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Other viral infections
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
The rate of congenital infection and the effect of transplacental infection appear to vary with gestational age at the time of infection. In a large prospective study of 1016 women with confirmed rubella infection, the rate of congenital infection was 81% in the first 12 weeks, 54% at 13 to 16 weeks, 36% at 17 to 22 weeks, 30% at 23 to 30 weeks, 60% at 31 to 36 weeks, and 100% from 37 weeks to delivery (55). No congenital anomalies were seen if infection occurred after 16 weeks. Another prospective study found no congenital anomalies if maternal infection occurred after 17 weeks of gestation (56,57).
Infection and immunology
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
Toxoplasmosis is caused by Toxoplasma gondii, which is a coccidian protozoan. It is an intracellular parasite which can multiply in all tissues of mammals and birds. Infection may be congenital, when it may manifest like any other congenital infection, or acquired. The latter may be asymptomatic or present with malaise, fever, myalgia, maculopapular rash, localized or generalized lymphadenopathy, hepatomegaly, encephalitis, pneumonia, myocarditis and choroidoretinitis. Although the organism is sensitive to sulphonamides, a combination of pyrimethamine and sulphonamides is superior.
Toxoplasma
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Fernanda Silva de Souza, Renato Augusto DaMatta
In most pregnant women, acute T. gondii infection is asymptomatic.73 A study performed with 131 mothers who had congenitally infected children showed that over half of them could not remember any clinical signs of toxoplasmosis during their pregnancy.90 The risk of vertical transmission increases in the later stages of pregnancy. Dunn et al.91 showed that the risk was 6% at 13 weeks of gestation and increased to 72% at 36 weeks. However, clinical signs are more evident after birth in children infected in early pregnancy.91 It is possible, although rare, that infected mothers before conception can transmit the parasite to the child.18 In the majority of cases, significant sequels may appear months or years after birth. Congenital infection can result in mental retardation, visual loss, hydrocephalus, retinochoroiditis, intracerebral calcification, loss of hearing, and even death.73,92
Molecular diagnosis of toxoplasmosis: recent advances and a look to the future
Published in Expert Review of Anti-infective Therapy, 2021
Marie Gladys Robert, Marie-Pierre Brenier-Pinchart, Cécile Garnaud, Hélène Fricker-Hidalgo, Hervé Pelloux
In the absence of a systematic follow-up program for CT during pregnancy, congenital infection is sometimes only suspected based on clinical signs at birth or even much later because symptoms can appear after several months or years [42]. In these situations, molecular diagnosis can be performed in peripheral blood, cerebro-spinal fluid (CSF) or urine and also profitably complement serology [43–46]. Sterkers et al. showed from a cohort of 12 newborns that PCR on neonatal peripheral blood could confirm the diagnosis of CT with a sensitivity of 83%, and that PCR could be the first positive test [43]. The sensitivity and specificity of CSF PCR were evaluated in a study on a cohort of infants born from an untreated mother. The authors reported an overall sensitivity of 46.5% and a specificity of 100%. The sensitivity was higher when the infants presented major clinical signs [44].
Immunogenicity and protection efficacy of enhanced fitness recombinant Salmonella Typhi monovalent and bivalent vaccine strains against acute toxoplasmosis
Published in Pathogens and Global Health, 2021
Fei-Kean Loh, Sheila Nathan, Sek-Chuen Chow, Chee-Mun Fang
It is estimated that one-third of the global human population has been exposed to Toxoplasma gondii [1], an opportunistic intracellular protozoan which stays active as tachyzoites but converts to bradyzoites in response to stress [2]. The parasite replicates sexually within the guts of feline families and the oocysts are excreted to the environment. The oocysts are then ingested and usually transmitted through food sources between the definitive hosts and intermediate hosts which include almost all mammals [2]. Most T. gondii infections are asymptomatic as the parasite is suppressed by effective host immune control. However, the tissue cysts can recrudesce in immunocompromised hosts and cause diverse complications. For instance, AIDS/HIV patients have an increased frequency of toxoplasma encephalitis [3]. In pregnant women, T. gondii may transmit across the placenta and cause miscarriage of the fetus. Infants with congenital infection have been diagnosed with manifestations including chorioretinitis, calcification and hydrocephalus [4]. Meta-analyses have also deduced positive correlation between T. gondii seropositivity and psychotic symptoms such as schizophrenia and bipolar disorder [5,6]. To date, there is only one live attenuated vaccine developed from the T. gondii S48 strain, Toxovax, mainly used to prevent sheep and goat abortions in United Kingdom, New Zealand, France and Ireland. All the drugs used in clinical practice are solely active against tachyzoites and are not able to clear cysts formed during chronic infection [7].
Congenital cytomegalovirus infection: epidemiology, prediction, diagnosis, and emerging treatment options for symptomatic infants
Published in Expert Opinion on Orphan Drugs, 2020
Nobuhiko Nagano, Ichiro Morioka
In some case of symptomatic infants, anti-viral treatments with IV GCV or oral VGCV, which are started from the neonatal period, have improved hearing and neurological prognosis. Therefore, if symptomatic infants with congenital infection are diagnosed, they should be consulted with doctors who specialize in neonatal or pediatric infection and should be considered to undergo treatments. However, GCV and VGCV are still off-label drugs for congenital CMV infection worldwide, because there are concerns about its safety during the treatment (myelosuppression, especially neutropenia that occurs at high rates). Long-term influences with fertility and carcinogenicity, which have been demonstrated in animal toxic experiments, have not yet been addressed in humans. The selection of infants to be treated must be done carefully. There is no established evidence for starting treatment after the neonatal period. Moreover, it should be remembered that there are cases where the effectiveness is remarkable, but treatment does not show an effect or hearing is worse even after receiving the treatment. At present, this treatment should be performed with a well-informed consent from the parents.