Transcript Campylobacter - Cal State LA

Campylobacteriaceae
(And Campylobacter-like species)
Campylobacter
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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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Campylobacter sp
Campylobacter sp.
Campylobacter sp
Campylobacter
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Five different species of Campylobacter may be
isolated from clinical specimens.
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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.
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Campylobacter
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Selective agar may be used to isolate the enteric
Campylobacter sp.
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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
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Oxidase +
Catalase + (except sputorum)
ID by above, growth requirements, and G stain
morphology
Campylobacter sp
Campylobacter sp
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Virulence factors
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Enterotoxin
Endotoxin
Adhesions
Intracellular survival
Ability to penetrate cells
Clinical significance
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Gastroenteritis
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Caused mainly by C. jejuni and C. coli
Campylobacter sp
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Acquired by ingestion of contaminated food or water or
contact with an infected animal (bird or mammal).
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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
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Systemic infections
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Usually due to C., fetus ssp. Fetus
Occur in debilitated or immunocompromised individuals
Campylobacter-like organisms – Helicobacter
pylori
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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
Helicobacter pylori
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Virulence factors
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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
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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
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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
Helicobacter pylori
Neutrophil activatiing
protein
Plus neutrophil activating protein
Helicobacter pylori
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Diagnosis –
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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:
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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
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The decrease in H. pylori is associated with an
increase in esophageal adenocarcinoma!
Summary of Campylobacter and
Helicobacter infections