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43 Cards in this Set
- Front
- Back
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Enterobacter family causes what human diseases
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bacteremias
UTIs (>70%) intestinal infections |
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What antigens are used for serotyping?
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LPS O antigen, Capsular K antigen, Flagellar H antigen
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certain strains are capable of systemic spread if they have what? why does this protect them?
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if they have a capsule, they are resistant to killing by complement in the serum
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which genera have flagella? how are the flagella distributed?
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esherichia and salmonella have flagella
distributed in peritrichous pattern (uniformly distributed over cell) |
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which genera do not have flagella?
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shigella, yersinia
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Enterobacteriaceae physiology/structure
Which antigen is common to them all? gram? shape? size? oxygen use nutritional requirements fermentation catalase oxidase spore formation |
All have O antigen in common
gram neg bacilli moderate size facultative anaerobes simple nutritional requirements- grow on many media types ferment glucose catalase pos oxidase neg don't form spores |
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Which genera ferment lactose? what color are they on MacConkey agar?
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Escherichia, Enterobacter
pink-purple on macconkeys |
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Which genera don't ferment lactose? what color on macconkey's
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Proteus, Salmonella, Shigella, Yersinia
clear on macconkeys |
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What are virulence factors commonly seen in the Enterobacteriaceae family?
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Endotoxin
Capsule Antigenic phase variation Type III Secretion Sequestration of growth factors Resistance to serum killing Antimicrobial resistance |
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Which genera produce Type III secretion systems?
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Escherichia, Salmonella, Shigella, Yersinia (YESS)
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How do type III secretion systems work?
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Like a bacterial flagellar body. Resembles a syringe through which bacterium (salmonella, shigella, yersinia, vibrio) can inject proteins into eukaryotic cells directly from bacterial cytoplasm.
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How do enterobacteriaceae obtain antimicrobial resistance?
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exchange of plasmids
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Hemorrhagic colitis
stools tissue invasion site orgs |
large amounts, blood (liquid blood), little or no pus
no tissue invasion large intestine EHEC |
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E. coli
as normal flora? as a frank pathogen? |
as normal flora, it's the most abundant facultative anaerobe in feces
as a frank pathogen, it's not a normal pathogen, and is associated w/diarrhea |
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Endogenous E. coli infections
origin of infection is what? its the MC cause of what illnesses? |
origin of disease is normal flora
MC cause of bacteremia and UTIs cystitis pyelonephritis prostatitis gastroenteritis |
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What surface antigens do E. coli UTI isolates express?
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P pili
Dr fimbriae Aggregative adherence fimbriae (AAF) Flagella (help ascend urinary tract) hemolysins |
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What are the 6 groups of E. coli that cause gastroenteritis?
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Enterotoxigenic (ETEC)
Enteropathogenic (EPEC) Enteroaggregative (EAEC) Enterohemorrhagic (EHEC) Enteroinvasive (EIEC) Diffuse aggregative (DAEC) |
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ETEC:
diseases caused? Source? |
travelers diarrhea
infant diarrhea in developing countries (watery diarrhea, vomiting, cramps, nausea, low-grade fever) source- fecal-contaminated food or water (no human-human) |
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ETEC:
clinical disease: persists for? look at intestines would show? localized to what part of intestines? pathogenesis |
persists for 3-5 days
no obvious inflammation seen in intestines localized to small intestines (not invasive) pathogenesis: enterotoxins stimulate hypersecretion of fluids/electrolytes |
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ETEC:
what are the two classes of enterotoxins (exotoxins)? where are they encoded? What are the adhesins? |
Enterotoxins encoded on transferable plasmids
1.Heat-labile toxins- LT1 & LT2 (only LT1 is associated w/disease) 2. Heat-stable toxins: Sta & Stb (only a assoc w/disease) Adhesins: (colonization factor adhesins) CFA/I, CFA/II, CFA/III (fimbriae that recognize specific host glycoprotein receptors and define host specificity) |
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ETEC
LT1 STa |
LT1: A subunit has ribosyltransferase activity
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ETEC
lab testing treatment |
lab: stool culture (need special test)
treatment: usu self limiting supportive care/rehydration therapy Abx rarely needed (use trimeth/sulfa or quinolones) |
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EPEC
what disease? source? clinical disease characteristics? localized to what area of intestines |
causes infant disease in developing countries
person-person spread (child care settings) clinical disease: watery diarrhea, fever, vomiting, non-bloody stools localized to small intestines, moderately invasive |
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ETEC
pathogenesis adhesins- how are they encoded characteristic lesions |
plasmid-mediated
