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[Cerebral toxoplasmosis. Neuroradiologic diagnosis and prognostic monitoring].

Cerebral toxoplasmosis remains the most frequent etiology of cerebral masses in AIDS. In most cases, the disclosure of multiple enhanced masses is suggestive of diagnosis of toxoplasmosis and leads to undertake presumptive therapy. Sometimes, the pattern is less suggestive, and the possibility of primary cerebral lymphoma (PCL) is a diagnostic dilemma, because this is a short term life-threatening lesion in the absence of an undelayed fitting therapy. However, apart from the periventricular form of PCL, where directly proceeding to biopsy should be suggested, there is no distinctive pattern of PCL. The most reliable features in distinguishing between PCL and toxoplasmosis are: solitary lesion, homogeneous enhancement of a lesion whose diameter is larger than 2 cm, situation in deep periventricular white matter and limited edema and mass effect. The presence of haemorrhagic foci in the lesion, if there is no steroid therapy is rather indicative of toxoplasmosis. The lack of enhancement on enhanced CT-scan does not allow to eliminate cerebral toxoplasmosis, and indicate MR examination, or empiric antitoxoplasmic treatment. The radiologic follow-up depends on clinical response and on initial pattern. The criteria of response to antitoxoplasmic treatment are: the decrease in volume or number of lesions, the decrease of edematous reaction and mass effect (if no steroid was administered). If the lesion was initially equivocal, the lack of growth in a 8-day delay is a criterion for toxoplasmosis, just as the occurring of haemorrhage in the lesions (if there is no steroid-therapy).

AIDS-Related Opportunistic Infections↗

Histologically confirmed clinical toxoplasmosis in cats: 100 cases (1952-1990).

Tissue sections from 119 cats that died or were euthanatized (1952-1990) because of toxoplasmosis-like illness were reexamined for Toxoplasma gondii by direct microscopy and immunohistochemical staining with anti-T gondii serum. Clinical and pathologic data from 100 of these cats with histologically verified toxoplasmosis were then analyzed. Of these 100 cats, 36 were considered to have generalized toxoplasmosis, 26 predominantly pulmonary lesions, 16 abdominal, 2 hepatic, 1 pancreatic, 1 cardiac, 2 cutaneous, 7 neurologic, and 9 had neonatal toxoplasmosis. In 14 cats, concurrent microbial infections or other maladies were seen. Cats were 2 weeks to 16 years old (median, 2 years; mean, 4 years). Sixty-five cats were males and 34 were females; sex was not recorded for 1 cat. Of 67 cats that had rectal temperatures recorded, 49 (73%) had fever (40.0 to 41.7 C). Dyspnea, polypnea, and signs of abdominal discomfort were frequently observed. Toxoplasmosis had been confirmed antemortem in 8 cats; 4 had a serum antibody titer to T gondii of > or = 1:1,024; and T gondii had been found in cytologic evaluation of tracheal aspirates from 2 cats and pleural fluid from 1 cat, as well as in a biopsy specimen of a mesenteric lymph node from another. Of the 15 cats with T gondii serum-antibody titers determined by the Sabin-Feldman dye test, 6 had no antibody detected in 1:4 dilution of their serum. Indirect fluorescent antibody titers were found in 10 of 10 cats' sera tested. Forty-one eyes from 27 of the cats were examined microscopically. Twenty-two of the 27 cats (81.5%) had evidence of intraocular inflammation in one or both eyes. Multifocal iridocyclochoroiditis was the most common lesion and was seen in 18 (81.8%) of the cats with ophthalmitis. The ciliary body was the most often severely affected portion of the uvea. Of the 22 cats with ocular toxoplasmosis, T gondii was found in eyes of 10. Toxoplasma gondii was found in the retina of 5 cats, the choroid of 2, the optic nerve of 1, the iris of 3, and the ciliary body of 4. Toxoplasma gondii was identified in 80% of 55 brains, 70.0% of 90 livers, 76.7% of 86 lungs, 64.4% of 45 pancreata, 62.7% of 59 hearts, 45.8% of 72 spleens, 41.5% of 65 intestines, 17.7% of 61 kidneys, and 60.0% of 30 adrenal glands.

Animals↗

[Pulmonary toxoplasmosis in patients with human immunodeficiency virus infection. 21 cases].

