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The purpose of this study was to determine the prevalence and incidence of toxoplasmosis in pregnant women in Denmark, and to estimate the incidence of congenital toxoplasmosis. Consecutive serum samples from 5,402 women were analysed for specific IgG and IgM Toxoplasma gondii antibodies by EIA. The prevalence of IgG antibodies was 27.4%. The seroconversion rate was estimated to be 1.16% per year (SE = 0.0017) in all age groups, consistent with an incidence of acute toxoplasmosis in pregnant women of 0.65%. Specific IgM antibodies were present in sera from 29 women. Based on an assumed maternofetal transmission rate of 50%, the incidence of congenital toxoplasmosis was estimated to be 0.33%. Based on these data it is predicted that about 410 pregnant women are infected with T. gondii every year in Denmark, and that about 200 children every year are infected in utero by T. gondii. There was no difference in the prevalence of antibodies in women from rural or urban areas, or from different parts of Denmark.
In the BALB/c mouse model, primary infection with Toxoplasma gondii during the second third of gestation leads to a high percentage of infected foetuses. However, immunity induced by infection contracted before pregnancy prevents parasites from crossing the placenta and completely protects the foetuses, as well as the pregnant women. In order to clarify the roles of CD4+, CD8+ T lymphocytes and IFN-gamma in this protection, pregnant BALB/c mice were treated with depleting monoclonal antibodies against CD4, CD8, IFN-gamma, or control antibody. Only the foetuses of the groups treated with anti-CD8 and anti-IFN-gamma antibodies developed congenital toxoplasmosis. The maternal production of IFN-gamma was depressed in the mice depleted of CD4 and CD8 cells (P < 0.001). Determination of the blood parasite load demonstrated that materno-foetal transmission of T. gondii correlates with maternal parasitaemia. Together, these results show that CD8+ T lymphocytes and IFN-gamma play an important role in protection against congenital toxoplasmosis during reinfection.
Infections with the zoonotic protozoan Toxoplasma gondii during pregnancy can result in severe fetal infections. To investigate the use of pigs as animal models for congenital toxoplasmosis, tachyzoites of 5 T. gondii strains, with low to intermediate virulence in mice, were intravenously inoculated into pregnant minipig gilts. Two strains caused abortions of uninfected fetuses following severe disease of the mothers. One strain caused no disease in the gilts but slightly elevated anti-T. gondii antibodies in 2 of 9 fetuses. One strain produced clinical disease with 4 mummified fetuses and 2 full-term, congenitally infected piglets in 1 gilt and no clinical disease but elevated specific fetal antibodies in both piglets of the other gilt. Infection with the fifth strain (SVS-O14), which was considered apathogenic to both pigs and mice based on the clinical course of this and previous experiments, resulted in significant numbers of congenitally infected piglets, as indicated by production of anti-T. gondii antibodies in all 12 fetuses; the parasite was identified in 3 of these fetuses. This pattern of infection indicates that pigs infected with SVS-O14 (or a similar strain) are relevant animal models for studies of transplacental transmission and pathogenesis of congenital toxoplasmosis.
Little is known about congenital toxoplasmosis in twins. As in singletons fetal infection occurs usually in mothers seroconverted during second or third trimester of pregnancy. Infection affects usually both siblings, but there is posible that one child is not infected, especially in dizygotic pregnancies. A distinct difference in clinical patterns between dizygotic and monozygotic twins is observed. In monozygotic pairs most often clinical course is similar, while in dizygotic twins discrepancies in clinical findings are frequent and marked. For almost thirty years of our own experience with congenital toxoplasmosis we observed only four pairs of twins with this intrauterine infection. All of them were dizygotic. In two pairs the clinical course was similar, and different in the other two.
Protective immunity in mice infected with Toxoplasma gondii is mainly mediated by NK cells, CD4 and CD8 T cells, and type 1 cytokines, such as gamma interferon (IFN-gamma). To clarify the roles of NK cells and IFN-gamma in protection against primary congenital toxoplasmosis, we used recombination activating gene 2 knockout (RAG-2(-/-)) mice, which lack T and B lymphocytes, in comparison with the wild-type BALB/c model. RAG-2(-/-) mice had a significantly lower risk of fetal toxoplasmosis than BALB/c mice (25 versus 63.9%; P = 0.003). This protection was associated with an increased number of maternal NK cells, IFN-gamma secretion by spleen cells, and decreased parasitemia. In the RAG-2(-/-) mice, NK cell depletion increased both the rate of fetal infection, to 56.5% (P = 0.02), and the blood parasite burden. Conversely, in the BALB/c mice, this treatment did not modify maternofetal transmission or the blood parasite burden. Neutralization of IFN-gamma in both infected RAG-2(-/-) and BALB/c mice decreased congenital Toxoplasma transmission, contrasting with an exacerbation of maternal infection. These data suggest that a partially protective immunity against congenital toxoplasmosis is achieved due to the increased number of NK cells in RAG-2(-/-) mice. However, it seems that IFN-gamma enhances, directly or indirectly, the transplacental transmission.
