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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although cerebral angiography should be approached with caution in the diagnosis of inflammatory cerebro-vascular disease there are some characteristic angiographic findings which may be helpful for classification and differential diagnosis. The proximal cerebral arteries are favourably affected by basal meningitis and thrombangiitis obliterans with resulting stenoses and occlusions. Whereas those inflammations originating from neighbouring skull structures mostly involve the intracavernous parts of the carotid artery, the tuberculous and mycotic arteritis prefer the supraclinoid carotid siphon. Peripheral vascular changes are found in luetic endangiitis, necrotizing and toxic angiitis and in collagenoses. Simultaneous involvement of the temporal arteries is of great diagnostic importance demonstrating the systemic character of the inflammatory process; in Horton's arteritis it can be a pathognomonic finding. Infectious endocarditis, some mycoses and malaria may lead to embolic occlusion of cerebral vessels. Mycotic aneurysms mostly have a broad base or a fusiform shape and do not prefer the localizations of congenital aneurysms. Angiographically, abscesses, tuberculomas and viral encephalitis may result in circumscribed hypervascularized areas. The characteristic angiographic findings are exemplified and discussed on the basis of 8 cases of inflammatory cerebro-vascular disease (tuberculosis, pneumococcal and unspecific bacterial meningitis, syphilis, mycosis, Takayasu-syndrome, panarteritis nodosa, temporal arteritis).
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PMID:[Inflammatory cerebro-vascular disease: angiographic findings and distribution patterns (author's transl)]. 0 27

Two Thai girls aged 10 and 13 years from the same rural area were admitted to Paholpolpayuhasena Hospital, Kanchanaburi, Thailand during the rainy season of 1989 with cerebral malaria. After several days of conventional treatment, both developed gangrene involving the feet and toes, but the lesions healed and no other complications were seen. In the absence of convincing clinical and laboratory evidence of vasculitis or coagulopathy, it seems likely that host factors (dehydration, sluggish peripheral circulation, platelet activation, subclinical intravascular coagulation) combined with strain-specific parasite factors (tissue sequestration of mature forms, rosette formation) may predispose to peripheral microvascular occlusion sufficient to produce infarction of tissue in susceptible children. However, despite the apparently ominous appearance of such lesions in a comatose child, the prognosis seems good.
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PMID:Peripheral gangrene in nonfatal pediatric cerebral malaria: a report of two cases. 194 78

We compared the performance of six complement tests: electrophoresis, immunofixation, immunoelectrophoresis, and nephelometric quantifications of C3, C4, and C3d. We used 123 blood samples from 60 control subjects and 63 patients with immune complex diseases: systemic lupus erythematosus, idiopathic thrombocytopenic purpura, rheumatoid arthritis, acquired immunodeficiency syndrome, renal diseases, vasculitis, cryoglobulinemia, Gram-negative bacteremia, Hashimoto's thyroiditis, rheumatic heart disease, malaria, and chronic active hepatitis. Immunofixation and quantification of C3d were better for detecting complement activation, their sensitivity rates (90.5% and 89.3%, respectively) being higher than those of the other tests studied. Immunofixation is a relatively simple and inexpensive test, provides good resolution of protein bands, and yields results that are easily quantified with a densitometer. Nephelometry of C3d provides more rapid and accurate quantitative results than immunofixation, but commercial reagents are not yet available. The causes of false-positive results in complement tests and the mechanisms of complement activation in AIDS are also discussed.
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PMID:Detection of complement activation in immune complex diseases: six methods compared. 294 96

Severe Plasmodium falciparum malaria is characterized by multiple organ involvement due to sequestration of infected erythrocytes in small vessels. Endothelial cell adhesion molecules play an important role in this interaction. During the course of a severe cerebral P. falciparum malaria infection we found very markedly elevated levels of the soluble adhesion molecules intercellular adhesion molecule-1, E-selectin, and vascular cell adhesion molecule-1, with a maximum increase of nine, seven, and eight times, respectively. These very high levels of soluble adhesion molecules point to an endothelial cell injury as an additional cause to physiological release or shedding due to receptor interactions. Soluble thrombomodulin (sTM) levels showed an extremely marked elevation up to 332 ng/ml (up to 13 times the normal value) as well. Malaria patients without severe organ involvement/cerebral manifestation showed only a mild elevation of sTM levels. TM is a parameter independent of the immunological system. It is regarded as a marker of vasculitis and endothelial cell destruction. Therefore, markedly elevated sTM levels document a substantial endothelial cell injury in severe malarial infection and may be of diagnostic and prognostic importance.
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PMID:Serum levels of adhesion molecules and thrombomodulin as indicators of vascular injury in severe Plasmodium falciparum malaria. 781 16

