Enterobacteriaceae Flashcards
Enterobacteriaceae
Category of bacteria residing in the GI tract (mostly) of humans and animals.
Enterobacteriaceae overt pathogens
Salmonella, shigella, yersinia, campylobacter and helicobacter
Enterobacteriaceae opportunistic pathogens (and commensals)
Escherisichia, klebsiella, enterobacter, Serratia, and proteus,
5 major factors of all Enterobacteriaceae
- All facultative anaerobes
- All ferment glucose (dextrose)
- All reduce nitrates to nitrites
- All are oxidase negative
- All except klebsiella, shigella and yersinia are motile
Enterobacteriaceae virulence and antigenic factors
Endotoxin, capsule, antigenic phase variation, sequestration of growth factors (any nutrient it can’t make itself), resistance to serum killing, antimicrobial resistance
Watery diarrhea
3 or more liquid stools within 24 hours; liquid stool with no inflammatory cells (PMN)
Inflammatory diarrhea
3 or more liquid stools within 24 hours, with PMN cells, mucus and possibly small amounts of blood
Dysentery
Inflammatory diarrhea with blood, mucus, and tissue in stool (extreme form of inflammatory diarrhea)
Bloody diarrhea
Brick red. Implies the presence of whole blood in the stool, without evidence of inflammation (no PMN)
Enterobacteriaceae diarrhea diagnosis
Look for fecal leukocytes
(20+ per high power field, 80% PMN)= inflammatory (Shigella)
Few fecal leukocytes with watery diarrhea= bacterial OR viral
Enterobacteriaceae diarrhea treatment
Sulfa/trimethoprim (or ciprofloxacin, but has harsh side effects)
May not require antibiotic and may make things worse (like in hemorrhagic E.Coli infection)
Electrolyte replacement and supportive therapy
Escherichia Coli fermenting ability
Ferments lactose, glucose, and xylose (by-products include acid and CO2)
Escherichia Coli motility
Motile
Escherichia Coli diseases
Wide range, but major cause of neonatal meningitis and septicemia, gastroenteritis, urinary tract infections and wound infections
5 types of Escherichia Coli GI infections
- Enteropathogenic (EPEC)
- Enterotoxigenic (ETEC)
- Enteroinvasive (EIEC)
- Enterohemorrhagic (EHEC)
- Enteroaggregative (EaggEC)
Enteropathogenic Escherichia Coli infection
Symptoms:
usually in hospital nurseries/ daycare
Watery diarrhea with mucous (no blood)
Fever and vomiting
Enteropathogenic Escherichia Coli infection
Diagnosis and treatment
Serotyping Rehydration therapy (no antibiotic intervention)
Enteropathogenic Escherichia Coli infection
Disease mechanism/ virulence factors
Virulence factor: bundle forming pili and intimin
- bacteria bind to cells with bundle forming pili, intimin allows tighter adherence. Results in effacement of enterocytes
Enterotoxigenic Escherichia Coli infection (ETEC)
Symptoms
Traveler’s diarrhea, diarrhea in malnourished infants (montezuma’s revenge)
Watery diarrhea, nausea, abdominal cramps, low-grade fever
Enterotoxigenic Escherichia Coli infection (ETEC)
Virulence factors
Adhere to small intestine via pilli (CFA 1 and 2)
And secrete heat stable (ST) or heat label (LT) toxin—> plasmid encoded necessary for disease. Messes with cAMP levels and causes hypersecretion of fluids and electrolytes
Enterotoxigenic Escherichia Coli infection (ETEC)
Treatment
TMP (trimethoprim) or SMX (sulfamethoxazole) and rehydration. Clam stomach with rice water!
Prophylaxis with doxycycline or high-dose peptobismol
Enteroinvasive Escherichia Coli infection (EIEC)
Symptoms
Found mostly in 3rd world in contaminated food and water
mild diarrhea to dysentery: watery, mucous, blood
Fever, abdominal cramps, malaise and toxemia
Enteroinvasive Escherichia Coli infection (EIEC)
Virulence
After attaching to colonic mucosa, Cells invade the mucosa and lamina propria (NO TOXINS PRODUCED)
Does not ferment lactose: identified via DNA probes
Moves from cell to cell like listeria (using cell’s cytoskeleton)
Enteroinvasive Escherichia Coli infection (EIEC)
Treatment
TMP (trimethoprim) or SMX (sulfamethoxazole) and rehydration. Clam stomach with rice water!
