Asymptomatic Congenital Infection Research Articles

One-year neurodevelopmental outcome in children with asymptomatic congenital CMV infection

IntroductionInfants with congenital CMV (cCMV) infection may show manifestations at birth and develop symptomatic disease, although the majority have no apparent clinical signs and should be considered asymptomatic (acCMV). Studies about neurodevelopmental and neurological sequelae in acCMV patients during childhood are few and contradictory, thus, the purpose of this study is to evaluate the neurological and neurodevelopmental outcomes in 1-year-old children with acCMV infections. MethodThirty-five infants with acCMV infections were followed-up for 12 months and were compared to healthy children matched for age and gender. The Bayley Scales of Infant Development III (BSID-III) were administered, and neurological examinations were performed. ResultsChildren with acCMV infection showed minimal to mild neurological signs and the score obtained from the Motor Scale was significantly lower than that of the control group. No significant differences between the two groups were found regarding the Cognitive and Language Scales. DiscussionAsymptomatic congenital infection of CMV may be associated with a decrease in motor skills that may become evident during the first year of life. Close monitoring is essential to determine if rehabilitative treatment is required for children with asymptomatic congenital cytomegalovirus (acCMV). Longer follow-up is necessary to provide further details about their neurodevelopmental outcomes.

Maternal-Fetal Infections (Cytomegalovirus, Toxoplasma, Syphilis): Short-Term and Long-Term Neurodevelopmental Outcomes in Children Infected and Uninfected at Birth.

(1) Background: Infections in pregnancy can lead to miscarriage, premature birth, infections in newborns, and developmental disabilities in babies. Infected infants, symptomatic at birth, can have long-term sequelae, and asymptomatic babies are also at increased risk of developing long-term sensorineural outcomes. Targeted therapy of the pregnant mother can reduce fetal and neonatal harm. (2) Aim of the study: To explore the association between symptoms and time of onset of long-term sequelae in infected children born from mothers who contracted an infection during pregnancy, by a long-term multidisciplinary follow-up. (3) Methods: For up to 2-4 years, we evaluated cognitive, motor, audiological, visual, and language outcomes in infants with symptomatic and asymptomatic congenital infections and in uninfected infants. (4) Results: 186 infants born from women who acquired Cytomegalovirus infection (n = 103), Toxoplasma infection (n = 50), and Syphilis (n = 33) during pregnancy were observed. Among them, 119 infants acquired the infection in utero. Infected infants, symptomatic at birth, obtained lower scores on the Cognitive and Motor Scale on Bayley-III compared to asymptomatic and uninfected infants (p = 0.026; p = 0.049). Many severe or moderate sequelae rose up within the first year of life. At 24 months, we observed sequelae in 24.6% (14/57) of infected children classified as asymptomatic at birth, compared to 68.6% (24/35) of symptomatic ones (χ2 = 15.56; p < 0.001); (5) Conclusions: Infected babies symptomatic at birth have a worse prognosis than asymptomatic ones. Long-term sequelae may occur in infected children asymptomatic at birth after the first year of life. Multidisciplinary follow-up until 4-6 years of age should be performed in all infected children, regardless of the presence of symptoms at birth.

Placental infection by Zika virus in French Guiana.

