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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 (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
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)
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.
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
Campylobacter sp • Virulence factors • Enterotoxin • Endotoxin • Adhesions • Intracellular survival • Ability to penetrate cells • Clinical significance • Gastroenteritis • Caused mainly by C. jejuni and C. coli
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
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)
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?
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.
Helicobacter pylori Neutrophil activatiing protein Plus neutrophil activating protein
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
Helicobacter pylori • The decrease in H. pylori is associated with an increase in esophageal adenocarcinoma!
