Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019214 (hepatosplenomegaly)
 4,408 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Mexican-American boy presented at birth with an extensive eruption consisting of 0.5 to 1.0 cm hyperpigmented macules with a distinct peripheral scale involving primarily the forearms, abdomen and lower back (Fig. 1). Rare intact vesicopustules were also identified. There was an unremarkable prenatal history, and the infant was a product of a normal vaginal delivery. With the exception of the skin lesions and moderate hepatosplenomegaly, the physical examination was normal. Gram stains of the pustules showed numerous neutrophils but no bacteria. Bacterial cultures, of the skin and blood, TORCH screen (toxoplasmosis, rubella, cytomegalic virus, and herpes virus) and a VDRL were negative. On the second day of life, the patient developed several pustules with surrounding erythema consistent with erythema toxicum neonatorum. Wright-stained smears of these lesions showed abundant eosinophils. Hepatosplenomegaly resolved by the third day of life and at the time of discharge only hyperpigmented macules persisted. Follow-up visit six weeks later showed no evidence of skin lesions.
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PMID:Transient neonatal pustular melanosis. 51 27

Toxoplasma pneumonia is being recognized with increased frequency, especially in patients with AIDS. We reviewed the English-, French-, and Spanish-language literature from January 1966 through February 1991 to identify cases of postnatally acquired pneumonia associated with Toxoplasma gondii. We identified two distinct clinical syndromes, one in immunocompetent patients and one in patients with defects in cell-mediated immunity. Shortness of breath and cough were the most common symptoms and fever and rales the most common signs in both groups of patients. Lymphadenopathy and hepatosplenomegaly were reported more frequently for immunocompetent patients. Chest roentgenographs usually revealed bilateral interstitial infiltrates, but a variety of other roentgenographic findings were reported. Serological findings were suggestive of active toxoplasmosis in immunocompetent but not in immunosuppressed patients. In early reports, identification of T. gondii as the etiologic agent of pneumonia was based on serology or autopsy findings. In more recent reports, open lung biopsy and especially bronchoalveolar lavage were used for diagnosis. Mortality among patients with toxoplasma pneumonia was 55%. However, in cases of T. gondii pneumonia diagnosed during life, mortality was 0 for immunocompetent patients and 40% for immunosuppressed patients. In immunosuppressed patients, improvement was associated with specific antitoxoplasma drug therapy. Unfortunately, relapses were common. We also reviewed data on series of patients with disseminated toxoplasmosis manifested predominantly in extrapulmonary sites and found that 33% of these patients had evidence of subclinical pulmonary involvement even though pneumonia had not been diagnosed clinically.
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PMID:Pulmonary toxoplasmosis: a review. 157 81

We present 21 cases of visceral Leishmaniasis diagnosed in our hospital during the past 8 years. The diagnostic method used was the visualization of the parasite in bone marrow aspiratory puncture. All cases presented fever at admission, hepatosplenomegaly, anemia elevated sedimentation rate and polyclonal gammapathy. Two of our patients were diagnosed of AIDS during the course of the disease. Cure was observed in all cases after one cycle treatment with pentavalent antimonials except for the two AIDS cases one of whom died due to cerebral toxoplasmosis. We point out visceral Leishmaniasis as an opportunistic infection in patients with AIDS and its resistance to the usual treatment.
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PMID:[Visceral leishmaniasis in Alicante. Analysis of 21 cases]. 224 57

To date, the acquired immunodeficiency syndrome (AIDS) has been identified in over 50 children in the US, including those with associated hemophilia, high-risk environmental factors (Haitian background, parental intravenous drug abuse, or prostitution), and blood transfusions. The evaluation of an infant or young child in whom AIDS is suspected requires exclusion of congenital disorders of immune function. A specific test is not currently available, but inclusion criteria for childhood AIDS have been developed. The diseases accepted as indicative of underlying cellular immunodeficiency children are the same as those used in defining AIDS in adults, with the exclusion of congenital infections such as toxoplasmosis or herpes simplex virus infection in the 1st month of life or cytomegalovirus infection in the 1st 6 months of life. Specific conditions that must be excluded in children are primary immunodeficiency diseases (e.g., DiGeorge syndrome, Wiskott-Aldrich syndrome, ataxia-telangiectasia, neutrophil function abnormality) and secondary immuno-deficiency associated with immunosuppressive therapy, lymphoreticular malignancy, or starvation. Almost all young children with AIDS have hepatosplenomegaly, interstitial pneumonitis, and poor growth. The average age of 36 US child AIDS victims studied in detail was 5 months at presentation with findings suggestive of severe immunodeficiency. Mucocutaneous candidiasis was present in 75% of these 36 children, and Pneumocystis carinii and cytomegalovirus were each isolated from 30% of cases. Normal T4:T8 ratios occur in about 15% of pediatric AIDS cases. Laboratory evidence of polyclonal hypergammaglobulinemia generally supports the AIDS diagnosis. Recurrent infection and malnutrition are major problems in the clinical management of child AIDS patients.
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PMID:Acquired immune deficiency syndrome in childhood. 298 8

