Bucher, Heiner C.

Guex, Anne-Catherine

Radziwill, Alexander J.

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602BRIEF REPORTSFigure 1. A, CT scan before empirical therapy for toxoplasmic encephalitis in an HIV-infected patient. B, CT scan 2.5 years later, after immunerestoration with highly active antiretroviral therapy and 8 months without maintenance therapy for toxoplasmic encephalitis.Discontinuation of Secondary Prophylaxisfor Toxoplasmic Encephalitis in HumanImmunodeficiency Virus Infection After ImmuneRestoration with Highly Active AntiretroviralTherapyToxoplasma gondii is one of the leading causes of neurologicalmorbidity and mortality in patients with advanced HIV infec-tion. Effective therapies for primary and secondary preventionof toxoplasmic encephalitis in HIV infection have been estab-lished [1, 2]. With the introduction of highly active antiretroviraltherapy (HAART), discontinuation of primary and secondaryprophylaxis for opportunistic infections in patients with HIVinfection and good response to HAART have become a focusof interest. We describe an HIV-infected patient with toxo-plasmic encephalitis and excellent response to HAART whodiscontinued secondary prophylaxis for toxoplasmosis.A 26-year-old woman with HIV infection presented to ourReprints or correspondence: Dr. Heiner C. Bucher, Medizinische Univer-sita¨ts-Poliklinik, Kantonsspital Basel, CH-4031 Basel, Switzerland (bucher@ubaclu.unibas.ch).Clinical Infectious Diseases 2000;30:602–3q 2000 by the Infectious Diseases Society of America. All rights reserved.1058-4838/2000/3003-0036$03.00clinic with headache in November 1996. She had acquired HIVinfection in 1986 by needle exchange, and, in the followingyears, did not seek regular medical assistance. She had notreceived any prophylaxis for opportunistic infections or treat-ment with antiretroviral drugs. Physical examination showedno neurological deficits. A CT scan revealed a 2.8-cm diametersolitary hypodense cerebral lesion with perifocal edema on theright parietotemporal hemisphere (figure 1A); this lesion wassuspected to be toxoplasmic encephalitis. IgG antibodies to T.gondii were positive at 34 U/mL, her CD4 cell count was 29/mm3, and the plasma viral load was 302,000 copies/mL. Thepatient was empirically treated with pyrimethamine, sulfadia-zine, and leucovorin.Four weeks later, a control CT scan showed regression ofboth the cerebral lesion and the perifocal edema. Because of asevere rash, sulfadiazine was changed to clindamycin, and after6 weeks, the patient received maintenance therapy. Antiretro-viral therapy with lamivudine, stavudine, and indinavir wasthen started. The response was excellent, and in the following18 months, the CD4 cell count progressively increased to 11100/mm3, and her plasma viral load was permanently suppressed(as measured by an ultrasensitive assay [Amplicor; Roche Di-agnostic Systems, Rotkreuz, Switzerland]).After 22 months, the patient insisted that her maintenanceCID 2000;30 (March) Brief Reports 603therapy for toxoplasmic encephalitis be discontinued to reduceher pill load of 20 tablets a day. At this time, a CT scan showeda 1.7-cm diameter cerebral lesion with calcification that wasidentical to that on a previous CT scan at a 12-month follow-up. Twelve months after discontinuation of secondary prophy-laxis for T. gondii infection, the patient had no clinical signs ofrelapse, and her CT scan remained unchanged (figure 1B).Data from observational studies on the discontinuation ofprimary prophylaxis for Pneumocystis carinii pneumonia in pa-tients with persistent CD4 lymphocyte counts 1200/mm3 andantibodies to T. gondii have shown that no relapses of P. cariniipneumonia and T. gondii infection occurred [3, 4]. However,the number of patients with antibodies to T. gondii was toosmall to allow for firm conclusions as to whether discontinu-ation of primary prophylaxis for toxoplasmic encephalitis issafe.Discontinuation of maintenance therapy for patients withestablished toxoplasmic encephalitis is not recommended [5].Relapse rates after discontinuation of maintenance therapy, asreported from the pre-HAART era, may be >50% [2]. However,secondary prophylaxis for toxoplasmic encephalitis is all butsatisfactory. Rates of breakthrough relapses associated with sul-fadiazine and pyrimethamine, the most effective drug combi-nation, are 10%–40%, and rates of drug-limiting toxicity as-sociated with this combination are 30%–43% [2].Because of side effects, high pill load, and drug interactions,discontinuation of maintenance therapy for