OBJECTIVE: Our purpose was to evaluate Toxoplasma gondii concentration in amniotic fluid (AF) samples as a prognostic marker of congenital toxoplasmosis. STUDY DESIGN: A retrospective study was carried out in 88 consecutive AF samples from 86 pregnant women, which were found positive by prospective polymerase chain reaction (PCR) testing. Parasite AF concentrations were estimated by real-time quantitative PCR and analyzed in relation to the clinical outcome of infected fetuses during pregnancy and at birth, taking into account the gestational age at maternal infection. RESULTS: A significant negative linear regression was observed between gestational age at maternal infection and T gondii DNA loads in AF. After adjusting for time at maternal seroconversion by multivariate analysis, higher parasite concentrations were significantly associated with a severe outcome of congenital infection (odds ratio [OR]=15.38/log (parasites/mL AF) [95% CI=2.45-97.7]). CONCLUSION: PCR quantification of T gondii in AF can be highly contributive for early prognosis of congenital toxoplasmosis. Maternal infections acquired before 20 weeks with a parasite load greater than 100/mL of AF have the highest risk of severe fetal outcome.
Primary infection with Toxoplasma gondii during pregnancy may affect the fetus and result in congenital toxoplasmosis. In Austria serological screening for detection of newly acquired infection during pregnancy was introduced in 1975. In this study we used polymerase chain reaction (PCR) for detection of fetal infection with Toxoplasma gondii. Amniotic fluid samples were analyzed from 11 women with serological indication of acute toxoplasmosis infection. Nine of these women had already received treatment prior to amnio-centesis and no evidence of Toxoplasma gondii DNA was detected with PCR in the respective amniotic fluid samples. Isolation of the organism by mouse inoculation was negative in these cases and follow-up serology as well as clinical examination of the infants confirmed these results. In 2 patients investigation of the amniotic fluid samples by means of PCR was positive; both women had not yet been treated at the time of amniocentesis. Our results indicate that identification of Toxoplasma gondii in amniotic fluid is a useful procedure for diagnosing or excluding fetal infection. Moreover, the current recommendations of the screening program appear to be successful in preventing congenital toxoplasmosis.
Congenital toxoplasmosis has been confirmed in Indonesia. Many newborn children in Indonesia have congenital anomalies attributable to Toxoplasma gondii. The parasite is widespread, with seroprevalence rates of 2-63% in humans, 35-73% in cats, 75% in dogs, 11-36% in pigs, 11-61% in goats, and less than 10% in cows. The prevalence of Toxoplasma antibodies in pregnant women in the Dr Cipto Mangunkusumo Hospital in Jakarta is 14.3%, and in 50 abortions it is 67.8%. In patients with a history of one or more abortions or stillbirths, the prevalence is 21.5% and 22.8%, respectively. No significant difference has been found in women with or without histories of habitual abortions or stillbirths. In adults and children with chorioretinitis, the prevalence of antibody is 60%; in patients with other eye lesions, it is 17%. The prevalence in hydrocephalic children is 10.6%; in children with mental retardation, 44.6%; in children with eye lesions, 44.6%; and in children with signs of systemic diseases, 9.5%. The diagnosis of an acute Toxoplasma infection using the ELISA should be based on a significant increase in IgG levels in paired sera or on detection of IgM.
An immunocapture assay was developed to detect Toxoplasma gondii-specific immunoglobulin E (IgE) in sera from adults with acute acquired infection or reactivation and from babies with congenital toxoplasmosis. The components of this assay were monoclonal antibody to human IgE, samples from patients, and T. gondii tachyzoites treated with Formalin. When T. gondii-specific IgE antibodies were present, visually detectable agglutination occurred. Sera, umbilical cord blood, fetal blood, cerebrospinal fluid, and amniotic fluid were tested by this method. Specific IgE antibodies were detected in sera from 25 (86%) of 29 adults who developed specific IgG antibody during pregnancy or had specific IgA and IgM antibodies. Specific IgE was present early during infection, at the time that IgM antibodies were present, and slightly preceding the presence of specific IgA antibodies. In 23 patients tested serially, IgE antibodies never persisted for longer than 4 months. No nonspecific anti-T. gondii IgE was detected in sera from uninfected individuals. Maternal IgE antibodies did not cross the placenta. In sera of patients with congenital toxoplasmosis, specific IgE antibodies were found at birth, during the first year of life, and during immunologic recrudescence following discontinuation of pyrimethamine-sulfonamide therapy. The IgE immunocapture assay is simple to perform. It is especially useful for determining when T. gondii was acquired by recently infected pregnant women.
