RESUMO
La toxoplasmosis, enfermedad conocida como “Parasitosis del Siglo XX”, cobra importancia en los neonatos cuyas madres se infectaron por primera vez durante la gestación. El objetivo del trabajo es presentar el caso de un recién nacido de 40 semanas con toxoplasmosis congénita. El peso al nacer fue de 3 500 g, Apgar 2/3. Requirió intubación orotraqueal y resucitación cardiopulmonar inmediata. Hubo presencia de líquido amniótico meconial, tiempo de rotura de membranas de 14 h, antecedentes maternos de sepsis vaginal, y con un descenso detenido de la presentación lo que llevó a cesárea de urgencia. A las 4 h de vida desarrolla cuadro de coagulación intravascular diseminada, acompañado de hipotonía marcada, mirada fija sin respuesta pupilar ni esfuerzo respiratorio. A las 48 h aparece insuficiencia renal aguda con evolución rápida a fallo múltiple de órganos. Ultrasonido de cráneo con aumento de la ecogenicidad cerebral, borramiento de las circunvoluciones cerebrales y ventrículos laterales dilatados. Evolución tórpida, sin recuperación neurológica, alteraciones del medio interno y trastornos del equilibrio ácido-base e hidroelectrolítico, empeoramiento progresivo de la función cardiaca y respiratoria, fallece a los 21 días de vida.
Toxoplasmosis, known as the "Twentieth century parasites disease", becomes important in infants whose mothers were infected for the first time during pregnancy. The aim of this work is to present the case of a 40 weeks newborn with congenital toxoplasmosis. The birth weight was 3 500 g, Apgar 2/3. Immediate endotracheal intubation and cardiopulmonary resuscitation was required. There were meconium, 14-hour membrane rupture time, maternal history of vaginal sepsis, detained presentation prompting emergency caesarean section. At 4 hours of life, disseminated intravascular coagulation develops, accompanied by marked hypotonia, staring with no pupillary response or respiratory effort. At 48 hours, acute renal failure appears with rapid progression of multiple organ failure. Skull ultrasound showed increased brain echogenicity, effacement of the cerebral convolutions and dilated lateral ventricles. Torpid evolution, with no neurological recovery, internal disorders and disorders of acid-base and electrolyte balance, progressive deterioration of the cardiac and respiratory functions, dies at 21 days of life. Decease occurs at 21 days of life.
Assuntos
Humanos , Feminino , Recém-Nascido , Toxoplasmose Congênita/complicações , Toxoplasmose Congênita/mortalidade , Toxoplasmose Congênita/transmissãoRESUMO
There is a lack of studies using Toxoplasma gondii strains isolated from human patients. Here, we present a pathological study of three strains obtained from human cases of congenital toxoplasmosis in Brazil using inbred mice after oral infection with 10 tissue cysts. Multiplex-nested PCR-RFLP of eleven loci revealed atypical genotypes commonly found in Brazil: toxodb #8 for TgCTBr5 and TgCTBr16 strains and toxodb #11 for the TgCTBr9 strain. BALB/c and C57BL/6 mice were evaluated for survival and histological changes during the acute phase of the disease. All mice inoculated with the non-virulent TgCTBR5 strain survived after 30 days, although irreversible tissue damage was found. In contrast, no mice were resistant to infection with the highly virulent TgCTBR9 strain. The TgCTBr16 strain resulted in 80% survival in mice. However, this strain presented low infectivity, especially by the oral route of infection. Despite being identified with the same genotype, TgCTBr5 and TgCTBr16 strains showed biological differences. Histopathologic analysis revealed liver and lungs to be the most affected organs, and the pattern of tissue injury was similar to that found in mice inoculated perorally with strains belonging to clonal genotypes. However, there was a variation in the intensity of ileum lesions according to T. gondii strain and mouse lineage. C57BL/6 mice showed higher susceptibility than BALB/c for histological lesions. Taken together, these results revealed that the pathogenesis of T. gondii strains belonging to atypical genotypes can induce similar tissue damage to those from clonal genotypes, although intrinsic aspects of the strains seem critical to the induction of ileitis in the infected host.
