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61 Cards in this Set
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Campylobacter phys/structure
Gram Shape Motility Fermentation? Catalase? Oxidase? Colony morphology Growth temp Growth time |
Gram neg
spiral shaped bacilli (S, comma, sea gull, ribbon shapes) Motile- has polar flagellum Microaerobic- req 5-8% O2 Non-fermenter Oxidase pos Catalase pos Small, convex, circular colonies Grow at 37-42C; no growth at 25 (C. jejuni) Takes 2-3 days to grow |
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Campylobacter virulence factors
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Cytolethal distending toxin
LPS OMPs: Enterotoxin Hemolysin Flagella Chemotaxis S protein in C. fetus |
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Cytolethal distending toxin
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blocks cells in G2 phase
cells slowly distend and die |
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LPS
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causes local inflammation
not as endotoxic as other enterics |
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Flagella
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important for motility in viscous environement and adherence
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Chemotaxis toward?
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mucins
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S protein
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C. fetus only
capsule-like protein that covers bact prevents C3b binding and prevents complement-mediated killing by serum allows C. fetus to spread from GI tract go blood/distant foci |
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Campylobacter epidemiology
hosts? how humans acquire it? what can decrease infective dose? human-human transmission? in what setting? how commonly does C. jejuni cause diarrhea? |
zoonotic, hosts - cows & poultry
acquired thru consumption of contaminated food, milk, or water foods(milk) & meds that decrease gastric acid secretion lower infective dose required human to human transmission via fecal-oral route (daycares) C. jejuni is MC cause of diarrhea on all 6 continents |
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Campylobacter pathology/immunity
probability of disease is influenced by? what kills campylobacter in the body? what affects severity of disease? |
probability of disease is influenced by dose
gastric acid kills it immune status affects severity (less severe in endemic areas (underdeveloped) b/c they have Abs, more severe in people w/hypergammaglobunlinemia) |
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campylobacter GI disease
causes what 4 things? these are signs of what? |
damage to mucosal surface of jejunum, ileum, and colon
mucosal surface is ulcerated, edematous, bloody crypt abscesses in epithelial glands infiltration of PMNs, macs, and esoinophils into lamina propria these are all signs of tissue invasion |
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Campylobacter in underdeveloped countries
when is it common severity of disease? |
symptomatic disease occurs in young children
adults have persistent, asymptomatic carriage people have Abs to it and thus have less severe disease (simple diarrhea only) |
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Campylobacter in developed countries
what is responsible for most infections? how many cases/yr in US? most common in what time of year? most common in what age group? severity of disease? |
contaminated poultry accts for 1/2 of C. jejuni/coli infection
C. upsaliensis is acquired from dogs 2.5 mill cases/year most common in warm months (but occurs throughout year) disease is severe (inflammatory diarrhea) most common in young adults |
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Reiter's syndrome
what is it? associated w/what genotype? when does it occur? |
a subtype of reactive arthritis
associated w/HLA B27 genotype occurs several wks after initial infection, can last several mos/yrs w/recurrences |
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Guillan-Barre Syndrome
what's the pathology? when does it develop? occurs w/what serotypes? |
peripheral neuropathy- autoimmune
antigenic cross-reactivity between oligosaccharide in bact. capsule and glycosphingolipids on surface of neural tissue occurs w/C. jejuni O:19 develops several days-wks after diarrhea begins, and symmetrical weakness develops over a period of days |
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C. fetus
how common? occurs in what groups of people? primarily what type of pathogen? what complications can occur? Most human infections are what? Thermophilia? Nalidixic acid reaction? Hydrolysis of hippurate? Treatment |
relatively uncommon
occurs in immunocompromised elderly adults (opportunistic) primarily a veterinary pathogen (causes fetal infection & abortion) can cause extra-intestinal infection, septic abortions in pregnant females Most human infections are systemic Non-thermophilic, Nalidixic acid-resistant, doesn't hydrolyze hippurate treatment- erythromycin, azithromycin |
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Diagnosis of campylobacter
Definitive diagnosis is via? What media? oxygen/CO2 requirement? Temp requirement? Growth speed? fermentation? oxidase/catalase? urease? nitrate 6? hippurate hydrolysis |
definitive diagnosis is by detection of organism
specialized media microaerophilic (reduced O2, increased CO2) Elevated temp (42) Slow growth (mean 3 days) non-fermenter oxidase & catalase pos nitrate 6 pos hippurate hydrolysis pos |
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Treatment:
gastroenteritis? severe gastroenteritis and septicemia? what Abx is it resistant to? |
gastroent. is usu self- limiting, manage w/fluid & electrolyte replacement
severe gastro/septicemia- tx w/erythromycin or azithromyin (second line is tetracyclin or quinolones) Bact are B-lactam resistant aso are showing increased resistance to fluoroquinolones (eg cipro) used for travelers diarrhea |
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Campylobacter clinical disease
infectious dose? asymptomatic disease- common where? |
Low infectious dose (500 bact / drop of chicken juice)
asymptomatc disease common in underdeveloped countries |
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Campylobacter GI disease
how soon does diarrhea set in? mode of transmission? affected population? stages of disease |
diarrhea onset is 16-48 hours usually (anywhere from 1-7 days)
transmission is via consumption affected population- young adults in US stages: prodromal diarrheal recovery |
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Campylobacter prodromal stage
onset? symptoms? |
abrubt onset
cramping abdominal pains acute enteritis (diarrhea, malaise, fever, myalgia)- can resemble flu-like symptoms |
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Diarrheal stage of campylobacter
# of stools/day nausea/vomiting? what can pain mimic? what can be present in stools? how long does it last? what other symtpoms/complications can arise? |
>50% of pts have >10 stools/day
nausea frequent, <10% have vomiting pain may mimic appendicitis stools may contain blood, mucus, & leukocytes self-limiting, but may last for week or more other Sx can include colitis, acute abdominal pain, septicemia |
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Recovery stage
how long into illness does it take for Sx to subside? how long can organisms be isolated from stool after Sx resolve? can chronic infections develop? |
3-4 days into illness, Sx begin to subside
can isolate stool for wks after Sx chronic infections can develop |
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Most common food borne pathogen?
