Treatment

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Treatment Since TE was the most common cause of focal CNS lesions in AIDS patients before the era of HAART (highly active antiretroviral therapy), empiric anti-T. gondii therapy used to be the standard approach. However, the incidence of TE in AIDS patients has significantly decreased since the introduction of HAART and the widespread use of prophylaxis. Therefore, this empiric therapeutic approach may miss or delay the appropriate work-up and management of important diagnosis like CNS lymphoma. Algoritum 31(A) illustrates the management approach to TE in HIV patient. 12 In general, the presence of multiple brain lesions with CD4 T-cell counts of less than 100/μL and positive anti-T. gondii antibodies in an HIV patient who is not taking anti-T. gondii prophylaxis is highly predictive of TE. Combination of pyrimethamine/sulfadiazine and folinic acid is considered the standard regime for the treatment of TE (Box 31.1). 8 Unfortunately sulfadiazine is not available in Hong Kong. Clindamycin can be used instead of sulfadiazine in this regard. Infected patient should be treated for at least 4-6 weeks after the resolution of all signs and symptoms. It is important to note that, as a result of the myelotoxicity of sulfonamides and pyrimethamine, "folinic acid" instead of "folic acid" should be used since the latter will reverse the action of pyrimethamine. The efficacy of Trimethoprim/sulfamethoxazole (co-trimoxazole) appears to be comparable to that of pyrimethamine/sulfadiazine in AIDS patients. 13 Short course of corticosteroid can be used in TE patient with significant cerebral oedema and elevated intracranial pressure. In one study 51% of patients with TE developed clinical response to anti-T. gondii therapy within the first 3 days and 91% by day 14. 6 Other investigation including brain biopsy should be considered if there is no improvement by 2 weeks or when there is deterioration by day 3. 6 Over 90% of patients have radiological response by 2 weeks of therapy. Monitoring brain CT/MRI every 4-6 weeks is suggested until there is complete resolution of the lesions. Prophylaxis

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Transcript of Treatment

Page 1: Treatment

Treatment

Since TE was the most common cause of focal CNS lesions in AIDS patients before the era of HAART (highly active antiretroviral therapy), empiric anti-T. gondii therapy used to be the standard approach. However, the incidence of TE in AIDS patients has significantly decreased since the introduction of HAART and the widespread use of prophylaxis. Therefore, this empiric therapeutic approach may miss or delay the appropriate work-up and management of important diagnosis like CNS lymphoma. Algoritum 31(A) illustrates the management approach to TE in HIV patient.12 In general, the presence of multiple brain lesions with CD4 T-cell counts of less than 100/μL and positive anti-T. gondii antibodies in an HIV patient who is not taking anti-T. gondii prophylaxis is highly predictive of TE.

Combination of pyrimethamine/sulfadiazine and folinic acid is considered the standard regime for the treatment of TE (Box 31.1).8 Unfortunately sulfadiazine is not available in Hong Kong. Clindamycin can be used instead of sulfadiazine in this regard. Infected patient should be treated for at least 4-6 weeks after the resolution of all signs and symptoms. It is important to note that, as a result of the myelotoxicity of sulfonamides and pyrimethamine, "folinic acid" instead of "folic acid" should be used since the latter will reverse the action of pyrimethamine. The efficacy of Trimethoprim/sulfamethoxazole (co-trimoxazole) appears to be comparable to that of pyrimethamine/sulfadiazine in AIDS patients.13 Short course of corticosteroid can be used in TE patient with significant cerebral oedema and elevated intracranial pressure.

In one study 51% of patients with TE developed clinical response to anti-T. gondii therapy within the first 3 days and 91% by day 14.6 Other investigation including brain biopsy should be considered if there is no improvement by 2 weeks or when there is deterioration by day 3.6

Over 90% of patients have radiological response by 2 weeks of therapy. Monitoring brain CT/MRI every 4-6 weeks is suggested until there is complete resolution of the lesions.

Prophylaxis

After the acute treatment of TE, maintenance therapy (secondary prophylaxis) should follow since the current anti-T. gondii therapy cannot eradicate tissue cysts. Normally the same medications used in the acute phase could be continued at half dose to this effect (Box 31.1).

