KP - 14 Flora Normal dan Patologis dalam mulut

• Pathogenic mechanisms of agents of GI infections include producing a toxin that affects fluid secretion, cell function, or neurologic function.
• Agents of GI infections can grow within or close to intestinal mucosal cells and destroy them, thus disrupting function.
• Agents of GI infections can invade the mucosal epithelium, causing cellular destruction and occasionally invading the bloodstream and going on to systemic disease.
• Agents of GI infections can adhere to intestinal mucosa, preventing the normal functions of absorption and secretion.
• Helicobacter pylori produces vacuolating cytotoxin, which causes epithelial cell damage and is associated with gastric atrophy and the development of gastric cancer.
• Helicobacter pylori produces urease, which changes urea (found in the stomach) into bicarbonate (CO2) and ammonia, neutralizing the stomach environment.
• Diagnosis of Helicobacter pylori infection can be done through non-invasive tests such as serology, urea breath test, and faecal antigen test.
• Invasive testing for Helicobacter pylori infection includes histologic biopsy specimens and CLO-test.
• Staphylococcus aureus produces toxin that can cause an onset of illness as quickly as 30 minutes.
• Clostridium botulinum produces botulinum toxin, which is the cause of botulism.
• Clostridium botulinum is an anaerobic, gram positive, rod-shaped bacteria that are 0.5 to 2.0 mcm in width and 1.6 to 22.0 mcm in length.
• Clostridium botulinum create spores that can remain dormant for 30 years or more.
• Spores of Clostridium botulinum are extremely resistant to environmental stressors, such as heat and UV light.
• In some cases, Shiga toxin can mediate damage to the glomerular endothelial cells, resulting in renal failure.
• Vibrio cholerae can cause asymptomatic colonization to fatal diarrhea, with onset 2-3 days after ingestion, abrupt onset of watery diarrhea and vomiting, rice water stools, severe fluid and electrolyte loss, and death 60% if untreated, 1% if treated for fluid loss.
• Vibrio cholerae causes non-invasive infection of small intestine, secretes enterotoxin, and causes watery diarrhea.
• Vibrio cholerae is oxidase positive, facultative anaerobe, tolerates alkaline conditions to pH9.0, is readily cultivated, and has simple nutritional requirements.
• C. difficile spores can survive for up to 5 months on environmental surfaces.
• Shigella dysenteriae produces Shiga neurotoxin, identical to verotoxin-1 produced by enterohemorrhagic strains of E. coli, and the primary manifestation of toxin activity is damage to the intestinal epithelium.
• Vibrio cholerae has a common heat-labile flagellar H antigen, O-lipopolysaccharide confers serologic specificity, and more than 150 O antigen serogroups are known.
• Vibrio cholerae is a Gram-negative rod with curved or comma-shaped non-spore-forming cells, is highly motile with a single polar flagella, and is associated with salt water.
• Contaminated hands of healthcare workers and environmental surfaces are reservoirs for C. difficile.
• Fecal-oral route is the transmission pathway for C. difficile.
• Core prevention strategies for C. difficile include Contact Precautions for duration of diarrhea, hand hygiene, cleaning and disinfection of equipment and environment, laboratory-based alert system for immediate notification of positive test results, and education of HCP, housekeeping, admin staff, patients, families, visitors.
• Bacteriological diagnosis of Vibrio cholerae involves stool, vomitus, stained smear, and culture on TCBS agar plate.
• Replication of Rota Virus involves attachment to cell receptors containing sialic acid, internalization and uncoating via endolysosomes, early transcription by viral RNA polymerase occurs inside sub-viral particle, and secondary transcription occurs in the cytoplasm in a conservative fashion.
• Diagnosis and treatment of Rota Virus include antigen enzyme immunoassay (EIA) of stool specimens and RT-PCR, with non-specific treatment being oral rehydration therapy to prevent dehydration.
• Morphology of Rota Virus is a family called Reoviridae with a 70-85 nm diameter, nearly spherical icosahedral particle, and is non-enveloped.
• Incubation period for acute dysentery is 1-2 days to 7 days.
• Common type of acute dysentery is an onset in sudden, shiver, high fever, abdominal pain, diarrhea, and stool mixed with blood, mucus, and pus.
• Blood picture in acute dysentery includes total WBC count increase, neutrophils increase.
• Prevention of Rota Virus includes hand washing, proper sanitation, safe drinking water and food, and the phrase “Boil it, cook it, peel it, or forget it”.
• Pathogenesis of Salmonella involves PMNs confining the infection to the gastrointestinal tract, but organisms may spread hematogenously to other body sites.
• Inflammatory response in Salmonella mediates the release of prostaglandins, stimulating cAMP and active fluid secretion with loose diarrheal stools; epithelial destruction occurs during the late stage of disease.
• Rota Virus is classified by cross-neutralization with polyclonal antibodies of antigenic specificities (glycoproteins), with VP4 antigen being P serotype and VP7 antigen being G serotype.
• Bacterial cells of Salmonella are internalized in endocytic vacuoles (intracellular) and the organisms multiply.
• Bacterial culture in acute dysentery is done using a sigmoidoscope to identify shallow ulcer, scar, and polyps.
• Stool examination in acute dysentery includes direct microscopic examination for WBC, RBC, pus cells, and bacteria.
• Pathogenesis of Salmonella involves penetrating mucus, adhering to and invading into the epithelial layer of the terminal small intestine and further into subepithelial tissue.
• E. coli protects the intestinal flora, produces our main source of vitamins B12 and K, and lives symbiotically with us.