Flashcards in GI Bacteria I and II Deck (82):
Where is there a dramatic increase in the flora present in the GI tract? What type of organisms are they?
-predominantly anaerobes and E. Coli
3 major mechanisms that lead to Gastroenteritis
1. ingestion of preformed toxin present in contaminated food
2. infection by toxigenic organisms, which proliferate in the gut lumen and elaborate an enterotoxin
3. infection by enteroinvasive organisms
Onsets of the 3 major mechanisms of gastroenteritis
1. ingestion of preformed toxin has rapid onset
2. infection by toxigenic organisms can have rapid or delayed onset of illness
3. infection by enteroinvasive organisms have delayed onset
Virtually all bacterial diarrheal diseases are treated with _________. Any exceptions?
-supportive care only
-exceptions are salmonella non-typhi in certain high risk. salmonella typhi always, Clostridium difficile, cholera, shigella
What causes Travelers' Diarrhea. How is it prevented and treated?
-ETEC as diagnosed by referral labs
-Drink only bottled beverages and steaming hot food when in endemic areas **no ice cubes in drinks**
-Treat via oral rehydration and potentially shorten its duration with antimicrobials and antimotility agents
Common prescriptions given for Travelers' Diarrhea
-fluoroquinolone +/- loperamide
Stool culture is the primary test for detection of what bacteria?
What is a common transport medium of stools called?
-contains inhibitors of Gram + bacterial growth (bile salts and CV), lactose, peptone, and pH indicator
Role of lactose, peptone, and bile salts of MacConkey Agar
-bile salts and Cv inhibit gram positive growth
-lactose: lactose fermentors use lactose, produce acid, lower pH, and make colonies pink/red.
-peptone: utilized by non-lactose fermenters, produce ammonia, raise pH, and make clear colonies
Sorbitol MacConkey helps identify ____________. How?
-shiga toxin producing EHEC
-by including sorbitol, which these strains cannot utilize so they grow as white circular colonies
-curved, gram negative, flagellated rod- rapidly motile
-secretes cholera toxin
Where does V. cholerae colonize, what does it secrete, and what is its action?
-proximal small intestine
-secretes cholera toxin
-CT increases intracellular cAMP in intestinal epithelial cells leading to increased secretion of chloride ions and decreases Na absorption--water flows out and causes diarrhea
V. cholera needs to survive harsh stomach acids to reach lumen of small intestine where it infects individuals. What can one infer about the inoculation size needed? What kinds of patients may be at higher risk?
-patients on medication for reduced stomach acid production
V. cholera can be found in water sources. Fresh or salt water?
Structure and mechanism of cholera toxin
-carried by CTXphi phage
-2 subunit toxin with the A subunit being catalytic/pathological portion
-toxin enters cell, retrograde transport through golgi and ER, A1 subunit acts of AC, increase cAMP, increase PKA activity which phosphorylates CFTR and get copious Cl-secretion and diarrhea
Transmission of cholera
-fecal-oral transmission via contaminated food or water
Subclinical infection of cholera effects
-short-term excretion following mild or subclinical infection
-majority of cases are subclinical
-lower stomach acidity
-leads to increases severed and lowers infectious dose
Can V. Cholera survive outside of a human host? If yes, what are its reservoirs?
-copepods, shellfish, algae, water hyacinths
-needs estuarine environments where there's mixing of salt and fresh water
Symptoms of severe dehydration due to V. Cholera infection
-loss of skin turgor (sign of severe dehydration)-aka skin tenting
-rice water stools: straw like color and flecks of intestinal mucus
How does one treat cholera?
-by replenishing fluids and electrolytes that are lost in the stool
-WHO formula oral rehydration salts
-addition of glucose to stimulate Na uptake
-Ringer's lactate via IV
Tetracycline treatment can shorten duration of diarrhea in V. cholera infections, but why is this not the first line of defense?
-patients may die from dehydration before antibiotics can work
-rehydration is the most important therapy
What is the leading bacterial cause of seafood-associated gastroenteritis in the US?