toxoplasmosis afterimmune restoration with HAART is likely to improve the qual-ity of life in patients with AIDS and to increase adherence toantiretroviral therapy. Therefore, studies evaluating whethersecondary prophylaxis for toxoplasmic encephalitis may be dis-continued for selected patients with excellent response toHAART seem timely.Anne-Catherine Guex,1 Alexander J. Radziwill,2and Heiner C. Bucher11Medizinische Universita¨ts-Poliklinik and 2NeurologischeUniversita¨tsklinik, Kantonsspital Basel, Basel, SwitzerlandReferences1. Bucher HC, Griffith L, Guyatt GH, Opravil M. Meta-analysis of prophylactictreatment against Pneumocystis carinii pneumonia and toxoplasma en-cephalitis in HIV-infected patients. J Acquir Immune Defic Syndr HumRetrovirol 1997;15:104–14.2. Katlama C, De Wit S, O’Doherty E, Van Glabeke M, Clumeck N. Pyrime-thamine/clindamycin vs. pyrimethamine/sulfadiazine as acute and long-term therapy for toxoplasmic encephalitis in patients with AIDS. Clin InfectDis 1996;22:268–75.3. Furrer H, Egger M, Opravil M, et al. Discontinuation of primary prophylaxisagainst Pneumocystis carinii pneumonia in HIV-1–infected adults treatedwith combination antiretroviral therapy. N Engl J Med 1999;340:1301–6.4. Weverling GJ, Mocroft A, Ledergerber B, et al. Discontinuation of Pneu-mocystis carinii pneumonia prophylaxis after start of highly active anti-retroviral therapy in HIV-1 infection. Lancet 1999;353:1293–8.5. USPHS/IDSA Prevention of Opportunistic Infections Working Group. 1997USPHS/IDSA guidelines for the prevention of opportunistic infections inpersons infected with human immunodeficiency virus. MMWR Morb Mor-tal Wkly Rep 1997;46(RR-12):1–46.Intestinal Involvement by NontuberculousMycobacteria After Heart TransplantationThe prevalence of disease due to nontuberculous mycobac-teria (NTM) in the United States is 1.8 cases per 100,000 pop-ulation [1]. In the general population, 5%–10% of mycobacteriacausing infections are NTM, whereas in transplant recipientsNTM cause 25%–40% of all mycobacterial infections [2]. Wedescribe a case of infection with Mycobacterium avium/Myco-bacterium intracellulare in a heart transplant recipient and re-view the literature on disease due to NTM [3–12].A 56-year-old man underwent orthotopic heart transplan-tation in June 1990 for ischemic cardiomyopathy. In November1992, he was admitted to the hospital because of fever (tem-perature, 397C) during treatment with cyclosporine, azathio-prine, and deflazacort. Physical examination disclosed a smallepitrochlear node and a tender periumbilical mass. His eryth-Reprints or correspondence: Dr. Miguel Yebra, Medicina Interna I, Clı´n-ica Puerta de Hierro, San Martı´n de Porres, 4, Madrid 28035, Spain (myebraf@nexo.es).Clinical Infectious Diseases 2000;30:603–5q 2000 by the Infectious Diseases Society of America. All rights reserved.1058-4838/2000/3003-0037$03.00rocyte sedimentation rate was 92 mm/h. Blood cultures andserological tests for Brucella, Salmonella, Yersinia, cytomega-lovirus, and HIV were negative. Ziehl-Neelsen staining of urineand sputum samples were negative, as were cultures of thesesamples on Lo¨wenstein-Jensen medium. Purified protein deriv-ative skin testing was also negative. A CT scan of the chestand abdomen revealed enlarged retroperitoneal and mesentericlymph nodes.Biopsy of the epitrochlear node revealed granulomas withscarce acid-fast bacilli, and culture of the node on Lowe¨nstein-Jensen medium was negative. Laparotomy showed mesentericand retroperitoneal lymphadenopathies. Histopathologic ex-amination of the nodes demonstrated noncaseating granulo-matous adenitis, whereas Ziehl-Neelsen staining of the nodesand culture of the nodes on Lo¨wenstein-Jensen medium werenegative. Azathioprine therapy was discontinued, and the cy-closporine dose was reduced. Subsequently, the fever subsided,the erythrocyte sedimentation rate normalized, and lymphad-enopathies regressed.The patient remained asymptomatic until December 1993,when he presented because of abdominal pain and a 5-kg weightloss. Gastrointestinal examination revealed a distorted duo-denum with duodenal and jejunal mucosal thickening. An ab-

Discontinuation of Secondary Prophylaxis for Toxoplasmic Encephalitis in Human Immunodeficiency Virus Infection After Immune Restoration with Highly Active Antiretroviral Therapy

Discontinuation of Secondary Prophylaxis for Toxoplasmic Encephalitis in Human Immunodeficiency Virus Infection After Immune Restoration with Highly Active Antiretroviral Therapy

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