Tema Toxoplasmose Congenita - Transmissão vertical

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Aluno: Rodrigo Lima de Albuquerque 
Curso: Enfermagem 
Período: Noturno 
RA: 201603327381 
 
 
RESUMO DE ARTIGO PROPOSTO SOBRE O TEMA TOXOPLASMOSE 
CONGÊNITA 
 
Introdução: 
A toxoplasmose é uma zoonose causada pelo parasita intracelular 
obrigatório Toxoplasma gondii, (protozoário intracelular pertencente à ordem 
Coccidia, capaz de infectar praticamente qualquer linhagem de células dos 
mamíferos ou aves) que acomete cerca de um terço da população mundial. 
Esta infecção pode ser adquirida pela ingestão de alimentos contaminados, 
transfusão sanguínea e de órgãos e por transmissão vertical (Derouin & Pellox, 
2008; Gelaye et al., 2015; Jones et al., 2009). Homens e os outros animais são 
apenas hospedeiros intermediários do parasita que penetra pelo tubo digestivo 
e, através da corrente sanguínea, pode alojar-se em diferentes tecidos do 
corpo e nos líquidos orgânicos (como saliva, esperma, líquido peritoneal). 
 Entretanto, não é encontrado nas hemácias. A infecção por T. gondii 
em seres humanos geralmente é assintomática e autolimitada e sua 
manifestação mais severa se consolida por meio da toxoplasmose congênita 
(TC). Os riscos de transmissão durante a gestação variam de 10% a 80%, 
dependendo da idade gestacional do feto, da virulência da cepa do parasito, da 
resposta imune da mãe, da permeabilidade placentária e do tratamento pré-
natal. (Chaudhy et al., 2014; Dunn et al., 1999). Geralmente, a transmissão 
para o embrião/feto se dá quando a mãe é acometida de toxoplasmose aguda. 
 
 
Ciclo Biológico do Parasita: 
Apresenta um ciclo biológico de duplo hospedeiro, em que o gato é o 
hospedeiro definitivo, no qual o ciclo reprodutivo é enteroepitelial. Outros 
mamíferos e aves são hospedeiros intermediários, que abrigam o ciclo 
proliferativo extraintestinal. Existem 3 estágios de desenvolvimento: 
1. Taquizoítos: Multiplicação rápida que determinam a lesão tecidual na 
infecção aguda e que provavelmente estão implicados na transmissão 
transplacentária em humanos. Encontrado dentro do vacúolo parasitóforo de 
várias células, como nos líquidos orgânicos, excreções, macrófagos, células 
hepáticas, pulmonares, nervosas e musculares. 
2. Bradizoítos: Formas de multiplicação lenta, delimitando uma infecção 
crônica. Encontrado dentro do vacúolo parasitóforo dos tecidos muscular 
esquelético, cardíaco, nervoso e retiniano. 
3. Esporozoítos: Presentes nos oocistos eliminados nas fezes de gatos. Em um 
período de 3 dias ocorre a esporulação e consequente formação dos 
esporozoítos, os oocistos tornam-se infectivos para mamíferos e aves. 
 
Processo de Invasão: 
Primeiramente, o taquizoíto entra em contato com a célula hospedeira. 
No momento da adesão do taquizoíto à superficie da célula hospedeiro, há 
secreção das proteínas dos micronemas e róptrias, logo depois forma-se a 
junção móvel. Ao formar a junção móvel o parasito sofre uma constrição, 
deformando seu corpo. Quando o parasito invade a célula, ocorre a formação 
do vacúolo parasitóforo. 
 
Toxoplasmose Congênita: 
Como o sistema imune do feto está "imaturo" a presença do parasita 
promove ações muito mais graves que em adultos, além do fato de que 
comprometer a formação do órgão já é uma condição de maior gravidade, daí 
ações hepáticas, neurológicas e motoras são possíveis. Outra condição muito 
grave gerada pela infecção é a contaminação dos pneumócitos que leva ao 
comprometimento pulmonar. O acometimento dos olhos merece destaque, pois 
o medo comum das gestantes em relação aos gatos é que eles podem fazer 
seus filhos nascerem cegos, e de fato a visão pode ser comprometida com a 
infecção, apesar de existirem inúmeras condições "mais graves". 
(BRASILEIRO FILHO, 2016; FIGUEIRÓ-FILHO, 2005)A TC pode levar ao óbito 
cerca de 40% a 50% dos fetos infectados e os que sobrevivem podem 
desenvolver múltiplas manifestações clínicas, tais como: convulsões, 
espasticidade, microcefalia, hidrocefalia, meningoencefalomielite, retardamento 
mental, coriorretinite, hepatoesplenomegalia, icterícia e erupções cutâneas 
(Prusa et al., 2012; Remington et al., 2001)Tríade clássica - coriorretinite, 
calcificações intracranianas e hidrocefalia - é muitas vezesacompanhada por 
convulsões. 
 
