1) Toxin Production Invitro/In Vivo

1) Toxin Production Invitro/In Vivo

<p>GI Pathogens</p><p>Mechanisms: </p><p>1) Toxin production invitro/in vivo</p><p>2) Adhesive/aggregative- occupy microvilli</p><p>3) Invasive- inflammation</p><p>Transmission: 7 Fs: feces, food, fluids, fingers, fomites, fornication, flies; depends on # CFUs required to cause disease</p><p>Defenses: </p><p>1) Stomach- low pH</p><p>2) Small Intestine: large volume; proteases, bile, IgA</p><p>3) Large Intestine: large # flora produces inhibitory substances and occupies adhesive sites</p><p>Bug General characteristics Epidemiology Transmission Virulence Factors Treatment V. Chorlea - net loss of water - Gulf coast/ Africa - Human pathogen Cholera toxin: encoded Abs can shorten Dehyration: rice water - Warm months - Consumption of phage duration of toxin stool contaminated - Bind to cells secretion and - Not invasive water/food - ADP-ribosylating enzyme decrease spread - Acid Sensitive - No person to person (↑ cAMP) - halophilic, can grow in transmision -turns off Na absorption Support with IV absence - increase Cl secretion fluids - caused by serotype O1/O139</p><p>V. para-hemolyticus - requires salt - Gastroenteritis year - consumption of See V. Chorlea round improperly cooked - Septicemia and wound seafood or raw infections in warm months oysters V. Vulnificus - severe wound infections - Eating raw oysters See V. Chorlea and sepsis (sepsis) - Protein capsule protects - Esp. affects ICH: cirrhosis, against phagocytosis and renal fail complement Entero-bacteriaceae Gram negative rods E. coli Motile Lactose fermenter Commensals, or acquired virulence ETEC Weanling diarrhea (ST) - exposure can induce - High infectious dose - Labile toxin similar to Antibiotics decrease Traveler’s diarrhea mucosal immunity (IgA) - Contaminated cholera toxin; activates duration/severity of - Watery diarrhea - asymptomatic carrier food/water (no adenylate cyclase ↑ cAMP diarrhea states person to person) - Stable toxin: ↑ cGMP, - Incubation: 14-50 stimulates CL secretion, Prevent: bismuth hrs inhibits NaCl abs. subsalicylate 4x/day EPEC Infant diarrhea, no - Oral/fecal, hands, Diagnosis: WBC; sometimes foods, tabletops phenotypic culture vomiting - Reservoir: HeLa cells; genotype - Effacing microvilli and asymptomatic kids/ PCR attaching cell adults membrane leads to Rehydrate and Abs activation of signal transduction - Mortality 25-50% EHEC - O157:H7 assoc w/ - age extremes, esp kids - Reservoir: animals - attach Gb3R to renal Diagnosis: culture HUS, causes bloody <10 yrs - contaminated beef, epithelium and damages stool on SMAC, diarrhea (4-10 days), lamb, pultry, apple glomeruli detect non 0157:H7 also fever, cramps (1st) jice, salami, by PCR or DNA - Hus: hemolytic mayonnaise, radish probes anemia, oliguric RF, sprouts thrombocytopenia - Person to person too Do not give - Hemorrhage and - Low infectious dose antimotility drugs or edema of transverse AB (makes it worse) and ascending colon “thumbprinting” Shigella - invasive enteric - s. dysenteriae: developing - human only - invades intestinal Fecal sample: pathogen contries (most severe, only - low infectious dose epithelium (inflammatory leukocyte + -watery diarrhea to 1 w/ shiga toxin) - direct contact, sex, leukocytes in LP) Diagnose w/ DNA Dysentery- freq stools of - s. sonnei: most common food and water - Release inflamm mediators probe/PCR small vol, w/ pus and US, mildest results in blood in lumen blood - s. flexneri/ boydii - Invade colonic mucosa, Treat: Abs reduce - nonmotile, lactose The rest have cytotoxins multiply intracellular and duration of illness nonfermenting - 70% of kids <15 spread from cell to cell, and period of Endemic in homosexual leads to focal mucosal