Campylobacter & Helicobacter
1
Campylobacter & Helicobacter
Campylobacter and Helicobacter species are gram-negative rods that are all widely
distributed in nature. The campylobacters are found in many species of animals.
Campylobacter : - Campylobacters cause both diarrheal and systemic diseases
and are among the most widespread causes of infection in the world.
Campylobacter jejuni & Campylobacter coli
Campylobacter jejuni and Campylobacter coli have emerged as common human
pathogens, causing mainly enteritis and occasionally systemic infection. C jejuni
and C coli cause infections that are clinically indistinguishable, and laboratories
generally do not differentiate between the two species. C jejuni and the other
campylobacters are gram-negative rods with comma, S, or "gull-wing" shapes.
They are motile, with a single polar flagellum, and do not form spores.
Antigenic Structure & Toxins
The campylobacters have lipopolysaccharides with endotoxic activity. Cytopathic
extracellular toxins and enterotoxins have been found.
Pathogenesis & Pathology
- The infection is acquired by the oral route from food, drink, or contact with
infected animals or animal products.
- C jejuni is susceptible to gastric acid, and ingestion of about 104 organisms
is usually necessary to produce infection.
- The organisms multiply in the small intestine, invade the epithelium, and
produce inflammation that results in the appearance of red and white blood
cells in the stools.
- Occasionally, the bloodstream is invaded and a clinical picture of enteric
fever develops. Localized tissue invasion coupled with the toxic activity
appears to be responsible for the enteritis.
1
Campylobacter & Helicobacter
2
Clinical Findings: - Clinical manifestations are acute onset of :- crampy abdominal pain, profuse diarrhea that may be grossly bloody,
headache, malaise, and fever.
- Usually the illness is self-limited to a period of 5–8 days, but occasionally it
continues longer.
Diagnostic Laboratory Tests
Specimens: - Diarrheal stool is the usual specimen.
Smears: - Gram-stained smears of stool may show the typical "gull wing"-shaped
rods. Dark-field or phase contrast microscopy may show the typical darting
motility of the organisms.
Culture: - Selective media are needed, and incubation must be in an atmosphere
with reduced O2 (5% O2) with added CO2 (10% CO2). A relatively simple way to
produce the incubation atmosphere is to place the plates in an anaerobe incubation
jar without the catalyst and to produce the gas with a commercially available gasgenerating pack or by gas exchange.
- Incubation of primary plates for isolation of C jejuni should be at 42 °C,
incubation at 42 °C prevents growth of most of the other bacteria present in
feces.
- Several selective media are: Skirrow's medium contains vancomycin,
polymyxin B, and trimethoprim to inhibit growth of other bacteria. Other
selective media also contain antimicrobials, including cephalothin or
cefoperazone, and inhibitory compounds. The colonies tend to be colorless
or gray. They may be watery and spreading or round and convex, and both
colony types may appear on one agar plate.
Epidemiology & Control Campylobacter enteritis resembles other acute
bacterial diarrheas, particularly Shigella dysentery. The source of infection may
be food (eg, milk, undercooked fowl) or contact with infected animals or
2
Campylobacter & Helicobacter
3
humans and their excreta. Outbreaks arising from a common source, eg,
unpasteurized milk may require public health control measures.
Helicobacter pylori
Helicobacter pylori is a spiral-shaped gram-negative rod. H. pylori is
associated with antral gastritis, duodenal (peptic) ulcer disease, gastric
ulcers, and gastric carcinoma. Other Helicobacter species that infect the
gastric mucosa exist but are rare.
H pylori has many characteristics in common with campylobacters. It is motile,
and is a strong producer of urease.
Pathogenesis & Pathology
- H pylori grows optimally at a pH of 6.0–7.0 and would be killed or not
grow at the pH within the gastric lumen. Gastric mucus is relatively
impermeable to acid and has a strong buffering capacity. On the lumen
side of the mucus, the pH is low (1.0–2.0) while on the epithelial side the
pH is about 7.4. H pylori is found deep in the mucous layer near the
epithelial surface where physiologic pH is present.
