Explore the vast range of titles available.

IntroductionChilaiditi syndrome is very seldom met in medical casuistry, having a frequency not more than 0.28% and it is described especially referring to people over 60 years old, mainly on males. Radiological diagnosis is represented by a loop of bowel interposition, frequently transverse colon in interhepato-diaphragmatic space.Case presentationPatient CS, male, aged 16 years and 3 months with psychomotor retardation, is brought in emergency with abdominal pain, vomiting and faintness. On admission, the overall condition is serious, hypotonic, afebrile with toxic facies, subicteric skin, a distended abdomen with superficial vascularisation evident at thoracico-abdominal level. Laboratory examinations highlights acidosis, severe anaemic syndrome with anisocytosis and anizocromie, neutrophilic leukocytosis, hypoproteinemia, hepatic cytolysis, hyperammonemia and IgG positive for CMV and Toxoplasma. After the surgical clinical examination, it is practiced a gastric aspiration, rebalancing electrolyte, atibiotics, supportive treatment of liver function, eubiotic and neuropsychiatric treatment. Due to a marked flatulence, abdominal sonographic examination was irrelevant and radiological examination put in evidence the distension of intestinal loops overlaid over the whole hepatic area, with a pneumoperitoneum aspect. CT scan reveals hepatic left lobe aplasia, transverse colon interposition between right hepatic lobe and diaphragm and ascites throughout the abdominal cavity. The response to the instituted treatment for colonic decompression was favourable, with the disappearance of Chilaiditi sign, the improvement of liver function and of general health condition.conclusionsThe particularity of this case seems to be the rare Chilaiditi syndrome associated with a previously undiagnosed mixed decompensated cirrhosis with liver left lobe aplasia at a teenager with psychomotor disabilities. We consider that the syndrome has been favoured by a decompensated cirrhosis.

IntroductionIn Ireland, 75% of pregnant women are seronegative for toxoplasma, making them susceptible to primary infection during pregnancy. First case: A female infant was conceived by IVF. Her mother received high dose steroids, humira and intravenous immunoglobulin at the initiation of, and during early pregnancy. The infant was neurologically abnormal at birth, had marked ventricular dilatation, intracranial calcification and bilateral retinal detachments. CT was confirmed with infant toxoplasma IgG and IgM positive. Maternal serology was consistent with primary maternal infection during pregnancy. Despite anti-toxoplasma therapy, the infant succumbed at six months of age. Second Case: A one-year-old girl was investigated for a convergent strabismus. Conceived by IVF, her mother received high dose steroids for the first four months of pregnancy. Developmentally normal, at nine months of age she developed a right strabismus. Dilated fundoscopy revealed an extensive right macular scar. Neuroimaging showed intracranial calcification. Although toxoplasma IgM was negative, CT was diagnosed based on strongly persistent Toxoplasma IgG Ab, without evidence of decline over time. Developmental progress has been reassuringly appropriate. The macular scar is currently inactive.DiscussionThe recognition of these two cases, one lethal infection in the setting of primary infection and one possible reactivation disease in women receiving immunosuppressive therapy to facilitate assisted reproduction raises a number of issues. Neither women were aware of toxoplasmosis, their toxoplasmosis status or measure to prevent its acquisition in pregnancy. Women under going immunosuppression in pregnancy should be aware of their status and advised regarding preventative measures.

Background and objectiveFrequency and clinical manifestations of congenital toxoplasmosis in Iran is not determined, object of study was to determine the Frequency of positive serologic neonates for Toxoplasma from birth and follow up of them.MethodsIn a cohort prospective study (2011-2012), Cord blood sample obtained from 270 neonates, toxoplasma serology tests (IgG, IgM) done, cases with positive toxo-IgM treated and followedFindingPositive IgM and IgG determined 1.5%, 44.1% respectively. The most common manifestation was Eye (50%) and brain (50%).ConclusionEarly treatment of infected neonates and wide variation of toxoplasma infection in country is so important. Adding the toxoplasma serologic tests to neonatal screening test is needed and recommended.