OBJECTIVE: To report on the role of infectious and inflammatory disorders as risk factors for stroke in a prospective and retrospective cohort of Saudi children. METHODS: Children, who presented with stroke, were evaluated at the Division of Pediatric Neurology or admitted to King Khalid University Hospital, College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia during the periods July 1992 to February 2001 (retrospective study) and February 2001 to March 2003 (prospective study). Investigations for suspected cases included hemostatic assays, microbiological and serological tests. Neuroimaging included cranial CT, MRI, magnetic resonance angiography (MRA), magnetic resonance venography (MRV) and single photon emission computed tomography (SPECT) brain scan. RESULTS: Of the 104 Saudi children with stroke, seen during the combined study periods of 10 years and 7 months, infectious and inflammatory disorders of the circulatory system were the identified risk factor in 18 (17.3%). Five children had stroke following acute bacterial meningitis at ages ranging between 5-21 months. The causative organism was identified in 3 of them and consisted of Haemophilus influenzae (in a 5-month-old girl), Streptococcus pneumoniae (in a 21-month-old girl complicated by subdural empyema and sinovenous thrombosis), and Staphylococcus aureus in a 6-month-old boy who had an underlying chronic granulomatous disease. Unspecified meningitis/meningoencephalitis affected 4 patients, whereas 3 children had an underlying congenital infection as a cause for their stroke. Two of the latter 3 children were diagnosed to have congenital toxoplasmosis, and the third had congenital rubella syndrome. Two girls had stroke following septicemia at ages of one and 2 months. Neurobrucellosis caused stroke in 2 boys at the ages of 4 1/2 and 4 years. In both patients, neuroimaging revealed lacunar and other infarcts involving mainly the deep cerebral nuclei, secondary to occlusion of small penetrating end arteries. Two patients presented with cerebrovascular disease following systemic lupus erythematosus. These were a 12-year-old girl and a 5-year-old boy. CONCLUSIONS: Several of the infectious diseases that caused stroke in this cohort of Saudi children are potentially preventable through childhood immunization programs or other maternity health programs. In particular, immunogenic conjugate vaccines against the 3 most common organisms causing acute bacterial meningitis (Haemophilus influenzae type b, Neisseria meningitidis and defined serotypes of Streptococcus pneumoniae) are needed to protect the young (<2 years) who are mostly affected.
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Toxoplasmosis is caused by the protozoan organism, Toxoplasma gondii. Infection with this organism primarily results from contact with infected cats and from ingestion of improperly cooked meat. Most adults with toxoplasmosis are asymptomatic. When symptoms are present, they typically resemble a mononucleosis or flulike illness. The diagnosis of toxoplasmosis in the pregnant adult is best made using serological techniques to detect IgM antibody and to document significant changes in the IgG antibody titer. Congenital toxoplasmosis usually occurs as a result of primary maternal infection. The most useful tests for confirmation of fetal infection are ultrasound examination, cordocentesis for detection of IgM-specific antibody, and amniocentesis for detection of toxoplasma DNA in amniotic fluid. Congenital toxoplasmosis can be treated with reasonable success by administration of antibiotics (spiramycin, sulfadiazine, and pyrimethamine) to the mother. In an effort to prevent acquisition of infection, pregnant women should be counseled to avoid contact with cat litter and improperly cooked beef, pork, or lamb.
In a study performed to define the prevalence of false positive toxoplasma IgM-IFA test results in sera containing RF, 8 (19.5%) of 41 sera which were positive for RF were positive in the toxoplasma DT and conventional toxoplasma IFA test. Three of these eight were also positive in the toxoplasma IgM-IFA test and in two, the results were considered to be false positives. Of the 33 sera remaining which were positive for RF but negative in both the DT and conventional IFA test, three were positive in the toxoplasma IgM-IFA test. Of 51 sera from patients with suspected rheumatoid arthritis or other collagen vascular disorders, all of which were negative when tested for RF, none was positive for toxoplasma IgM antibodies in the IgM-IFA test. Sera from 15 adults with the acute lymphadenopathic form of toxoplasmosis and 13 infants with congenital toxoplasmosis were tested for the presence of RF. Whereas none of the sera from the acquired cases had demonstrable RF, two of the congenital cases had RF, and their titers were both 1:320. False positive IgM-IFA test results became negative after treatment of sera with heat-aggregated IgG. In contrast, IgM-IFA test titers in cases of acute congenital or acquired toxoplasmosis were unaffected by this treatment. Thus, treatment with heat-aggregated IgG can be used to differentiate false positive IgM-IFA test titers due to RF from those due to specific IgM toxoplasma antibody.
