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Study the pathogenicity of Providencia Vermicola in mice

Bibliographic Data

ID15794773
AuthorsAhmed Kazem Al Ameer (University of Baghdad, corresponding author), Nagham Mohammed Al‐Gburi (0000-0003-2783-5916, University of Baghdad), Nagham Mohammed Al-Gburi
Year2022
Pages6895-6906
Publication date2022-06-30
Open AccessYes
TypeARTICLE
VenueInternational Journal of Health Sciences (JOURNAL)
Journal identifiersISSN: 2550-696X • E-ISSN: 2550-6978
PublisherUniversidad Tecnica de Manabi (PUBLISHER • EC)
DOI10.53730/ijhs.v6ns4.10020
OpenAlexW4288926863
LanguageEN
References cited1

P. vermicola is an opportunistic pathogen of human and animals. To estimate the pathogeneses of P.vermicola in mice infected orally and I/P with 1x108 CFU/ml).The histopathological changes at 24 hrs showed infiltration of inflammatory cells and apoptosis in hepatocytes in the liver, infiltration of inflammatory cells around a congested blood vessel and interstitial tissue of kidney; lung revealed congestion of blood vessels, infiltration of inflammatory cells and alveolar emphysema; intestine appeared infiltration of mononuclear cells in mucosa layer with hyperplasia of goblet cells. In mice infected I/P, the liver showed infiltration of inflammatory cells in a necrotic area with granulomatous lesion formation, the spleen showed depletion of white pulp. The kidney revealed dilatation of bowman’s space with vacuolation of glomeruli. The intestine appeared infiltration of inflammatory cells in mucosa and submucosa layers with hyperplasia of goblet cells, also, the lung showed infiltration of inflammatory cells in interalveolar septa and alveolar emphysema

Biology · Cellular infiltration · Hyperplasia · In vitro · Infiltration (HVAC · Inflammation · Kidney · Lung · Mononuclear cell infiltration · Pathology · Peripheral blood mononuclear cell · Spleen · Submucosa · Biliary and Gastrointestinal Fistulas · Chemistry · Medicine · Oral and gingival health research · Therapeutic Uses of Natural Elements · Endocrinology · Immunology · Internal Medicine

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Highly citedNo
Open DOIOpen Access
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