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المرجع الالكتروني للمعلوماتية

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علم الاحياء : الأحياء المجهرية : البكتيريا :

Campylobacter, Helicobacter and Spirillum

المؤلف:  Fritz H. Kayser

المصدر:  Medical Microbiology -2005

الجزء والصفحة: 

7-3-2016

2448

Campylobacter, Helicobacter and  Spirillum

 

Campylobacter, Helicobacter, and Spirillum belong to the group of spiral, motile, Gram-negative, microaerophilic bacteria. C. jejuni causes a form of enteritis. The sources of infection are diseased animals. The pathogens are transmitted to humans in food. The diseases are sometimes also communicable among humans. The pathogens are identified for diagnostic purposes in stool cultures using special selective mediums. Helicobacter pylori contribute to the pathogenesis of type B gastritis and peptic ulcers. Spirillum minus causes rat bite fever, known as sodoku in Japan where it is frequent.

The genera Campylobacter, Helicobacter, and Spirillum belong to the group of aerobic, microaerophilic, motile, Gram-negative rod bacteria with a helical/ vibrioid form . Human pathogens are found in all three genera.

Campylobacter

Classification. For several years now, Campylobacter bacteria have been clas-sified together with Arcobacter (medically insignificant) in the new family Campylobacteriaceae (fam. nov.). The genus Campylobacter comprises numerous species, among which C. jejuni (more rarely C. coli, C. lari) as well as C. fetus have been observed as causative pathogens in human infections.

Morphology and culture. Campylobacter are slender, spirally shaped rods 0. 2-0.5 µm thick and 0.5-5 µm long. Individual cells may have one spiral winding or several. A single flagellum is attached to either one or both poles.

Campylobacter can, under microaerophilic conditions, and in an atmosphere containing 5% O2 and 10% CO2, be cultured on blood agar plates. The optimum proliferation temperature for C. fetus is 25 °C and for C. jejuni 42 °C.

Pathogenesis and clinical pictures. The details of the pathogenic mechanisms of these pathogens are largely unknown. C. jejuni produces an entero-toxin similar to the STa produced by E. coli as well as a number of cytotoxins. C. jejuni causes a form of enterocolitis with watery, sometimes bloody diarrhea and fever. The incubation period is two to five days. The manifest illness lasts less than one week.

C. fetus has been identified in isolated cases as a pathogen in endocarditis, meningitis, peritonitis, arthritis, cholecystitis, salpingitis, and sepsis in im-munocompromised patients.

Diagnosis. To isolate C. jejuni in stool cultures, mediums are used containing selective supplements (e.g., various anti-infective agents). The cultures are incubated for 48 hours at 42 °C in a microaerophilic atmosphere. Identification is based on growth requirements as well as detection of catalase and oxidase. C. fetus is readily isolated in most cases, since it is usually the only organism found in the material (e.g., blood, cerebrospinal fluid, joint punctate, pus, etc.).

Therapy. Severe Campylobacter infections are treated with macrolides or 4- quinolones. Resistance is known to occur.

Epidemiology and prevention. Campylobacter jejuni is among the most frequent enteritis pathogens worldwide. The bacteria are transmitted from animals to humans via food and drinking water. Direct smear infection transmission among humans is possible, especially in kindergarten or family groups. There are no specific preventive measures.

Helicobacter pylori

Morphology and culture. H. pylori are spirally shaped, Gram-negative rods with lophotrichous flagellation. Cultures from stomach biopsies are grown on enriched mediums and selective mediums under microaerobic conditions (90% N2, 5% CO2, and 5% O2) for three to four days. Identification is based on detection of oxidase, catalase, and urease.

Pathogenesis and clinical pictures. H. pylori occurs only in humans and is transmitted by the fecal-oral pathway. The pathogen colonizes and infects the stomach mucosa. The pathogenicity factors include pronounced motility for efficient target cell searching, adhesion to the surface epithelial cells of the stomach, urease that releases ammonia from urea to facilitate survival of the cells in a highly acidic environment and a vacuolizing cytotoxin (VacA) that destroys epithelial cells.

Once the pathogen has infected the stomach tissues an acute gastritis results, the course of which may or may not involve overt symptoms. Potential sequelae include:

1. Mild chronic gastritis type B that may persist for years or even decades and is often asymptomatic.

2. Duodenal ulceration, sometimes gastric ulceration as well.

3. Chronic atrophic gastritis from which a gastric adenocarcinoma sometimes develops.

4. Rarely B cell lymphomas of the gastric mucosa (MALTomas). 

Diagnosis. Histopathological, cultural and, molecular identification of the bacteria in stomach lining biopsies. A noninvasive breath test involving ingestion of 13C-labeled urea and measurement of 13CO2 in the expelled air. Antigen detection in stool. Antibodies can be identified with an ELISA or Western blotting.

Therapy. In patients with ulcers and/or gastritis symptoms, a triple combination therapy with omeprazole (proton pump blocker), metronidazole, and clarithromycin lasting seven days is successful in 90% of cases.

Epidemiology. Based on sero-epidemiological studies we know that H. pylori occur worldwide. Generalized contamination of the population begins in childhood and may reach 100% in adults in areas with poor hygiene. The contamination level is about 50% among older adults in industrialized countries. Transmission is by the fecal-oral route.

Spirillum minus

This species is a motile bacterium only 0.2 µm thick and 3-5 µm long with two to three spiral windings. It cannot be grown on culture mediums. S. minus causes spirillary rat bite fever, also known as sodoku. This disease occurs worldwide, with a high level of incidence in Japan. The organism is transmitted to humans by the bites of rats, mice, squirrels, and domestic animals that eat rodents. Following an incubation period of seven to 21 days a febrile condition develops with lymphangitis and lymphadenitis. Ulcerous lesions develop at the portal of entry. Diagnosis can be done by using dark field or phase contrast microscopy to detect the spirilla in blood or ulcerous materiel. Penicillin G is used to treat the infection.

 

 

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