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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?

-Large bowel
-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?



MacConkey Agar

-semi-selective agar
-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


Vibrio cholerae

-causes cholera
-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?

-larger inoculation
-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

-sunked eyeballs
-wrinkled fingers
-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?

-Vibrio parahaemolyticus
-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


ETEC features

-important in developing countries: children, travelers
-watery diarrhea
-short duration
-fecal-oral route
-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?

-fecal-oral route


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
-petting zoos
-person-to-person transmission


Does EHEC need a low or high inoculum?



EHEC pathogenesis

-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


What is the most common cause of renal failure in children?

-Hemolytic-uremic syndrome


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

-WBC count
-anti-motility agents


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

-watery diarrhea
-mucous with/without blood
-intestinal colic
-growth retardation


Describe Shigella species bacterium

-Gram-negative rods
-facultative anaerobe
-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

-acute inflammation
-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


Salmonella description

-gram-negative rod
-oxidase negative
-non-lactose fermenter on MacConkey agar


2 types of salmonella to watch out for

Salmonella enteritidis
Salmonella Typhi


Transmission of salmonella

-fecal-oral pathogen
-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


Campylobacter reservoirs

-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


Guillain-Barre Syndrome

-ascending paralysis
-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


Clostrodium difficile

-gram-positive bacillus
-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


CDI diagnosis

-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

-oral cavity
-GI tract
-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


There are many species of anaerobes. Thus, most anaerobic infections are ________.