Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immunodepressive effect of Toxoplasma gondii infection in mice was studied, using sheep erythrocytes (SRBC) as the testing antigen and serum hemagglutinins, hemolysins, and both direct and indirect splenic plaque-forming cells (PFC) to SRBC as assays. In the primary antibody response, immunoglobulin M (IgM), hemagglutinins, and hemolysins and both IgM- and IgG-secreting PFC were depressed in animals immunized after infection. Maximum immunodepression occurred during the first 3 weeks of Toxoplasma infection. When the secondary antibody response was studied, results varied. Mice immunized with SRBC after being infected with T. gondii had a depression in both IgM and IgG PFC. Mice immunized with SRBC before being infected with T. gondii and then given a challenge dose of SRBC had a delay, but no an actual depression, in IgG hemagglutinins and hemolysins and IgG-secreting PFC. These studies show that the immunodepression associated with Toxoplasma infection is complicated, and they provide no definitive explanation for the mechanism.
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PMID:Depressed antibody responses to a thymus-dependent antigen in toxoplasmosis. 31 57

Entry by tachyzoites of Toxoplasma gondii, the causative agent of toxoplasmosis, into peritoneal cells was investigated with transmission and scanning electron microscopy. The process of entry is initiated by the parasite contacting the host cell with its anterior end, creating a small depression in the plasmalemma of the host cell. Occasionally, a small portion of the host cell cytoplasm protrudes and contaccts the anterior end of the parasite. A cylindrical structure (35 nm in diameter) extends from the pellicle of the parasite to the host cell. Such structures appear to assist host cell entry by T. gondii. As the entry process progresses, pseudopods of the host cell surround theparasite and finally T gondii becomes intracellular, being located in a vacuole separated from the host cell cytoplasm by a unit membrane. (Am J. Pathol 87:285-296, 1977).
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PMID:Transmission and scanning electron microscopy of host cell entry by Toxoplasma gondii. 85 Nov 68

Toxoplasmosis is known to complicate diseases with impaired cellular immunity. For treatment of toxoplasma infections atoxic drugs should be used to avoid depression of the bone marrow. The hitherto recommended treatment, pyrimethamine in combination with sulphonamides, is often associated with severe side-effects. The present study presents the results of treatment with trimethoprim and sulphamethoxazole in 7 patients, clinically and serologically diagnosed as having toxoplasmosis. Good therapeutic results were observed in 5 patients with lymphoglandular toxoplasmosis and a significant reduction of the dye test titres were found in 6 patients. In one patient, however, a relapse of clinical symptoms and a reversion to high dye test titres were observed 6 1/2 months after the end of the treatment. Treatment had to be discontinued in one patient due to an allergic reaction.
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PMID:Treatment of toxoplasmosis with trimethoprim-sulphamethoxazole. 114 37

A prospective study of possible aetiological factors for neuropathy associated with HIV infection was performed in 80 patients and 28 homosexual controls. At entry to the study twelve patients (15 per cent) had evidence of a generalized neuropathy not due to any other cause and a further three patients developed symptomatic neuropathy during a mean (SD) follow-up of 20 (7.5) months. All but two of these neuropathies were of the distal symmetrical sensory type. Electrophysiology was consistent with an axonal pathology and nerve biopsy confirmed this as the major pathological change. Warming threshold was the diagnostic test most frequently abnormal, sometimes in the absence of other electrophysiological abnormalities. No association was seen with opportunistic infection (cytomegalovirus, herpes simplex, Pneumocystis pneumonia, toxoplasmosis, Cryptococcus infection or tuberculosis). HIV proviral DNA could not be detected in paraffin sections of peripheral nerve in six patients with neuropathy. The presence of the neuropathy did not show significant correlation with depression of the number of CD4+ T cells in the blood, impaired T cell function tests, or IgG, IgM, or IgA levels. Immune complexes containing C1q, but not those containing IgG, IgM, IgA or C3c, were significantly more common among neuropathic patients (p = 0.01).
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PMID:A study of neuropathy in HIV infection. 144 48

A 13-month-old Doberman Pinscher was evaluated because of slowly progressive paraparesis and signs of depression. The dog had temporal, supraspinatus, and infraspinatus muscle atrophy, bilateral enophthalmos, superficial inguinal lymphadenopathy, tachycardia with pulse deficits, and lesions of active and inactive chorioretinitis. Neurologic abnormalities included hyperreflexic patellar reflexes, lack of conscious proprioception, signs of superficial pain in the hind limbs, and depressed hopping reflexes in the forelimbs. Cranial nerve abnormalities included decreased sensation in the left nostril and a delayed gag reflex. Results of cerebrospinal fluid analysis were characteristic of nonsuppurative inflammation. A diagnosis of multifocal neurologic disease was made. The dog did not have serum titers for fungal diseases, canine distemper, Ehrlichia canis infection, borreliosis, Rocky Mountain spotted fever, or toxoplasmosis. The dog did not respond to various antimicrobial treatments, and only slightly responded to corticosteroid treatment. The dog died during an anesthetic procedure. The postmortem diagnosis of Trypanosoma cruzi infection (canine Chagas disease) was made on identification of the amastigote form of the organism in sections of brain, spinal cord, and myocardium.
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PMID:Neurologic manifestations of trypanosomiasis in a dog. 189 57