Prophylaxis with doxycycline or high-dose peptobismol
Enteroaggregative E. Coli (EaggEC) infection
Symptoms
Persistent watery diarrhea, low grade fever, vomiting, dehydration if no fluid replacement
Enteroaggregative E. Coli (EaggEC) infection
Virulence
Bacteria adhere to discrete areas and clump “like stacked bricks”
Release shigella-like toxin called EAST (entero aggregating stable toxin)0 causes mucosal cells to swell and RBC to coagulate in intestinal capillaries
Enteroaggregative E. Coli (EaggEC) infection
Treatment
Treat the same as for ETEC and EIEC
Enterohemorrhagic E. Coli (EaggEC) infection
Symptoms
Cattle are primary reservoir, as well as contaminated produce in US
4 days post exposure: watery diarrhea and cramps. Then 40% develop copious bloody diarrhea and even worse cramping. Usually no fever
10% develop hemolytic uremic syndrome w/ acute renal failure
Enteroaggregative E. Coli (EaggEC) infection
Virulence factors
After attaching, secrete verotoxin 1 and 2
- verotoxin 1: just like shigella toxin. Inhibits protein synthesis and results in cell death
- verotoxin 2: structurally different but functionally the same
Enteroaggregative E. Coli (EaggEC) infection
treatment
Same as ETEC, EIEC and EaggEC, but fluoroquinolones (siprofloxin) can worsen the disease by activating phage.
Bacteriophage can integrate into host chromosome (will kill cells)
Hemolytic uremic syndrome (HUS)
Caused by EHEC. Blood vessels in epithelium of glomeruli damaged by toxin. Causes kidney failure and platelet lysis (thrombocytopenia)
Treatments can include transfusions and dialysis
Lethal in 5-10%, neurological deficits in 5-10%
Uropathogenic E. Coli
Recurrent bladder infections due to pod-like formations protecting bacterial colonies in bladder epithelial cells.
Can lead to acute cystitis (bladder infection) and pyelonephritis (kidney infection)
Klebsiella
Opportunistic capsule-protected bacteria
One of the leading causes of drug resistant nosocomial infections
(Causes pneumonia, as well as bacteremia, meningitis, wound infections, and UTI’s)
Enterobacter
Ubiquitous soil/ plant bacteria, as well as digestive tracts of animals and humans
Can contaminated dairy products (opportunistic infectsions)
Causes opportunistic nosocomial infections in immunocompromised patients
Almost never see community acquired infections of this strain
Proteus
Facultative anaerobe
Proteus mirabilis most commonly seen in human disease
Highly motile with tendency to swarm. Urinary tract infections in those with catheters and other indwelling units
Resistant to many antimicrobial drugs
Common characteristics of Salmonella, shigella, and yersinia
Overt pathogens
Produces type 3 secretion systems (hypodermic meddle type protein insertion into host cell)
Proteins inhibit phagocytosis, rearrange cytoskeleton (cell to cell motility) and induce apoptosis
Salmonella general characteristics
Resistant to bile salts and produce H2S!
Motile gram negative facultative anaerobes
DO NOT ferment lactose
Salmonella transmission
Animals main reservoir
Ingestion of contaminated food (eggs and poultry)
Fecal-oral route (especially in children)
Disease of consumption
Clinical syndromes of salmonealla
Generic= salmonellosis Enteritis= acute gastroenteritis Enteric fever= severe form is typhoid fever Septicemia Asymptomatic carriage
Salmonella enteritis
Most common form of salmonellosis
High infectious dose
6-48hr incubation period
Nausea, vomiting, non-bloody diarrhea, fever, cramps, myalgia (tiredness), headache common
Salmonella enteritis virulence factors
Due to invasive ness, intracellular survival and multiplication in macrophages, and endotoxin lipid A
Events in salmonellosis (non-typhoid)
- Penetrate mucus,
- Internalized into GI M-cells, and multiply
- PMN’s take up, to confine infection to GI, but travel in macrophages to other areas
- Inflammatory response (and cAMP) causes diarrheal symptoms
Salmonella enteric fevers
Slightly lower infectious dose (10^6 vs 10^8)
10-14 day incubation period. Show signs signs of sepsis w/ week+ long fever BEFORE abdominal symptoms come in. Fever break and build nearly every day, climbing up to a peak of 104-105ºF
Colonize in liver, spleen and BONE MARROW as mode of sepsis
Lipid A cause of fever (pyrogenic)
Asymptomatic carriers
Chronic carriage in 1-5% of cases—> shedding of bacteria in feces up to 20 weeks after symptoms clear up. Gall bladder main reservoir. Chronic carriage very very rare («1% of cases)
Salmonella syndromes treatment
Enteritis: supportive care (antibiotics not recommended)
Enteric fever: antibiotics, mostly to avoid carrier state
Vaccination can reduce risk of disease for travelers to endemic areas
Shigella strains
Shigella Sonnei: most common in industrial world
Shigella flexneri: most common in developing world
Shigella boydiii
Shigella dysenteriae: greatest clinical impact/ most dangerous
Shigella diagnostic characteristics
Non-lactose fermenting Gram-negative facultative anaerobe Resistant to bile salts Low infectious dose (10-100 organisms!) Humans only reservoir
