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Session 2 Microbio15
Microbio -15- GI #1 Infection Hartley
| Question | Answer |
|---|---|
| What type of bacteria are the majority of GI pathogenic bacteria | Gram Negative Bacteria |
| Why would you use MacConkey agar in a fecal culture | it inhibits gram positive growth. And you get a color change based on lactose fermentation |
| Why would you use Hektoen Enteric Agar for a fecal culture | it inhibits the growth of common colon flora and help selectively recover salmonella and shigella spp. if they are present and you have indicators to detect H2S production |
| Why would you use Campylobacter blood agar in a fecal culture | agar enriched to recover campylobacter spp. from stool |
| Apart from a fecal culture what other tests can you run to differentiate what is causing the GI infection | CBC with Diff. UA Stool Analysis (microscopic, fecal leukocytes, fecal lactoferrin(indicates neutrophils are present)) |
| What antigen is found on the outer membrane of gram negative bacteria | O-antigen |
| What Antigen is found on the flagella of gram negative bacteria | H- antigen |
| When they have a capsule what type of antigen is found on gram negative bacteria | K antigen |
| Why do we care what antigen is found on gram negative bacteria | helps to characterize and identify the bacteria |
| What are the most common route of GI infection | Fecal to oral route of contamination is most common also could be inadequately cleaned or cooked foods or water contaminated with fecal matter |
| What is the general progression of bacterial infections of the GI tract | bacteria passes through the intestines -attaches to mucouse layer or intestinal epithelia -secret toxin -induce diarrhea and other symptoms -then hopefully cleared by host immune system |
| What are the general s/sx of GI infections | Diarrhea, Cramps and Vomiting |
| What are some of the causes of acute diarrhea lasting less than 7-14 days | drugs infectious agents feeding after a long fast fecal impaction |
| What is the tx for acute diarrhea | monitor electroylytes and hydration and use fluid replacement therapy as needed also bismuth compound or anti-nausea meds can be offered as needed |
| Are there vaccines available for GI bacteria | NO GALT(gut associated lymphoid tissue) will normally clear bacteria with innate immunity and IgA |
| Gram Negative Bacillus most strain rapidly ferment lactose and produce indole. Many strains are actually a normal GI flora so it can be hard to discriminate them from pathogenic strains | E. Coli |
| What is significant of the following strains of E. Coli Enterotoxigenic E. coli (ETEC) Enteropathogenic E.coli (EPEC) Enterohemorrhagic E.coli (EHEC) Enteroinvasive E.coli (EIEC) Enteroaggregative E.coli (EAEC) | They are pathogenic strains of E. Coli |
| What is the typical source of infection of Enterotoxigenic E. coli (ETEC) | lack of good hygienic practices (ingesting contaminated food or water) Major Cause of Travelers Diarrhea |
| What is the major cause of traveler's diarrhea | Enterotoxigenic E. coli (ETEC) |
| What is the progression of infection of Enterotoxigenic E. coli (ETEC) | ETEC is ingested and attach to intestinal epithelia by pili in the small intestines -secretes one or both of two types of toxins causing symptoms -immune system clears infection after 3-4 days |
| what are the s/sx of infection with Enterotoxigenic E. coli (ETEC) | WATERY Diarrhea, cramps, Vomiting, malaise, low grade fever More severe symptoms if ETEC secretes both types of toxins |
| in what age group are infections of Enterotoxigenic E. coli (ETEC) most common | under 5 or over 15 yrs old |
| How do you differentiate ETEC from enterobacteria or plain E. Coli | The toxins it secrets |
| What are the two toxins that Enterotoxigenic E. coli (ETEC) can secrete | ST- small toxin LT- heat labile toxin (made of A and B subunits A pierces membrane B aids in membrane Binding) |
| what is the treatment with infection of Enterotoxigenic E. coli (ETEC) | hydration as needed for symptoms only can give supportive care antibiotics will only shorten symptoms by 1 day. Although some physicians will take or prescribe antibiotics as prophylatic for traveling |