Four of 30 patients with Plasmodium falciparum infection in Bangkok, Thailand, were positive for anti-neutrophil cytoplasmic antibodies by indirect immunofluorescence 1 month after antimalarial therapy. No myeloperoxidase, proteinase 3, lactoferrin, or elastase reactivity was found. Since no evidence of vasculitis was seen in these patients, anti-neutrophil cytoplasmic antibody production in malaria-infected susceptible patients probably represents a secondary response, indicating neutrophil activation.
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PMID:Detection of anti-neutrophil cytoplasmic antibodies after acute Plasmodium falciparum malaria. 877 May 17

B cell deficient animals obtained by various strategies of gene targeting were used to study the B cell development and examine the role of different immune compartments in the immune response to microbes. Study of muMT, JHD, lambda 5T and JHT models of B cell deficiency, was essential in order to understand the role of pre-B cell receptor in B cell development, allelic exclusion and variable gene rearrangement regulation. In the immune response to influenza virus, a protective role of T cells in a total absence of B cell compartment, was revealed by studying the JHD -/- model. Further, it was established that a T cell compartment is sufficient to mediate the recovery from influenza infection. Examination of immune response in muMT and JHD models of definitive B cell deficiency to various blood stage Plasmodia species, showed that whereas B cells are not required for recovery from infection with P. chabaudi adami, P. vinckei petteri and P. chabaudi chabaudi (CB), B cell compartment is important in the later stages of infection with P. chabaudi chabaudi (AS). Studies carried out in muMT model suggested a possible role for T gamma delta subpopulation in the immune response to blood stage malaria parasite. B cell deficiency models are valuable for understanding the normal and pathological immune response. Studies carried out in muMT model indicated that T cell responses are not significantly affected in the absence of B cells. These data can neither rule out a role for B cells in T cell priming, nor in triggering an effective T cell help for humoral response. Study of double homozygous mice deficient for B cells and FAS or IL-2 gene, pinpointed the role of B cells in pathogenesis of lupus-like nephritis and vasculitis from lpr mouse and in hemolytic anemia from IL-2 -/- mouse model, respectively.
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PMID:Immunoglobulin deficient mice generated by gene targeting as models for studying the immune response. 888 29

At age 46, Francisco de Goya (1746-1828) suffered from a severe illness that lasted several months. It caused loss of vision and hearing, tinnitus, disorientation, weakness, abdominal distress, and general malaise. After a few months he recuperated but was left deaf forever. In addition to the physical effects, his emotional health and artwork were affected. The precise cause of this illness has long been debated. One early, but unlikely, hypothesis was that he had syphilis. Later conjectures have included Vogt-Koyanagi-Harada disease and lead toxicity. Cogan's syndrome and vasculitis are additional possibilities, although neither is likely to have been Goya's diagnosis. An infectious disease such as meningitis, encephalitis, or malaria is far more likely. Quinine toxicity (cinchonism) may have complicated the illness.
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PMID:What ailed Goya? 1054 Nov 54