Background and aimsDespite progress made for the diagnosis of congenital Toxoplasma infection in utero and at birth, serological follow-up in first year of life remains required to exclude or confirm congenital infection. To reduce the constraints of this follow-up, we developed a test to detect anti-Toxoplasma IgG in oral fluid.MethodsIn 362 patients referred for Toxoplasma serology oral fluid was collected on two micro-sponges in parallel to blood sampling. A pilot study on 212 patients aged >15 months (274 samples) was performed to validate sampling procedures and develop an in-house indirect ELISA for the detection of anti-T. gondii IgG in oral fluid. It was then applied to 150 children aged 0-15 months (341 samples) born from 133 women who seroconverted during pregnancy and 17 who remained seronegative. IgG on oral fluid were compared to serum IgG detected with MEIA AxSYM registered Toxo IgG (Abbott Laboratories).ResultsThe pilot study validated the acceptability and the safety of the test and the adequate duration of sampling. IgG detected in serum and in oral fluid had a parallel kinetics among newborns (correlation coefficient: 0.59, p < 0.0001), with a concordant decline in the non-infected ones (n = 110), and matching raising or stable IgG in those who were congenitally-infected (n = 23).ConclusionsCollection of oral fluid is painless and inexpensive. Our new test provides a simple and rapid method to detect anti-Toxoplasma gondii IgG and to manage newborn at risk for congenital infection. It could have many other applications in pregnant women and other groups of patients.

Toxoplasmosis, caused by the obligate intracellular protozoan Toxoplasma gondii , is an important zoonosis with medical and veterinary importance worldwide. The disease is mainly contracted by ingesting undercooked or raw meat containing viable tissue cysts, or by ingesting food or water contaminated with oocysts. The diagnosis and genetic characterization of T. gondii infection is crucial for the surveillance, prevention and control of toxoplasmosis. Traditional approaches for the diagnosis of toxoplasmosis include etiological, immunological and imaging techniques. Diagnosis of toxoplasmosis has been improved by the emergence of molecular technologies to amplify parasite nucleic acids. Among these, polymerase chain reaction (PCR)-based molecular techniques have been useful for the genetic characterization of T. gondii . Serotyping methods based on polymorphic polypeptides have the potential to become the choice for typing T. gondii in humans and animals. In this review, we summarize conventional non-DNA-based diagnostic methods, and the DNA-based molecular techniques for the diagnosis and genetic characterization of T. gondii . These techniques have provided foundations for further development of more effective and accurate detection of T. gondii infection. These advances will contribute to an improved understanding of the epidemiology, prevention and control of toxoplasmosis.

Key Points The parasite Toxoplasma gondii is extremely widespread in animals and is a common cause of food- and water-borne infection in people. Although most infections are benign, they can have severe consequences in immunocompromised patients and following congenital infection. T. gondii is regarded as a model intracellular parasite for which forward- and reverse-genetics tools are available. In combination with the mouse model of toxoplasmosis (including the many genetic knockout and transgenic mouse lines that are available), these tools for genetic manipulation of the parasite have enabled researchers to explore the molecular determinants of T. gondii pathogenesis and host defence. Forward-genetics crosses conducted in T. gondii , using strains of different genotypes and virulences in mice, revealed that acute virulence is largely mediated by a family of effector proteins that are secreted into the host cell cytoplasm during parasite invasion. These proteins are derived from a secretory organelle called the rhoptry and, hence, are called ROP effectors. ROPs include a family of serine/threonine kinases that affect host targets and have important roles in infection in the mouse. Among these, ROP18 phosphorylates immunity-related GTPases, thus promoting parasite survival in activated macrophages, whereas ROP16 phosphorylates signal transducer and activator of transcription 3 (STAT3) and STAT6 and, hence, alters host gene transcription. Curiously, the activity of ROP18 is mediated by another family member called ROP5, which is a pseudokinase. Although a limited subset of ROP kinases can largely explain the virulence of T. gondii in the mouse, their role in other hosts has not been established. The genome encodes more than 40 ROPs, and these different proteins might have distinct roles during infection in the wide range of hosts infected by T. gondii . Understanding these patterns might help in the prevention and treatment of human infections. The intracellular parasite Toxoplasma gondii can infect a range of hosts and occasionally causes serious disease in humans. In this Review, Hunter and Sibley summarize recent studies that implicate rhoptry kinases and a dense-granule protein as mediators of acute virulence in the mouse model. They also describe the complex interplay between these parasite effector proteins and the innate immune system. Toxoplasma gondii is a common parasite of animals and humans and can cause serious opportunistic infections. However, the majority of infections are asymptomatic, possibly because the organism has co-evolved with its many vertebrate hosts and has developed multiple strategies to persist asymptomatically for the lifetime of the host. Over the past two decades, infection studies in the mouse, combined with forward-genetics approaches aimed at unravelling the molecular basis of infection, have revealed that T. gondii virulence is mediated, in part, by secretion of effector proteins into the host cell during invasion. Here, we review recent advances that illustrate how these virulence factors disarm innate immunity and promote survival of the parasite.

