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    Rev Bras Oftalmol. 2010; 69 (3): 184-207

    Toxoplasmose ocular adquiridaToxoplasmose ocular ps-natal

    Acquired ocular toxoplasmosisPost-birth ocular toxoplasmosis

    Fernando Orfice1, Ruy Cunha Filho2, Alda Lcia Barboza3, Juliana Lambert Orfice4, Daniela Calucci5

    1Doutor, Professor Titular da Universidade Federal de Minas Gerais - UFMG - Belo Horizonte (MG), Brasil; Diretor da Diviso deUvete do Centro Brasileiro de Cincias Visuais - CBCV - Belo Horizonte (MG), Brasil;

    2Mdico Estagirio do Centro Brasileiro de Cincias Visuais e do Servio de Uvete do Hospital So Geraldo do Hospital das Clinicasda Universidade Federal de Minas Gerais - UFMG - Belo Horizonte (MG), Brasil;

    3Doutora da Universidade Federal de Minas Gerais - UFMG - Belo Horizonte (MG), Brasil;4Doutora, Diretora da Diviso de Imagens do CBCV; Assistente voluntria do Servio de Uvete do Hospital So Geraldo do Hospitaldas Clnicas da Universidade Federal de Minas Gerais - UFMG - Belo Horizonte (MG), Brasil;

    5Tecnloga em Oftalmologia do CBCV - Centro Brasileiro de Cincias Visuais - CBCV - Belo Horizonte (MG), Brasil.

    Recebido para publicao em: 30/4/2009 - Aceito para publicao em 24/3/2010

    ARTIGO DE REVISO

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    INTRODUCTION

    The T.gondii, etiologic agent of toxoplasmosis, isan obligate intracellular protozoan, withworldwide distribution. This parasite has shown awide geographic distribution and behaves as a high in-fectivity and low pathogenicity agent, as observed thathalf of the population is infected and only a reduced pro-portion of it presents the disease (Holland, 1999a). InBrazil, 50 to 83% of the adult population is soropositivefor T.gondii (Orfice; Bahia-Oliveira, 2005).

    The most common presentation form of post-birthsystemic toxoplasmosis (PNST) an asymptomatic one thathappens in 80-90% of all cases (Akstein; Wilson; Teutsch,1982; Mansur; Jones; Lempert, 1978; Stagno; Dykes; Amos,1980). The ocular compromise of this infection may occurduring the acute phase or several years after the systemicdisease, and in latency interval is quite variable. This char-acteristic makes the diagnosis of post-birth ocular toxo-plasmosis (PNOT) difficult, as long as the cases with ocularcompromising at the inactive stage of the disease can bemisunderstood with late manifestation of congenital infec-tion (Akstein; Wilson; Teutsch, 1982; Couvreur; Thulliez,1996; Mansur; Jones; Lempert, 1978; Melamed, 1994).

    Although two and five cases of PNOT reportedof by Hogan (1958) and Hogan e Kimura (1964) re-spectively, Perkins (1973) considered that ocular in-volvement of post-birth systemic toxoplasmosis (PNST)occurs in 2-3% of cases and that in United Kingdom,almost all cases of ocular toxoplasmosis had a congeni-tal origin. Besides that, the complications of systemictoxoplasmosis are more frequent when central nervoussystem is involved. These conceptions prevailed for longyears. Nevertheless, Glasner, Silveira and Kruszon-Moran (1992), Gilbert and Standford (2000) empha-sized the relevance of post-birth systemic toxoplasmo-sis (PNST). Besides that, the high prevalence of post-birth infection showed in southern Brazil suggests thatthe post-birth infection may be a common form of trans-mission of the disease (Glasner; Silveira; Kruszon-Moran, 1992). Another study made in the same regionproved that 8.3% of the individuals with post-birth in-fection, who have not developed retinochoroiditis, pre-sented scar passed a period of 7 years (Silveira et al.,2001). Gilbert and Standfort (2000) reported that twothirds of the cases of ocular toxoplasmosis in the UnitedKingdom are from post-birth origin.

    The PNST may cause serious consequences toimmunosupressed individuals, fetus of pregnant womencarrying negative serology of the disease and may cause

    irreversible damage to the vision, mainly when the opticnerve and macula are involved (Lieb et al., 2004).

    The diagnosis of the systemic post-birth diseaseand the recognition of the origin of infection are essentialto understand the basic mechanisms of the disease, princi-pally for protection of high risk patients, to preventionplanning programs and to guidance about therapeuticconsequences (Bosch-Driessen; Rothova, 1999).

    The specific treatment of PNOT consists in theuse of pirimetamin, sulfadiazin and folinic acid. When-ever an intense inflammation occurs, the use of systemiccorticosteroids is indicated. Thus, the precise diagnosis ofPNST is quite important, once it is known that the use ofsteroids during parasythemia (with no specific drugs fortoxoplasmosis) may cause severe destruction of the retinaand uncontrolled dissemination of the infection (Rondayet al. 1995).

