GI Microbiology Flashcards
Outcomes of enteric infections? (4)
diarrhoea, dehydration, malabsorption, repeat infections
Outline water flux including values?
Input 9L - oral intake 2L, salivary, gastric, biliary, pancreatic 7L
Reabsorbed 8.8L - SI 7.5L, LI 1.3L
Excreted 0.2L
Secretion - pulls water into small intestine due to digestion of high osmolar food and active secretion of electrolytes (Cl pump pulling Na pulling water
Absorption - coupled Na/glucose transporter with Na into submucosa attracting water to follow, basis of oral rehydration solutions
4 mechanisms of diarrhoea production?
- Inflammatory - Increased active secretion of electrolyte and therefore water
- Secretory - Damage to brush boarder resulting in malabsorption of nutrients and electrolytes and water goes into bowel
- Osmotic - Damage to brush boarder leading to loss of disaccharide activity and increased osmolarity of stool
- Motility - Altered motility so less time for water reabsorption
Pathogenesis of Vibrio Cholera and type of diarrhoea?
Secretory diarrhoea
Ingested vibrio that aren’t killed by stomach acid adhere to SI enterocytes and release toxin subunit B which binds to receptor and subunit A which alters molecules to enhance adenyl cyclase enzyme resulting in over production on cAMP which overstimulates Cl into lumen, followed by Na, followed by water
Pathogenesis of Shigella and type of diarrhoea?
Inflammatory diarrhoea which is a cause of bacillary dysentery (blood/pus in stool) and inflammatory colitis.
1. M cells engulf shigella and invasion plasmid antigens enter host
2. Ipa protein (actin) cause cells to form filopods which carry bacteria which is released into sub-epithelial tissue
3. Engulfed by macrophages and activated to produce IL1 and attracts PMNL to area which disrupt cell barriers and move into lumen
4. icsA genes on plasmid encode actin to push bacteria into joining cells
5. Damage is caused by inflammatory processes and from cytokines
Single organ infection? (7)
- Liver abscess - pyogenic bacterial from biliary tree/portal circulation/systemic, fungal from candidiasis, helminthic from Echinococcus granulosus, protozoal from entamoeba histolytica (anchovy sauce pus)
- Splenic abscess - from systemic circulation, endocarditis mainly
- Pancreatitis - inflammation mainly from blockage of bile duct and self digestion due to blockage
- Cholangitis - infection of biliary due to blockage of common bile duct or growth of bacteria from duodenum
- Cholecystitis - obstruction of cystic duct or bacteria from duodenum leading to inflammation and infection of gallbladder
- Diverticulitis - sac like projections from colonic wall becoming blocked and infected due to increased pressure or abrasion from food. Local erosion, inflammation, necrosis, perforation
- Appendicitis - narrow lumen easily blocked due to enlarged lymphoid tissue cuased by onstruction leading to luminal wall thickening, bacterial invasion, inflammation and ishaemia, perforation
2 infections due to leakage of gastrointestinal contents?
- Intra-abdominal abscess - develop when leakage is contained by mesentery and classified by location (sub-phrenic/hepatic, paracolic, mesenteric
- Peritonitis - inflammation of peritoneal tissue reacting to blood, bile, urine, gastric fluids and infection.
2a. Primary - spontaneous bacterial peritonitis seen in patients with ascites and end liver disease or CAPD patients
2b. Secondary - usually polymicrobial which is acute (community aquired, perforation, ischaemic bowel), post-op or post-traumatic
2c. Tertiary - in critically ill patients which persists or recurs
What antibiotic covers gram, negative, gram positive, enterococcus and anaerobic organisms
Gram negative - gentamycin
gram positive - vancomycin
enterococcus - amoxycillin
anaerobic - metronidazole
What is the common flora from stomach to colon?
Stomach/duodenum - lactobacilli (gram +ve)
jejunum - lactobacilli, streptococcus
Ileum/appendix/colon - enterbacteria, enterococcus, clostridia, lactobacilli
Alpha vs Beta diversity?
