1. (And Campylobacter-like species)
Campylobacteriaceae
(And Campylobacter-like species)

2. Campylobacter Classification –family Campylobacteriaceae.
They are curved, oxidase +, non-spore forming, microaerophilic, Gram-negative rods
Motile by polar flagella
Non-fermentative
Can’t grow under strictly aerobic conditions

3. Campylobacter sp

4. Campylobacter sp.

5. Campylobacter sp

6. Campylobacter
Five different species of Campylobacter may be isolated from clinical specimens.
C. sputorum, biovar sputorum – is part of the normal oral flora of humans
C. fetus, ssp. fetus
C. fetus, ssp. venerealis
C. jejuni
C. coli
They are so small that they will pass though .65 uM filters that filter out most enteric bacteria
They grow best at reduced O2 and increased CO2 concentrations of 10% (is capnophilic)

7. Campylobacter
The enteric species (C. coli and C. jejuni) are best isolated at 420 C since this is their optimal growth temperature and the higher temperature will suppress the growth of many other enteric organisms.
The organisms grow well on CBA a chocolate, and poorly on Mac plates.
It may take 48 hours for the small, translucent colonies to appear.

8. Campylobacter Biochemistry
Selective agar may be used to isolate the enteric Campylobacter sp.
CampyBAP – Brucella agar base with 10% sheep blood, vancomycin, trimethoprim, polymyxin B, amphotericin B, and cephalothin to supress NF.
Skirrows media – contains lysed, defiriinated horse blood and vancomycin, polymyxin B, and trimethoprim.
Biochemistry
Oxidase +
Catalase + (except sputorum)
ID by above, growth requirements, and G stain morphology

9. Campylobacter sp

10. Campylobacter sp Virulence factors Clinical significance Enterotoxin
Endotoxin
Adhesions
Intracellular survival
Ability to penetrate cells
Clinical significance
Gastroenteritis
Caused mainly by C. jejuni and C. coli

11. Campylobacter sp
Acquired by ingestion of contaminated food or water or contact with an infected animal (bird or mammal).
The organism invades the epithelium of the lower small intestine and multiplies.
The invasion produces an inflammatory response that may be responsible for many of the symptoms.
Symptoms start 1-10 days after ingestion with vague abdominal cramps that progress to crampy abdominal pain, bloody diarrhea, chills, and fever for 3-6 days
Untreated patients may excrete the organism for several months
Erythromycin is used in severe cases

12. Campylobacter sp Campylobacter-like organisms – Helicobacter pylori
Systemic infections
Usually due to C., fetus ssp. Fetus
Occur in debilitated or immunocompromised individuals
Campylobacter-like organisms – Helicobacter pylori
Small, gram-negative, curved rod
Grown on same media and under same conditions as Campylobacter, but may take 5 days to grow.
Differentiated from Campylobacter based on strong urease + test (may become - in as short as 10 minutes)

13. Helicobacter pylori

14. Helicobacter pylori Virulence factors Adhesions – BapA and HpaA
Vacuolating Cytotoxin (VacA) - forms a pore in host cell membranes and induces apoptosis
Neutrophil-Activating protein (NAP) - activates neutrophils and mast cells that damage local tissues
Endotoxin
Urease – facilitates survival in the stomach by raising the pH, provides access to nitrogenous nutrients needed by the bacteria for growth, and the NH4+ endproduct may cause cell damage and inflammation
Flagella – allow bacteria to penetrate through gastric mucous
Collagenase/Mucinase –degrades gastric collagen and mucous,exposing gastric epithelium to gastric acid
CagA – is injected into host epithelial cells where it activates host signal transduction pathways that can stimulate growth→ cancer?

15. Helicobacter pylori Clinical significance
Responsible for chronic, active gastritis and peptic ulcers – symptoms include nausea, vomiting, anorexia, and epigastric pain
There is an association between H. pylori and carcinoma of the stomach
possibly due to chronic inflammation
Possibly due to the activity of CagA.
Activates signal transduction pathways that cause an increase in cell cycling that can contribute to the development of cancer.

16. Helicobacter pylori

17. Helicobacter pylori Neutrophil activatiing protein
Plus neutrophil activating protein

18. Helicobacter pylori Diagnosis –
Biopsy
Non-invasive urea breath test – oral 14C labeled urea is given and the breath is monitored for 14CO2
Treatment – administration of several antimicrobial agents, including meteonidazole, tetracycline, amoxicillin, and clarithromycin
New ecological studies with H. pylori:
Has been a part of normal human flora as far back as been studied
Changes associated with modern life have lead to a decrease in the number of humans who harbor the organism

19. Helicobacter pylori
The decrease in H. pylori is associated with an increase in esophageal adenocarcinoma!

20. Summary of Campylobacter and Helicobacter infections