Campylobacter Microbiology properties Curved (comma- or S-shaped) Gram-negative rods Microaerophilic (growing in 5% oxygen) Nonfermenting Motile(darting motility) with single flagellum Oxidase positive

Important species Campylobacter jejuni : Gastroenteritis Campylobacter fetus: An opportunistic organism Bacteremia in compromised hosts and self-limited diarrhea in previously healthy individuals. Campylobacter coli:

Transmission Source of the organisms: Domestic animals, such as cattle, chickens and dogs Person-to-person transmission: oral-fecal

Epidemiology The major cause of bacterial diarrhea in developed countries (4.6% of patients with diarrhea, compared with 2.3 and 1% for salmonella and Shigella) Campylobacter jejuni & C. coli are endemic worldwide and hyperendemic in developing countries. Infant and young adults are most often infected. The incidence peak in the summer. Sporadic outbreaks are associated with contaminated animal products or water.

Pathogenesis Invasion to the epithelial cells and colonization the small and large intestines often occurs, accompanied by blood in stool causing inflammatory diarrhea and fever. Systematic infections, e.g. bacteremia, occur most often in neonates or debilitated adults.

Acts in the same manner as cholera toxin Campylobacter jejuni Virulence factors Endotoxin Flagellum is not only facilitates motility but secretion of Campylobacter invasive antigens (Cia) Enterotoxin (Cytolethal distending toxin) Acts in the same manner as cholera toxin

Clinical findings Enterocolitis: watery, fuel-smelling diarrhea bloody stools fever severe abdominal pain. Systemic infections, most commonly bacteremia, are caused by C. fetus showing symptoms of fever and malaise.

Detection of C jejuni and related enteric bacteria.

Laboratory diagnosis for Campylobacter A stool specimen Blood agar culture Microaerophilic atmosphere (5% O2 and 10% CO2) Skirrow’s medium (containing vancomycin, trimethoprim, cephalothin, polymyxin, and amphotericin B.)

The identification of C. jejuni is confirmed by: Ability to grow at 42 C Failure to grow at 25 C Oxidase positive Sensitivity to nalidixic acid The identification of C. fetus is confirmed by: Failure to grow at 42 C Ability to grow at 25 C Resistance to nalidixic acid

Treatment Erythromycin in C. jejuni enterocolitis An aminoglycoside in C. fetus bacteremia

Prevention No vaccine Proper sewage disposal Personal hygiene (Hand washing)

Helicobacter pylori Multiple flagella (lophotrichous): Darting motility Gram-negative curved (comma- or S-shaped) rods Microaerophilic (growing in 5% oxygen) Oxidase & Catalase positive Nonfermenting Urease

Seventy-two hour culture of H pylori showing typical thin, comma- or S-shaped forms

Virulence Factors

Pathogenesis H. pylori is associated with type B gastritis (antral stomach inflammation/ peptic ulcer). It shelters from gastric acid in the gastric mucous layer and probably is able to adhere to gastric epithelial cells. Production of urease and cytotoxin is associated with injury to the gastric epithelium.

Epidemiology The prevalence of infection increases with age. The source and mode of transmission are not known. H. pylori is in the mucosa of the stomach of 20% people under 30 years but in 40 – 60 % of 60 years old.

Detection methods for H pylori

Laboratory diagnosis Invasive methods: Histological examination Culture PCR (polymerase chain reaction) A rapid urease test on the sample

Skirrow’s medium (containing vancomycin, trimethoprim, polymyxin, and amphotericin B.) A selective blood agar medium

Laboratory diagnosis Non-invasive methods: Serological tests for antibodies on blood or saliva 13C or 14C urea breath tests Fecal antigen testing

The Carbon urea breath test (CUBT) The breath tests are performed by asking the patient to swallow carbon-labeled urea which is metabolised by H. pylori’s urease to produce labeled carbon dioxide. Two forms of urea breath tests by using 13C urea or 14C urea is available. This is absorbed into the blood stream and then exhaled in the breath of infected individuals.

13C or 14C urea breath tests (CUBT) for Helicobacter pylori detection

The rapid urease test Least expensive and can be performed on endoscopic biopsy specimens. The urease produced by the organism converts urea to ammonia resulting in a PH change detected by phenol red. The tests usually give a rapid result but typical sensitivity at 1 hour is 71% which increases to 96% at 6 hours.

Serology Testing IgG is the most sensitive as seen in 95%. Testing IgA responses in 68-80%. Testing IgM responses in only 14% of infected patients.

Serological tests for H. pylori Elisa Complement fixation Latex agglutination

Control A three drug treatment for 2 weeks: 1. A proton pump inhibitor (such as lansoprazole and omeprazole decreasing stomach's production of acid allowing the ulcer to heal) 2. Metronidazole 3. Tetracycline