Alpha - mean diversity within a sample group
Beta - diversity between sample groups
Factors affecting a microbiome?
Environment, interactions between microbes, evolution and speciation, stochastic (unpredictable) factors (diet, pharm, geography, lifecycle, birthing process, infant feeding, stress)
What is dysbiosis and what are disorders due to it?
Imbalance in microbial community associated with disease. Due to overgrowth of commensals, loss of commensals, loss of diversity and can lead to atherosclerosis, obesity, IBD, diabetes, neurodegeneration, autoimmune, colon cancer, metabolic changes
Interventions to impact microbiota? (3)
- Prenatal - placenta
- Neonatal - delivery, gestational age
- Postnatal - feeding, geographic location, family members, maternal diet
Hepatitis A: transmission, epidemiology, vaccine, diagnosis, treatment
Faecal-oral route, found worldwide with epidemic areas, risk group in Australia (MSM, IVDU, child-care, travellers). Vaccine very effective with lifelong protection. Diagnosed by IgA for acute (lasts 6-9 mo.) and IgG for immunity after natural infection
Hepatitis E: transmission, epidemiology, vaccine, diagnosis, treatment
enteric transmission in contaminated food and water with illness similar to HAV (jaundice, neurological, DIC in pregnancy) but no vaccine in Australia
Hepatitis B: transmission, epidemiology, vaccine, immune clearance, consequences, treatment
Vertical and horizontal transmission (sexual) with universal childhood vaccine.
Immune clearance when viral load (HBV DNA) falls and liver recognizes and produces ALT enzyme.
Consequences of fibrosis-cirrhosis-hepatocellular carcinoma
Treatment by entecavir and tenofovir to suppress but cannot cure and HBsAg remains
Vaccine is subunit and universal for all infants
Hepatitis D: transmission, epidemiology, vaccine, diagnosis, treatment
Defective satellite RNA virus but must be infected with HBV, no vaccine
Hepatitis C: transmission, epidemiology, vaccine, diagnosis, treatment
usually from contaminated blood (IVDU, tattoo, transfusion, sexual if ulceration)
actue/asymptomatic to chronic/clear infection to cirrhosis to HCC/liver failure
Diagnosis - HCV antibodies and PCR for active infection
Treatment - Epclusa, maviret, vosevi
Fibrosis/cirrhosis staging markers and HCC standard recommendations?
Fibrosis staging - serum markers, fibroscan, liver biopsy
Cirrhosis staging - Child-Turcotte Pugh score, MELD, INR and creatinine
HCC - Asian males older than 40, Asian females older than 50, all Africans older than 20, all patients with cirrhosis or family history of HCC
Risk factors for UTI?
age, gender, pregnancy, sexual activity, spermicides, menopause, congenital abnormalities, calculi, ureteral occlusion, incomplete emptying, faecal incontinence, poor hygiene
What is the vesico-ureteric reflex?
When bladder contracts, urine backflow to kidneys due to inadequate detrusor muscle contraction stopping this. UTI in children high association woth tract abnormality. Leads to reflex nephropathy/recurrent UTI leading to renal scarring then hypertension/renal failure
Outcomes of pregnancy UTIs?
asymptomatic can lead to low birth weight, preterm birth, perinatal mortlity OR cystitis, pyelonephritis, maternal morbidity, preterm birth
Pathogenesis of UTI? Source (3), causative bacteria acquired from where?
Source - bacteria from urethra, haematogenous seeding of kidney by S. aureus or candida or from bowel
Community aquired - E. coli, S. sapropphyticus, Proteus, Klebsiella
Hospital acquired - E. coli, enterobacteriacae, Morganella, S. epidermidis
Clinical features of UTIs? (3)
- Cystitis - dysuria, frequency, bloody and bad smell urine
- Acute pyelonephritis - inflammation of parenchyma and collecting system of kidney causing flank pain, fever, chills, rigor suggesting bacteriaemia with headache, nausea, vomiting, dysuria, frequency, urgency
- Atypical presentation in children (non specific fever, nausia, vomiting, abdominal pain) elderly (bacteriaemia and shock)