To describe placental findings on prenatal ultrasound and anatomopathological examination in women with Zika virus (ZIKV) infection, and to assess their association with congenital ZIKV infection and severe adverse outcome, defined as fetal loss or congenital Zika syndrome (CZS). This was a prospective study of pregnancies undergoing testing for maternal ZIKV infection at a center in French Guiana during the ZIKV epidemic. In ZIKV-positive women, congenital infection was defined as either a positive reverse transcription polymerase chain reaction result or identification of ZIKV-specific immunoglobulin-M in at least one placental, fetal or neonatal sample. Placental ZIKV-infection status was classified as non-exposed (placentae from non-infected women), exposed (placentae from ZIKV-infected women without congenital infection) or infected (placentae from ZIKV-infected women with proven congenital infection). Placentae were assessed by monthly prenatal ultrasound examinations, measuring placental thickness and umbilical artery Doppler parameters, and by anatomopathological examination after live birth or intrauterine death in women with ZIKV infection. The association of placental thickness during pregnancy and anatomopathological findings with the ZIKV status of the placenta was assessed. The association between placental findings and severe adverse outcome (CZS or fetal loss) in the infected group was also assessed. Among 291 fetuses/neonates/placentae from women with proven ZIKV infection, congenital infection was confirmed in 76 cases, of which 16 resulted in CZS and 11 resulted in fetal loss. The 215 remaining placentae from ZIKV-positive women without evidence of congenital ZIKV infection represented the exposed group. A total of 334 placentae from ZIKV-negative pregnant women represented the non-exposed control group. Placentomegaly (placental thickness > 40 mm) was observed more frequently in infected placentae (39.5%) than in exposed placentae (17.2%) or controls (7.2%), even when adjusting for gestational age at diagnosis and comorbidities (adjusted hazard ratio (aHR), 2.02 (95% CI, 1.22-3.36) and aHR, 3.23 (95% CI, 1.86-5.61), respectively), and appeared earlier in infected placentae. In the infected group, placentomegaly was observed more frequently in cases of CZS (62.5%) or fetal loss (45.5%) than in those with asymptomatic congenital infection (30.6%) (aHR, 5.43 (95% CI, 2.17-13.56) and aHR, 4.95 (95% CI, 1.65-14.83), respectively). Abnormal umbilical artery Doppler was observed more frequently in cases of congenital infection resulting in fetal loss than in those with asymptomatic congenital infection (30.0% vs 6.1%; adjusted relative risk (aRR), 4.83 (95% CI, 1.09-20.64)). Infected placentae also exhibited a higher risk for any pathological anomaly than did exposed placentae (62.8% vs 21.6%; aRR, 2.60 (95% CI, 1.40-4.83)). Early placentomegaly may represent the first sign of congenital infection in ZIKV-infected women, and should prompt enhanced follow-up of these pregnancies. Copyright © 2019 ISUOG. Published by John Wiley & Sons Ltd.

Trophoblast communication with distant cells – messaging via extracellular vesicles and non-coding RNA

Cytomegalovirus (CMV) infection is the most common cause of congenital viral infections in humans. The unusual structure of the placenta plays a pivotal role in CMV transmission from mothers to fetuses. The aim of this study was to evaluate the histopathological findings of placentas with congenital CMV infections.We obtained placental specimens from 35 women who had newborns with congenital CMV infections. Placental specimens, extraplacental membranes, and umbilical cords were stained with hematoxylin and eosin, and subjected to immunohistochemical analysis. We evaluated the localization of CMV-infected cells and other histological parameters.Thirty (86%) of the 35 placentas tested positive for CMV-infected cell proteins by immunohistochemistry. A majority of CMV-positive cells were present in fibroblasts and endothelial cells in the villi. The number of CMV-infected cells was inversely correlated to gestational age at delivery. The frequency of chronic villitis (65% vs. 11%; p < 0.01) and changes of the villi (38% vs. 0%; p < 0.05) in the placentas from mothers with symptomatic congenital CMV infections was higher than those observed in samples from mothers with asymptomatic congenital infections. The frequency of changes of the decidua (43% vs. 5%; p < 0.01) in the placentas from mothers with non-primary CMV infections was higher than those from mothers with primary infections.Chronic villitis and changes of the villi were associated with symptomatic congenital CMV infections. The changes of the decidua were associated with congenital CMV infections, in mothers with non-primary CMV infections.

Histopathological analysis of placentas with congenital cytomegalovirus infection

IntroductionCytomegalovirus (CMV) infection is the most common cause of congenital viral infections in humans. The unusual structure of the placenta plays a pivotal role in CMV transmission from mothers to fetuses. The aim of this study was to evaluate the histopathological findings of placentas with congenital CMV infections. MethodsWe obtained placental specimens from 35 women who had newborns with congenital CMV infections. Placental specimens, extraplacental membranes, and umbilical cords were stained with hematoxylin and eosin, and subjected to immunohistochemical analysis. We evaluated the localization of CMV-infected cells and other histological parameters. ResultsThirty (86%) of the 35 placentas tested positive for CMV-infected cell proteins by immunohistochemistry. A majority of CMV-positive cells were present in fibroblasts and endothelial cells in the villi. The number of CMV-infected cells was inversely correlated to gestational age at delivery. The frequency of chronic villitis (65% vs. 11%; p < 0.01) and changes of the villi (38% vs. 0%; p < 0.05) in the placentas from mothers with symptomatic congenital CMV infections was higher than those observed in samples from mothers with asymptomatic congenital infections. The frequency of changes of the decidua (43% vs. 5%; p < 0.01) in the placentas from mothers with non-primary CMV infections was higher than those from mothers with primary infections. DiscussionChronic villitis and changes of the villi were associated with symptomatic congenital CMV infections. The changes of the decidua were associated with congenital CMV infections, in mothers with non-primary CMV infections.

