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

Plasmodium brasilianum causes chronic quartan malaria in the common marmoset Callithrix jacchus, whereas Epstein-Barr virus (EBV) infection is followed by an infectious mononucleosis-like syndrome that resolves. We infected weanling marmosets with one or both of these pathogens. Timing of the infections influenced outcome. Six animals were simultaneously infected with both agents; four became seriously ill (with accompanying proteinuria and edema) and either died or were killed. Histopathology indicated that glomerulonephritis had developed. The two survivors had more-prolonged parasitemia than did animals infected with P. brasilianum alone, as did animals infected with EBV before P. brasilianum. Five of the six simultaneously infected animals had absent or low titers of antibody to Epstein-Barr viral capsid antigens when compared with the other EBV-infected animals. Our results suggest that combined infection may be part of the etiology of quartan malarial nephropathy.
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PMID:Glomerulonephritis in common marmosets infected with Plasmodium brasilianum and Epstein-Barr virus. 284 17

The renal pathology of 9 squirrel monkeys (Saimiri sciureus) with acute Plasmodium falciparum infection was studied by light and electron microscopy. Endocapillary proliferative glomerulonephritis was the major pathological change observed. The peroxidase anti-peroxidase method demonstrated the presence of IgG, IgM, and P. falciparum antigens in the mesangium and basement membrane. These findings were consistent with those seen in humans with acute P. falciparum infection and indicates that squirrel monkeys are likely to be a good model for the study of renal pathology in malaria research.
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PMID:Glomerulopathy in squirrel monkeys with acute Plasmodium falciparum infection. 327 66

Renal biopsies were performed on 21 of 27 Melanesian patients presenting with significant proteinuria in Vanuatu from 1983 to 1985. All patients had more than 2 g of proteinuria per 24 hours or clinical evidence of the nephrotic syndrome. The average age of the patients who were biopsied was 31 years. Three of the 21 patients had evidence of active malaria at the time of presentation, and all of these patients had Plasmodium falciparum. Renal histopathology revealed that six patients (29%) had amyloidosis and five patients (24%) had mesangiocapillary glomerulonephritis (type 1). Of particular note was the fact that only one patient had membranous glomerulonephropathy and only one patient had minimal change nephrotic syndrome, the two most common lesions reported in nephrotic patients in Europe and the United States. Thus, the spectrum of renal histopathology in patients presenting in Vanuatu with significant proteinuria is very different from that seen in Western Countries.
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PMID:The spectrum of renal histopathology in patients with significant proteinuria in Vanuatu. 349 88

A splenectomized aotus monkey infected with human quartan malaria (Plasmodium malariae) developed oedema and proteinuria. Histological examination revealed a generalized diffuse glomerulonephritis and immunofluorescent staining showed granular deposits of IgM in the glomeruli. The pathological picture resembled that shown by human patients with the quartan malaria nephrotic syndrome.
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PMID:Nephrotic syndrome in monkey infected with human quartan malaria. 500 May 4

This paper describes the immunopathologic findings in acute malaria-associated glomerulonephritis in the rat. Young Sprague-Dawley rats were infected with Plasmodium berghei berghei. The subsequent parasitemia and elevation of circulating Clq-reactive immune complexes were transient while the appearance of anti-plasmodial antibody in the serum was persistent. Sequential examination of renal tissue and urine revealed the following glomerular alterations: (a) granular, predominantly mesangial deposits of IgG, IgM, and C 3, (b) electron dense deposits in the mesangial matrix, (c) glomerular deposition of plasmodial antigen(s) and of anti-plasmodial antibody as demonstrated by acid elution studies, (d) hypercellularity of the glomerular tufts and (e) increased urinary excretion of high molecular weight proteins. All renal abnormalities were transitory, disappearing within one to three months. The results indicate that this form of acute malarial glomerulonephritis in rats is mediated by immune complexes involving plasmodial antigen. The disease resembles the transient glomerular injury complicating cases of Plasmodium falciparum infection in humans. As an easily reproducible model, rat malarial glomerulonephritis appears most suitable for further immunopathologic and functional studies of post-infectious glomerular disease.
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PMID:Rat malarial glomerulonephritis. An experimental model of post-infectious glomerular injury. 611 79

Nonspecific immunity (NSI) was manifested in rats injected intravenously with killed Corynebacterium parvum and challenged with Trypanosoma lewisi, Plasmodium chabaudi, or Babesia rodhaini. The NSI became evident some 5 days after infection as a suppressed parasitemia, a more rapid recovery from patent infection and as enhanced survival among rats infected with B. rodhaini. The C. parvum injections produced anemia and thrombocytopenia with splenomegaly and signs of glomerulonephritis in rats. The signs became evident about 5 days after injection and were accompanied by reduced titers of lytic complement, elevated titers of antibody against fibrinogen products (Anti-F), antibody against soluble serum antigen of malaria and babesiosis (ABSA), and antibody against the third component of fixed complement or immunoconglutinin (IK). These were the autoantibodies associated with anemia and reduced parasitemia of infection-induced NSI. In as much as immunoconglutination of blood cells or parasites coated with complement fixing immune complexes was implicated as a functional mechanism in infection-induced NSI, it is possible that these same factors might function in C. parvum induced NSI.
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PMID:Anemia and thrombocytopenia from Corynebacterium parvum-stimulated resistance against malaria, trypanosomiasis, and babesiosis. 635 27

