Helicobacter pylori
Bacterial Specificity

Author: Gianpiero Pescarmona
Date: 09/11/2008

2011-06-13T09:21:36 - Annamaria Vernone

Route of transmission

It seems that the transmission is oral-oral and fecal-oral.
Box 1 | A speculative model of the evolution and transmission of Helicobacter pylori [June 2001]

CagA protein is phosphorilated on tyrosine residues by a host cell membrane-associated tyrosine kinase. CagA then allosterically activates protein tyrosinephosphatase/protooncogene Shp2 that act on different pathways.

The Helicobacter pylori VacA toxin is a urea permease that promotes urea diffusion across epithelia [2001]
Urease and the cytotoxin VacA are two major virulence factors of the human pathogen Helicobacter pylori. Results: VacA increases the transepithelial diffusion of urea.

Binds to and inhibits PAR1/MARK resulting in an increased cellular proliferation:
presence of Gly 955 instead of Lys 955 allows a more potent inhibition

EPIYA Motif Is a Membrane-targeting Signal of Helicobacter pylori Virulence Factor CagA in Mammalian Cells [2005]

Higher number of Helicobacter pylori CagA EPIYA C phosphorylation sites increases the risk of gastric cancer, but not duodenal ulcer - [BMC Microbiology 2011].

The protein–protein interaction map of Helicobacter pylori

Treatment provides lansoprazole (30mg), clarithromycin (500mg) and amoxicillin (1000mg) twice a day for seven days.

Patients with no eradication undergo a retreatment with Omeprazole (20mg) twice a day and furazolidone (200mg) and tetracycline (500mg) three times a day for seven days


Rapid urease test.

Culture: Agar media sufficient for identification, typing and antibiotic studies Liquid culture possible with ß-cyclodextrin and FBS.
OBIS and Fluka test.HP like all members of Epsilonproteobacterian was found to lack the L-alanine aminopeptidase.


Urea breath test

Immunochromatographic-detection of Helicobacter antigen

Detection of Helicobacter antigen by ELISA

Detection of Helicobacter DNA by PCR

Cigarette smoking and Helicobacterpylori infection [1993]

Salt intake and gastric cancer risk according to Helicobacter pylori infection, smoking, tumour site and histological type [British Journal of Cancer (2011)] - Results: salt intake is an important dietary risk factor for gastric cancer, and confirms the evidence of no differences in risk according to H. pylori infection and virulence, smoking, tumour site and histological type.

2008-11-28T14:27:29 - Gianpiero Pescarmona

Helicobacter pylori e ulcera peptica
Il gene homB può essere considerato come co-marcatore dei ceppi di Helicobacter pylori associati all'ulcera peptica, differenziandoli da quelli associati a dispepsia non ulcerosa. Il gene, che codifica per una proteina della membrana esterna del batterio, era già stato associato in studi precedenti all'ulcera peptica del bambino. La proteina da esso codificata risulta importante per la patogenicità dell'Helicobacter nel contesto dell'ulcera peptica, in quanto si tratta di un'adesina che induce infiammazione, ed inoltre è presente negli stessi ceppi degli altri fattori patogeni già noti. Fra i vari genotipi di virulenza dell'H. pylori analizzati, il cagA, marcatore del cagPAI, è il solo fattore predittivo dello sviluppo di ulcera peptica sia nei bambini che negli adulti. Ciò risulta coerente con quanto rilevato da altri studi, e conferma pertanto che il cagPAI sia uno dei principali fattori di virulenza del batterio. (J Infect Dis 2008; 198: 1379-87

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