Primary prophylaxis should be considered in HIV patient with CD4 cell counts less than 100/μL. Use of co-trimoxazole for the prophylaxis of Pneumocystis jiroveci pneumonia (PCP) could also provide protection against toxoplasmosis. Other alternatives include high dose dapsone alone or dapsone plus pyrimethamine. Both primary or secondary prophylaxis can be discontinued when the patient's CD4 cell count has returned to over 200/μL for at least 6 months.14

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Prevention of toxoplasmosis in HIV/AIDS

HIV-infected persons should be tested for baseline IgG antibodies to Toxoplasma to detect latent infection with T. gondii. All HIV-infected persons should be counseled regarding exposure to toxoplasmic infection:15

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(a) Avoid eating raw or undercooked meat, including undercooked mutton, beef, pork, or venison

(b) Wash hands after contact with raw meat, after gardening or other contact with soil

(c) Wash fruits and vegetables well before eating them raw

(d) Avoid handling cats' litter and wash hands thoroughly after changing the litter box

(e) Keep cats inside, and do not to adopt or handle stray cats

(f) Feed cats only with canned or dried commercial food or well-cooked table food, not raw or undercooked meats

Further reading

1. Montoya JG, Kovacs JA, Remington JS. Toxoplasma gondii. In: Mandell GL, Bennett JE, Dolin R, 6th eds. Principles and Practice of Infectious Diseases. Philadelphia: Churchill Livingstone, 2005;3170-98.

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2. Hunter CA & Reichmann G. Immunology of toxoplasma infection. In Joynson DHM, Wreghitt TG. Toxoplasmosis: a comprehensive clinical guide. Cambridge: Cambridge University Press, 2001;43-57.

3. Montoya JG, Liesenfeld O. Toxoplasmosis. Lancet 2004;363:1965-76.

References

1. Tenter AM, Heckeroth AR, Weiss LM. Toxoplasma gondii: from animals to humans. Int J Parasitol 2000;30:1217-58.

2. Ko RC, Wong FW, Todd D, Lam KC. Prevalence of Toxoplasma gondii antibodies in the Chinese population of Hong Kong. Trans R Soc Trop Med Hyg 1980;74:351-4.

3. Grant IH, Gold JW, Rosenblum M, Niedzwiecki D, Armstrong D. Toxoplasma gondii serology in HIV-infected patients: the development of central nervous system toxoplasmosis in AIDS. AIDS 1990;4:519-21.

4. Luft BJ, Remington JS. Toxoplasmic encephalitis in AIDS. Clin Infect Dis 1992;15:211-22.

5. Department of Health. Hong Kong STD/AIDS Update: a quarterly surveillance report. July 1998;4(3):7.

6. Luft BJ, Hafner R, Korzun AH, et al. Toxoplasmic encephalitis in patients with the acquired immunodeficiency syndrome. Members of the ACTG 077p/ANRS 009 Study Team. N Engl J Med 1993;329:995-1000.

7. Torrey EF, Yolken RH. Toxoplasma gondii and schizophrenia. Emerg Infect Dis 2003;9:1375-80.

8. Montoya JG, Kovacs JA, Remington JS. Toxoplasma gondii. In: Mandell GL, Bennett JE, Dolin R, 6th eds. Principles and Practice of Infectious Diseases. Philadelphia: Churchill Livingstone, 2005;3170-98.

9. Levy RM, Rosenbloom S, Perrett LV. Neuroradiologic findings in AIDS: a review of 200 cases. AJR Am J Roentgenol 1986;147:977-83.

10. Dunn IJ, Palmer PE. Toxoplasmosis. Semin Roentgenol 1998;33:81-5. 11. Parmley SF, Goebel FD, Remington JS. Detection of Toxoplasma gondii in

cerebrospinal fluid from AIDS patients by polymerase chain reaction. J Clin Microbiol 1992;30:3000-2.

12. Wong KH. Toxoplasmosis. In: Chan K, Wong KH, Lee SS. HIV manual 2001. Red Ribbon Centre 2002;193-8.

13. Torre D, Casari S, Speranza F, et al. Randomized trial of trimethoprim-sulfamethoxazole versus pyrimethamine-sulfadiazine for therapy of toxoplasmic encephalitis in patients with AIDS. Italian Collaborative Study Group. Antimicrob Agents Chemother 1998;42:1346-9.

14. Mofenson LM, Oleske J, Serchuck L, et al. Treating opportunistic infections among HIV-exposed and infected children: recommendations from CDC, the National Institutes of Health, and the Infectious Diseases Society of America. MMWR Recomm Rep 2004;53(RR-14):1-92.

15. 1999 USPHS/IDSA guidelines for the prevention of opportunistic infections in persons infected with human immunodeficiency virus. U.S. Public Health Service (USPHS) and Infectious Diseases Society of America (IDSA). MMWR Recomm Rep 1999;48(RR-10):1-59, 61-6.