Helicobacter pylori:an overview

Helicobacter   pylori

Helicobacter pylori is a spiral bacteria discovered by  two Australian scientists Warren and Marshall in 1983. Today H pylori colonies the stomach of  half the human population of the world. Usually it infects from early childhood . Helicobacter pylori  is adapted to human gastric mucosa. The presence of helicobacter was detected  even in the intestine of pre Columbian mummies in USA. Helicobacter pylori was originally named as Campylobacter pylori  but as there was differences from Campylobacter it was renamed as Helicobacter pylori.

Morphological characters

Helicobacter pylori is a gram negative spiral  bacteria , motile by lophotrichous  flagella. In old culture it appears  in coccoid form.

Biochemical characters

It produces oxidase , catalase , phosphatase and hydrogen sulphide. A distinctive property of this bacteria is abundant production of urease. This property is used as a rapid diagnostic tool with gastric biopsy samples. It does not ferment carbohydrates or reduce  nitrate .

Cultural characters

It grows on chocolate agar  and Campy BAP media  under microaerophilic condition with 5-20 %carbon dioxide and pH 6-7.usually colonies  develop within 2-7  days.  

Epidemiology

Helicobacter pylori seen globally, mainly in developing countries. Poverty overcrowding, poor hygiene favor transmission and the transmission is likely  to be  oral-oral route and fecal- oral route.

Pathogenicity

Infection of  Helicobacter pylori differ  among  individuals . In  some  people  it is seen as  mild gastritis which may last for about two weeks and in  others  it  may  seen as transient forms which persist  for years or decades  and usually such patients are  asymptomatic and can be demonstrated  histologically .  Helicobacter pylori may seen  on  overlying mucus and do not invade the mucosa .In intestine, common site of colonisaion is gastric antrum. The bacteria is also seen in  areas of gastric metaplasia and heterotopia in duodenum . Bacterial protease, toxins, ammonia  released by  urease activity  or auto immune  response  to  gastric  antigens may initiate  the infection.

Peptic ulcer  disease  is  seen  initially, in  later  stages chronic  atopic  gastritis  is perceived.  Helicobacter pylori is  a risk  factor  for gastric  malignancies  such as  adeno carcinoma  and MALT  ( mucosa   associated  lymphoid tissue ) lymphoma.Such MALT lymphomas regress  after elimination of this bacteria by treatment. Infection  induces  IgM , IgG, IgA  and celluar immune responses  but they are not protective.

Lab diagnosis

Diagnosis includes  invasive  and noninvasive tests .

Invasive tests

 It includes endoscopic biopsy  of gastric mucosa, its microscopic  examination,  culture  and urease test .Gram stained smears  or silver staining of biopsy  sections  is indeed  a  useful  method .  Culture is also  a sensitive  method  but  it requires  expertise  and  a   long  duration  of  incubation  .Urease test is done by dipping  a  bit of  biopsy  material in  medium  shows result  within  minutes.

Noninvasive tests

It  includes  Elisa test  and  urea  breath  test.

Urea  breath test

The patient  drinks   urea solutions  containing  labelled carbon  which  can  be detected  in the  breath  .The  advantage  is, it  is  a sensitive  and  reliable method .

Limitations  include  using the facility to use isotope  

Treatment

Standard  treatment  includes  combination  of  bismuth subsalicylate  tetracycline  or amoxicillin and  metronidazole  for  two weeks . Omeprazole and clarithromycin  is  also used for  treatment .

 

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