Cat-scratch fever.
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Intracellular invasion is an important aspect of Carrión's disease caused by Bartonella bacilliformis. Both the hematic and tissue phases of the disease involve the initial attachment of the organism to erythrocytes and endothelial cells, respectively. Using two different approaches, preliminary evidence is provided that B. bacilliformis interacts with multiple surface-exposed proteins on human erythrocytes. Utilizing Western blot analysis, it was demonstrated that the organism binds several biotinylated erythrocyte proteins with approximate molecular masses of 230, 210, 100, 83 and 44 kDa. There was enhanced Bartonella binding to the 44 kDa protein and binding to a 25 kDa protein following exposure of intact red cells to trypsin. Moreover, there was a complete abrogation of binding to these proteins following exposure of erythrocytes to sodium metaperiodate oxidation, indicating the significance of carbohydrate moieties in the interactions of Bartonella with the erythrocyte. In a second approach, similar binding proteins or putative receptors were identified when Bartonella was co-incubated with isolated membrane proteins from red cell ghosts. A comparison of the molecular weights of these putative receptors with known erythrocyte proteins and their immunoreactivity to specific antisera suggested that the 230 and 210 kDa proteins are the alpha and beta subunits of spectrin; the 100 and 83 kDa proteins are band 3 protein and glycophorin A, respectively; and the 44 and 25 kDa proteins are the respective dimeric and monomeric forms of glycophorin B. Consistent with this notion was the binding of Bartonella to purified preparations of alpha and beta spectrin and glycophorin A/B.
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R. Koch showed in 1882 in his so-called fundamental experiment that tuberculous guinea pigs exhibit a vigorous immunity against re-infection. In investigations in 1930--40 we showed that this immunity is not mediated by humoral antibodies. It is a cellular process, a local and general activation of the macrophage system (the system of mononuclear phagocytes). The tuberculous granuloma consists of activated macrophages and their descendants (epitheloid and giant cells), which inhibit the growth and spreading of tubercle bacilli. The role of the specific and unspecific activation of the macrophage system could be demonstrated in experiments on rats, infected with Bartonella muris ratti. These early results are related to the recent knowledge concerning cellular immunity and granulomatous inflammation, especially to the cooperation between the lymphatic and macrophage system.
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We describe a 13-year-old boy who presented with hematuria and intermittent low-grade proteinuria at the time when he was diagnosed with cat scratch disease. Two months before presentation, he had a negative urinalysis during a routine physical evaluation. He continued to have microscopic hematuria for the next 6 months, when he developed gross hematuria and recurrence of low-grade proteinuria. The renal biopsy showed evidence of mild/moderate IgA nephropathy. We speculate that the immunological changes associated with cat scratch disease in this patient may have triggered the development of IgA nephropathy. A history or serological evidence of infection with Bartonella henselae may need to be sought in patients presenting with IgA nephritis.
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Bartonella bacilliformis invades the endothelial lining of the cardiovascular system. Damage to the red blood cells and white blood cells, the effects of the toxins, invasion of the brain and electrical charges induced by the organism so interfering with normal electrical stimulation of the heart may explain many of the features of cardiovascular disease (1-5).
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Although cats and their arthropod parasites can sometimes be important sources of zoonotic diseases in humans, the extent of exposure among various cat populations to many potential zoonotic agents remains incompletely described. In this study, 170 domestic cats living in private homes, feral cat colonies, and animal shelters from California and Wisconsin were evaluated by serology to determine the levels of exposure to a group of zoonotic vector-borne pathogens. Serological positive test results were observed in 17.2% of cats for Rickettsia rickettsii, 14.9% for R akari, 4.9% for R typhi, 11.1% for R felis, and 14.7% for Bartonella henselae. Although vector-borne disease exposure has been documented previously in cats, the evaluation of multiple pathogens and diverse cat populations simultaneously performed here contributes to our understanding of feline exposure to these zoonotic pathogens.
OBJECTIVES: Rickettsiae, which causes vasculitis, has not been linked to atherosclerotic cardiovascular disease in contrast to Chlamydia pneumoniae whose association with coronary artery disease and with sclerotic heart valves in patients undergoing aortic valve replacement is well established, even if causality is yet to unproven. In the search for any of these infectious agents, 84 pathological and 15 normal aortic heart valves of patients undergoing forensic autopsy were analysed by PCR and DNA-sequencing. METHODS: Two to four pieces of all valves were examined by semi-nested PCR, with primers specific for 16S rDNA, citrate synthase (gltA) and 17 kDa outer membrane protein (OMP) genes. RESULTS: Genetic material from Rickettsia spp. and C. pneumoniae was found in 17 (20.2%) and 22 (26.2%), respectively, of the 84 pathological aortic valves. In 35 (41.7%) of these 84 valves either C. pneumoniae or Rickettsia spp. were detected by PCR and in six cases (7.1%) these two organisms co-existed. In one case with Lambl's excrescences, previously considered as aseptic, presence of rickettsia-like organisms also was demonstrated by light microscopy, immunohistochemistry and sequencing of the amplified PCR product showing 100% homology with the published sequence for R. helvetica. In three of the 15 control valves, genetic material from only C. pneumoniae was detected compared to Rickettsia spp. that was significantly detected only in the pathological valves (Fisher's Exact test, 1-sided p = 0.046). CONCLUSIONS: The findings suggest that Rickettsia spp. also have a role in the pathogenesis of aortic valve disease.
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