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campylobacter, then salmonella, then shigella
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C. upsalialensis
catalase? thermophilia? how acquired? what does it cause in animals? what kind of people might it infect? |
catalase negative (or weakly pos)
thermotolerant acquired from domestic dogs causes gastroenteritis & bacteremia in animals opportunistic infections in immunocompromised |
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3 Helicobacter spp
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H. pylori
H. cinaedi H. fennelliae |
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H. pylori
hosts human disease caused frequency |
humans, pigs, primates (humans are the only significant reservoirs)
gastritis, peptic ulcers, gastric adenocarcinoma, MALT B-cell lymphoma common |
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H. cinaedi
hosts human disease caused frequency |
humans, hamsters
gastroenteritis, septicemia, procolitis, cellulitis uncommon |
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H. fennelliae
hosts human disease caused frequency |
humans
gastroenteritis, septicemia, procolitis uncommon |
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Helicobacter physiology/structure
gram? shape? motility/flagella? stomach helicobacters produce? oxygen requirement? fermentation? oxidase? catalase? media required? colony morphology? growth temp? growth time? |
Gram neg
spiral bacilli when young, coccoid when old highly motile- corkscrew motility w/4-6 polar flagella stomach spp make urease microaerobic- 5-8% O2 non-fermenters oxidase pos, catalase pos supplement media w/blood, hemin or charcoal (protects from free O2 radicals, H2O2, & fatty acids) small, convex, circular colonies growth temp 30-37 growth time- 2-3 days |
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H. cinaedi & H. fennellae
where do they colonize what do they cause? in what populations? HIV+ homosexual males may present with? |
colonize the intestinal tract (enterohepatic helicobacters)
cause gastroenteritis/bacteremia in immunocompromised pts HIV males may present w/proctitis, proctocolitis, and enteritis |
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H. pylori
characteristics of disease |
gastric inflammation
altered gastric acid secretion tissue damage |
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H. pylori epidemiology
first isolated? source of infection? prevalence? what % of pop are colonized in developing countries? fraction of worlds pop? % of US adults colonized? |
first isolated from culture 1984
humans are only source of infection most common chronic bacterial infection of humans 87-90% of people in developing countries 2/3 of worlds population 30-50% of US adults colonized |
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Difference in colonization between developing countries and developed countries?
due to what? |
Developing- 70-90% are colonized, most colonized before the age of10
Developed- incidence low during childhood, ~45% of adults difference due to hygiene |
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What % of pts w/gastritis, gastric ulcers, of duodenal ulcers are infected w/H. pylori?
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70-100%
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H. pylori transmission routes- 3
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fecal-oral route: fecal contamination
oral-oral route: dental plaque & saliva gastro-oral route: contaminated vomit |
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H. pylori is associated w/protection from what 2 diseases?
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gastroesophageal reflux
adenocarcinomas of esophagus and gastric cardia |
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H. pylori initial colonization- 3 steps
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1. bacterial acid-inhibitory protein blocks stomach acid production
2. urease neutralized gastric acid by breaking urea down into CO2 and ammonia (enhanced by HspB) 3. actively motile bacteria pass thru mucus and ahdere to gastric epithelial cells |
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H. pylori adherence
do most pylori adhere or not? adherence is specific forwhat? where is adherence restricted to in stomach? (unless what) |
most H. pylori found in mucus, only a few adhere
adherence is specific for gastric epithelium adherence restricted to less acidic antrum (unless pts are on long-term acid suppression therapy) |
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local tissue damage of H.pylori is mediated by? (4 things)
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urease byproducts
mucinases phospholipases vacuolating cytotoxin (VacA)- damages cells by making vacuoles |
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H. pylori is protected from phagocytosis and intracellular killing by what two things?