Several observations suggest that bacteria induce autoimmunity in primary biliary cirrhosis (PBC). Since no PBC-specific bacterial species could be identified, it can be speculated that the triggers are non-species-specific bacterial proteins. This hypothesis would imply that several or even all bacterial species can trigger PBC. Therefore, we investigated whether PBC exhibits immune reactions to non-species-specific bacterial antigens. Yersinia enterocolitica O3 was screened for the presence of proteins that were labeled by immunoblotting using PBC sera. We focused our investigations on a 160-kDa protein, which was further enriched and characterized by partial N-terminal amino acid sequencing. The prevalence of antibodies to this protein was determined by immunoblotting in a variety of diseases. The 160-kDa protein was identified as the beta-subunit of bacterial RNA-polymerase, a highly conserved bacterial protein with a very high degree of sequence identity among all bacterial species. Antibodies to the beta-subunit of bacterial RNA polymerase were specific for this protein. Until now no mammalian protein could be found that cross-reacts with these antibodies. The prevalence of antibodies to the beta-subunit of bacterial RNA polymerase (ARPA) using the protein from Yersinia enterocolitica O3 (serum dilution 1:1000) was: healthy controls (HC, N = 101) 7.9%, primary biliary cirrhosis (PBC, N = 61) 32.8%, autoimmune hepatitis type 1 (AIH, N = 46) 26.1%, alcoholic liver cirrhosis (ALC, N = 44) 9.1%, Crohn's disease (CD, N = 38) 7.9%, ulcerative colitis (UC, N = 24) 8.3%, primary sclerosing cholangitis + UC (PSC/UC, N = 11) 0%, acute yersiniosis (Yers, N = 36) 19.4%, acute infection with Campylobacter jejuni (Camp, N = 10) 0%, acute Q-fever (QF, N = 16) 6.25%, chronic hepatitis C (HCV, N = 39) 7.7%, c-ANCA-positive vasculitis (Vasc, N = 40) 15%, systemic lupus erythematosus (SLE, N = 28) 10.7%, and malaria tropica (MT, N = 24) 16.7%. There was no significant difference between PBC and AIH. The group of autoimmune liver diseases (PBC + AIH, N = 107, 29.9%) differed highly significantly from HC, chronic inflammatory bowel diseases (CD + UC + PSC/UC, N = 73, 6.8%), ALC, and HCV and also differed significantly (P = 0.01) from the group with bacterial and parasitic diseases (Yers + Camp + QF + MT, N = 86,13.95%) and from the group with Vasc + SLE (N = 68,13.2%). Testing of ARPA using the protein from E. coli yielded nearly identical results. In conclusion, an increased prevalence of antibodies to the beta-subunit of bacterial RNA polymerase, a highly conserved non-species-specific bacterial protein, can be found in primary biliary cirrhosis, but also in autoimmune hepatitis type I. These findings do not add an argument for a bacterial trigger of PBC. Rather, they suggest that ARPA belong to the pool of natural antibodies that are up-regulated in autoimmune liver diseases.
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PMID:Identification of beta-subunit of bacterial RNA-polymerase--a non-species-specific bacterial protein--as target of antibodies in primary biliary cirrhosis. 1275 71

This cross-sectional study was carried out to determine the possible causes of chronic renal failure (CRF) in Ibn Sina Teaching Hospital (ISTH) in Hadramout, Yemen. Fifty-one CRF patients (29 men and 22 women) on regular hemodialysis were included in the study. Glomerulonephritis (25.4%) was the commonest cause of CRF, followed by obstructive nephropathy (13.7%), hypertension (11.8%), pyelonephrits (11.8%), diabetic nephropathy (7.8%), arthritis, malaria, vasculitis and postpartum hemorrhage (5.9% each) and the least common one was Alport's syndrome (3.9%). There were more men than women (57% and 43%, respectively). The mean age range of the patients was 42 years. More patients were the from coast of Mukalla than from the valley and desert (59% and 41%) respectively.
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PMID:Causes of Chronic Renal Failure in Hemodialysis Unit: a single center experience in Yemen. 1729 42

Antineutrophil cytoplasmic antibody (ANCA) is often used in the laboratory to confirm paucicellular vasculitis like Wegener's granulomatosis, Churg Strauss syndrome or polyarteritis nodosa in the presence of suggestive clinical features. In tropical countries, tuberculosis, leprosy and, occasionally, malaria can produce clinical features similar to a vasculitic illness and all the three infections are known to be associated with auto antibodies. We tested 318 patients suffering from malaria, tuberculosis or leprosy for ANCA positivity. ANCA positivity was found in 19%, 32% and 30% of malaria, tuberculosis and leprosy patients (Pradhan V, Badakere S, Shankarkumar V, Iyer Y, Ghosh K, Karnad D, Indian J Malariol, 39:51-59, 2002; Pradhan V, Badakere S, Ghosh K, Pawar A, Indian J Med Sci, 58:283-288, 2004a; Pradhan V, Badakere S, Shankarkumar V, Lepr Rev, 75:50-56, 2004b), respectively, raising the possibility that ANCA positivity with clinical features suggestive of vasculitis in tropical countries may even be related to the background noise of this seropositivity caused by one of these three infections rather than confirming the diagnosis of paucicellular vasculitis. Hence, one should be careful about the background noise of ANCA positivity caused by these infections while diagnosing a vasculitic illness.
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PMID:Background noise of infection for using ANCA as a diagnostic tool for vasculitis in tropical and developing countries. 1829 72


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