Nya:NYLAR albino mice infected with Toxoplasma gondii gradually developed a chronic and progressive wasting syndrome characterized by facial and body alopecia, corneal opacities, necrotic lesions of ears and tail, signs of neurologic disease and death within six to eight months after infection. Haematologic changes included a transient normochromic, normocytic anaemia, and persistent lymphopenia and neutrophilia. Changes in serum proteins were manifested by hypoalbuminaemia and pronounced hypergammaglobulinaemia. Serum thyroxine concentrations fell sharply during the first month of infection, then gradually returned to control concentrations. Gross changes included loss of body weight, hepatosplenomegaly, ovarian and uterine atrophy, and a marked involution of the thymus. The predominant histopathologic change in the brain was a mononuclear cell vasculitis, particularly affecting the hippocampus and the choroid plexus, ependyma, and periventricular areas of the lateral and third ventricles. These preliminary observations indicate that mice can serve as a practical animal model of great potential for study of the pathogenesis of chronic toxoplasmosis.
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PMID:Chronic murine toxoplasmosis: clinicopathologic characterization of a progressive wasting syndrome. 340 Oct 69

A toxin associated with Toxoplasma gondii infection was obtained from the trophozoites and culture medium used to propagate the parasite in cell cultures. The toxin, named Toxofactor (TF), administered parenterally or nonparenterally in adult mice, produces transient symptoms of lethargy, ruffled fur, and body weight loss. Organ changes which accompanied the outward symptoms included hepatosplenomegaly and involuted thymus. TF activity was detected in extracts of the blood, peritoneal fluid, liver, and spleen of infected mice. Severe damage to embryonal and fetal development was induced when TF was administered during pregnancy. Resorption, abortion, and congenital abnormalities were produced, dependent upon the stage of development at the time of exposure. Adult mice which had reacted to and recovered from an initial intraperitoneal injection to TF were protected against a secondary challenge from TF. Fetal development was also protected from damage when TF was used to challenge adults previously exposed to TF. Mouse and rabbit anti-TF sera neutralized TF activity in the adult. In no instance did control mice show any deleterious effect when exposed to soluble cell lysate from the uninfected cell line (BHK-21) used to propagate the organism plus the used medium from these same uninfected cells. TF activity was not attributed to bacterial, myocoplasmal, or viral contamination. TF toxic activity is labile to elevated temperature and high or low pH, which also destroy its protective properties. TF activity was sensitive to trypsin and was obtained in the elution fraction (alpha-methyl-D-mannoside) from affinity chromatography (concanavalin A-Sepharose 4B). Ultrafiltration indicated the molecular weight to be between 50,000 and 100,000. TF, apparently a glycoprotein, was quantitated for activity by a weight loss assay. A unit of activity was defined as the minimum quantity of TF (highest dilution) which produced at least a 10% average body weight loss in adult Nya:NYLAR female mice between days 7 and 12 post-intraperitoneal injection.
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PMID:Toxofactor associated with Toxoplasma gondii infection is toxic and teratogenic to mice. 668