| How do you diagnose some one with an infection of Enterotoxigenic E. coli (ETEC) | They will have Characteristic symptoms -watery diarrhea -abdominal cramping -low grade fever WITH ONLY lactose fermenting organisms on fecal cultures |
| what is the source of infection of Enteropathogenic E. coli, EPEC | fecal oral contamination from poor hygienic practices. Adults are generally carriers and Infants get the disease |
| what is the progression of infection of Enteropathogenic E. coli, EPEC | -EPEC is ingested and attaches to epithelial cells by pili in small intestines -Secretes factors that alter host cells -creates a pedestal for bacterial cell -induces diarrhea by loss of villi and lack of absorption -immune system clears the infectio |
| what are the s/sx of infection w/ Enteropathogenic E. coli, EPEC | Fever vomiting WATERY diarrhea that may have large amounts of MUCUS Associated with clusters in the US |
| What E. Coli infection is associated with CLUSTERS in the US e.g. nursery and hospital outbreaks | Enteropathogenic E. coli, EPEC |
| Enteropathogenic E. coli, EPEC are groupd with what type of pathogens | Attachement and Effacement pathogens- all have a type III secretion system that is highly conserved |
| What are the stages of infection w/ Enteropathogenic E. coli, EPEC | A- initial adherence B- Injection- type III secretion system C- Tight Adherence- Pedestal formation D- Diarrhea |
| What is the Type III secretion system like | it is like a hypodermic needle at the cellular level and is the most complex bacterial secretion system |
| Since adults are carriers of Enteropathogenic E. coli, EPEC that means they don't develop a lasting immunity but since they don't have sympotms how are they dealing with the Enteropathogenic E. coli, EPEC | likely have developed a resistance or tolerance to the bacteria |
| What is the tx for Enteropathogenic E. coli, EPEC infections | hydration as needed antibiotics are generally not needed you can give bismuth compounds for symptomatic relief |
| What are the likely source of infection of Enterohemorrhagic E. coli, EHEC | ingestion of insufficiently cleaned or cooked foods. Resevoir is usually adult cattle wich are asymptomatic |
| What is the progression of infection w/ Enterohemorrhagic E. coli, EHEC | -EHEC are ingested and attach to epithelial cells via pili in the large intestines -Secrete factors that alter host cell -for a pedestal for the bacterial cell -secrete toxins that damage or kill host cells -immune system clears the infection |
| What are the s/sx of Enterohemorrhagic E. coli, EHEC infection | !!! water diarrhea that progresses to BLOODY diarrhea -abdominal cramps -+/- fever -may also have hemolytic uremic syndrome |
| What is hemolytic uremic syndrome HUS | toxin release into bloodstream lysis erythorcytes, thrombocytes and destroys glomerular capillary endothelial cells. can be fatal if kidney failure is not prevented |
| what is Enterohemorrhagic E. coli, EHEC O157:H7 most commonly associated with | HUS hemolytic uremic syndrome |
| how is Enterohemorrhagic E. coli, EHEC similar to EPEC | they both are A/E pathogens and carry a type III secretion system to induce pedestal formation |
| What is the mortality rate of patients w/ infection of Enterohemorrhagic E. coli, EHEC that develop HUS | 3-17% 30% will have permanent disabilities (chronic renal insufficiency, hypertension, and neurological defects) |
| What are Enterohemorrhagic E. coli, EHEC toxins functionally similar to | Shiga Toxin they have AB type toxins |
| what is the tx for Enterohemorrhagic E. coli, EHEC infection | MONITOR for RENAL FAILURE hydration as needed antibiotics are usually not required |
| How can you tell your patient is infected w/ Enterohemorrhagic E. coli, EHEC | cultures FAIL to ferment sorbitol (macConkey agar using sorbitol) Culture of O157 are sero positive -MUG assay EHEC typically don't produce Beta-Glucoronidase while 92% of other strains do |
| What are Enteroinvasive E. coli, EIEC biochemically, genetically and pathogenically related to | Shigella Spp. |