 
Profilaxia: 
A profilaxia para a toxoplasmose congênita depende exclusivamente de 
certos cuidados básicos para evitar a infestação do parasita no organismo da 
gestante. A toxoplasmose pode ser adquirida pelo ser humano adulto através 
de duas vias: Por ingestão dos protozoários defecados pelos gatos na terra, no 
lixo ou na areia, veiculados pelo contato manual ou através de vetores, como 
moscas, baratas e minhocas. Por ingestão de carne crua ou mal passada de 
animais contaminados. Para prevenir a infestação na gestante não imunizada, 
é necessário evitar o contato desta com gatos e a sua presença no ambiente 
doméstico; manter perfeita limpeza da casa e arredores, eliminando os insetos 
vetores; habituar a gestante ao uso de luvas para manipular carnes cruas, o 
solo, a areia e o lixo, lavando muito bem as mãos após o contato com este tipo 
de material; finalmente, cozinhar bem as carnes (o aquecimento acima de 
sessenta e seis graus centígrados mata o toxoplasma). A espiramicina é um 
antibiótico macrolídeo similar à eritromicina, que não atravessa a barreira 
placentária, portanto não ajudando na infecção fetal. A dose recomendada é de 
3g/dia, divididos em três tomadas, sem alimentos, até o final da gestação. Com 
ele há a diminuição de cerca de 60% da transmissão vertical e o tratamento 
precoce reduz a frequência e a gravidade das sequelas. 
 
 
Diagnóstico no Embrião: 
A toxoplasmose pode ser diagnosticada pela USG fetal, porém não é 
muito eficaz pois geralmente é inespecífico e, em muitos casos, nenhuma 
alteração é visível. Por essa razão, é importante o acompanhamento 
ultrassonográfico seriado dos fetos infectados e também dos casos suspeitos. 
Os principais achados são hidrocefalia, calcificações intracranianas, 
hepatoesplenomegalia, ascite fetal e espessamento da placenta. Quando há 
evidências de acometimento fetal, pode ser realizada pesquisa de DNA do 
Toxoplasma no líquido amniótico. Já as alterações neonatais são: coriorretinite, 
hepatoesplenomegalia, linfadenopatia, icterícia, anemia, anormalidades 
liquóricas, estrabismo, crises convulsivas, erupção cutânea, hidrocefalia, 
calcificações cerebrais, macro ou microcefalia, restrição do crescimento 
intrauterino, prematuridade, distermias e sangramentos. (Secretaria de Estado 
da Saúde, 2015). 
Quando a USG não dá sinais de alterações é importante pesquisar a 
Toxoplasmose pós-natal no RN, trazendo alguns exames necessários para 
essa pesquisa como: hemograma completo com plaquetas, sorologia para 
toxoplasmose (IgG, IgM), líquor no RN sintomático, RX do crânio do RN 
(calcificações cerebrais), ecografia cerebral transfontanelar (calcificações 
cerebrais, necroses, dilatação ventricular), exame oftalmológico e, tendo sinais 
de coriorretinite, iniciar tratamento com corticóides. (GOES, 2012). A maioria 
dos RN não apresenta sintomas ao nascimento. Em grande parte das crianças 
afetadas as sequelas aparecem depois de meses ou anos como diminuição da 
acuidade visual, deficiência cognitiva de gravidade variável e epilepsia, sendo 
coriorretinite a manifestação mais prevalente, podendo acometer até 90% dos 
infectados. 
 
 
Tratamento: 
Por ser patologia suscetível ao tratamento por antibiótico totalmente 
seguro durante a gestação (espiramicina), o médico assistente deve estar 
atento aos seus sintomas na mãe. O diagnóstico é feito através de sorologia 
específica, mas a simples suspeita durante a gravidez, na falta ou no atraso do 
recurso laboratorial, justifica o tratamento. A gravidade da doença e a 
segurança da medicação, que não oferece nenhum risco teratogênico, 
fundamentam a conduta. A coleta rotineira de sorologia para toxoplasmose, 
antes e durante a gestação, é tema de controvérsias. No entanto, a sorologia 
anterior negativa, seguida de quadroclínico compatível e de nova sorologia 
positiva, confirma o diagnóstico de toxoplasmose adquirida e auxiliam o médico 
na decisão terapêutica. Por outro lado, a sorologia francamente positiva 
realizada antes da gravidez é sinal de imunidade e o risco de transmissão da 
doença para o feto por via transplacentária praticamente inexiste. 
O tratamento materno com espiramicina (3 gramas por dia fracionadas 
em três tomadas) deve acontecer nas situações em que haja confirmação de 
infecção materna, em caso de soroconversão (positivação do IgG após IgM 
positivo) e teste de avidez baixo, ou seja, o tratamento deve ser iniciado com o 
objetivo de reduzir o risco de transmissão fetal em caso de infecção materna e 
está indicado no primeiro trimestre de gestação. A combinação de sulfadiazina, 
pirimetamina e ácido folínico é indicada para o tratamento de grávidas com 
diagnóstico de infecção aguda pelo toxoplasma adquirida no final do segundo 
trimestre ou durante o terceiro trimestre de gestação. O tratamento do RN, filho 
de mãe com toxoplasmose, deve ser iniciada e só interrompida quando, dois 
resultados sorológicos negativos, obtidos com um mês de intervalo, 
demonstrarem que não houve infecção. Tal como na grávida com 
toxoplasmose, a terapêutica do RN é feita com pirimetamina e sulfadiazina. 
 
Referências: 
 
Artigo: Programas de Controle da Toxoplasmose Congênita. Autores: Fabiana Maria 
Ruiz Lopes, Regina Mitsuka-Breganó, Jaqueline Dario Capobiango, Inácio Teruo 
Inoue, Edna Maria Vissoci Reiche, Helena Kaminami Morimoto, Antônio Marcelo 
Barbante Casella, Laura Helena França De Barros Bittencourt, Roberta Lemos Freire, 
Italmar Teodorico Navarro. Publicado em: Rev Assoc Med Bras 2011; 57. 
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