OBJECTIVES: Assess expression of pulmonary toxoplasmosis, the second most frequent localization after brain, in patients infected with the human immunodeficiency virus (HIV). METHODS: Twenty-one HIV-infected patients (18M, 3F) were admitted for pulmonary toxoplasmosis between September 1987 and February 1995. Mode of HIV transmission was unprotected homosexual sexual activity (n = 16), intravenous drug abuse (n = 3) and transfusion (n = 2). RESULTS: Isolated pulmonary toxoplasmosis was found in 11 patients. In 10 patients pulmonary toxoplasmosis was associated with cerebral (n = 4), bone marrow (n = 2), ocular (n = 1) and multifocal (n = 3) localizations. Seven patients were admitted for acute pulmonary distress. Fever (reported for 20 patients) and nonproductive cough (reported for 16 patients) were the most common clinical symptoms. Chest roentgenogram revealed bilateral pulmonary infiltrates in 16 (76%) patients. Mean absolute CD4 count was 25 +/- 57 (range 0-110). Serologic evidence of past infection was observed in 18 patients. Serology tests were not done for two patients and negative for one. Two patients presented co-infection with Pneumocystis carinii. Fourteen patients had elevated serum lactic dehydrogenase (LDH) concentration. Among those, 4 patients whose LDH concentration was elevated more than ten fold died of respiratory distress. Patients received pyrimethamine and sulfadiazine (n = 13) or clindamycin (n = 8). Seven patients died during the first month after diagnosis was made. For the other patients, mean survival was 8 months. No relapse of toxoplasmosis was observed. All the patients took a secondary prophylaxis. CONCLUSION: No difference between patient with isolated pulmonary toxoplasmosis and patients with associated extra-pulmonary localization was noted for clinical, biological, radiological presentations and outcome.

AIDS-Related Opportunistic Infections↗

[Toxoplasmosis-chorioretinitis: clinical course and treatment of seven patients].

Toxoplasmosis is a major and preventable cause of severe visual loss and blindness in young people. Ocular toxoplasmosis is the leading cause of posterior uveitis and in most cases it represents a late manifestation of a congenital infection. The clinical picture and anti-Toxoplasma therapy of seven patients referred to the Department of Infectious Diseases, Hvidovre Hospital is described. All patients had clinical ocular toxoplasmosis at initial examination with unilateral focal necrotizing retinitis associated with typical old, pigmented scars. All patients had anti-toxoplasmosis IgG antibodies. After anti-Toxoplasma therapy with sulfadiazine, pyrimethamine and corticosteroid the ocular lesions were healed to atrophic scars and the inflammatory activity disappeared. We conclude that when the clinical picture is compatible with toxoplasmosis, antibodies to Toxoplasma gondii are demonstrated and there is no other diagnosis, anti-Toxoplasma treatment should be considered. It is important to inform pregnant women about prophylactic measures, and to perform a serological screening of newborns, since treatment of congenital toxoplasmosis from birth improves the prognosis.

Adolescent↗

[Toxoplasmosis and immunosuppression].

Toxoplasmosis is a widely distributed zooanthroponosis, caused by the ubiquitous obligatory intracellular protozoan parasite Toxoplasma gondii. Once infected, the host acquires lifelong immunity induced by the persistence of the parasite in an encysted form. While T. gondii infection in pregnancy has long been known as a significant cause of perinatal morbidity and mortality (congenital toxoplasmosis), its significance as an opportunistic agent has been increasingly recognized during the last decade, particularly with the outbreak of AIDS. Reactivation of a previously latent infection results in a wide clinical spectrum, predominantly within the central nervous system. The paper reviews recent data on the significance of toxoplasmosis as an opportunistic infection in immunosuppressed individuals, such as patients with malignant and systemic diseases treated with immunosuppressive drugs, organ transplant recipients, and, first and foremost, patients with AIDS. A high prevalence of latent toxoplasmosis in Yugoslavia indicates a high local exposure to infection reactivation. While a definitive diagnosis of toxoplasmosis is difficult in the immunosuppressed, its treatability as opposed to a fatal outcome, if untreated, demands that physicians caring for the above categories of patients keep in mind toxoplasmosis and its possible clinical presentations and include them in the differential diagnosis of these conditions.

Humans↗

[Toxoplasmosis in families. II. Clinical analysis].