| What are S. flexneri S. boydii S. sonnei S. dysenteriae | Strains of Shigella Spp. |
| what are the sources of infection w/ Enteroinvasive E. coli, EIEC | Fecal oral contamination contaminated food or water outbreaks reservoirs involve human sources |
| What is the progression of infection of Enteroinvasive E. coli, EIEC | -EIEC is ingested and attach to large inetsine epith cells w/ pili -secret factor that induce uptake and transmission by M cells -Entry into the inf. or lat. sides of intest. epithelial cells -replication in epithelial cells -immune system clears inf |
| what are the s/sx of infection w/ Enteroinvasive E. coli, EIEC | many are asymptomatic w/ transient fever early symptoms- fever, severe cramps, WATERY diarrhea late symptoms- reduced fever increased diarrhea with BLOOD, urgency, tenesmus |
| How are Shigella Dysenteriae type 1 different from Shigella Spp and EIEC | IT secrets shiga toxin whil Shigella spp. and EIEC do not |
| What is the tx for Enteroinvasive E. coli, EIEC infection | antibiotics in severe cases to decresae length of symptoms -hydration as needed (severe dehydration is possible) |
| How do you dx infection w/ Enteroinvasive E. coli, EIEC | culture on differential and selective media (Hektoen enteric agar, MacConkey) DNA probes for EIEC are commercially available |
| What is the source of infection w/ Enteroaggregative E. coli, EAEC | little is known. fecal to oral is likely also linked with foodborne outbreaks |
| what is the progression of infection w/ Enteroaggregative E. coli, EAEC | =EAEC are ingested and attach to large intestin epithelia -Bacteria replicate and aggregate in a unique Stacked Brick fashion -secrete several toxins leading to inflammation and intestinal damage -immune system clears the infection |
| what are the s/sx of infection w/ Enteroaggregative E. coli, EAEC | WATERY diarrhea (some cases may include blood or mucus in the feces) abdominal cramps EAEC may cause diarrhea for greater than 14 days especially in HIV patients and travelers. |
| What toxins does Enteroaggregative E. coli, EAEC secrete | ShET1(shigella enterotoxin 1) similar to toxin in most shigella flexneri strains -- causes diarrhea w/ mechanism other than cAMP, cGMP or Ca2+ EAST1- similar to ETEC toxin ST PET- serine protease that alters enterocyte cytoskeleton |
| Why is there no vaccine against E. Coli | many strains are non pathogenic and actually resident members of the normal GI flora |
| What is the TX for Enteroaggregative E. coli, EAEC | antibiotics may be helpful for prolonged disease and give hydration as needed |
| What is the key in differential diagnosis between different strains of E coli. | key differential is whether diarrhea contains blood or mucus |
| If the Diarrhea is WATERY what strains would you suspect | EPEC, ETEC, most viral, (EAEC) |
| If the diarrhea is Bloody what strains would you suspect | EHEC, Shigella spp./EIEC, (EAEC) |
| If the diarrhea is water + mucus what strain would you suspect | EPEC |
| If your patient has recently traveled what cause of dirrhea would you suspect | ETEC, EAEC, Rotavirus, EIEC |
| If your patient recently ate a meal of beef and now has Diarrhea what would be your suspected cause | EHEC |
| If you patient has had diarrhea for the past 7 days what would you suspect | EAEC, Shigella/EIEC, ETEC |
| Gram Positive Bacillus, Obligate Anaerobe readily forms spores | Clostridium dificle |
| Where do you typically get an infection from clostridium dificle | typically no socomial infection but can be community acquired as 3% of humans are normal carriers |
| What acounts for 30% of all antibiotic associated diarrheas | Clostridium dificle |
| What is the progression of infection from clostridium dificle | 1. Ingest contaminated food ( prior to or after antibiotic clearance of normal GI flora) 2. Colonization of gut and secretion of toxins 3. Extent of Ab production to toxin A determine outcome of infection |
| What are the s/sx of infectino with clostridium dififcle | diarrhea may be mild and watery or be bloody -cramps -fever -leukocytosis -pseudomembranous colitis |
