A brief descriptions of Curved GNR, Pseudomonas & Bordetella

1. Vibrio, Campylobacter, Helicobacter,
Pseudomonas & Bordetella
Aman Ullah
B.Sc. MLT
M. Phil Microbiology
Master in Health Research
Certificate in Health Professional Education

2. Vibrio cholerae
Common characteristics
• Gram-negative
• Short, curved rod
• Rapidly motile due to single polar flagellum
• Facultative anaerobes
• Growth of many Vibrio species requires or is
stimulated by NaCl

3. Pathogenesis/Clinical Significance
• V. cholerae is transmitted by contaminated water and food
• In the aquatic environment, a number of reservoirs have
been identified, including crustaceans, phytoplankton and
protozoa
• Outbreaks of V. cholerae infection have been associated
with raw or undercooked seafood harvested from
contaminated waters
• Following ingestion, V. cholerae infects the small intestine
• Adhesion factors are important for colonization and
virulence
• The organism is not invasive, and causes disease through
the action of an enterotoxin (cholera toxin)
• This initiates an outpouring of fluid into the intestine

4. Pathogenesis/Clinical Significance
Cholera
• Full-blown cholera is characterized by massive
loss of fluid and electrolytes from the body
• After an incubation period ranging from hours to
a few days, profuse watery diarrhea (rice-water
stools) begins
• Untreated, the death from shock may occur in
hours to days
Lab diagnosis
• Stool C/S

5. Campylobacter jejuni
Common characteristics
• Gram-negative
• Curved, spiral, or S-shaped rods
• Single, polar flagellum results in characteristic
darting motion
• Microaerophilic

6. Pathogenesis/Clinical Significance
• C. jejuni is widely distributed in nature, existing as part
of the normal flora of many vertebrate species,
including both mammals and fowl, wild and domestic
• Transmission is via the fecal-oral route through direct
contact, or exposure to contaminated meat (especially
poultry) or to contaminated water
• C. jejuni infects the intestine, where it can cause
ulcerative, inflammatory lesions in the jejunum, ileum,
or colon
• An enterotoxin related to cholera toxin and a cytotoxin
are important virulence factors

7. Pathogenesis/Clinical Significance
Acute enteritis
• Symptoms may be both systemic (fever, headache,
myalgia) and intestinal (abdominal cramping and
diarrhea, which may or may not be bloody)
• Rare complications include Guillain-Barré syndrome
Lab diagnosis
• Presumptive diagnosis can be made on the basis of
finding curved organisms with rapid, darting
motility in a wet mount of feces

8. Helicobacter pylori
Common characteristics
• Gram-negative
• Curved or spiral rods
• Multiple polar flagella give the organism rapid,
corkscrew motility

9. Pathogenesis/Clinical Significance
• H. pylori is unusual in its ability to colonize the stomach,
where low pH normally protects against bacterial infection
• Transmission is thought to be from person to person (the
organism has not been isolated from food or water)
• H. pylori colonizes gastric mucosal cells in the stomach,
surviving in the mucous layer that coats the epithelium
• The organism is noninvasive, but recruits and activates
inflammatory cells, thus causing a chronic inflammation of
the mucosa
• H. pylori secretes urease, producing ammonium ions that
neutralize stomach acid in the vicinity of the organism, thus
favoring bacterial multiplication
• Ammonia can damage the gastric mucosa

10. Pathogenesis/Clinical Significance
Acute gastritis
• Initial infection with H. pylori results in
decreased mucous production, and leads to
acute gastritis
• Both duodenal ulcers and gastric ulcers are
closely correlated with infection by H. pylori
• The organism appears to be a risk factor for
development of gastric carcinoma and gastric
Bcell lymphoma

11. Lab diagnosis
• Characteristic corkscrew movement can be
seen in smears of biopsied gastric mucosa.
• Urease-positivity can be measured by a breath
test (radioactively labeled urea is cleaved by
bacterial enzyme, releasing radioactive CO2 in
expired breath)
• Serologic tests are available, including enzyme
linked Immunosorbent assay (ELISA) for serum
antibodies to H. pylori

12. Pseudomonas aeruginosa
Common characteristics
• Gram-negative
• Motile rods (polar flagella) with alginate capsule
• Aerobic
• Oxidase-positive
• Produces diffusible green and blue pigments
• Does not ferment carbohydrates (Non-fermenter)

13. Pathogenesis/Clinical Significance
• P. aeruginosa is widely distributed in nature (soil, water, plants, animals)
• It is a significant opportunistic pathogen and a major cause of nosocomial
infections
• P. aeruginosa is regularly a cause of nosocomial pneumonia; nosocomial
infections of the urinary tract, surgical sites, and severe burns; and of
infections of patients with cystic fibrosis, and those who are undergoing
either chemotherapy for neoplastic diseases or antibiotic therapy for other
infections.
• P. aeruginosa can grow in distilled water, laboratory hot water baths, hot
tubs, wet intravenous tubing, and other water-containing vessels
• This explains why the organism is responsible for so many nosocomial
infections
• P. aeruginosa disease begins with attachment and colonization of host tissue.
Virtually any tissue/organ may be affected
• Pili mediate adherence, and extracellular proteases, cytotoxin, hemolysins,
and pyocyanin promote tissue damage and local invasion and dissemination
of the organism
• Systemic disease is promoted by an antiphagocytic capsule, and endo- and
exotoxins

14. Pathogenesis/Clinical Significance
Localized infections:
• Localized P. aeruginosa infections may occur in the eye, ear,
skin, urinary tract, respiratory tract, gastrointestinal tract
(GI). In most cases, localized infections have the potential
to lead to disseminated infection
Systemic infection
• The GI tract is a particularly common site for penetration.
• The resulting systemic infections may include bacteremia,
secondary pneumonia, bone and joint infections,
endocarditis, and infections of the skin/soft tissue and CNS
Lab diagnosis
• Specimen depend on the site of infection
• Specimen for C/S

15. Bordetella pertussis
Common characteristics
• Gram-negative
• Small coccobacilli that grow singly or in pairs
• Encapsulated
• Aerobic

16. Pathogenesis/Clinical Significance
• B. pertussis is transmitted primarily by
droplets spread by coughing
• B. pertussis binds to ciliated epithelium in the
upper respiratory tract
• There, the bacteria produce a variety of toxins
and other virulence factors that interfere with
ciliary activity, eventually causing the death of
these cells

17. Pathogenesis/Clinical Significance
Pertussis (“whooping cough”)
• The incubation period for this disease ranges from 1 to 3 weeks
• The disease can be divided into two phases:
1) Catarrhal phase, which begins with relatively nonspecific
symptoms, and then progresses to include a dry, nonproductive
cough; and
2) Paroxysmal phase, in which the cough worsens, causing
paroxysms of coughing followed by a “whoop” as the patient
inspires rapidly. Large amounts of mucus are typically produced
• During the 3–4 week convalescent period, secondary complications,
such as encephalopathy, seizures, and/or pneumonia, may occur
Lab diagnosis
• Nasopharyngeal specimen for C/S
• Antibodies detection in nasopharyngeal sepecimen

18. Questions/Suggestions
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