[Intestinal cryptosporidiosis at an early age and its negative consequences].
This review calls the attention of physicians, primarily pediatricians, to cryptosporidiosis, a still little known intestinal infection caused by the protozoan pathogen Cryptosporidium parvum (Coccidia, Sporozoa). By using 10--14-day rats as a model, the authors have first provided evidence that even 4-day intestinal cryptosporidiosis may trigger obvious negative changes in the liver and heart, i.e. in the organs where the parasite does not develop. In the infected rats, growth retardation was registered, in addition to liver hypertrophy and partial heart atrophy, and growth retardation. Light and electron microscopies, absorption and fluorescence cytometry, quantitative morphometry, and image analysis were applied. In both hepatocytes and cardiomyocytes, the polyploid cell fraction was seen much increased, with the occurrence of 4c, 8c, and even 16c nuclei. Besides, in the hepatocytes, the amount of glycogen decreased whereas the level of protein increased, along with enhanced nucleolar activity in the nuclei. Unlike, the cardiomyocytes of the infected rats were characterized by protein decrease, in addition to almost two-fold cell body elongation. This is the first documented evidence for serious pathological changes in the extraintestinal organs, caused by the intestinal pathogen C. parvum. Within the first 4 days of infection, both the liver and heart of the host seem to work under stress. It is plausible that on modulating liver and heart ploidy, the intestinal parasitic infection (cryptosporidiosis) may bring about functional impairments of these organs, untypical of early age, leading eventually to long-term consequences in further life of formerly infected individuals.
Beĭer
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Sidorenko
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Anatskaia
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D000818:Animals; D000833:Animals, Suckling; D048429:Cell Size; D002675:Child, Preschool; D003457:Cryptosporidiosis / Q000378:metabolism / Q000503:physiopathology*; D016785:Cryptosporidium parvum / Q000502:physiology; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology; D022781:Hepatocytes / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008112:Liver Glycogen / Q000378:metabolism; D009206:Myocardium / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D011123:Polyploidy; D014176:Protein Biosynthesis; D051381:Rats
D008112:Liver Glycogen