Assuntos
Toxoplasma/patogenicidade , Toxoplasmose Animal/patologia , Toxoplasmose Congênita/patologia , Animais , Encéfalo/parasitologia , Encéfalo/patologia , Feminino , Técnicas de Genotipagem , Humanos , Íleo/patologia , Recém-Nascido , Intestinos/patologia , Fígado/patologia , Pulmão/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Reação em Cadeia da Polimerase Multiplex , Polimorfismo de Fragmento de Restrição , Baço/patologia , Análise de Sobrevida , Toxoplasma/classificação , Toxoplasma/genética , Toxoplasmose Animal/mortalidade , Toxoplasmose Animal/parasitologia , Toxoplasmose Congênita/mortalidade , Toxoplasmose Congênita/parasitologia , VirulênciaRESUMO
Aims: To review the present knowledge about congenital toxoplasmosis in South America and to advance some hypothesis for future research. Source of data: Medline and Scielo database search for papers reporting clinical characteristics of cohorts of children in South America and comparative studies between South America and other continents. Summary of findings: Systematic analysis of primary data obtained during screening programs showed that the risk of ocular lesions in congenital toxoplasmosis was much higher in the South American cohorts (47%; 18/38) than in Europe (14%, 79/550). The crude risk of intracranial lesions was much higher in the cohorts from South America (53%, 20/38) than those from Europe (9%, 49/550). In a Colombian cohort it was found 11% of mortality. Additionally, a comparative prospective cohort of congenitally infected children from Brazil and Europe found that in Brazilian children eye lesions were larger, more numerous and more likely to affect the area of the retina responsible for central vision that their counterpart in Europe. The presence of Toxoplasma strains genetically different to those found in North America and Europe could explain the higher severity of congenital toxoplasmosis in South America. Conclusions: Congenital toxoplasmosis in South America seems to be more frequent and infected children are more symptomatic than in Europe and in North America. Research for new drugs and candidate vaccines are a priority to improve indicators of health in children of South America.
Objetivos: revisar o conhecimento atual sobre toxoplasmose congênita na América do Sul e traçar algumas hipóteses para futura pesquisa. Fonte de dados: busca nas bases de dados Pubmed e Scielo por artigos sobre características clínicas de coortes de crianças com toxoplasmose congênita na América do Sul e estudos comparativos entre América do Sul e outros continentes. Síntese dos dados: uma análise sistemática de dados primários obtidos durante programas de triagem mostrou que o risco de lesões oculares foi muito maior na coorte de crianças da América do Sul (47%, 18/38) do que nas européias (14%, 79/550). O risco bruto de lesões intracranianas foi muito maior na coortes da América do Sul (53%, 20/38) do que nas da Europa (9%, 49/550). Em uma coorte colombiana constatou-se 11% de mortalidade. Adicionalmente, uma coorte prospectiva, que comparou crianças com toxoplasmose congênita do Brasil e da Europa, mostrou que nas crianças brasileiras as lesões oculares foram maiores, mais numerosas e com maior probabilidade de atingir o polo posterior da retina do que nas européias. A presença de cepas de Toxoplasma gondii diferentes das da Europa e dos Estados Unidos pode explicar a maior gravidade da toxoplasmose congênita na América do Sul. Conclusões: a toxoplasmosis congênita na América do Sul parece ser mais frequente e as crianças infectadas são mais sintomáticas do que na Europa e na América do Norte. A pesquisa sobre novas drogas e vacinas deve ser prioritária, para melhorar os indicadores de saúde nas crianças da América do Sul.
Assuntos
Polimorfismo Genético , Predisposição Genética para Doença , Toxoplasma/classificação , Toxoplasma/genética , Toxoplasma/patogenicidade , Toxoplasmose Congênita/complicações , Toxoplasmose Congênita/epidemiologia , Toxoplasmose Congênita/mortalidade , Toxoplasmose OcularRESUMO
Fatal cases of toxoplasmosis seen at the Hospital Infantil de México between 1943 and 1973, together with postmortem studies are reviewed. There were five postmortem studies where it was possible to identify toxoplasma in histologic lesions. Clinical manifestations were grouped in pictures; thus, the infectious picture, the intracranial hypertensive, the neurological and the meningeal pictures were made up. In all five cases of this small group, toxoplasma was identified within and without parasitized cells and was found specially abundant in the central nervous system. Considering the early initiation of neurological manifestations and the intensity of encephalic lesions, it may be assumed that all five cases of prenatal toxoplasmosis. The reason why an infection so usually light in the mother is able to cause a disease so severe in the fetus seems to have an explanation on the fact that toxoplasma increases in virulence when reaching the product as second-step infection. In all five cases, the intensity of the lesions agrees with the severeness of the clinical picture and with the early manifestations following birth. The parasite was identified in the brain in all cases and in some of them, in the liver and lungs.