-multiple outbreaks in coastal states associated with crabs, oysters, shrimp
Symptoms of Vibrio parahaemolyticus infection
-watery, self-limited diarrhea with cramps, nausea, vomiting, sometimes bloody diarrhea
-wound infection after exposure to warm seawater are also seen
When do vibrio parahaemolyticus infections peak?
-when seafood becomes more regular
2 methods of acquiring Vibrio vulnificus infection
1. ingesting raw seafood
2. wound infection after exposure to seawater during warm months
Vibrio vulnificus wound infection: symptoms and progression
1. cellulitis, sometimes with vesicles or bullae follwed by necrosis
2. sometimes progresses to bactermemia and death, particularly in those with liver disease
3. often after exposure of wound to seawater during warm months
Vibrio vulnificus "primary sepsis": how does one get it? symptoms?
-infected by eating raw seafood
-organism invades bloodstream from the intestine causing a syndrome characterized by fever, chills, prostration, and hypotension
-usually have secondary skin lesions on the extremities, with erythematous or ecchymotic areas-vesicles or bullae- necrotic ulcers
-high death rate -50-60%
Who is most at risk for primary sepsis from Vibrio vulnificus?
-people with pre-existing hepatic or other chronic disease
-Cirrhosis, AIDS, malignancy, hemochromatosis, immunosuppressive meds
-estrogen can be protective, so more than 90% of cases in males
Enterobacteriaceae is a large family of what kind of bacteria?
-gram negative rods found mostly, but not exclusively, in the gut lumen where they live as facultative anaerobes
True/False: all strains of E.coli cause diarrhea.
false; have extraintestinal and diarrheagenic strains
-important in developing countries: children, travelers
-plasmic virulence factors
2 plasmid virulence factors of ETEC
1. Heat-labile enterotoxin: same mechanism of cholera toxin; raise cAMP, resulting in intense and prolonged hypersecretion of Cl and Water, while also inhibiting Na absorption
2. Heat-stable enterotoxin:
strain with both toxins associated with more severe disease
How is ETEC transmitted?
EPEC is usually seen in what patient population?
-infants in developing countries
Signs and symptoms of EPEC infection
-watery diarrhea and vomiting (fever sometimes)
-usually short duration, but can be protracted and deadly
-atypical strains emerging in developed countries with chronic diarrhea
Transmission of EPEC
-person to person
-why it can occasionally cause outbreaks in infant daycares in US
EHEC (enterohemorrhagic E. Coli) reservoir and how/where people can acquire it?
-reservoir is cattle
-contaminated food: ground beef, produce, juice
-water: drinking, swimming
Does EHEC need a low or high inoculum?
-Shiga toxin that injured intestinal cell walls and blood vessels leading to bleeding
-once in blood stream the toxin damages other vessels, especially those in the kidney leading to kidney failure
-diarrhea is this main issue, it is the damage to other organs
Shiga toxin encoding and structure
-encoded by lambda-like bacteriophages
-5 identical B, 1 A subunit
Mechanism and action of shiga toxin
-B subunits bind GB3 which is present on many cell types
-transported retrograde to ER
-A subunit is an N-glycosidase
-depurinates 28S ribosomal subunit
-PROTEIN SYNTHESIS CEASES
What is the most common cause of renal failure in children?
Hemolytic-Uremic Syndrome can follow what infection? what is it?
-thrombotic microangiopathy: blocking small blood vessels due to parts of destroyed RBCs
-can affect any organ
Risk factors of hemolytic-uremic syndrome
Enteroaggregative E.Coli (EAEC) epidemiology
-childhood diarrhea in developing countries: can be persistant, associated with growth retardation
-Emerging pathogen in developed countries
Clinical features of EAEC
-mucous with/without blood
Describe Shigella species bacterium
-oxidase-negative, non-motile, appears as non-lactose fermenter on MacConkey agar
How many species of Shigella? Which is most common in the US?
-S. dysenteriae Serogroup A
-S. flexneri serogroup B
-S. boydii Serogroup C
-S. sonnei Serogroup D** most common in US
Symptoms of Shigella species and how infectious is it?
-HIGHLY infection: ~10 organisms
-locally invasive organism, fever, abdominal cramps, bloody/mucoid diarrhea
Is Shigella found outside of humans?