Clinical and serological analysis was conducted on 102 families including index-cases of lymphonodular toxoplasmosis (102 patients-group A) and 286 family members (group B). The studies included a total of 388 persons (167 children and 221 adults), originating mainly from Wielkopolska region (West Poland). The lymphonodular form of toxoplasmosis represented the dominating pattern among adult cases but among children the clinical pathology pattern was variable: in 14 out of 49 children (group A) lymphadenopathy was not dominating sign and clinically signs and symptoms of central nervous system or organ of vision involvement prevailed; in 6 cases clinical pattern pointed to congenital toxoplasmosis and in 8 cases it indicated sequele of acquired toxoplasmosis. In group B, among 35 children with lymphadenopathy, 7 presented also neurological signs/symptoms, in 5 children the pattern suggested acquired neurotoxoplasmosis in 2 cases congenital form of toxoplasmosis. In 11 adults of the group, lymphonodular form of the disease was diagnosed. In both groups (A and B), the pattern lymphonodular toxoplasmosis was detected also in 5 pregnant women (1.3% of studied persons and 2.7% of all adults). Four of the pregnant women manifested active stage of the disease, confirmed by the presence of IgM class antibodies. Thus, among 286 family members clinical pathology was demonstrated in 46 patients (16.1%) and in 35 patients (12.2%) activity of the disease presented indications for a specialistic therapy.

Adolescent↗

Risk factors for Toxoplasma gondii infection in mothers of infants with congenital toxoplasmosis: Implications for prenatal management and screening.

OBJECTIVE: The purpose of this study was to determine whether demographic characteristics, history of exposure to recognized transmission vehicles, or illness that was compatible with acute toxoplasmosis during gestation identified most mothers of infants with congenital toxoplasmosis. STUDY DESIGN: Mothers of 131 infants and children who were referred to a national study of treatment for congenital toxoplasmosis were characterized demographically and questioned concerning exposure to recognized risk factors or illness. RESULTS: No broad demographic features identified populations that were at risk. Only 48% of mothers recognized epidemiologic risk factors (direct or indirect exposure to raw/undercooked meat or to cat excrement) or gestational illnesses that were compatible with acute acquired toxoplasmosis during pregnancy. CONCLUSION: Maternal risk factors or compatible illnesses were recognized in retrospect by fewer than one half of North American mothers of infants with toxoplasmosis. Educational programs might have prevented acquisition of Toxoplasma gondii by those mothers who had clear exposure risks. However, only systematic serologic screening of all pregnant women at prenatal visits or of all newborn infants at birth would prevent or detect a higher proportion of these congenital infections.

Adult↗

Recognition of tissue cyst-specific antigens in reactivating toxoplasmosis.

Current serological tests do not discriminate between asymptomatic latent Toxoplasma gondii infection and reactivating toxoplasmosis, but timely therapeutic intervention before the development of symptoms would lead to major reductions in morbidity and permanent disability. This study developed a new enzyme-linked immunosorbent assay (ELISA) for antibody to T. gondii tissue cyst antigens and screened tissue cyst antigens by Western blot analysis to test the hypothesis that antibody recognition of T. gondii tissue cyst-derived antigen is a good indicator of reactivation disease. A total of 187 sera was tested by Sabin-Feldman dye test and tissue cyst ELISA, AIDS patients and patients with ocular disease were considered separately, as the exposure to parasite antigens may be different in these two groups. The dye test did not discriminate between immunocompetent and immunocompromised T. gondii seropositive patients or between active and quiescent toxoplasmosis. Tissue cyst ELISA demonstrated a raised specific antibody response in immunocompetent T. gondii seropositive patients and in quiescent HIV positive sera. These data support th view that the tissue cyst population is in a state of dynamic equilibrium. It is proposed that, in the immunocompetent host, tissue cyst development and rupture are under some degree of immune control, but that in the immunocompromised host this equilibrium is disturbed and reactivation disease results. Data from patients with reactivating ocular toxoplasmosis demonstrate that tissue cyst-specific antibody levels are not different in active and quiescent disease and indeed they are not significantly different from immunocompetent T. gondii seronegative sera. In the Western blot analysis of 57 HIV positive patient sera, eight antigens (65, 57, 49, 47, 36, 28, 26 and 18 kDa) were consistently recognised by one third or more of the sera tested, but no single antigen was diagnostic of quiescent or active toxoplasmosis. It is concluded that tissue cyst-derived antigens are not a reliable serological marker of reactivating toxoplasmosis.

AIDS-Related Opportunistic Infections↗

[Rudolf-Virchow Prize 1998. Award lecture. Toxoplasmosis: a model infection for studying systemic and intracerebral immune reactions].