- H pylori also produces a protease that modifies the gastric mucus and
further reduces the ability of acid to diffuse through the mucus.
- H pylori produces potent urease activity, which yields production of
ammonia and further buffering of acid.
- H pylori is quite motile, even in mucus, and is able to find its way to the
epithelial surface. H pylori overlies gastric-type but not intestinal-type
epithelial cells.
- In human volunteers, ingestion of H pylori resulted in development of
gastritis and hypochlorhydria. There is a strong association between the
presence of H pylori infection and duodenal ulceration. Antimicrobial
therapy results in clearing of H pylori and improvement of gastritis and
duodenal ulcer disease.
- Toxins and lipopolysaccharide may damage the mucosal cells, and the
3
Campylobacter & Helicobacter
4
ammonia produced by the urease activity may directly damage the cells
also.
- Histologically, gastritis is characterized by chronic and active
inflammation. Polymorphonuclear and mononuclear cell infiltrates are
seen within the epithelium and lamina propria. Vacuoles within cells are
often pronounced. Destruction of the epithelium is common, and
glandular atrophy may occur. H pylori thus may be a major risk factor
for gastric cancer.
Clinical Findings
Acute infection can yield an upper gastrointestinal illness with nausea and
pain; vomiting and fever may be present also. The acute symptoms may last for
less than 1 week or as long as 2 weeks. Once colonized, the H pylori infection
persists for years and perhaps decades or even a lifetime. About 90% of
patients with duodenal ulcers and 50–80% of those with gastric ulcers have H
pylori infection. H pylori also may have a role in gastric carcinoma and
lymphoma.
Diagnostic Laboratory Tests
Specimens -Gastric biopsy specimens can be used for histological
examination. Blood is collected for determination of serum antibodies.
Smears: The diagnosis of gastritis and H pylori infection can be made
histologically. A gastroscopy procedure with biopsy is required. Routine stains
demonstrate gastritis, and Giemsa or special silver stains can show the curved
or spiraled organisms.
Antibodies
Several assays have been developed to detect serum antibodies specific for H
pylori. The serum antibodies persist even if the H pylori infection is eradicated.
4
Campylobacter & Helicobacter
5
Special Tests Gastric biopsy material can be placed onto a urea-containing
medium with a color indicator. If H pylori is present, the urease rapidly splits
the urea (1–2 days) and the resulting shift in pH yields a color change in the
medium. In vivo tests for urease activity can be done also. 13C- or 14C-labeled
urea is ingested by the patient. If H pylori is present, the urease activity
generates labeled CO2 that can be detected in the patient's exhaled breath.
Immunity
Patients infected with H pylori develop an IgM antibody response to the
infection. Subsequently, IgG and IgA are produced, and these persist, both
systemically and at the mucosa, in high titer in chronically infected persons.
Early antimicrobial treatment of H pylori infection blunts the antibody
response; such patients are thought to be subject to repeat infection.
Treatment
- Triple therapy with metronidazole and either bismuth subsalicylate or
bismuth subcitrate plus either amoxicillin or tetracycline for 14 days
eradicates H pylori infection in 70–95% of patients. An acid-suppressing
agent given for 4–6 weeks enhances ulcer healing. Proton pump
inhibitors directly inhibit H pylori and appear to be potent urease
inhibitors.
- Either 1 week of a proton pump inhibitor plus amoxicillin and
clarithromycin or of amoxicillin plus metronidazole also is highly
effective.
Epidemiology & Control H pylori is present on the gastric mucosa of less
than 20% of persons under age 30 but increases in prevalence to 40–60% of
persons age 60, including persons who are asymptomatic. In developing
countries, the prevalence of infection may be 80% or higher in adults. Personto-person transmission of H pylori is likely because intrafamilial clustering of
infection occurs. Acute epidemics of gastritis suggest a common source for H
pylori.
5
Campylobacter & Helicobacter
6
6