Persistent Cytomegalovirus Infection in Amniotic Membranes of the Human Placenta

Human cytomegalovirus (HCMV) is the leading viral cause of birth defects, including microcephaly, neurological deficits, hearing impairment, and vision loss. We previously reported that epithelial cells in amniotic membranes of placentas from newborns with intrauterine growth restriction and underlying congenital HCMV infection contain viral proteins in cytoplasmic vesicles. Herein, we immunostained amniotic membranes from 51 placentas from symptomatic and asymptomatic congenital infection with HCMV DNA in amniotic fluid and/or newborn saliva, intrauterine growth restriction, preterm deliveries, and controls. We consistently observed HCMV proteins in amniotic epithelial cells (AmEpCs) from infected placentas, sometimes with aberrant morphology. Primary AmEpCs isolated from mid-gestation placentas infected with pathogenic VR1814 proliferated and released infectious progeny for weeks, producing higher virus titers than late-gestation cells that varied by donor. In contrast to intact virion assembly compartments in differentiated retinal pigment epithelial cells, infected AmEpCs made dispersed multivesicular bodies. Primary AmEpCs and explants of amniochorionic membranes from mid-gestation placentas formed foci of infection, and interferon-β production was prolonged. Infected AmEpCs up-regulated anti-apoptotic proteins survivin and Bcl-xL by mechanisms dependent and independent of the activated STAT3. Amniotic membranes naturally expressed both survivin and Bcl-xL, indicating that fetal membranes could foster persistent viral infection. Our results suggest strengthening innate immune responses and reducing viral functions could suppress HCMV infection in the fetal compartment.

Human cytomegalovirus UL55, UL144, and US28 genotype distribution in infants infected congenitally or postnatally.

Cytomegalovirus (CMV) is the most common cause of congenital infection. This pathogen exhibits extensive genetic variability in the genes that encode structural envelope glycoproteins, regulatory proteins, and proteins that contribute to immune evasion. However, the role of specific viral strains in the outcome of congenital CMV infection is unclear. Variation in the UL55 gene encoding glycoprotein B (gB), the UL144 gene encoding TNF α-like receptor, and the US28 gene encoding β-chemokine receptor was determined in 60 newborn infants with congenital CMV infection and 90 infants with postnatal or undefined CMV infection. CMV polymorphisms were studied in relation to disease outcome and viral load. Genotyping was performed by a sequencing analysis of PCR-amplified fragments, and the viral load was measured by quantitative real-time PCR. The results demonstrated that (1) the UL55 and US28 genotype distributions were similar among the group of congenital and postnatal CMV infection; (2) the UL144 B1 genotype was more prevalent in congenital than in postnatal infection and was detected in 70% of newborns with asymptomatic congenital infection; and (3) none of the examined genotype was significantly linked with symptomatic CMV infection. No relationship was observed between genotype and viral load. The results revealed that UL55, UL144, and US28 polymorphisms are not associated with the outcome of CMV infection in infants, but the presence of UL144 B1 genotype might be virological marker of asymptomatic infection at birth.

Antibody Kinetics in Infants Exposed to Chikungunya Virus Infection During Pregnancy Reveals Absence of Congenital Infection

To search for serological evidence of congenital infection in apparently healthy neonates born to women infected with the Chikungunya virus (CHIKV) during pregnancy, monitoring for CHIKV-specific antibodies was performed within the CHIMERE cohort study (Reunion island, 2006-2008). CHIKV-specific antibody kinetics showed no evidence of asymptomatic congenital infection as neonates were tested negative for CHIKV-specific IgM antibodies at birth and 368 infants with CHIKV-specific IgG antibodies seroreversed completely (mean seroreversion time: 7.7 months). Seroreversion time of transplacental CHIKV IgG antibodies was inversely correlated with the stage of pregnancy at which exposure took place and end-term small for gestational infants seroreversed earlier.

