Livramento, J.A.; Machado, L.R.; Nóbrega, J.P.S.; Vianna, L.S.; Spina-França, A.

doi:10.1590/S0004-282X1993000100013

Resumos

Foram estudadas 113 amostras de LCR de 8 pacientes no período compreendido entre setembro-1980 e agosto-1992. Todos os pacientes apresentavam quadro clínico e do LCR compatível a processo meningoencefalitico de evolução protraída. Nenhum deles apresentava a síndrome de imunodeficiência adquirida. Em todos foi feito o diagnóstico de histoplasmose do SNC; em todos foram detectados anticorpos a Histoplasma capsulatum no LCR; em um foi isolada a levedura por cultura em meio de Sabouraud. As principais características do LCR por ocasião do diagnóstico foram: pleocitose moderada com predomínio de células lin-fomononucleadas porém com presença de neutrófilos e por vezes eosinófilos; hiperproteinor-raquia moderada; hipoglicorraquia; aumento moderado do teor de globulinas gama. Os pacientes foram acompanhados durante períodos que variaram de 7 a 102 meses e submetidos a exames periódicos de LCR, em função da sintomatologia clínica. O número de células do LCR e a concentração de proteínas totais apresentaram evolução caracterizada pela ocorrência de episódios de exacerbação com perfil parcialmente dissociado, favorecendo as proteínas. As concentrações de glicose eram moderadamente baixas sendo os menores valores coincidentes aos períodos de exarcebação do número de células. Os teores de globulinas gama apresentaram também oscilações, porém menos evidentes. Submetidos os pacientes a tratamento eficaz, ocorreu no LCR: rápida diminuição do número de células; aumento da taxa de glicose; lento decréscimo dos aumentos de proteínas e de globulinas gama.

histoplasmose; sistema nervoso central; líquido cefalorraqueano; meningite crônica

One hundred and thirteen samples of CSP from eight patients with chronic meningitis were studied in a 12 years period (September, 1980 - August, 1992). None of them had AIDS. In all, CNS histoplasmosis diagnosis was made by CSF examination. All eases, tested positive for antibodies to Histoplasma capsulatum in CSF; in one case the yeast gro-wed in Sabouraud culture in three different occasions. The main findings in CSF by the time of the diagnosis were: moderate hypercytosis marked by lymphocytes and monocytes, neutrophils-being present and in some cases eosinophil cells; moderate increase of total proteins content; decrease in the glucose content; and moderate increase of gamma globulins sometimes with oligoclonal reaction. Patients were followed-up from 7 to 102 months, and periodically submitted to CSF examinations according to clinics. Cell number and total protein content of CSF showed marked episodes of exarcebation in the follow-up, with a dissociated profile favoring total protein content which got higher with the chronification of the disease. Changes in the CSF pattern with treatment were: rapid decrease of hypercytosis; disappearence of neutrophil and eosinophil cells; increase in glucose content; and slow reduction of the increased contents of total proteins and gamma globulins.

histoplasmosis; central nervous system; cerebrospinal fluid; chronic meningitis

J.A. Livramento^I; L.R. Machado^I; J.P.S. Nóbrega^I; L.S. Vianna^II; A. Spina-França^III

^ICIN, Centro de Investigações em Neurologia, Departamento de Neurologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP)/LSF (Laboratório de Neurodiagnóstico): Médico Assistente

^IICIN, Centro de Investigações em Neurologia, Departamento de Neurologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP)/LSF (Laboratório de Neurodiagnóstico): Médico Pesquisador

^IIICIN, Centro de Investigações em Neurologia, Departamento de Neurologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP)/LSF (Laboratório de Neurodiagnóstico): Professor Emérito

RESUMO

Foram estudadas 113 amostras de LCR de 8 pacientes no período compreendido entre setembro-1980 e agosto-1992. Todos os pacientes apresentavam quadro clínico e do LCR compatível a processo meningoencefalitico de evolução protraída. Nenhum deles apresentava a síndrome de imunodeficiência adquirida. Em todos foi feito o diagnóstico de histoplasmose do SNC; em todos foram detectados anticorpos a Histoplasma capsulatum no LCR; em um foi isolada a levedura por cultura em meio de Sabouraud. As principais características do LCR por ocasião do diagnóstico foram: pleocitose moderada com predomínio de células lin-fomononucleadas porém com presença de neutrófilos e por vezes eosinófilos; hiperproteinor-raquia moderada; hipoglicorraquia; aumento moderado do teor de globulinas gama. Os pacientes foram acompanhados durante períodos que variaram de 7 a 102 meses e submetidos a exames periódicos de LCR, em função da sintomatologia clínica. O número de células do LCR e a concentração de proteínas totais apresentaram evolução caracterizada pela ocorrência de episódios de exacerbação com perfil parcialmente dissociado, favorecendo as proteínas. As concentrações de glicose eram moderadamente baixas sendo os menores valores coincidentes aos períodos de exarcebação do número de células. Os teores de globulinas gama apresentaram também oscilações, porém menos evidentes. Submetidos os pacientes a tratamento eficaz, ocorreu no LCR: rápida diminuição do número de células; aumento da taxa de glicose; lento decréscimo dos aumentos de proteínas e de globulinas gama.