The disposal of immune complexes by the glomerulus and the participation of infiltrating monocytes were studied in acute malaria-associated glomerulonephritis. Young Sprague-Dawley rats were infected with Plasmodium berghei. Parasitemia reached a maximum after 8 to 12 days, ending by day 20. In all infected rats, renal immunofluorescence microscopy showed in all glomeruli granular deposition of rat IgG, IgM, and C3 in a mesangial distribution. The staining was strongest from days 8 to 12, then diminished and disappeared after day 32. By contrast, electron-dense deposits were rarely seen before day 16 when they became detectable in the mesangial matrix, particularly along the inner aspect of the glomerular basement membrane. They were most conspicuous on days 20 and 34 and disappeared by day 100. Few monocytes were detected in the glomeruli by electron microscopy and by histochemistry for nonspecific esterase. Highest counts of esterase-positive monocytes were found on day 10 (means 2.9 per glomerulus, range 0 to 5; normal control range 0 to 1). Total glomerular cell counts were transiently elevated on days 10 and 20. Renal functional damage of malarial rats was mild as reflected by a transient increase of urinary protein excretion, whereas serum urea values remained in the normal range. The results suggest that elimination of glomerular immune deposits in acute malarial glomerulonephritis of rats involves their gradual condensation and degradation in the mesangium which reduces detection by immunofluorescence while leading to formation of transient electron-dense deposits. In this model, the efficient disposal of glomerular immune deposits by the mesangium appears to minimize the infiltration of monocytes and to prevent aggravation of the glomerular injury.
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PMID:Mesangial disposal of glomerular immune deposits in acute malarial glomerulonephritis of rats. 703 93

The renal complications in course of malaria have notably increased in number during the last years, as well as the cases of malaria in the world. This subject and a case of malaria in the world. This subject and a case of renal complication in course of malaria we could recently observe led us to re-examine the papers in which this problem was debated. Only the Pl. malaria and the Pl. falciparum can cause renal complications, as the first can produce a nephrosic syndrome and the second an acute renal insufficiency functional or organic, or a glomerulonephritis more often acute transitory, which can rarely develop into a nephrosic syndrome or into an acute renal organic insufficiency. Then the various physiopathologic causes of the acute renal insufficiency, of the glomerulonephritis, of the nephrosic syndrome are described, followed by a case description of an acute renal functional insufficiency in course of malaria caused by Pl. falciparum.
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PMID:[Renal changes in malaria]. 704 51

Pathogenic organism can be considered as pro-oxidant agents because they produce cell death and tissue damage. In addition organism can be eliminated by specific cell defense mechanism which utilize in part, reactive oxygen radicals formed by oxidative stress responses. The cause of the necessarily defense process results in cell damage thereby leading to development of inflammation, a characteristic oxidative stress situation. This fact shows the duality of oxidative stress in infections and inflammation: oxygen free radicals protect against microorganism attack and can produce tissue damage during this protection to trigger inflammation. Iron, a transition metal which participates generating oxygen free radicals, displays also this duality in infection. We suggest also that different infectious pathologies, such as sickle cell anemia/malaria and AIDS, may display in part this duality. In addition, it should be noted that oxidative damage observed in infectious diseases is mostly due the inflammatory response than to the oxidative potential of the pathogenic agent, this last point is exemplified in cases of respiratory distress and in glomerulonephritis. This review analyzes these controversial facts of infectious pathology in relation with oxidative stress.
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PMID:[Oxidative stress and infectious pathology]. 779 23

MRL-lpr/lpr mice spontaneously develop an autoimmune disease resembling systemic lupus erythematosus and rheumatoid arthritis. One of the unique serological abnormalities in this strain is remarkably high concentrations of cryoglobulins. Analysis of immunoglobulin components in their cryoglobulins has shown selective enrichment of a particular IgG subclass, IgG3. As IgG3 enrichment is also found in two other cryoglobulins, which are induced after injection with bacterial lipopolysaccharides or infection with malaria, IgG3 apparently represents a major source of murine cryoglobulins. Studies on murine IgG3 monoclonal antibodies (mAbs) have clearly shown that murine IgG3 have the unique physiochemical property to self associate through non-specific IgG3 Fc-Fc interaction, and that most of them can generate monoclonal cryoglobulins. Most strikingly, IgG3 monoclonal cryoglobulins with rheumatoid factor (RF) activity induce extensive pathological manifestations: skin vascular purpura and glomerulonephritis with 'wire loop' lesions. Although the cryoglobulin activity of IgG3 RF mAb is solely responsible for the generation of glomerular lesions (both RF and cryoglobulin activities are necessary for skin vascular lesions), the absence of nephritogenic activity by some IgG3 cryoglobulins supports the idea that qualitative features of cryoglobulins are critical to determine their pathogenic activity. The demonstration of a positive correlation between the production of IgG3 cryoglobulins and the development of lupus nephritis in MRL-lpr/lpr mice further substantiates the pathological importance of cryogenic autoantibodies. On the other hand, it should be emphasised that non-cryogenerating IgG3 autoantibodies may not be harmful, but even protective, as a result of their interaction with pathogenic IgG3 cryoglobulins. Finally, the development of an experimental model of cryoglobulinaemia associated with vascular and glomerular disease certainly represents an invaluable opportunity to study the molecular mechanisms responsible for the generation of cryoglobulins and their associated tissue lesions, and also to assess various therapeutic approaches. Our demonstration that anti-idiotypic mAb can prevent the pathogenic effects of the cryoprecipitable IgG3 RF mAb suggests strongly that such a therapeutic approach might be successful in similar diseases in man.
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PMID:IgG3 cryoglobulins in autoimmune MRL-lpr/lpr mice: immunopathogenesis, therapeutic approaches and relevance to similar human diseases. 848 Oct 59


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