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Campylobacteriaceae

Campylobacteriaceae. (And Campylobacter -like species). 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.

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Campylobacteriaceae

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  1. 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 • 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 • 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 • 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

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