but its etiology remains obscure. Peripheral facial palsy in the late stage of HIV infection is characterized by an advanced immunological deficit and generally it is secondary to an opportunistic infection of the CNS, such as neurotoxoplasmosis and lymphoma. However, this peripheral attack of the facial nerve is not very common at this late stage of HIV infection. Bilateral peripheral facial palsy as a complication of non-Hodgkin s lymphoma is considered an extremely rare entity. There are no published reports of bilateral peripheral facial palsy secondary to lymphomas or other neoplasms of the CNS in immunosuppressed patients. Non-Hodgkin s lymphoma (NHL) has been considered a late and relatively common manifestation of HIV infection, but an exact cause for the higher incidence of this malignant neoplasm in HIV/AIDS patients is still uncertain.- - - - - - - - - - ranking = 0.1382193053053keywords = toxoplasmosis (Clic here for more details about this article) |
9/25. Reactivation of retinal toxoplasmosis despite evidence of immune response to highly active antiretroviral therapy.We report a case of retinal toxoplasmosis that occurred in a patient with acquired immunodeficiency syndrome who had a previous diagnosis of cerebral toxoplasmosis, despite the patient having had a robust immune response to highly active antiretroviral therapy. Clinical decisions about whether to discontinue secondary prophylaxis for opportunistic infections continue to be challenging.- - - - - - - - - - ranking = 0.82931583183182keywords = toxoplasmosis (Clic here for more details about this article) |
10/25. Upward gaze paralysis as the initial manifestation of HIV-infected patient: a case report.Upward gaze palsy developed in a 23-year-old man without any other abnormal findings except pupillary light-near dissociation in ocular examination. The neuroradiologic examination was consistent with cerebral toxoplasmosis--the most frequent opportunistic infection of the brain in AIDS patients. The serologic work-up revealed a positive HIV test. Symptoms and neuroradiologic abnormality improved after treatment for cerebral toxoplasmosis. HIV infection should be considered in patients who have upward gaze paralysis and neuroimaging compatible with cerebral toxoplasmosis. Empirical treatment may alleviate the upward gaze palsy.- - - - - - - - - - ranking = 0.41465791591591keywords = toxoplasmosis (Clic here for more details about this article) |
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