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superoxide dismutase
catalase |
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H. pylori virulence factors (12)
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urease
HspB acid-inhibitory protein flagella adhesins mucinase phospholipids superoxide dismutase catalase vacuolating cytotoxin cytotoxin-associated genes (cag) Cag PAI |
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H. pylori- urease
function? neutralizes what? stimulates chemotaxis of what cells? stimulates production of what? |
hydrolyzes urea into ammonia & CO2
ammonia then neutralizes gastric acids and buffers cytosol stimulates chemotaxis of monocytes, PMNs stimulates production of inflammatory cytokines |
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H. pylori HspB
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enhances expression of urease
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H. pylori acid-inhibitory protein
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induces hypochlorhydria during acute infection by blocking acid secretion by parietal cells
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H. pylori flagella
function structure |
allow penetration into gastric mucus layer and protection from aid environment
membranous sheath: protection from stomach proteases capped by terminal bulbs: protect flagela from depolymerization in acid |
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H. pylori adhesins
function examples |
binding to host cells
ex: hemagglutinins, sialic acid binding proteins, lewis blood group antigens Lewis B-binding Adhesin- binds to lewis b histo-group antigen on gastric epithelial cells sialic acid binding adhesin- binds to sialyated lewis x-containing glycolipids on gastric epithelial cells |
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H. pylori- mucinase & phospholipid functions
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disrupts gastric mucus (reduce viscosity)
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H. pylori
Superoxide dismutase Catalase functions |
Superoxide- neutralizes oxygen metabolites, prevents phagocytic killing
catalase- neutralizes peroxides, prevents phagocytic killing |
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H. pylori vacuolating cytotoxin (VacA)
function does what to neutrophils critical for what for organism interferes w/what by host how does it help release nutrients to bact? |
induces vacuole formation in epithelial cells
stimulates neutrophil migration into mucus not critical for initial colonization, but is critical for promoting persistence interferes w/processing of antigens by host, thus helps resist clearance by immune system permeabilization of epithelial monolayer helps release nutrients to bacteria |
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H. pylori cytotoxin associated genes (cag)
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encodes a type IV secretion system that injects the cagA gene product into host epithelial cells
Cag A protein interferes w/normal cytoskeletal sturcture |
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Cag PAI (phosphoribosylanthranilate isomerase)
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induces IL-8 production which attracts neutrophils
neutrophils release proteases and ROS that may contribute to gastritis and gastric ulcers |
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Some other poorly defined aspects of H. pylori virulence
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stimulate gastric mucosal cells to produce PAF (stimulates gastric acid secretion)
induces nitric oxide synthase in gastric epithelial cells (mediates tissue injury) induces death of gastric epithelial cells |
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Peptic ulcer disease
what are two other causes symptoms severe symptoms |
NSAID use and autoimmune disease (cause 10% of PUD)
gnawing, burning upper abdominal pain between meals or at night Bloating Heart burn Nausea/vomiting Severe: Dark or black stool Vomiting blood Weight loss Severe pain |
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H. pylori- gastric adenocarcinoma
where does it rank in causes of all cancers? accts for what % of gastric cancers? |
second most common cause of cancer morbidity and mortality
95% of gastric cancers |
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H. pylori and MALT lymphoma
what % of gastric cancers H. pylori presence increases risk of developing lymphomas by how much? only known malignancy that what? |
5% of all gastric cancers (more in men)
H. pylori increases risk 6 fold only known malignancy for which regression occurs upon elimination of an invading microbe |
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H. pylori diagnosis
microscopy examine what section? what stain? specificity/sensitivity? |
examination of gastric biopsy
warthin-starry stain is most sensitive histologic examination is 100% specific/sensitive |
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H. pylori diagnosis
urease test benefits sensitivity/specificity |
rapid, can be measured directly from clinical specimen or after org has been isolated
high level of urease produced by h. pylori allows for detection w/in 2 hours sensitivity 75-95% specificity 100% so pos test is evidence of active infection |
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H. pylori diagnosis
culture catalase/oxidase/urease? growth conditions needed? |
cat/ox/urease pos
needs specialized media, microaerobic environment, 30-37 temp grow slowly - 2 or more days |
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H. pylori diagnosis
serology |
Humoral immune response persists as a result of continuous exposure to the bacteria.
Can persist for several years, so can not be used to distinguish between current and past infection Titer does not correspond to severity of disease or response to therapy HpSA Test (H. pylori stool antigen test): Measurement of H. pylori antigens excreted in stool of host |
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H. pylori treatment
triple therapy: duration |
bactericidal drug (two Abx)
acid reducers (H2 blockers block histamind binding, PPIs suppress pumping of acid into stomach) protective therapy: bismuth protects stomach lining duration: 2 wks more than 90% effective if pt is compliant |
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Drugs used to treat H. pylori ulcers
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Abx: Macrolide + B-lactam (eg, clarithromycin & amoxicillin)
Second line Abx: metronidazol, tetracyline H2 blockers: cimetidine PPI: omeprazole Stomach lining protector: bismuth subsalicylate resistance to metronidazole, clarithromycin, and tetracycline becoming more prevalent |