Intracellular parasites like Toxoplasma gondii scavenge host nutrients, particularly lipids, to support their growth and survival. Although Toxoplasma is known to adjust its metabolism based on nutrient availability, the mechanisms that mediate lipid sensing and metabolic adaptation remain poorly understood. Here, we perform a genome-wide CRISPR screen under lipid-rich (10% Fetal Bovine Serum (FBS)) and lipid-limited (1% FBS) conditions to identify genes critical for lipid-responsive fitness. We identify the Toxoplasma protein GRA38 as a lipid-dependent regulator of parasite fitness. GRA38 exhibits phosphatidic acid (PA) phosphatase (PAP) activity in vitro, which is significantly reduced by mutation of its conserved DxDxT/V catalytic motif. Disruption of GRA38 leads to the accumulation of PA species and widespread alterations in lipid composition, consistent with impaired PAP activity. These lipid imbalances correlate with reduced parasite virulence in mice. Our findings identify GRA38 as a metabolic regulator important for maintaining lipid homeostasis and pathogenesis in Toxoplasma gondii . Here, using a genome-wide CRISPR screen, Bitew et al . identify GRA38, a phosphatidic acid phosphatase, as a key factor in Toxoplasma gondii adaptation to lipid-rich conditions via keeping lipid balance, sustaining growth, ultimately ensuring survival.

Toxoplasma gondii is a parasite that infects a wide range of animals and causes zoonotic infections in humans. Although it normally only results in mild illness in healthy individuals, toxoplasmosis is a common opportunistic infection with high mortality in individuals who are immunocompromised, most commonly due to reactivation of infection in the central nervous system. In the acute phase of infection, interferon-dependent immune responses control rapid parasite expansion and mitigate acute disease symptoms. However, after dissemination the parasite differentiates into semi-dormant cysts that form within muscle cells and neurons, where they persist for life in the infected host. Control of infection in the central nervous system, a compartment of immune privilege, relies on modified immune responses that aim to balance infection control while limiting potential damage due to inflammation. In response to the activation of interferon-mediated pathways, the parasite deploys an array of effector proteins to escape immune clearance and ensure latent survival. Although these pathways are best studied in the laboratory mouse, emerging evidence points to unique mechanisms of control in human toxoplasmosis. In this Review, we explore some of these recent findings that extend our understanding for proliferation, establishment and control of toxoplasmosis in humans.Toxoplasmosis caused by the parasite Toxoplasma gondii is a common opportunistic infection with high mortality in individuals who are immunocompromised, most commonly due to reactivation of infection in the central nervous system (CNS). In this Review, Sibley and colleagues explore the interaction between host immune defences and parasite virulence factors with emphasis on bradyzoite differentiation and survival of T. gondii within the CNS.

The coccidian subgroup of Apicomplexa possesses an apical complex harboring a conoid, made of unique tubulin polymer fibers. This enigmatic organelle extrudes in extracellular invasive parasites and is associated to the apical polar ring (APR). The APR serves as microtubule-organizing center for the 22 subpellicular microtubules (SPMTs) that are linked to a patchwork of flattened vesicles, via an intricate network composed of alveolins. Here, we capitalize on ultrastructure expansion microscopy (U-ExM) to localize the Toxoplasma gondii Apical Cap protein 9 (AC9) and its partner AC10, identified by BioID, to the alveolin network and intercalated between the SPMTs. Parasites conditionally depleted in AC9 or AC10 replicate normally but are defective in microneme secretion and fail to invade and egress from infected cells. Electron microscopy revealed that the mature parasite mutants are conoidless, while U-ExM highlighted the disorganization of the SPMTs which likely results in the catastrophic loss of APR and conoid.