Distribution of UL144, US28 and UL55 genotypes in Polish newborns with congenital cytomegalovirus infections

Human cytomegalovirus (HCMV) is the most common congenital infection. HCMV strains display genetic variability in different regions. Distribution of HCMV genotypes in the population of congenitally infected newborns from Central Poland and viral load in newborns' blood is described and discussed. HCMV isolates were analysed by sequencing at three sites on the genome: the UL144 tumour necrosis factor-alpha (TNFα)-like receptor gene, the US28 beta-chemokine receptor gene and the UL55 envelope glycoprotein B (gB) gene. The newborns' blood was examined for HCMV DNA with a nested (UL144, UL55) or heminested (US28) polymerase chain reaction, and the genotypes were determined by sequence analysis. HCMV DNA was detectable in 25 out of 55 examined newborns born by HCMV-infected mothers (45.5%). The blood viral load in mother-infant pairs was determined. Most of the newborns had identical virus genotype, gB2 (96%), UL144 B1 (88%) and US28 A2 (84%). These genotypes were detected in all newborns with asymptomatic congenital infection. The occurrence of UL144 B1 or US28 A2 genotypes in the babies examined was significant in comparison to other genotypes (p=0.0002 and p=0.040 respectively). There was no association between specific gB subtypes in all patients groups (p=0.463). There was no correlation between HCMV genotypes and the outcome.

Prognostic markers of symptomatic congenital human cytomegalovirus infection in fetal blood

To identify fetal cord blood prognostic markers of symptomatic congenital human cytomegalovirus infection (HCMV). Retrospective observational study. Fetal medicine unit in Milan and Medical virology unit in Pavia, Italy. HCMV-infected and -uninfected fetuses of mothers with primary HCMV infection during the period 1995-2009. Overall, 94 blood samples from as many fetuses of 93 pregnant women experiencing primary HCMV infection were examined for multiple immunological, haematological and biochemical markers as well as virological markers. Congenital HCMV infection was diagnosed by detection of virus in amniotic fluid, and symptomatic/asymptomatic infections were determined by ultrasound scans, nuclear magnetic resonance imaging, histopathology or clinical examination at birth. Blood sample markers were retrospectively compared in symptomatic and asymptomatic fetuses with congenital infection. A statistical analysis was performed to determine the value of each parameter in predicting outcome. Univariate analysis showed that most nonviral and viral markers were significantly different in symptomatic (n = 16) compared with asymptomatic (n = 31) fetuses. Receiver operator characteristics analysis indicated that, with reference to an established cutoff for each marker, the best nonviral factors for differentiation of symptomatic from asymptomatic congenital infection were β(2) -microglobulin and platelet count, and the best virological markers were immunoglobulin M antibody and DNAaemia. β(2) -Microglobulin alone or the combination of these four markers reached the optimal diagnostic efficacy. The determination of multiple markers in fetal blood, following virus detection in amniotic fluid samples, is predictive of perinatal outcome in fetuses with HCMV infection.

Cytomegalovirus Blood Viral Load and Hearing Loss in Young Children With Congenital Infection

This study was designed to determine whether elevated viral load in infants and young children is associated with congenital cytomegalovirus (CMV)-related hearing loss. Blood samples were obtained from 135 children with congenital CMV infection. CMV DNA in the peripheral blood was quantitated with a real-time polymerase chain reaction assay. Viral load measurements were analyzed in 3 different age groups (<2 months, 2-12 months, 12-36 months). In children with symptomatic and asymptomatic infection, CMV DNA levels were not different between children with hearing deficit and those with normal hearing in all 3 age groups. In children with asymptomatic infection, the positive predictive value of a peripheral blood viral load >3500 genomic equivalents per milliliter (ge/mL) at <2 months and 2 to 12 months of age is 8%, and at 12 to 36 months of age is 11.8%. However, the negative predictive value of a viral load <3500 ge/mL is 94.4% at <2 months of age, and 100% at 2 to 36 months of age. Peripheral blood viral load is not associated with hearing loss in children with congenital CMV infection. However, a viral load of <3500 ge/mL is associated with a lower risk of hearing loss in children born with asymptomatic congenital infection.

