Helicobacter

Rabia Chaudhry
 Historical Background
• 1892: Italian pathologist Giulio Bizzozero first
described “spirilli” in dog’s stomach

• Several reports over the next century

• 1954: Palmer biopsy study established dogma

of sterile stomach environment

• 1979: Robin Warren found spiral bacteria in

human stomach; association with gastritis

• 1983: Barry Marshall isolated and cultured

Bizzazero’s original drawings bacteria
(Figura, 2002)
 Historical Background
• Initially named Campylobacter pylori

• 1985 - 1987: Marshall and Morris inoculated

themselves and developed gastritis

• 1989: New spiral bacteria named Helicobacter

pylori

• Scientific community extremely slow to

accept link between H. pylori and peptic ulcer
disease

• 2005: Warren and Marshall win Nobel Prize H. heilmannii in a patient with
dyspepsia (Figura, 2002)
 A New Genus: Helicobacter
• Currently has 18 formally validated species

• Non-spore forming, Gram negative, motile,

spiral/ curved, microaerophilic bacteria

• Human stomachs are primarily colonized by

Helicobacter pylori as well as H. heilmannii to a
lesser degree

• Nearly all mammals have associated

Helicobacter species e.g. H. felis (cats and dogs)
and H. mustelae (ferrets) H. pylori and H. felis (Mobley, 2001)

• Infection of a mammal from a different

Helicobacter species is possible
Helicobacter pylori
• Causes gastritis; correlated with peptic ulcers
and progression to cancer

• Present in roughly half the world’s population

• Most infections are asymptomatic

• Most common human infectious agent; higher

prevalence in developing regions

• Often colonizes lower stomach or upper

duodenum; named after pylorus

• Colonizes host for life; well adapted to stomach

niche environment
 H. pylori: Pathogenisis
• Propels itself to the mucus layer

• Protects itself from stomach acids by

producing urease during transmission

• Colonizes the gastric mucosa and mucus

layer of the gastric epithelium

• Inflammation of the gastric mucosa

provides nutrients as well as urea

• Has a number of adhesion capabilities

and molecular mimicry techniques to
Montecucco, 2001 evade immune system
 H. pylori: Pathogenisis
• Not an acidophile

• Causes acute and chronic gastritis

(inflammation of the stomach lining)

• Peptic ulcer disease: gnawing gastric pain;

occasionally nausea, vomiting, loss of
appetite or bleeding

• Associated with gastric lymphoma of the

mucosal-associated lymphoid tissue

• About 10% infections develop ulcer and

Montecucco, 2001 even fewer progress to cancer
 H. pylori: Detection & Treatment
• Non invasive: Urea breath testing,
ELISA, Stool antigen testing

• Invasive: endoscopic biopsy to obtain

tissue sample; identification, culture
and PCR

• Various antibiotic regimens to treat

the infection

• No vaccines have been developed

yet
 H. pylori Transmission
• Infective dose (data from Rhesus monkeys): 10^4

• Animals and water potential environmental sources

- Studies about animal hosts inconclusive

- Never been cultured from water; maybe VBNC.

- PCR techniques have detected H. pylori in environmental water; viable?

• Person-to-person most likely more important; not sure how

- Gastro-oral, oral-oral or fecal-oral

- Mixed results for trying to culture

 Current Research Areas
• Pathogenicity of H. pylori resulting
in many asymptomatic cases

• Transmission routes

• Mechanisms of gastric cancer

• Understanding of viability and

infectivity outside the gastric
environment
 Five Things to Remember
• H. pylori first isolated and cultured by Warren and
Marshall in 1983

• Can cause gastritis, peptic ulcers and cancer

• Half the world’s population is infected but many are

asymptomatic

• Protects itself against stomach acid by secreting urease

• Can be treated with antibiotics; no vaccine yet

 References
Figura, N., Bianciardi, L. (2002). Helicobacters were discovered in Italy in 1892: AN episode in the scientific life of an eclectic pathologist,
Giulio Bizzozero. In B. Marshall (Ed.), Helicobacter Pioneers (pp. 1-11). Victoria, Australia: Blackwell Science Asia Pty Ltd.

Fukuda, Y., Shimoyoma, T., Shimoyoma, T., Marshall B. J. (2002) Kasai, Kobayashi and Koch’s postulates in the history of Helicbacter pylori. In
B. Marshall (Ed.), Helicobacter Pioneers (pp. 15-23). Victoria, Australia: Blackwell Science Asia Pty Ltd.

Giao, M. S., Azevedo, N. F., Wilks, S. A., Vieira, M. J., Keevil, C. W. (2010). Effect of Chlorine on Incorporation of Helicobacter pylori into
Drinking Water Biofilms. Applied And Environmental Microbiology, 76 (5), 1669–1673.

Marshall, B. J. (2002). The discovery that Helicobacter pylori, a spiral bacterium, caused peptic ulcer disease. In B. Marshall (Ed.), Helicobacter
Pioneers (pp. 165-201). Victoria, Australia: Blackwell Science Asia Pty Ltd.

Mobley, H. L.T., Mendz, G. L., Hazell, S. L., (Ed.). (2001). Helicobacter pylori. Washington (DC): American Society for Microbiology Press.

Montecucco, C., Rappuoli, R. (2001). Living dangerously: how helicobacter pylori survives in the human stomach. Nature Reviews Molecular
Cell Biology, 2, 457-466.

Solnick, J. V., Hansen, L. M., Canfield, D. R., Parsonnet, J. (2001). Determination of the Infectious Dose of Helicobacter pylori during Primary
and Secondary Infection in Rhesus Monkeys (Macaca mulatta). Infection and Immunity, 69 (11), 6887 – 6892.

Yamamoto, Y., Friedman, H., Hoffman, P. (2002). Helicobacter pylori Infection and Immunity. New York, NY: Kluwer Academic/ Plenum
Publishers.

Yamaoka, Y. (2008). Helicobacter pylori: Molecular genetics and cellular biology. Norfolk, UK: Caister Academic Press.