GIHEPL2 GNB SalmShigHP24Stud.pdf

Aerobic Gram-Negative Bacilli (GNB) 2 Dr Aoife Kearney Clinical Lecturer Dept of Clinical Microbiology, RCSI  RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn Gram-negative bacilli: Salmonella, Shigella, Helicobacter Class Year 2 Semester 1 C...

Aerobic Gram-Negative Bacilli (GNB) 2 Dr Aoife Kearney Clinical Lecturer Dept of Clinical Microbiology, RCSI  RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn Gram-negative bacilli: Salmonella, Shigella, Helicobacter Class Year 2 Semester 1 Course Undergraduate Medicine Lecturer Dr Aoife Kearney Date 11th September 2023  How much do you need to get an infection? (infective dose) Salmonella(∼ 105) Shigella (∼ 10) E. coli 0157:H7 < 10 Campylobacter jejuni (∼ 500) HIGH V. LOW i,e, need very little to get an infection! 3. Helicobacter pylori  H. pylori Curved Gram-negative bacillus Asymptomatic coloniser of stomach but causes gastritis & duodenal ulcers Commonest chronic bacterial infection in humans? – 50% of the world’s population – 70% peptic ulcer cases colonised with H. pylori More common in resource-poor countries – Highest prevalence in Africa (70%), South America (69%), and Western Asia (66%) – Lowest prevalence in Oceania (24%), Western Europe (34%), and Northern America (37%) Mode of spread unclear – person-to-person & faecal-oral routes both occur  Main virulence factors of H. pylori Urease production – Hydrolyses urea  ammonia  neutralises gastric acid Motility – Spiral shape, flagella and mucolytic enzymes Facilitate passage through the mucus layer to the gastric epithelium Ability to adhere to gastric epithelium – specific receptor-mediated adhesion  H. pylori Pathogenesis Adheres to mucosa of the stomach – Only adheres to gastric-type epithelium flagella/ adhesins – Colonisation may be patchy Urease activity – Helps survive in an acid environment Causes chronic inflammation of the underlying mucosa – Gastritis  stomach acid and pepsin overwhelm mechanisms that protect mucous membranes  ulceration – Lymphocytic infiltration  MALTomas It does not invade  Clinical features & complications of infections caused by H. pylori Asymptomatic Acute gastritis – Dyspepsia Chronic gastritis Gastric atrophy – Fe deficiency anaemia – ITP – Vit B12 deficiency Gastric Cancer (adenocarcinoma) – 1994 – WHO Class I carcinogen Duodenal ulcer > Gastric ulcer Mucosa Associated Lymphoid Tissue tumour (MALT lymphoma ) ? Other GI cancers  Detection of H. pylori Laboratory a. Faecal antigen testing b. Serology (positive for life even after eradication) c. Culture = difficult (microaerophilic) + rarely done Also 2. Endoscopy biopsy – Rapid urease test (CLO test) – Histology 3. Urea breath test  Treatment Smith et al. The Irish Helicobacter pylori Working Group consensus for the diagnosis and treatment of H. pylori infection in adult patients in Ireland, European Journal of Gastroenterology & Hepatology: May 2017 - Volume 29 - Issue 5 - p 552-559  Treatment decision schematic Smith et al. The Irish Helicobacter pylori Working Group consensus for the diagnosis and treatment of H. pylori infection in adult patients in Ireland, European Journal of Gastroenterology & Hepatology: May 2017 - Volume 29 - Issue 5 - p 552-559  Prevention of acquisition & spread of infections caused by H. pylori Mode of spread unclear – person-to-person & faecal-oral routes both occur Prevention of acquisition – Practice good hygiene and hand washing, especially with food preparation Prevention of spread – All patients with chronic GI symptoms should be tested and treated to prevent exposure to family members – Patients should complete the full course of therapy (antibiotics and acid blockers) to maximize the potential for a cure