Physical and intellectual development in children with asymptomatic congenital cytomegalovirus infection: A longitudinal cohort study in Qinba mountain area, China

Background Although about 90% of congenital cytomegalovirus (CMV) infection is asymptomatic in newborn, some of them could show sequelae later in life. Qinba mountain area is a place with high incidence of mental retardation and a high rate of CMV intrauterine transmission in China. The correlation between asymptomatic congenital CMV infection and developmental outcomes of children in this area remain unclear. Objectives To investigate the impact of asymptomatic congenital CMV infection on physical and intellectual development of children during the first 6 years of life in Qinba mountain area. Study design Longitudinal cohort study. Forty-nine of all the 54 children with asymptomatic congenital CMV infection were followed prospectively in a study for surveying physical growth and intellectual developments. Results Either in neonatal or in infant period, no significant difference was noted between the asymptomatic congenital CMV infection children and the controls in average weight, height and head circumference (both p > 0.05). The intellectual development was disproportion in asymptomatic congenital infected children. Compared with the control group, both global development quotient (DQ) and full-scale intelligence quotient (IQ) scores of asymptomatically infected children were worse ( t = 2.19, p = 0.031; t = 2.48, p = 0.015), especially on language DQ scores ( t = 3.25, p = 0.002) and verbal IQ scores ( t = 3.88, p = 0.000). However, the incidence rates of mental retardation (DQ/IQ < 70) were similar in two groups ( χ 2 = 1.03, p > 0.05). Conclusions Although asymptomatic congenital CMV infection did not have significant influence on the neonatal physical development or incidence of mental retardation later in life, it is obviously an important factor correlating with long-time cognitive outcomes, especially on the development of language. It is necessary to survey CMV congenital infection and monitor the early intellectual development of children with asymptomatic congenital CMV infection in this area.

Diagnóstico retrospectivo de infección congénita por citomegalovirus en un caso clínico infantil

10-15% of asymptomatic congenital infections by cytomegalovirus (CMV) in the neonatal period develop persistent problems with varying degrees of severity, fundamentally involving neurological disorders, neurosensory hypoacusis and hypovision, which appear from the age of 6-9 months onwards, when a diagnosis is no longer possible. The PCR (polymerase chain reaction) technique can detect DNA of CMV in blood samples on filter paper used for screening hypothyroidism and metabolic pathologies that were kept from the neonatal period. A child aged 3 years and 8 months with delayed intrauterine growth, autism, mental retardation, microcephalus and neurosensory hypoacusis; periventricular calcifications, leukoencephalopathy and bilateral malformation of the temporal lobe; and a diagnosis of congenital CMV confirmed by detection of DNA by PCR in the blood sample on filter paper saved from the neonatal period. The retrospective study of congenital infection by CMV should be considered when faced with severity and varying association of delayed intrauterine growth, microcephalus, neurosensory hypoacusis, chorioretinitis, mental retardation, autism or other behavioural disorders, intracranial calcifications, encephaloclastic alterations, leukoencephalopathy, cortical dysplasia and malformations of the temporal lobe and the hippocampus. Since the filter papers from neonatal screening are not kept for ever, perhaps the idea of doing so ought to be considered, given the possibilities they offer for retrospective studies.

Chronological changes of incidence and prognosis of children with asymptomatic congenital cytomegalovirus infection in Sapporo, Japan.

BackgroundChronological changes of the incidence of congenital cytomegalovirus (CMV) infection and the longitudinal prognosis in children with asymptomatic congenital infection were investigated.MethodsCongenital CMV infection, as demonstrated by isolation of the virus within the first week of life, was diagnosed in infants born in Sapporo, Japan, during the 26-year period between 1977 and 2002.ResultsCongenital infection was diagnosed in 37 (0.31%) of 11,938 infants. Thirty-two infants were (86.5%) asymptomatic and 5 (13.5%) were symptomatic at birth.ConclusionsAlthough a decrease in the total incidence of congenital CMV infection has been seen in recent years, screening of congenital infection at birth seems to be necessary to detect late-onset neurodevelopmental sequelae.

Immunological evaluation and clinical aspects of children with congenital cytomegalovirus infection.

To determine the ability of immunological response to human cytomegalovirus (CMV), the flow cytometric assay was evaluated as a tool for real-time monitoring of specific cellular immunity in children with congenital CMV infection. Longitudinal cohort study of 2 children with asymptomatic and 2 with symptomatic congenital CMV infection evaluated at birth and followed up with serial age-appropriate neurodevelopmental testing. Frequencies of CMV-specific CD4 (+) T cell in these children were detected by intracellular cytokines (ICC), interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, staining. Findings detected by CT and MRI were the most sensitive predictor for neurodevelopmental prognosis. Frequencies of CMV-specific CD4(+) T cells detected by ICC, both IFN-gamma and TNF-alpha, were higher in 2 children with symptomatic congenital CMV infection than those in 2 children with asymptomatic congenital infection. Frequencies of CMV-specific CD4(+) T cells in 2 children with symptomatic congenital infection were significantly higher than those in 6 healthy children of 1 to 5-years of age with serum anti-CMV IgG antibody without serum anti-CMV IgM antibody and viral excretion in to urine (p < 0.01). The ICC assay reflects immunological activity against CMV infection in children with asymptomatic or symptomatic congenial infection. Categorizing findings obtained by the ICC assay may helps to determine the prognosis of children with congenital CMV infection.

