YERSINIA&HELICOBACTER

1. YERSINIA&HELICOBACTER Prepared by Dr. Najdat B. Mahdi

2. YERSINIA The genus Yersinia includes three species of medical importance: Yersinia enterocolitica and Yersinia pseudo tuberculosis, both potential pathogens of the GI tract , and Yersinia pestis, the etiologic agent of bubonic plague. Y. enterocolitica and Y. pseudo tuberculosis are both motile when grown at 25 C but not at 37 C. Multiple serotypes of both species exist, and, as with Y. pestis, the type III secretion system and Yop proteins are virulence factors for avoidance of phagocytosis. In contrast to most pathogenic Enterobacteriaceae, these strains of Yersinia grow well at room temperature as well as at 37o C. Most strains are Lac–.

3. A. Pathogenesis and clinical significance Infection occurs via ingestion of food that has become contaminated through contact with colonized domestic animals, abattoirs, or raw meat (especially pork), Y. pseudotuberculosis is even rarer. Infection results in ulcerative lesions in the terminal ileum, necrotic lesions in Peyer patches, and enlargement of mesenteric lymph nodes. Enterocolitis caused by Yersinia is characterized by fever, abdominal pain, and diarrhea. When accompanied by right lower quadrant tenderness and leukocytosis, the symptoms are clinically indistinguishable from appendicitis. Symptoms commonly resolve in 1 to 3 weeks. Sequelae may include reactive poly - arthritis and erythema nodosum. Other, less common clinical presentations include exudative pharyngitis and, in compromised patients, septicemia.

5. B. Laboratory identification Yersinia can be cultured from appropriate specimens on MacConkeyor cefsulodin-irgasan-novobiocin (CIN, a medium selective for Yersinia) agars. Identification is based on biochemical screening. In the absence of a positive culture, serologic tests for anti-Yersinia antibodies may assist in diagnosis.

6. C. Treatment and prevention Reducing infections and outbreaks rests on measures to limit potential contamination of meat, ensuring its proper handling and preparation. Antibiotic therapy (for example, with ciprofloxacin or trimethoprim -sulfamethoxazole) is essential for systemic disease (sepsis), but is of questionable value for self-limited diseases such as enterocolitis.

7. HELICOBACTER Members of the genus Helicobacter are curved or spiral organisms . They have a rapid, corkscrew motility resulting from multiple polar flagella. Helicobacter pylori, the species of human significance, is microaerophilic, and produces urease. It causes acute gastritis and duodenal and gastric ulcers. H. pylori (and several other Helicobacter species) are unusual in their ability to colonize the stomach, where low pH normally protects against bacterial infection. H. pylori infections are relatively common and worldwide in distribution.

8. A. Pathogenesis Transmission of H. pylori is thought to be from person to person, because the organism has not been isolated from food or water. Untreated, infections tend to be chronic, even lifelong. H. pylori colonizes gastric mucosal (epithelial) cells in the stomach and metaplastic gastric epithelium in the duodenum or esophagus but does not colonize the rest of the intestinal epithelium. The organism survives in the mucus layer that coats the epithelium and causes chronic inflammation of the mucosa . Although the organism is noninvasive, it recruits and activates inflammatory cells. Urease released by H. pylori produces ammonia ions that neutralize stomach acid in the vicinity of the organism, favoring bacterial multiplication. Ammonia may also both cause injury and potentiate the effects of a cytotoxin produced by H. pylori.

9. Lippincott’s Illustrated Reviews:Microbiolog Third Edition 2013

10. B. Clinical significance Initial infection with H. pylori causes acute gastritis, sometimes with diarrhea that lasts about 1 week. The infection usually becomes chronic, with diffuse, superficial gastritis that may be associated with epigastricdiscomfort. Both duodenal ulcers and gastric ulcers are closely correlated with infection by H. pylori. [Note: H. pylori infection is found in more than 95 percent of duodenal ulcer patients and in nearly all patients with gastric ulcers who do not use aspirin or other nonsteroidalanti-inflammatory drugs, both risk factors for gastric ulcers.] H. pylori infection appears to be a risk factor for development of gastric carcinoma and gastric B-cell lymphoma (mucosaassociatedlymphoid tumors, or MALTomas).

11. C. Laboratory identification Noninvasive diagnostic tests include serologic tests (enzyme-linked immunosorbent assay, commonly known as ELISA, for serum antibodies to H. pylori,) and breath tests for urease. [Note: Breath tests involve administering radioactively labeled urea by mouth. If H. pylori are present in the patient's stomach, the urease produced by the organism will split the urea to CO2 (radioactively labeled and exhaled) and NH3.] Invasive tests involve gastric biopsy specimens obtained by endoscopy. H. pylori can be detected in such specimens histologically, by culture, or by a test for urease.

12. D. Treatment and prevention Elimination of H. pylori requires combination therapy with two or more antibiotics. Although H. pylori is innately sensitive to many antibiotics, resistance readily develops. A typical regimen includes amoxicillin plus clarithromycin plus a proton pump inhibitor such as omeprazole. Gastrointestinal Gram-negative Rods • Curved or spiral rods • Multiple polar flagella, which give organism rapid, corkscrew motility • Urease positive • Culture on selective medium containing antibioticsHelicobacter pylori colonies on an agar plate Helicobacter pylori (Note: Young cultures grown in vitro frequently stain gram-positive) . Helicobacter pylori • Acute gastritis1 1 Clarithromycin1 Proton pump inhibitor1 Amoxicillin 1A number of alternate multi-drug regimens have have been shown to be effective in eradicating H. pylori. Gram (–) rods Helicobacter species 1 Indicates first-line drugs.

13. Lippincott’s Illustrated Reviews: Microbiology Third Edition