    Outbreaks of PNST have been described in sev-eral countries (Burnett et al. 1998, Mansur; Jones;Lempert, 1978; Moura et al., 2006). In fact, speaking ofepidemiology, the PNST has assumed an important roleall over the world. It reasserts not only about the impor-tance of diagnosis in the patient infected with the sys-temic disease, but also about the need of investigationof the origin f acute disease: how many persons werecontaminated, when it happened and what were its com-plications. Luft and Remington (1984) proved that theacute toxoplasmic infection in family members of pa-tients with lymphadenopathy caused by T.gondii is com-mon. They also showed that toxoplasmosis can be foundin groups or persons infected from the same origin(Akstein; Wilson; Teutsch, 1982; Gonalves et al., 1995;Teutsch et al.,1979). Additionally, the presence of ocu-lar toxoplasmosis has been verified in more than onebrother / sister in the same family (Pinheiro; Orfice,1990; Silveira et al., 1988).

    Recent studies have been discussing the truerole of the post-birth systemic infection in ocular dis-ease. Some authors (Bahia-Oliveira et al., 2003; Bowieet al., 1997; Burnett et al., 1998; Ross et al., 2001;Silveira et al., 2001) have suggested that the post-birthsystemic infection might be an important cause of ocu-lar toxoplasmosis.

    Orfice et al. (2009) evaluated cases with clinical,serologic and epidemiologic evidences of post-birth ocu-lar toxoplasmosis and episodes of ocular affection as theonly manifestation of the systemic infection where therewere no other clinical evidences of PNST. Researchesabout this subject with such a large sample are rare in theworld literature, once this is a difficult diagnosis diseaseand with cases of conflicting diagnosis (tables 1,2).

    Rev Bras Oftalmol. 2010; 69 (3): 184-207

    Toxoplasmose ocular adquirida - Toxoplasmose ocular ps-natal

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    INTRODUO

    O T.gondii, agente etiolgico da toxoplasmose, um protozorio intracelular obrigatrio, de dis-tribuio mundial. O parasito tem ampla dis-tribuio geogrfica e comporta-se como agente de altainfecciosidade e baixa patogenicidade, visto que 50,0%ou mais da populao esto contaminados pelo T.gondiie apenas uma proporo reduzida apresenta a doena(Holland, 1999). No Brasil 50,0 a 83,0% da populaoadulta soropositivo (Orfice; Bahia-Oliveira, 2005).

    A forma de apresentao mais comum datoxoplasmose sistmica ps-natal (TSPN) a formaassintomtica que acomete 80-90% dos casos (Akstein;Wilson; Teutsch, 1982; Mansur; Jones; Lempert, 1978;Stagno; Dykes; Amos, 1980). O comprometimento ocu-lar nessa infeco pode ocorrer durante a fase aguda oumuitos anos aps a doena sistmica, sendo o intervalode latncia muito varivel. Isso torna difcil o diagnsti-co da toxoplasmose ocular ps-natal (TOPN), j que oscasos com comprometimento ocular na fase inativa dadoena podem ser confundidos com infeco congnitade aparecimento tardio (Akstein; Wilson; Teutsch, 1982;Couvreur; Thulliez, 1996; Mansur; Jones; Lempert, 1978;Melamed, 1994).

    Apesar do relato de dois em cinco casos de TOPNdescritos por Hogan (1958) e por Hogan e Kimura(1964), Perkins (1973), respectivamente afirmarem queo envolvimento ocular na TSPN ocorre em 2 a 3% doscasos e que no Reino Unido, quase todos os casos detoxoplasmose ocular eram de origem congnita. Ade-mais, que as complicaes da toxoplasmose sistmicaso mais frequentes quando h envolvimento do SNC.Esses conceitos prevaleceram por vrios anos. Entretan-to, Glasner, Silveira e Kruszon-Moran (1992) e Gilberte Standford (2000) ressaltaram a importncia da infec-o sistmica ps-natal na toxoplasmose ocular. Almdisso, a alta incidncia da infeco ps-natal documen-tada no sul do Brasil sugere que a infeco ps-natalpode ser uma forma comum de transmisso da doena(Glasner; Silveira; Kruszon-Moran, 1992). Outro estudona mesma regio comprovou que 8,3% dos indivduoscom infeco ps-natal, que no tinham retinocoroidite,apresentaram cicatriz aps perodo de sete anos (Silveiraet al., 2001). Gilbert e Standfort (2000) relatam que doisteros dos casos de toxoplasmose ocular do Reino Uni-do so de origem ps-natal.

    A TSPN pode trazer srias consequncias aimunodeprimidos, fetos de mulheres grvidas comsorologia negativa da doena, alm de comprometer aviso, levando a danos irreversveis, principalmente quan-

    do o nervo ptico e mcula so envolvidos (Lieb et al.,2004).

    O diagnstico da doena sistmica ps-natal e oreconhecimento da origem da infeco so essenciaispara o entendimento dos mecanismos bsicos da infec-o, principalmente para a proteo dos pacientes derisco, para o planejamento de programas de prevenoe para orientao quanto s consequncias teraputicas(Bosch-Driessen; Rothova, 1999).

    O tratamento especfico da TOPN consiste no usode pirimetamina, sulfadiazina e cido folnico. Quandoh intensa reao inflamatria, est indicado o uso decorticosterides via sistmica. Assim, importante ocorreto diagnstico da TSPN porque sabido que a ad-ministrao de corticosterides durante a parasitemia(sem medicao especfica para toxoplasmose) podecausar acentuada destruio da retina e disseminaodescontrolada da infeco (Ronday et al., 1995).

    Surtos de TSPN tm sido descritos em vrios