Palavras-chave: histoplasmose, sistema nervoso central, líquido cefalorraqueano, meningite crônica.

SUMMARY

One hundred and thirteen samples of CSP from eight patients with chronic meningitis were studied in a 12 years period (September, 1980 - August, 1992). None of them had AIDS. In all, CNS histoplasmosis diagnosis was made by CSF examination. All eases, tested positive for antibodies to Histoplasma capsulatum in CSF; in one case the yeast gro-wed in Sabouraud culture in three different occasions. The main findings in CSF by the time of the diagnosis were: moderate hypercytosis marked by lymphocytes and monocytes, neutrophils-being present and in some cases eosinophil cells; moderate increase of total proteins content; decrease in the glucose content; and moderate increase of gamma globulins sometimes with oligoclonal reaction. Patients were followed-up from 7 to 102 months, and periodically submitted to CSF examinations according to clinics. Cell number and total protein content of CSF showed marked episodes of exarcebation in the follow-up, with a dissociated profile favoring total protein content which got higher with the chronification of the disease. Changes in the CSF pattern with treatment were: rapid decrease of hypercytosis; disappearence of neutrophil and eosinophil cells; increase in glucose content; and slow reduction of the increased contents of total proteins and gamma globulins.

Key words: histoplasmosis, central nervous system, cerebrospinal fluid, chronic meningitis.

Full text available only in PDF format.

Texto completo disponível apenas em PDF.

Agradecimento Os autores agradecem ao Prof. Dr. Carlos da Silva Lacaz (Laboratório de Micologia, LIM 52, FMUSP) pela gentil assistência para identificação de fungos em culturas, no decorrer destes anos e pelo fornecimento dos antígenos para identificação dos fungos estudados.

Aceite: 39-agosto-1992.

Dr. José Antonio Livramento Caixa Postal 5190 - 01061-970 São Paulo SP - Brasil.

1. Bellim EL, Silva M, Lawyer T Jr. Central nervous system histoplasmosis in a Puerto Rican. Neurology 1962, 12:148-152.
2. Cooper RA, Goldstein E. Histoplasmosis of the central nervous system: report of two cases and review of the literature. Am J Med 1963, 35:45-57.
3. Fishmian RA. Cerebrospinal fluid in diseases of the central nervous system. Ed 2. Philadelphia: Saunders, 1992, p 276-277.
4. Gelfand JA, Bennet JE. Active histoplasma meningitis of 22 years duration. JAMA 1975, 233:1294-1295.
5. Gilden DH, Miller EM, Johnson WG. Central nervous system histoplasmosis after rhinoplasty. Neurology 1974, 24:874-877.
6. Greer D, Geraci JE, Corbin JB, Miller RH, Weed LA. Disseminated histoplasmosis presenting as a brain tumor and treated with amphotericin B: report of a case. Mayo Clin Proc 1964, 39:490-494.
7. Huang CT, McGarry T, Cooper S. Disseminated histoplasmosis in the immunodeficiency syndrome: report of five cases from a nonendemic area. Arch Intern Med 1987, 147:1181-1184.
3. Jardim E, Takayanagui OM. Mielopatia por histoplasmose. Arq Neuro-Psiquiat (São Paulo) 1981, 39:115-118.
9. Johnson PC, Sarosi GA. AIDS and progressive disseminated histoplasmosis. JAMA 1987, 258:202.
10. Karalakulasingam R, Arora KK, Adams G, Serratoni F, Martin DG. Meningoencephalitis caused by Histoplasma capsulatum: occurrence in a renal transplant recipient and a review of the literature. Arch Intern Mod 1976, 136:217-220.
11. Livramento JA, Machado LR, Nobrega JPS, Gomes HR, Vianna LS, Spina-França A. CSF in 85 patients with AIDS and CNS cryptococcosis. Arq Neuro-Psiquiat (Sao Paulo) 1992, 50:491-496.
12. Plouffe JF, Fass RJ. Histoplasma meningitis: diagnostic value of cerebrospinal fluid serology. Ann Intern Med 1980, 92:189-191.
13. Sathtapatayavongs B, Batteiger BE, Wheat LJ, Slama TG, Wass JL. Clinical and laboratory features of disseminated histoplasmosis during two large urban outbreaks. Medicine 1983, 62:263-270.
14. Smith JW, Utz JP. Progressive disseminated histoplasmosis. Ann Intern Med 1972, 76: 557-565.
15. Terry BS, Rosenow EC III, Roberts CD. False-positive complement fixation serology in histoplasmosis: a retrospective study. JAMA 1978, 239:2453-2456.
16. Tucker T, Ellner JJ. Chronic meningitis. In Scheld WM, Whitley RJ, Durack DT (eds): Infections of the central nervous system, New York: Raven Press, 1991, p 703-728.
17. Wheat LJ, Batteiger BE, Sathapatayavongs B. Histoplasma capsulatum infection of the central nervous system, a clinical review. Medicine 1990, 69:2444-260.
18. Wheat LJ, Connolly-Stringfield P, Kohler RB, Frame PT, Gupta MR. Histoplasma capsulatum polysaccharide antigen detection in diagnosis and management of disseminated histoplasmosis in patients with acquired immunodeficiency syndrome. Am J Med 1989, 87:396-400.
19. Wheat LJ, French MLV, Batteiger BE, Kohler RB. Cerebrospinal fluid histoplasma antibodies in central nervous histoplasmosis. Arch Intern Med 1985, 145:1237-1240.
21. Wheat LJ, Kohler RB, Tewari RP, Garten M, French MLV. Significance of histoplasma antigen in the cerebrospinal fluid of patients with meningitis. Arch Intern Med 1989, 149:302-304.