Ocular toxoplasmosis can be a progressive and recurring disease that can threaten visual function. Retinochoroiditis develops gradually weeks to years after subclinical congenital toxoplasmosis; this is the preponderant form, which is frequently bilateral; with healing, white or dark-pigmented scars may result. Toxoplasmosis acquired in older children and adults rarely progresses to retinochoroiditis; it is generally unilateral. We report the results of a clinical study concerning 16 patients with ocular toxoplasmosis observed for the first time in the period from 1992 to 2004 and followed up until today. The patients came to the Department of Infectious Diseases of the Second University of Naples. We studied 16 patients, 10 of whom were females; 11 cases presented ocular signs of congenital toxoplasmosis, while in 5 cases ocular impairment was related to an acquired toxoplasmosis. Only one case of congenital toxoplasma chorioretinitis was symptomatic at birth: it was complicated by microphthalmia and strabismus, calcifications in the brain and epilepsy; 10 congenital cases were asymptomatic at birth and were recognized after several years because of a reactivation of infection. In 5 patients congenital chorioretinitis was bilateral, with presence of scars in the contralateral eye. The 5 cases of acquired toxoplasma retinitis were ascertained by anamnestic, serologic and ophthalmologic examinations; in 4 of them the lesion was typical and unilateral; the 5th case was a 6-year-old boy with acquired toxoplasma bilateral neuroretinitis. 13/16 cases of ocular toxoplasmosis were treated with the combination of pyrimethamine, sulfadiazine; they were followed up and re-treated if necessary. The therapy was curative in each case. Our experience confirms that late-onset retinal lesions and relapse can occur many years after birth but that the overall ocular prognosis is satisfactory when congenital damage is recognized early and treated appropriately. Prevention of congenital and acquired toxoplasmosis is very important in controlling ocular toxoplasmosis.
Termination of pregnancy is usually recommended to pregnant women who have infection with Toxoplasma gondii before 26 weeks of pregnancy if the fetus is infected. No prospective studies are available on the outcome if such pregnancies are allowed to continue with anti-parasitic treatment. We prospectively studied 163 mothers with acute toxoplasma infection before 28 weeks of amenorrhoea. All received anti-parasitic treatment with 9 million IU spiramycin orally. 23 also received pyrimethamine and sulphadiazine. All had cordocentesis and regular obstetric ultrasound examinations. The 162 liveborn infants were followed up for 15 to 71 months. 3 fetuses died in utero. 27 of 162 liveborn infants had proven congenital toxoplasmosis: 10 had one or more clinical signs of congenital toxoplasmosis; 5 had isolated or multiple intracranial calcifications; 7 had peripheral chorioretinitis; and 2 had moderate ventricular dilations. All 27 are free from symptoms and have normal neurological development at 15 to 71 months of age. We conclude that in first and second trimester pregnancies with acute fetal toxoplasma infection, the pregnancy need not be interrupted if repeated fetal ultrasound is normal, and antiparasitic treatment is given.
The development of glomerulonephritis as a complication of neonatal lupus or congenital toxoplasmosis is extremely rare. We report a case of membranous glomerulonephritis occurring in a neonate with toxoplasmosis and atypical congenital lupus, including high-titer antinuclear antibodies and hypocomplementemia. This case illustrates that glomerulonephritis in the neonate may be induced by passively transferred maternal antibodies.
Toxoplasmic retinochoroiditis usually presents during the first three decades of life as a consequence of intra-uterine infection by Toxoplasma gondii. The ingestion of infected undercooked meat, or foodstuffs contaminated by infected cat faeces, constitute the primary sources of infection for the non-immune mother. It is thought that following congenital infection, Toxoplasma cysts remain dormant in otherwise normal retina and that acute retinochoroiditis is the result of reactivation of the parasite, perhaps by cyst rupture. Treatment is indicated for sight threatening disease and comprises anti-Toxoplasma agents. The addition of steroids may be required to diminish the inflammatory response. Photocoagulation of normal retina around focal lesions probably decreases the incidence of recurrent inflammation. Women should be advised not to eat undercooked meat and to avoid contact with cat excrement during pregnancy. These measures will decrease the incidence of both eye disease and the more severe manifestations of congenital toxoplasmosis, which include congenital abnormalities, mental retardation, hydrocephalus and blindness.