Toxoplasmosis has gained particular attention in the AIDS era as the most common opportunistic encephalitis in HIV-infected patients. Since there are important parallels between the human and rodent infection, experimental murine toxoplasmosis is widely used to study the immune reactions to this protozoal parasite. Oral application of low-virulent Toxoplasma (T.) gondii cysts leads to a biphasic disease characterized by an acute, generalized phase followed by a chronic stage confined to the brain, where an encephalitis with persistence of the parasite develops. Immunity to T. gondii is T cell mediated, and there is increasing evidence for a critical role of cytokines for an effective immune response. In order to address the functional role of interferon (IFN)-gamma in toxoplasmosis, we took advantage of mice lacking the IFN-gamma-receptor. Inactivation of the IFN-gamma-receptor rendered mice highly susceptible to T. gondii, and they died of a fulminant acute toxoplasmosis. Among the various organs affected, hepatitis was severe enough to cause death. In contrast to wild type animals, IFN-gamma-receptor-deficient mice were unable to activate their macrophages as evidenced by a lack of major histocompatibility complex (MHC) class II antigen induction and the absence of an upregulation of tumor necrosis factor (TNF)-alpha and inducible nitric oxide synthase (iNOS) mRNA transcripts, two macrophage effector molecules. These observations prompted the investigation of TNF- and TNF-receptor-mediated effects in toxoplasmosis by use of mice deficient in either the TNF-receptor type 1 (TNFR1) and/or the TNF-receptor type 2 (TNFR2). The lethal outcome of T. gondii-infected TNFR1/2- and TNFR1-deficient mice, but not of TNFR2-deficient and wild type animals, illustrated the important role of TNF-alpha and TNFR1-mediated signalling, respectively, in this infection. Histopathology attributed death of TNFR1- and TNFR1/2-deficient mice to a severe, necrotizing encephalitis. Unrestricted intracerebral parasite replication in these strains was associated with reduced numbers of iNOS+ leukocytes and a lack of iNOS mRNA induction in their brains as compared to resistant wild type and TNFR2-deficient mice. To precisely identify the cellular sources of cytokines in the brain, flow cytometry of leukocytes isolated from the brain, in situ hybridization, immunohistochemistry and RT-PCR analysis of cytokine mRNA transcripts of magnetically purified leukocyte populations were performed. These studies disclosed that both CD4+, CD8+ T lymphocytes and macrophages recruited to the brain as well as resident cell populations of the CNS including neurons, astrocytes and microglia contributed to the intracerebral cytokine synthesis. Each population was characterized by a specific cytokine pattern. Interestingly, activation of brain cells is a hallmark of Toxoplasma encephalitis. The marked induction of a variety of immunologically important cell surface molecules as MHC class I and II antigens, cell adhesion molecules and their ligands on microglia points to a particular important role of this cell type for the immune response to T. gondii, since the expression of these molecules is a prerequisite for cellular interactions with T cells. The observation of a prominent interleukin (IL)-10 production in the T. gondii-infected brain initiated studies addressing the function of this powerful immunosuppressive mediator in chronic Toxoplasma encephalitis. Neutralization experiments revealed that IL-10 facilitates persistence of the parasite in the brain by downregulating the intracerebral immune response. On the other hand, IL-10 may exert a regulatory role and may be necessary to prevent immunopathological effects of an uncontrolled immune response. In conclusion, these studies demonstrate the important role of the cytokines IFN-gamma and TNF-alpha and their receptors, respectively, for an effective control of T. gondii. In the CNS, the target organ of the parasite, a

Animals↗

[Toxoplasmosis after antineoplastic therapy in non-Hodgkin lymphoma. Demand of preventive measures].

BACKGROUND. Toxoplasmosis is an opportunistic infection reported in several groups of inmunosupressed patients. It is considered uncommon in patients with lymphoproliferative disorders and in bone marrow transplant recipiets (BMT). Nevertheless, recent reviews have reported cases of cerebral and disseminated toxoplasmosis in BMT recipients, particularly among patients with IgG antibodies to Toxoplasma sp. prior to BMT and antineoplastic treatment. PATIENTS AND METHODS. Two cases of toxoplasmosis are reported of patients with non-Hodgkin lymphoma who did not have graft-versus-host-disease and with positive antitoxoplasma serologic response. In the first patient, the predominant clinical picture was febrile neutropenia without source, with good response to specific treatment for toxoplasmosis; in the second patient, and autologous BMT was performed and six months later the patient developed a retino-choroiditis by toxoplasmosis reactivation. CONCLUSIONS. The excessive morbidity and mortality associated with toxoplasmosis reactivations in lymphomyeloproliferative neoplasms with antineoplastic therapy and both allogenic and autologous BMT, demand preventive measures. The pretransplant serologic tests can be helpful in evaluating the potential risk of suffering a reactivation by Toxoplasma sp. and considering the administration of chemoprophylaxis in selected patients with positive serology.