Histoplasmose do sistema nervoso central: estudo do líquido cefalorraqueano em 8 pacientes

Central nervous system histoplasmosis: cerebrospinal fluid study of eight patients

Datas de Publicação

Publicação nesta coleção
19 Jan 2011
Data do Fascículo
Mar 1993

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. Bellim EL, Silva M, Lawyer T Jr. Central nervous system histoplasmosis in a Puerto Rican. Neurology 1962, 12:148-152.

[2] 2. Cooper RA, Goldstein E. Histoplasmosis of the central nervous system: report of two cases and review of the literature. Am J Med 1963, 35:45-57.

[3] 3. Fishmian RA. Cerebrospinal fluid in diseases of the central nervous system. Ed 2. Philadelphia: Saunders, 1992, p 276-277.

[4] 4. Gelfand JA, Bennet JE. Active histoplasma meningitis of 22 years duration. JAMA 1975, 233:1294-1295.

[5] 5. Gilden DH, Miller EM, Johnson WG. Central nervous system histoplasmosis after rhinoplasty. Neurology 1974, 24:874-877.

[6] 6. Greer D, Geraci JE, Corbin JB, Miller RH, Weed LA. Disseminated histoplasmosis presenting as a brain tumor and treated with amphotericin B: report of a case. Mayo Clin Proc 1964, 39:490-494.

[7] 7. Huang CT, McGarry T, Cooper S. Disseminated histoplasmosis in the immunodeficiency syndrome: report of five cases from a nonendemic area. Arch Intern Med 1987, 147:1181-1184.

[8] 3. Jardim E, Takayanagui OM. Mielopatia por histoplasmose. Arq Neuro-Psiquiat (São Paulo) 1981, 39:115-118.

[9] 9. Johnson PC, Sarosi GA. AIDS and progressive disseminated histoplasmosis. JAMA 1987, 258:202.

[10] 10. Karalakulasingam R, Arora KK, Adams G, Serratoni F, Martin DG. Meningoencephalitis caused by Histoplasma capsulatum: occurrence in a renal transplant recipient and a review of the literature. Arch Intern Mod 1976, 136:217-220.

[11] 11. Livramento JA, Machado LR, Nobrega JPS, Gomes HR, Vianna LS, Spina-França A. CSF in 85 patients with AIDS and CNS cryptococcosis. Arq Neuro-Psiquiat (Sao Paulo) 1992, 50:491-496.

[12] 12. Plouffe JF, Fass RJ. Histoplasma meningitis: diagnostic value of cerebrospinal fluid serology. Ann Intern Med 1980, 92:189-191.

[13] 13. Sathtapatayavongs B, Batteiger BE, Wheat LJ, Slama TG, Wass JL. Clinical and laboratory features of disseminated histoplasmosis during two large urban outbreaks. Medicine 1983, 62:263-270.

[14] 14. Smith JW, Utz JP. Progressive disseminated histoplasmosis. Ann Intern Med 1972, 76: 557-565.

[15] 15. Terry BS, Rosenow EC III, Roberts CD. False-positive complement fixation serology in histoplasmosis: a retrospective study. JAMA 1978, 239:2453-2456.

[16] 16. Tucker T, Ellner JJ. Chronic meningitis. In Scheld WM, Whitley RJ, Durack DT (eds): Infections of the central nervous system, New York: Raven Press, 1991, p 703-728.

[17] 17. Wheat LJ, Batteiger BE, Sathapatayavongs B. Histoplasma capsulatum infection of the central nervous system, a clinical review. Medicine 1990, 69:2444-260.

[18] 18. Wheat LJ, Connolly-Stringfield P, Kohler RB, Frame PT, Gupta MR. Histoplasma capsulatum polysaccharide antigen detection in diagnosis and management of disseminated histoplasmosis in patients with acquired immunodeficiency syndrome. Am J Med 1989, 87:396-400.

[19] 19. Wheat LJ, French MLV, Batteiger BE, Kohler RB. Cerebrospinal fluid histoplasma antibodies in central nervous histoplasmosis. Arch Intern Med 1985, 145:1237-1240.

[20] 21. Wheat LJ, Kohler RB, Tewari RP, Garten M, French MLV. Significance of histoplasma antigen in the cerebrospinal fluid of patients with meningitis. Arch Intern Med 1989, 149:302-304.