ulcers infectivity, AB males and inflammation resistance is Epidemics in DCC, jails - Shiga toxin inactivates 60S common ribosomal subunit stops protein synthesis Salmonella typhi - Typhoid fever - Host-human - invades across mucosa and - Isolate org from - High daily fevers 4-8 - Person to person hids in mononuclear cells in blood, stool, or (S. typhimurium is most weeks - Low ID, more lymph nodes urine common in US) - invased gallbladder common in PPI and - Multiples and causes (carrier), kidney, and antacid use bacteremia that spreads to - Amp, cefriaxone, reinvasion of gut liver and spleen bactrim mucosa (causes - Multiplys in macrophages inflammation and can in liver and spleen (not killed For carriers use lead to diarrhea) intracellularly) amp+ probenecid or - doesn’t adhere to - Increases then released Bactrim x6 wks endothelium and causes continuous - Motile, lactose bactermia w/ high fevers nonfermenter Salmonella choleraesuis - focal infection: - conditions impairing - Host: pigs - Multiplies in LP - nonlactose vascular endothelium phagocytosis are - more common in - induce fluid secretion by ↑ fermenter and endocarditis or vascular susceptible to bacteremia PPI and antacid use cAMP and prostaglandins biochem properities infections (HbSS, AIDS, leukemia) - get from food, - Enters BS (rapid kill by - Treat ICH and - Diarrhea water, zoonosis phagocytes) bacteremia w/ AB - adheres well (turtles and chickens) Salmonella enteritides - Osteomyelitis (in HbSS) See above - Host: humans/ See above - no AB, due to ↑ and diarrhea animals (2000+) shedding duration - adheres well can cause - more common in I.E., intravascular PPI and antacid use infections - get from food, water, zoonosis Yersinia enterocolitica - Plasmids w/ virulence genes - Resist phagocytosis Yersinia pseudo- - Diarrhea, fever, ab - common in Scandinavian - Zoonotic infections - Plasmids w/ virulence Treat w/ Cipro, 3rd tuberculosis pain for 2 wks and Europe in contaminated genes gen cephalopsporin, - Chronic disease can foods like milk, meat, - Resist phagocytosis bactrim develop water (Belgian - can grow at 4C - Affects mainly terminal chocolates) ileum, if mesenteric - Blood transfusion lymph nodes involved - Incub: 1-10 days (can mimic appendicitis) - nonmotile, lactose nonfermenter</p><p>H. pylori - spiral, gram neg rod w/ - highest colonization due - human primary - Urease + (neutralizes Diagnose: IgM, IgG, corkscrew motility to poor sanitation source stomach acid) IgA antibody ELISA - Gastritis, peptic ulcers, - colonization in US ↑ w/ - fecal-oral trans - pass through gastric - Titer no correlate gastric carcinoma, MALT age (protects against mucosa cause epithelial w/ severe associated lymphoma esophageal reflux) damage - warthin-starry - Stimulates inflame silver stain response (ulcers) - Biopsy specimen: urease+ - urease breath test</p><p>Treat: PPI+ tetra+ metronidazole+ bismuth or amox, clarithro</p>

View Full Text

Details

  • File Type
    pdf
  • Upload Time
    -
  • Content Languages
    English
  • Upload User
    Anonymous/Not logged-in
  • File Pages
    4 Page
  • File Size
    -

Download

Channel Download Status
Express Download Enable

Copyright

We respect the copyrights and intellectual property rights of all users. All uploaded documents are either original works of the uploader or authorized works of the rightful owners.

  • Not to be reproduced or distributed without explicit permission.
  • Not used for commercial purposes outside of approved use cases.
  • Not used to infringe on the rights of the original creators.
  • If you believe any content infringes your copyright, please contact us immediately.

Support

For help with questions, suggestions, or problems, please contact us