English Abstract↗

[Cerebral CT scan alterations in children with ocular lesions caused by congenital toxoplasmosis]

OBJECTIVE: To evaluate the frequency and the types of cerebral CT scan alterations in patients with ocular lesions caused by congenital toxoplasmosis. METHODS: The patients should fit one of the following criteria: reagent IgM serology for toxoplasmosis at birth and mother with positive serology for toxoplasmosis; age less than ten years, with bilateral funduscopic lesions compatible with toxoplasmic retinochoroiditis; or reagent IgG serology for toxoplasmosis and mother with positive serology for toxoplasmosis. All patients were submitted to noncontrast cerebral CT scan. RESULTS: Twenty-two patients participated in this study (44 eyes). Thirteen eyes presented macular lesions (29.5%), eight had peripheral lesions (18.2%) and 22 eyes had concomitant macular and peripheral lesions (50%). Seventeen patients presented radiological alterations (77.3%). Among these, sixteen patients (94.1%) presented brain calcifications, two patients (11.7%) presented ventricular dilation, two patients (11.7%) had hydrocephalus, one had hydranencephaly (5.9%), one presented porencephalic cyst (cerebral hemiatrophy) (5.9%), one had arachnoid cyst (5.9%) and one had mild dilation of ventricles and subarachnoid cistern (5.9%). CONCLUSIONS: Patients diagnosed with congenital toxoplasmosis and ocular lesions should be investigated for concomitant neuroradiologic alterations.

Journal Article↗

Ocular manifestations in congenital toxoplasmosis.

BACKGROUND: Retinochoroiditis is the most common ocular manifestation of congenital toxoplasmosis, but other associated ophthalmological pathologies can also occur. The aim of this study was to determine the nature of the latter in treated cases of the disease and to assess their impact on visual function. METHODS: Four hundred and thirty consecutive children with serologically confirmed congenital toxoplasmosis were included in this study. Data were prospectively collected using standardized ophthalmological assessment forms. The presence of retinochoroiditis and of associated pathologies was ascertained, and their impact on visual function was assessed. RESULTS: After a median follow-up of 12 years [range 0.6-26 years], 130 children manifested retinochoroiditis. We detected 22 foci of retinochoroiditis at birth and 264 additional ones during the follow-up period. Of these, 48 (17%) were active when first diagnosed. Twenty-five of the 130 children (19%) had other associated ocular pathologies. Of these, 21 (16%) had a strabismus, which was due to macular lesions in 86% of the cases; 7 (5.4%) presented with unilateral microphthalmia, and 4 (3%) with cataracts. Most of these events were detected after the onset of retinochoroiditis. None of the children presented with ocular involvement in the absence of chorioretinal lesions. Macular lesions occurred more frequently in children with associated pathologies (p<0.0001), and associated pathologies were likewise more common in individuals with macular lesions (p=0.0003). Visual impairment occurred in 31/130 cases, and in all but 3 of these eyes it was due not to an associated pathology but to macular retinochoroiditis. CONCLUSIONS: At the end of the follow-up period, ocular involvement existed in 30% of the treated children with congenital toxoplasmosis. Associated eye pathologies were manifested less frequently than anticipated. They may occur later in life and are an indirect marker of the severity of congenital toxoplasmosis, but they do not have a direct impact on visual acuity. The overall functional prognosis of congenital toxoplasmosis is better than would be expected on the basis of literature findings, with only 2 of the 130 children suffering bilateral visual impairment.

Adolescent↗

Outbreak of toxoplasmosis in a family and documentation of acquired retinochoroiditis.

An outbreak of toxoplasmosis in one household is described. It demonstrates the potential for a common source infection with Toxoplasma gondii to cause multiple cases. Six of seven members of a household investigated for toxoplasmosis demonstrated high antibody titers consistent with recent infection; five of these members (83%) were symptomatic. The most common manifestations were fever and lymphadenopathy, which developed from seven to 18 days (mean 11 days) after a common source ingestion of infected meat. Since inadequately cooked lamb, pork and beef are probably the most common sources of infection in the United States, outbreaks of multiple cases may occur more frequently than is generally appreciated. As more outbreaks of febrile illnesses are examined, especially in families and closed communities, it is likely that more common source epidemics of toxoplasmosis will be recognized. Retinochoroiditis is an unusual manifestation of adult acquired toxoplasmosis. In the index case in this epidemic the patient manifested vision threatening retinochoroiditis 129 days after infection with toxoplasmosis. He represents the ninth well-documented case of toxoplasma retinochoroiditis associated with adult acquired disease.

