EHEC long answer

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Parties jouées 11 %Précision 71 Temps moyen 42:11

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Jessica

United Kingdom

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Compléter EHEC long answerVersion en ligne Fill in the blanks par Jessica 1 EHEC strains differ from E . coli due to the acquisition of additional virulence - associated genetic elements . Genetic variation between pathogenic and non - pathogenic strains arises through acquisition , plasmid transfer , , genomic rearrangements , deletions , and point . Firstly , EHEC contains the of ( LEE ) , a pathogenicity island integrated into the . This region encodes a type III system , receptor and adhesin proteins that enable and ( A / E ) lesion formation on intestinal epithelial cells . Secondly , Shiga toxin genes ( and / or ) are encoded on lysogenic integrated into the bacterial . These phage - encoded toxins are present in non - pathogenic strains and are central to severe disease . 2 After ingestion , EHEC colonises the intestine . The LEE - encoded type secretion system injects Tir and other effector proteins into host epithelial cells . Tir integrates into the cell membrane and binds the bacterial outer membrane protein . This interaction results in intimate . Binding of intimin to Tir triggers the formation of - like structures on host cell membane . are effaced , reducing the absorptive surface of the intestine . These and ( A / E ) lesions contribute to and mucosal inflammation . 3 EHEC also produces Shiga toxin . Under stress conditions , ( e . g . certain ) , the bacterial SOS response can trigger induction , leading to increased transcription of genes and enhanced production . The toxin then travels in the . The toxin enters host cells halts synthesis and leads to cell death . Shiga toxins bind to the receptor globotriaosylceramide ( Gb3 ) on host cells . Gb3 is highly expressed on epithelial cells and endothelial cells . This damage to endothelial cells in the renal microvasculature may lead to ( HUS ) , characterised by acute kidney injury , haemolytic , and . 4 Diagnosis is typically performed using samples . On sorbitol MacConkey agar with cefixime and tellurite ( CTSMAC ) , O157 : H7 does not ferment and produces colonies , whereas commensal strains appear . Selective chromogenic media can detect O157 strains based on specific reactions , producing characteristic coloured colonies . These media improve and ease of identification Molecular tests such as detect Shiga toxin ( stx1 , stx2 ) and other EHEC markers directly from stool samples and provide rapid , diagnosis . Serological testing can confirm O157 and H7 using latex tests that detect the and antigens . Visible agglutination indicates the of the specific surface antigen .

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EHEC long answerVersion en ligne

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EHEC strains differ from E . coli due to the acquisition of additional virulence - associated genetic elements . Genetic variation between pathogenic and non - pathogenic strains arises through acquisition , plasmid transfer , , genomic rearrangements , deletions , and point .

Firstly , EHEC contains the of ( LEE ) , a pathogenicity island integrated into the . This region encodes a type III system , receptor and adhesin proteins that enable and ( A / E ) lesion formation on intestinal epithelial cells .

Secondly , Shiga toxin genes ( and / or ) are encoded on lysogenic integrated into the bacterial . These phage - encoded toxins are present in non - pathogenic strains and are central to severe disease .

After ingestion , EHEC colonises the intestine . The LEE - encoded type secretion system injects Tir and other effector proteins into host epithelial cells . Tir integrates into the cell membrane and binds the bacterial outer membrane protein . This interaction results in intimate . Binding of intimin to Tir triggers the formation of - like structures on host cell membane . are effaced , reducing the absorptive surface of the intestine . These and ( A / E ) lesions contribute to and mucosal inflammation .

EHEC also produces Shiga toxin . Under stress conditions , ( e . g . certain ) , the bacterial SOS response can trigger induction , leading to increased transcription of genes and enhanced production . The toxin then travels in the . The toxin enters host cells halts synthesis and leads to cell death . Shiga toxins bind to the receptor globotriaosylceramide ( Gb3 ) on host cells . Gb3 is highly expressed on epithelial cells and endothelial cells . This damage to endothelial cells in the renal microvasculature may lead to ( HUS ) , characterised by acute kidney injury , haemolytic , and .

Diagnosis is typically performed using samples .
On sorbitol MacConkey agar with cefixime and tellurite ( CTSMAC ) , O157 : H7 does not ferment and produces colonies , whereas commensal strains appear .
Selective chromogenic media can detect O157 strains based on specific reactions , producing characteristic coloured colonies . These media improve and ease of identification
Molecular tests such as detect Shiga toxin ( stx1 , stx2 ) and other EHEC markers directly from stool samples and provide rapid , diagnosis .
Serological testing can confirm O157 and H7 using latex tests that detect the and antigens . Visible agglutination indicates the of the specific surface antigen .

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EHEC long answer

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EHEC long answerVersion en ligne

par Jessica

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