Shigella transmission
Person to person, fecal-oral route
At-risk people: children, daycares, nurseries; male homosexuals;
Incubation period: 1-3 days
Shigella clinical presentation
Watery diarrhea (can develop into dysentery) Leading cause of infant diarrhea and mortality due to rapid dehydration. Inflammation of intestines (especially colon) with severe abdominal cramps, straining to defecate (tenesmus) and low-volume stools containing blood, mucus, and fecal leukocytes
Shigella invasion
- Shigella attaches to M cell. Endocytosis
- Bacteria lyses phagosome and replicates in the cell
- Develops actin tails to move cell to cell- cell to cell engulfment
- Causes apoptosis of PMN’s to reinfect
- Loss of epithelial cells destroys the integrity of the mucosal surface
- Red blood cells leak into the lumen, resulting in bloody diarrhea
Shigella virulence factors
-Invasiveness: attachment and internalization, and a large virulence plasmid
-Exotoxins: enterotoxin, neurotoxin, and cytotoxin
AB type toxin (binding and action)
Similar to shiga-like toxin encoded by lysogenic bacteriophage
Yersinia gram stain
Gram negative
Yersinia oxygen requirements
Facultative anaerobe
Yersinia oxidase usage
Oxidase negative
3 most important Yersinia species
Yersinia pestis (plague) Yersinia enterocolitica (enteropathogenic) Yersinia pseudotuberculosis (enteropathogenic)
Yersinia enterocolitica and Yersinia pseudotuberculosis acquisition
Ingestion of contaminated food
Yersinia enterocolitica and Yersinia pseudotuberculosis reservoirs
Rodents and domestic animals
Yersinia enterocolitica and Yersinia pseudotuberculosis diseases
Yersinia enterocolitica commonly causes a disease in humans, Yersinia pseudotuberculosis commonly is a disease of other animals
Yersinia enterocolitica and Yersinia pseudotuberculosis disease symptoms
Both cause fever and abdominal pain, but ENTEROCOLITICA causes bloody diarrhea
Yersinia enterocolitica and Yersinia pseudotuberculosis disease process
Bacteria invade the intestinal epithelium by invasion of M cells. They are then released at the basal surface, where they can invade the underlying lymphoid tissue (multiplying both inside and outside host cells)
Yersinia enterocolitica and Yersinia pseudotuberculosis serological identification
Side agglutination to identify cultures with specific antibodies based on the “O”-antigen
Yersinia enterocolitica and Yersinia pseudotuberculosis treatment
Mild-diarrheal disease is self-limiting and can often be treated at home with the help of fluids.
For severe cases (meningitis/ sepsis) antibiotic treatment should be started as soon as possible (rosephrin and streptomycin)
Yersinia enterocolitica and Yersinia pseudotuberculosis prevention
No preventative measures available beyond general hygiene
Yersinia pestis Cell morphology
Tiny, gram-negative bacilli (unusual bipolar staining)
Yersinia pestis virulence factors
- Capsule and envelope proteins (protect against phagocytosis and foster intracellular growth)
- Coagulase- clots plasma
- Endotoxin- responsible for many of the damaging symptoms
- Murine toxin- causes edema and necrosis in mice and rats (has not been shown to play a role in human disease)
Yersinia pestis epidemiology/ history
Zoonotic infection- humans accidental hosts
Very very contagious and with a very short treatment window
Three epidemiological cycles of Yersinia pestis
Sylvatic (wild) plague
Urban (domestic) cycle of plague
Human cycle of plague
Sylvatic plague cycle
Wild rodents serve as the reservoir (prairie dogs, mice, rabbits etc.) with a wild rodent flea as the vector
urban cycle of plague
Reservoir: domestic (urban) black rat
Vector: oriental rat flea (xenopsylla Cheopis)
Human cycle of plague
Bubonic plague acquired from contact with either sylvatic or urban reservoirs (or arthropod vector bite)
- then further transmitted in human populations via airborne droplets to spread pneumonic plague
Bubonic plague (Yersinia pestis)
Swollen, painful lymph nodes, fever, septic shock in later stages (transmission= from vector to host through bite)
Pneumonic plague (Yersinia pestis)
Host-to-host transmission via inhaled bacterial material (cough)
Flu-like illness progressing to mucous, bloody sputum, dyspnea, cyanosis and is rapidly fatal
Bubonic plague pathology
- Very low infectious dose- travel in blood to nearest lymph node, where are taken up by macrophages. -Then lymph nodes (especially arm-pit and groin) swell as bacteria proliferate and stimulate inflammatory response.
- lysis of the bacteria leads to LPS release, causing septic shock. This toxin causes DIC (blood clots in capillaries and systemic bruising- hence Black Death)
Pneumonic plague pathology
Infection localized to the lungs, highly contagious, toxin permeates rapidly and is almost always fatal without treatment. Bacteria grows within macrophages.
Yersinia pestis treatment and prevention
Streptomycin, tetracycline, or chloramphenicol (and quarantine)
Vaccine not widely available but exists, and given in rare occasions
