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what are the two types of infections caused by Escherichia coli
- gastroenteritis: infections acquired exogenously or from normal microbiome thru plasmids, bacteriophage DNA (transduction)
- non-gastroenteritis (extraintestinal infections): acquired endogenously
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what are the 6 types of e.coli gastroenteritis
- entertoxigenic (ETEC)
- enteroaggregative (EPEC)
- shiga toxin producing (STEC)
- enterohemorrhagic (EHEC)
- enteroinvasive (EIEC)
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what are the heat stable toxins of ETEC (enterotoxigenic e.coli)
- STa and STb
- STa leads to increase in cellular cGMP levels and hypersecretion of fluids and reduced absorption of fluids
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what are the heat labile toxins of ETEC (enterotoxigenic e. coli)
- LT-I, LT-II, LT-III
- increases cAMP levels causing enhanced secretion of chloride and decreased absorption of sodium chloride
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what is the pathogenicity of enteropathogenic e.coli (EPEC)
- bacteria attaches to epithelial cells
- contains a cluster of 40 virulence genes in a pathogenicity island called locus of enterocyte effacement (LEE)
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what is LEE (locus of enterocyte effacement)
40 virulence genes of EPEC that contains T3SS and virulence effector proteins
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How does EPEC cause pathogenesis
EPEC adheres to enterocytes by adhesins and pili which forms an actin microfilament pedestal
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how does shiga toxin cause pathogenecity
shiga toxin inhibits host cell protein synthesis that disrupts systemic absorption
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what are the non gastrointestinal E.coli infections (3)
- UTI: caused by hemolysin HllyA, adhesins
- neonatal meningitis: caused by K1 capsular antigen e.coli's
- septicemia
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how is e.coli treated
- strong lactose fermentation
- antibiotic therapy (resistance to penicillins)
- proper cooking of beef to prevent STEC
- avoiding unnecessary catheters
- high hygienic standards
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how is E.coli ID'd in lab
- strong lactose fermentation
- STEC strains: does not ferment sorbital, direct detection of shiga toxin from feces
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what are enterocytes
intestinal absorptive cell in epithelial lining of gut
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peyer's patch
lymph follicles beneath the epithelium that interact with antigens in the gut. contains peyer's patch cells
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what are peyer patch cells
MQ, denderitic cells, B cells, T cells
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what are M cells in the gut
- microfold cell
- cells above Peyer's Patches that take up antigen from the gut and present them to immune cells
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how does Y. enterocolitica cross the gut epithelium
- crosses by M cells or enterocytes.
- can mimic psuedoappendicitis and cause enterocolitis
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how does shigella cross the gut
- shigella cells do not directly invade enterocytes from gut lumen
- attaches and invades M cells before invading enterocytes
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how does salmonella cross the gut epithelium
- three ways
- 1. invasion by endocytosis by M cells, then M cells pass the bacteria to macrophages in the Peyer's patch
- 2. bacteria enter enterocytes by endocytosis
- 3. bacteria are directly taken up in the lumen via phagocytosis by dendritic cells that extend projections across the epithelium
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where do salmonella replicate in the cell
phagosome
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what are the pathogenicity islands that regulate the attachment, engulfment, and replication of salmonella
- pathogenicity island I (PAI I): encodes salmonella secreted invasion protein (SsP) and T3SS I that injects proteins into host cell
- pathogenicity island II (PAI II): encodes genes for invading host immune response and T3SS II
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what are the host inflammatory response to salmonalla infection
- effects mainly GI tract
- releases prostaglandins
- stimulates cAMP production, resulting in fluid release into gut, causing diarrhea
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what do typhoid strains of salmonella cause and where do they colonize
transported by MQ to the liver, spleen, and bone marrow where they replicate and lead to development of enteric typhoid fever
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non typhoid strains of salmonella can colonize what reservoirs
all animals and humans
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how is non typhoid strain acquired
- ingestion of contaminated foods
- high inoculum
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who are the patients at risk from non typhoid salmonella
- ppl that eat contaminated foods
- patients with reduced gastric acid levels
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how is typhoid strains of salmonella acquired
- contaminated foods
- fecal-oral spread in children
- low inoculum
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what are the two significant salmonella strains
- salmonella typhi
- salmonella paratyphi
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what are the pathogenesis of s. typhi and s. paratyphi
- typhoid fever/ paratyphoid fever
- colonizes gall bladder, may be asymptomatic
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what are the clinical diseases of salmonella
- gastroenteritis: non blood diarrhea
- septicemia: seen in s. typhi, paratyphi, and choleraesuis
- enteric fever: s. typhi produces typhoid fever
- asymptomatic colonization in gall bladder (s. typhi and s. paratyphi)
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how is salmonella ID'd in lab
isolation from stool
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how is salmonella treated
- antibiotic treatment not recommended for enteritis
- S. typhi and S. paratyphi should be treated with antibiotics
- proper cooking of food
- vaccines
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what are the 4 clinical species of shigella
- shigella dysenteriae: produces shiga toxin
- shigella flexneri: infectous in developing countries
- shigella sonnei: infections in developed countries
- shigella boydii: not commonly isolated
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how does shigella cause pathogenesis
- invade inside host cells of the colon
- secrete virulence effector proteins IpaA, IpaB, IpaCm and IpaD by T3SS
- resists phagocytosis by inducing apoptosis
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what molecule is released by shigella during apoptosis and how does it cause damage to colon
IL-18 which attracts polymorphonuclear leukocytes (PMNs) that destabilize integrity of intestinal wall, allowing for more shigella cells to cross the epithelial barrier and reach deeper tissues
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describe the shiga toxin
- A-B enterotoxin
- disrupts protein synthesis by cleaving ribosome
- toxin activity primarily damages epithelium
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what is the reservoir for shigella
only humans
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how is shigellosis transmitted
- low inoculum
- transmitted person to person, fecal-oral in low sanitary and personal hygiene standards
- occurs mainly in day care centers, nurseries,
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what is shigellosis and symptoms
- enterocolitis, a pediatric disease
- profuse watery diarrhea
- cramps
- tenesmus (straining to defecate)
- pus and blood in stool
- can progress to severe shigella dysenteriae
- symptoms occur 1-3 days after ingestion
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what is the sample to analyze shigella cases
stool
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how is shigella treated
antibiotic therapy
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klebsiella significant physiology
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what disease does klebsiella pneumoniae and klebsiella oxytoca cause
- necrotic destruction of alveolar spaces
- cavitation
- production of blood tinged sputum
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what does klebsiella granulomatis cause
- granuloma inguinale
- transmitted by sex or nonsexual trauma to genitalia
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what disease does klebsiella rhinoscleromatis cause
granulomatous disease of nose
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what disease does klebsiella ozaenae cause
chronic atrophic rhinitis
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what disease does proteus mirabils cause
- UTI
- infections in bladder or kidney
- produces large quantities of urease which increases pH of urine and kidney stones
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are proteus species motile
yes they swarm
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what is the clinical significance of enterobacter
- nosocomial infections affecting neonates or immunocompromised pts
- can colonize any body site
- linked to surgical wounds or pts who stay in ICUs
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what is the clinical significance of citrobacter
- nosocomial infections
- affecting neonates and immunocompromised patients
- causes meningitis and brain abscess in neonates
- UTI
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what is the clinical significance of morganella
- nosocomial
- UTI
- wound infections
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what is the clinical signficance of serratia
- nosocomial
- colonizes urinary and respiratory tracts
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what are the tests used to detect shiga toxin or shiga toxin genes
- immunoassays
- molecular probes
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