Prevention of Congenital Cytomegalovirus Disease

To the Editor-Yow [1] considers that prevention of congenital cytomegalovirus (CMV) disease is a NOW problem. Two of the preventative strategies she proposes require careful evaluation before they are implemented on a large scale. First, the efficacy of ganciclovir therapy in congenital CMV disease must be established in placebo-controlled trials. Uncontrolled trials will not provide conclusive results, because neonatal congenital CMV disease may resolve spontaneously without sequelae [2] and only ~5 % of neonates with initially asymptomatic congenital infection develop handicaps in later life [3]. Failure to evaluate ganciclovir therapy in properly controlled trials will perpetuate current uncertainties concerning the drug's efficacy [4, 5]. Second, the effectiveness of good hygienic practices as a means of preventing primary CMV infection in CMV-seronegative women of child-bearing age must be determined before all women are screened for CMV antibody and the seronegatives offered advice on these practices. Seronegative women working in a supervised hospital environment and using good hygienic practices such as handwashing, avoidance of intimate personal contact, and careful handling and disposal of potentially contaminated wastes have CMV seroconversion rates similar to those seen in control groups [6-8], but it is unclear whether this observation reflects the implementation of infection control policies. As the intimate personal contact occurring in the home is probably efficient in transmitting CMV [9], preventive measures effective in the hospital may not be effective in the home. Moreover, avoidance of intimate personal contact between a woman and her children could be psychologically damaging to the children. If good hygienic practices are impracticable or ineffective in the home, informing seronegative women that they are at risk of bearing CM Vdamaged babies may merely generate anxiety.

Indications for treatment

Parasites produce damage to man by 1) Consumption of nutrients 2) Destruction of tissues 3) Traumatic lesions 4) Toxic action 5) Immunoallergic reactions. Humans react against parasitic attack with their natural and acquired defences. Age, race, sex, genetic endowment and nutritional status are some of the factors which influence natural immunity. Acquired cellular immunity is responsible for the state of premunition which avoids superinfection in some parasitoses. The development of an infection or of the clinical disease in an individual will depend on the interaction between the aggressive factors of the parasite and the defensive capacities of the host. In the great majority of cases an equilibrium will result: in other words, an infection. When there is a great load of parasites with great pathogenicity affecting a susceptible host, a disease will develop which can eventually result in death. Treatment should be administered on the basis of clinical, epidemiological or prophylactic considerations. In amebiasis the virulence of the races is the main parasitic factor. The difference between virulent races is quantitative and not qualitative and can be demonstrated by phagocytosis of red blood cells, “toxin” production and by inoculation into the liver of newborn hamsters. The cytotoxin has at least two components: collagenase and amebapore. The nutritional status, intestinal lumenal pH and redox potential, secretory IgA and mucus and plasma complement are some of the host factors which influence the pathogenicity of amebae. Curative treatment is indicated on intestinal or extraintestinal invasive amebiasis. Prophylactic treatment should be administered to infected food handlers and infected persons in developed countries. In toxoplasmosis, curative treatment is indicated in patients with clinical manifestations of acquired or congenital infection, in acute, sub-acute or chronic, reactivated periods. The clinical symptomatology must be correlated with serological testing which indicates “activity”. In some acquired lymph node toxoplasmosis, without general compromise, asthenia, adynamia or fever, treatment is not needed because of its good prognosis. Chronic inactivated cases, or sequelae do not require treatment. Prophylactic treatment is indicated: in: 1) Pregnant women with seroconversion to avoid congenital infection. 2) In apparently healthy children with asymptomatic congenital infection, to avoid late ocular lesions. 3) In individuals who receive immunosupressive therapy and have serological evidence of toxoplasmosis activity. In the larva migrans syndrome, treatment is indicated in patients with symptomatology oreosinophilia. The therapy may produce remission of the clinical picture or of the eosinophilia.