bact attach to epithelial cells of SI and destroy microvilli via attaching and effacing lesions Bundle forming pili (Bfp): mediates initial aggregation to form microcolonies on epithelial cell surface Locus of enterocyte effacement (LEE) pathogenicity island is responsible for subsequent attachment -encodes Type III secretion to insert Translocated intimin receptor (Tir) onto epithelial cells this serves as receptor for EPEC intimin intimin to Tir binding causes polymerization of actin, accumulation of cytoskeletal elements under bacteria = loss of cell surface integrity & death |
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EAEC
disease caused? associated with what sequelae? localized to what part of intestines? invasive? |
persistent, watery diarrhea w/dehydration in infantsin developing countries & travelers diarrhea
associated w/chronic diarrhea & growth retardation in children localized to small intestine |
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EAEC
pathogenesis adhesins toxins |
plasmid-mediated aggregative adherence of rods ('stacked bricks') w/shortening of microvilli, mononuclear infiltration, and hemorrhage
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EAEC treatment
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usu self-limiting
supportive care/rehydration therapy |
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EHEC
most common where? in what time of year? in what population? source? how many orgs to cause disease? localized to what part of intestines? invasive? |
MC strain in developed countries
MC in warm months highest incidence in kids under 5 source: undercooked meat, water, unpast. milk/juice, uncooked veggies/fruit |
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EHEC
adhesins exotoxins |
adhesins: Bfp, intimin
exotoxins: Shiga toxins (Stx 1 & 2) |
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EHEC
clinical diseae range of symptoms? a few % of pts can develop two sequelae? |
initial watery diarrhea followed by grossly bloody diarrhea (hemorrhagic colitis), little to no fever, 1/2 have vomiting
5% may develop small vessel damage: Hemolytic Uremic syndrome and Thomobotic thrombocytopenic purpura (damage to vessels of brain, usu in older adults) |
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EHEC: HUS
MC cause of what? characterized by? highest incidence in what pop? mortality rate? severe sequelae? |
MC cause of acute renal failure in kids in US
Characterized by acute renal failure, thrombocytopenia, macroangiopathic hemolytic anemia highest incidence in kids under 5 mortality rate 5-10% severe sequelae: renal impairment, CNS manifestations, HTN |
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HUS appears to be assciated w/what toxin?
what is the toxin receptor? what does A subunit of toxin do? |
Shiga toxin 2 (Stx2)
receptor is globotriaosylceramide)-- high conc. in renal endothelial cells A subunit binds to 28S ribosomes (cleaves adenine residue) and inhibits protein synthesis |
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Most common strain of EHEC?
unable to ferment what? transmission via? infectious dose? posseses homolog to a gene ofwhat other e. coli strain? |
E. coli O157:H7 (STEC or VTEC)
unable to ferment sorbitol (unlike other E. coli) transmitted from animals to humans (zoonotic) tiny infectious dose has homolog of EPEC genes for A/E activity-- mediates actin and cytoskeletal rearrangements leading to A/E lesions |
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EHEC:
Shiga toxins 1 & 2 share same enzymatic specificity and binding site as toxin from what other bacteria? acquired via what? structure? where to the subunits bind? stimulate expression of what? |
same specificity/binding site as Shigella dysenteriae type 1
acquired by lysogenic bacteriophages have one A subunit and 5 B subunits A subunit binds to 28S ribosome to stop protein synthesis B subunit binds to globotriaosylceramide (GB3- highest conc. in intestinal villus and renal endothelial cells) stimulate expression of inflammatory cytokines |
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What EHEC strains are the most pathogenic?
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those that express both Shiga toxins and have attaching/effacing activity
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EHEC
testing treatment |
stool culture, sorbitol-containing macconkey agar to see if they ferment sorbitol (will be colorless if not): E. coli O157:h7 needs speical media
commercial kits for shiga toxins Treatment: supportive care, rehydration therapy monitor renal fcn, Hb, platelets Abx may promote development of HUS? |
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EIEC
where does it occur? source? disease symptoms localization in GI? invasive? |
rare in US, causes shigella-like disease in underdeveloped countries
food/water borne watery diarrhea, fever, may progress to dysentery (scantly bloody stools w/lymphocytes) localized to large intestines, invasive w/much cell destruction |
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EIEC
similar to what other bact? what genes regulate invasion? how does invasion/ replication occur? |
similar to shigella
pINV genes on a plasmid regulate invasion into colonic epithelium bact are phagocytosed, then lyse the phagosome and replicate in host cytoplasm most into adjacent cells w/actin tails this can all lead to colonic ulceration |
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EIEC
adhesins exotoxins |
adhesins: invasive plasmid antigen (Ipa)
exotoxin: hemolysin A (HlyA) |
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EIEC treatment
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usu self-limiting
supportive care/rehydration therapy |
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Which two groups of E. coli use Bfp/intimin to create pedestals to attach?
what is a major difference? |
EPEC and EHEC both use Bfp/intimin, but then EHEC secretes shiga toxins that are taken up via coated pits, go to golgi, and destroy 28SrRNA
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How does ETEC intract w/ gut epithelial cells?
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binds loosely via fimbriae (CFAs), then secretes toxins (LT1, Sta) that gain entry into cells w/o disruption of cytoplasm
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How does EIEC interact w/gut epithelial cells?
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gains entry into cell, digests phagosome, grows/divides in cytoplasm, gains entry into neighboring cells by bursting thru/digesting membranes
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