Campylobacter genus and Helicobacter pylori Flashcards
General Features and habitat of Campulobacter jejuni
Gram –
Curved Rod shape (comma-shaped)
Motile with peritrichous (many) flagella
Reservoir- intestinal tracts of human and
Intestinal tract of animals- zoonosis (especially poultry, but also cow, dog…)
Biochemical Properties of Campulobacter jejuni
Thermophilic- grows well in 42C (used to distinguish from Helicobacter)
Microaerophilic- likes less O2 and more CO2
Acid resistant- only few number of organisms are required to cause infection
Oxidase +
Catalase +
Pathogenesis of Campulobacter jejuni
Transmitted by fecal-oral primarily from poultry meat contaminated by feces
Incubation time of 1-2 days
Campylobacter penetrate the mucosa of the colon and destroy it surface causing inflammatory diarrhea (few number of bacteria is required since it is acid resistant)
Clinical Features (gastroenteritis) of Campulobacter jejuni
Bloody diarrhea
Fever
Strong abdominal pain
Complications: Reactive arthritis (Reiter’s syndrome)
Guillain-Barré Syndrome:
Autoimmune response causing demyelination of peripheral nerves which leads to ascending paralysis (opposite from botulism)
Occurs after being infected by C. jejuni species
Diagnosis of Campulobacter jejuni
Specimens- stool, food or blood (hemoculture)
Gram staining of fecal (stool) sample
Culture on Skirrow’s medium or Campy medium: 42C, microaerophilic with VPN
Selective for Campylobacter (other bacteria like H. pylori can’t grow)
Treatment of Campulobacter jejuni
Self-limiting (3-5 days)- often require supportive treatment
Erythromycin or Fluoroquinolones (bacteria are penicillin resistant)
General habitat and features of Helicobacter Pylori
Gram –
Curved rod shape (spiral or helical, hence the name)
Habitat- human, generally in gastric near pylori (~50% are carriers, ~80% are asymptomatic)
Motile with peritrichous (many) flagella
Biochemical Properties of Helicobacter Pylori
Urease + (used to distinguish from Campylobacter)
Oxidase +
Catalase +
Microaerophilic- likes less O2 and more CO2
Transmitted by fecal-oral or oral-oral
Pathogenesis of Helicobacter Pylori
Transmitted by fecal-oral or oral-oral
Adhesins used to adhere to stomach
Mucinase aids the penetration into the mucous layer of the stomach
Urease allow to cleave urea into ammonium and CO2 (Urea + H2O → NH3 + CO2)
This neutralize the stomach acidity (act as buffer, NH3 + H+ → NH4+); thus, lowering the acidity (increases the pH) allowing H. pylori to survive in stomach
Clinical Features (Gastritis) of Helicobacter Pylori
Chronic Gastritis and duodenal ulcers- chronic infection increase acid production by either reducing somatostatin or increasing gastrin production
Untreated ulcers are associated with several types of gastric adenocarcinoma-
does not resolve with the treatment of H. pylori
Associated also with gastric mucosa-associated lymphoid tissue lymphoma (known as MALT-oma)- will resolve with the treatment of H. pylori
Diagnosis of Helicobacter Pylori
Urea Breath Test (UBT)-
Patients swallow urea-labelled radioactive carbon (14C).
The urease activity of the bacteria produces NH3 and CO2. The CO2 that is formed contains the radioactive carbon and is exhaled, which can be detected
Biopsy during endoscopy- used to check for urease using biochemical tests (urease test)
ELISA- from urine or blood sample, negative IgG exclude infection (Western Blot to confirm)
Direct microscope- using silver impregnation or Giemsa stain
Culture- Skirrow medium: 42C, microaerophilic environment (selective-H. pylori can’t grow)
Treatment of Helicobacter Pylori
Triple (or Quadruple if Clarithromycin resistant) treatment includes all of the following:
Proton Pump Inhibitor (PPI)- e.g. Omeprazole
Amoxicillin and Metronidazole
Macrolide- specifically Clarithromycin + Metronidazole (if resistant- use Bismuth salts)