Adolescent↗

Congenital toxoplasmosis: prevention, screening and treatment.

Congenital toxoplasmosis is an established cause of abortion, neonatal disease and ocular defects presenting in later life. Preventative options include health education, immunization and screening of pregnant women and infants with appropriate management of cases found to be at risk. Screening requires a knowledge of the disease, the test, the treatment and the administration of the proposed programme. Treatment can be directed towards the acutely infected mother, the infected fetus or infant and the patient with an acute exacerbation of ocular toxoplasmosis following congenital infection. Harm-benefit assessment of screening programmes designed to prevent congenital toxoplasmosis has produced conflicting results. Further research is required into the incidence of acute toxoplasmosis in pregnancy and subsequent congenital infection, the frequency of neonatal handicap, precise tests for the diagnosis of recent maternal infection and the presence of congenital toxoplasmosis and improved treatment of the infection.

Female↗

Toxoplasmosis.

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.

Adult↗

Toxoplasmosis.

Toxoplasmosis in dogs and cats can cause chorioretinitis, anterior uveitis, or both. Ocular lesions are a common manifestation of generalized toxoplasmosis. The prevalence of toxoplasmosis as a cause of idiopathic anterior uveitis in cats is not clear, although there is a significant association between exposure to T. gondii and feline anterior uveitis. The pathogenesis of ocular toxoplasmosis may be different in humans and cats, and the anterior uveitis may represent a type of immune-mediated inflammation. A diagnosis is made by observing compatible clinical findings and obtaining supportive findings on serologic tests. Despite improved diagnostic techniques, including determination of IgM class antibodies and PCR testing, definitive diagnosis of ocular toxoplasmosis remains a challenge. Topical anti-inflammatory therapy should be used in cats with anterior uveitis, a positive serum titer, and no concurrent systemic signs. Systemic clindamycin should be given to cats with ocular and systemic signs and to cats with suggestive serology and idiopathic anterior uveitis that fails to respond to topical therapy alone.

Animals↗

Congenital toxoplasmosis in England, Wales, and Northern Ireland: some epidemiological problems.

It has been suggested that congenital toxoplasmosis could be prevented by antenatal serological screening, followed by treatment or by termination of pregnancy if infection occurs. The only study of the incidence of congenital toxoplasmosis in England, Wales, and Northern Ireland took place more than 10 years ago. To obtain more recent figures laboratory reports of cases occurring from 1975 to 1980 were analysed. A total of 91 cases were reported over the six years. By criteria established to classify these infections only 34 were congenital, 20 were acquired postnatally, and 37 were unclassifiable. The mean annual number of cases of congenital toxoplasmosis was considerably smaller than that found in other recent studies. The condition could be underdiagnosed or rates of placental transmission could be lower in Britain than in other countries. Variation in reporting criteria of the laboratories made the data difficult to interpret. Improved diagnosis of congenital toxoplasmosis would not only clarify the epidemiology but would also help clinicians in management of suspected cases. Further antenatal surveys are necessary to assess the role of screening in the prevention of congenital toxoplasmosis.

Child, Preschool↗

IgA antibody response during acquired and congenital toxoplasmosis.

Toxoplasma gondii specific IgA and IgM antibodies were quantitated by an antibody capture agglutination assay in 260 patients with acquired toxoplasmosis and from 94 fetuses suspected of congenital toxoplasmosis and 30 infected children. In acquired toxoplasmosis, IgA antibodies to T gondii were found in 95% of the cases. In congenital toxoplasmosis IgA antibodies were more frequently detected (75%) in cord blood than IgM antibodies (61%). They persisted after birth, in some cases for up to 24 months. IgA antibodies were also detected in fetuses whose mothers had toxoplasmosis during their pregnancy. In infected fetuses IgM and IgA antibodies were detected in fetal blood as early as week 24 of pregnancy. Detection of IgA T gondii antibodies may be useful for the diagnosis of some recently acquired infection and for the diagnosis and follow up of the infection in the fetus and neonate.

Adult↗