Describe Shigella enterocolitis
-pale, granular and inflamed mucosa with patches of coagulated exudate
-massive recruitments of PMNs inducing rupture of epithelial barrier
Cellular pathogenesis of Shigella. How does it cross the epithelial barrier? What happens once inside?
-translocation by the bacteriun of the intestinal epithelium and development of the infectious process leads to bacillary dysenteru
-cross M cells as well
-taken up by macrophages in which they induce apoptosis which produced proinflammatory cytokines and PMN recruitment
-enter enterocytes basolaterally
T/F: Shigella is invasive, and therefore, causes bacteremia.
False; no bacteremia
-non-lactose fermenter on MacConkey agar
2 types of salmonella to watch out for
Transmission of salmonella
-leading foodborne pathogen
Reservoirs and infectious dose of salmonella
-many host reservoirs (birds, mammals, reptiles, amphibians)
-infectious dose is large
Symptoms of salmonella typhi
-bacteremia, fever, systemic dissemination constitute typhoid fever
-may result in chronic infection of biliary tree, joints, bones, meninges
Salmonella pathogenesis mechanism
-enter GI by ingestion of contaminated food
-attach to M cells or pass between cells
-cause influx of immune cells (can survive inside macrophages or kill them)
Ultimate control of salmonella infection requires _________.
-functioning T/B cells, liver, and spleen
-salmonella lives within macrophages (doesn't leave them like shigella) and traffics with macrophages to lymphatic sites
Salmonella injects efforts via what system and what is their effect?
-by type III secretion system
-rearrange actin cytoskeleton
Typhoidal vs. Non-typhoidal (Typhimurium) Salmonella invasive disease
S.typhi bacteremic spread in immunocompetent hosts (enteric fever)
S. non-typhi bacteremic spread in immunocompromised hosts with greater immune activation (neutrophila and septic shock)
Symptoms of Salmonella enteriditis
-gastroenteritis, enteric fever, endovascular infections, focal metastatic infections (osteo, abscess), asymptomatic
-curved, gram negative (sea gull shaped)
-flagellated (motility important for colonization and virulence)
-extensive genetic variation
Extensive genetic variation of Campylobacter
-intra and extragenomic recombination
-variable LOS, variable capsule, flagellin modifications
-water and animals
-commensal in avian GI tract and pathogen in human GI tract
-huge foodborne pathogen via poultry
Campylobacter jejuni enteritis treatment and OTHER diseases
-can be managed with antibiotics if caught early
-oral replacement with fluids and electrolytes
-can cause Guillain-Barre syndrome
Symptoms of C. jejuni
-may have fever, no abdominal pain, diarrhea
-can be acquired from C. jejuni by virtue of cross-reacting surface antigens
-most common cause of acute neuromuscular paralysis
-some LOS structures trigger antibodies that cross-react with gangliosides
When do GBS appear?
-about 1-3 weeks after infection with C. jejuni
-obligate spore forming, anaerobe
When does one usually see a Clostrodium difficile break out? What locations can this happen in?
-after antibiotic treatment
-antibiotic associated diarrhea, pseudomembranous colitis
-can cause community and hospital acquired infections
Spectrum of illness for Clostrodium difficile
-mild to severe diarrhea, fever, abdominal cramping, leukocytosis
Natural history of C.difficile transmission
-spores ubiquitous in environment, and are ingested
-spores quiscent in colon
-perturbation of gut flora means increased nutrients for spores
-germination of spores and toxin production
What causes the diarrhea and inflammation in CDI (C. difficile infection)
-Toxin A and B
-not readily cultures bc present in low numbers
-detect via toxins presence: ELISA to see if glutamate Dh is present, and if it is, PCR for genes for toxins
CDI and treatment
-mild disease needs no treatment
-moderate disease may require some therapy (bloody stool, but not severe CDI)
-Severe disease uses Vancomyocin (oral, not IV) or Metronidazole
Major sites for anaerobes
-female genital tract
-spore-formers may be in gut, but more common in "soil"
Pathogenesis of anerobic infection
-generally results from disruption of mucosal surface followed by infiltration of resident flora into a sterile site