| What are the 3 toxins that clost. Dif. can secrete | toxin A- Glucosyl Transferase targeting small GTPasees (Ras and Rho) Toxin B- similar to A but not enterotoxigenic Binary Toxin- ADP ribosylating enzyme targeting actin similar to C2 toxin and Iota Toxin |
| What are the antibiotics used to treat infection with C. Dificle | Vanco, or Metronidazole |
| how do you dx infection w/ C. DIF | Culture Gram Staining- is a gram pos bacillus Detection of Endospores |
| Gram Neg Bacillus that is not halophilic | V. Cholera and V. Mimicus |
| Where do you typically get V. Cholera from | lack of good hygenic practices ingesting contaminated water or food |
| What products have been associated with outbreaks of V. cholera | Fish, Seafoods, milk, ice cream, and unpreserved meats |
| Why are infections with cholera associated with a high dose of the organism to cause infection | V. Cholera is killed by acid so you need a lot to get past the stomach acid and cause infeciton |
| What is the progression of infection with V. Cholera | 1. Cholera are ingested and attach to intestinal epithelia 2. Secretion of Toxin and assumption of sx 3. Immune system clears the infection |
| Does Cholera damage the enterocytes | no |
| What are the associated s/sx of V. Cholera infection | Severe Water Diarrhea Vomiting at onset Muscle Cramps due to dehydration |
| Are there any vaccines available for V. Cholera | Yes oral vaccines available outside of US -live attenuated strain -killed vaccine + B subunit Vaccine |
| If you give immediate hydration therapy to a patient infected w/ V. Cholera what do you reduce to mortality risk to | Reduces mortality risk to less than 1% |
| Gram Neg Bacillus that is curved, motile microaerophilic fastidious | Campylobacter jejuni |
| What are the typical sources of infection from Campylobacter jejuni | Direct contact with infected animals such as dogs, cats, birds indirect through eating contaminated water or milk or undercooked poultry associated w/ large outbreaks |
| What is the leading cause of bacterial gastroenteritis | Campylobacter jejuni |
| What is the progression of infection w/ Campylobacter jejuni | 1- C. Jejuni attaches to GI epithelium 2- Invades enetrocytes directly or passes through to lamina propria 3- Induces diarrhea uk method 4- immune system clears infection in 2-5 days |
| What are the s/sx of infection w/ Campylobacter jejuni | abdominal Pain within 2-10 of infection cramps diarrhea- bloody fever chills Rarely any nausea or vomiting |
| What happens in .1% of infections w/ Campylobacter jejuni | get Guillain-Barre syndrome esepcially HLA-B27 positive patients |
| what plays a role in providing immunity from Campylobacter jejuni | Immunoglobulins give protective immunity |
| what is the tx for infection w/ Campylobacter jejuni | fluid and electrolyte replacement |
| How do you dx infection w/ Campylobacter jejuni | oxidase positive motile gram neg bacillus Culture on CAMPY-BAP Growth at 42C (inhibits growth of other enetrics) Microaerophilic |
| Gram Neg. Spirilum microaerophilic multiple sheathed flagella produces urease to create ammonia to neutralize stomach acids | Helicobacter pylori |
| What is the progression of infection w/ H. Pylori | 1- Ingest Bacteria which migrates through gastric mucus layer 2- Inflammation of epithelium and halt mucus production 3- thining of mucus layer leads to damage of epithelium by gastric secretions (ulcers) 4- infection may persist for years or life |
| What are the s/sx of infection w/ Helicobacter pylori | Belching to vomiting epigastric pain/burning/gnawing (2-3 hours after meals) Relieved by eating, atacids, antisecretion agents Small% of infections lead to gastric cancer |
| How can you prevent infection w/ Helicobacter pylori | no effective or proven method to prevent infection |
| What is the tx for H. Pylori | combine antibiotics with antisecretory agents |
| How do you dx infection w/ h. pylori | serology/ELISA it is difficult to culture |
| What is key in differnetiating which organism is causing infection with GI symptoms | Get a Good H&P |
Created by:
smaxsmith
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