Prenatal diagnosis of fetal toxoplasmosis is possible with the use of fetal blood sampling, amniocentesis and ultrasound examination. The purpose of this study was to describe T lymphocyte subsets (CD3, CD4 and CD8) in mothers and their fetuses when Toxoplasma gondii infection occurred during pregnancy. Maternal and fetal blood samples were obtained in 86 cases and 9 fetuses showed T. gondii infection. Control groups consisted of 30 healthy nonpregnant women and 30 pregnant women. Pregnant women with T. gondii infection showed an increase in the suppressor (CD8) T subpopulation and a significant depression in the total helper (CD4) T cells. These alterations were more important in mothers whose fetus was infected. We showed the progressive maturation of the fetal immune system with a regular increase of all T lymphocyte subsets. Marked alterations were observed in the 9 infected fetuses (depression of CD4 population and lower CD4/CD8 ratio). In the future these differences might be used as a new marker of the severity of fetal lesions and become a useful diagnostic tool.
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PMID:Toxoplasma gondii infection during pregnancy: T lymphocyte subpopulations in mothers and fetuses. 198 May 40

The lung is directly affected by HIV virus early in the disease and is the site of a specific lymphocytic alveolitis. Neoplastic pulmonary disease linked to the virus occurs (Kaposi sarcoma, lymphoma and epidermoid tumour) but it is principally following opportunistic infections that patients with AIDS come under the care of a respiratory physician. Certain of the responsible infectious agents causing opportunistic pneumonia are probably present in a latent fashion before the disease presents and are reactivated by the immuno-depression. They may occur successively such as tuberculosis, toxoplasmosis (in this case pulmonary), infection to CMV and pneumocystis. Other infectious agents are transported by the environment and lead to recurrent bacterial infections, mycotic infections or infections with atypical mycobacteria. The clinical management of these different diseases has advanced greatly from a diagnostic therapeutic prophylactic and curative viewpoint.
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PMID:[Clinical management by the respiratory physician of patients with HIV infections]. 227 Mar 40

Acute renal failure due to tubulo-interstitial nephritis developed in a 12 year old boy. It was accompanied by an inflammatory syndrome consisting of a markedly increased erythrocyte sedimentation rate and high levels of C. reactive protein and fibrin. The association of these anomalies with an uveitis are typical of the Tinu syndrome (tubulo-interstitial nephritis uveitis) first described by Dobrin and al. in 1975. The interest of this case lies in the observation of focal chorioretinitis, as yet never described. The possibility of toxoplasmosis is discussed; it could be a direct etiologic factor or could represent a concurrent phenomenon. However no evidence of toxoplasmic infection could be demonstrated in this case, nor in any case previously reported. Light microscopic examination of a renal biopsy reveals diffuse monocellular interstitial infiltration and epithelioid granulomas. In some cases, non-specific bone marrow and lymph node granulomas have been found. In the Tinu syndrome, the nephropathy is completely reversible, either spontaneously or following steroid treatment; this contrasts with the tendency towards relapse of the uveitis. The possible pathogenesis and the relationship with other idiopathic acute nephritis and uveitis are discussed. As in some previous publications, the presence of circulating immune complexes in our patient would suggest the involvement of the immune system. Temporary depression of cellular immunity was also observed in some cases. But the etiology and the pathogenesis of this syndrome are still unknown.
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PMID:[Interstitial tubulo-nephritis and uveitis (Nitu syndrome). Apropos of a case]. 262 76

Fuchs' heterochromic iridocyclitis is a rare but significant cause of visual impairment. This form of uveitis is misdiagnosed more than any other in the entire field of uveitis. This is particularly true among brown-eyed individuals in whom gross heterochromia may not be diagnosed for many years. The clinical presentation of Fuchs' heterochromic iridocyclitis may include a number of generally unrecognised variants among which are Koeppe nodules, transient synechia formations, and blood-filled cysts. Recently the relationship of heterochromic iridocyclitis to posterior inflammatory lesions, such as those of toxoplasmosis, has been explored. Although the disease was once thought to be a degenerative or trophic disorder, current investigations reveal that it is a true inflammation of immunologic origin. The disorder may be related to a depression of suppressor T-cell activity. The aetiology of the disease is still obscure, but in some cases an association with simple heterochromia has been found among families in whom multiple members are affected by either simple heterochromia or Fuchs' heterochromic iridocyclitis. Corticosteroid treatment of Fuchs' heterochromic iridocyclitis is not effective and should be reserved for those patients in whom inflammatory products obstruct the visual axis. Most patients should be treated by observation alone. Cataract and glaucoma are the most important complications. Treatment of the glaucoma is particularly difficult and often unsuccessful.
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PMID:Doyne lecture. Heterochromic iridocyclitis. 389 9

The effect of antithymocyte serum (ATS) on mice infected with high-virulent or low-virulent strains of Toxoplasma gondii was studied. Treatment with ATS reduced the survival time of mice infected with high-virulent Toxoplasma and aggravated the disease; treatment prolonged parasitemia in animals infected with low-virulent Toxoplasma. Although ATS adversely affected the humoral antibody response, its main effect on toxoplasmosis was probably due to depression of cell-mediated immunity. ATS appeared to be able to activate chronic Toxoplasma infection, but this effect was much less pronounced than that on acquisition of immunity. The results suggest that Toxoplasma infection should be routinely looked for in patients treated with antilymphocyte serum.
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PMID:Effect of antithymocyte serum on experimental toxoplasmosis in mice. 453 27


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