During 1979, three brothers had antibody titers for toxoplasmosis of 1:1,024, 1:64, and 1:16, respectively, by IgG indirect immunofluorescent antibody (IgG-IFA) test. The first child also had a fever and lymphadenopathy. In August 1980 the three children had lymphadenopathy and IgG-IFA test titers between 1:4,096 and 1:16,000. Two other brothers, first examined at that time, had IgG-IFA test titers between 1:1,024 and 1:4,096, one with ascending titers and the other with IgM antibodies to Toxoplasma gondii. The latter had lymphadenopathy, fever, and hepatosplenomegaly. Clinical and serologic examinations during March, April, and September 1981 revealed good health and decreasing IgG-IFA test titers in most of the brothers. The simultaneous increase of antibody titers during August 1980 in the three initial patients lead to the consideration of a probable reinfection. A simultaneous reactivation of the disease was considered less probable because acute toxoplasmosis occurred in two other brothers at the same time.
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PMID:Concomitant cases of acquired toxoplasmosis in children of a single family: evidence of reinfection. 704 53

Clinical, serologic, and epidermiologic evidence documents an outbreak of toxoplasmosis involving ten of 30 members of an extended family. The index patient had unusual clinical manifestations including brain abscesses, progressive chorioretinitis, seizures, neurologic deficits, hepatosplenomegaly, pneumonitis, and eosinophilia. Toxoplasmosis was confirmed by demonstrating the organism in brain tissue and cerebrospinal fluids; clinical and serologic evidence also indicated infection with Toxocara (viscd children. Of the 11 such children, seven (68%) were seropositive, six of whom had high acute-phase titers (greater than or equal to 1024) to Toxoplasma and a disease consistent with acute toxoplasmosis. All six of the latter group required specific chemotherapy. Geophagia was associated statistically with acute toxoplasmosis among the children; it also increased the risk of infection with Toxocara and enteroparasites. Two school-aged children and two adults had serologic evidence of acute toxoplasmosis, but only one of the group was symptomatic. Epidemiologic evidence indicates that this outbreak was probably caused by ingesting oocysts from cat feces. We suggest that the severe and unusual clinical manifestations of the index patient resulted from simultaneous infection with Toxoplasma and Toxocara.
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PMID:An outbreak of toxoplasmosis linked to cats. 718 77

Generally speaking, with rapid international travel, it is very common to diagnose infectious diseases in areas where they were not known before. Nowadays, visceral leishmaniasis (VL) is documented in Egypt mainly in Al Agamy, Alexandria. Another case of infantile visceral leishmaniasis was identified in an adult farmer (unusual host) in Banha. Other studies all over Egypt (based on clinical and or serological diagnosis rather than demonstration of the parasites) raised the possibility of adult affection with visceral leishmaniasis. The point is that visceral leishmaniasis, shares many clinical manifestations with other diseases known in Egypt as schistosomiasis mansoni, hepatic amoebiasis, toxoplasmosis, and malaria. In the present study, out of 22 human cases with hypersplenism and suggesting manifestations, four gave seropositivity for VL, by the indirect haemagglutination tests (128 & more). Two of these four patients gave seropositivity by dot-ELISA (1:8000). Amastigotes of Leishmania parasite were demonstrated in the splenic smears obtained during splenectomy. One culture obtained from these two cases grew promastigotes. Typing is ongoing. It was concluded that visceral leishmaniasis should be in mind and considered in the differential diagnosis of patients with hepatosplenomegaly or hypersplenism in Egypt.
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PMID:Visceral leishmaniasis among hypersplenic patients in Dakahlia Governorate, Egypt. 837 75

Toxoplasmosis, caused by the intracellular protozoan Toxoplasma gondii, has as its major routes of acquisition either ingestion (of the cyst or oocyte) or transplacental infection (by trophozoites). Transplacental transmission occurs to the fetus in utero or to the newborn at vaginal delivery. Maternally acquired infections can infect the embryo as early as the 7th week of gestation. It has been estimated that 15-17% of maternal infections acquired between the 7th and 14th weeks of gestation are transmitted to the embryo (Lynfield R, Eaton RB., Teratology 1995;52:176-180.). We present a 7-wk-old white male, delivered at 38 wk of gestation, who shortly after birth was found to have hepatosplenomegaly and anemia; he developed liver failure and ascites with persistent anemia during the first week of life. After an extensive, but nondiagnostic, work-up, a paracentesis was performed which led to a diagnosis of congenital toxoplasmosis. This case demonstrates the utility of exfoliative cytology in determining the cause of neonatal ascites, especially of an infectious etiology. To our knowledge, this represents the first reported case of Toxoplasma gondii diagnosed by exfoliative cytology in a pediatric patient.
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PMID:Congenital toxoplasmosis: diagnosis by exfoliative cytology. 958 73


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