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Medical Microbiology > Enterobacteriaceae > Flashcards

Enterobacteriaceae Flashcards

1
Q

Enterobacteriaceae

A

Category of bacteria residing in the GI tract (mostly) of humans and animals.

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2
Q

Enterobacteriaceae overt pathogens

A

Salmonella, shigella, yersinia, campylobacter and helicobacter

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3
Q

Enterobacteriaceae opportunistic pathogens (and commensals)

A

Escherisichia, klebsiella, enterobacter, Serratia, and proteus,

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4
Q

5 major factors of all Enterobacteriaceae

A
  1. All facultative anaerobes
  2. All ferment glucose (dextrose)
  3. All reduce nitrates to nitrites
  4. All are oxidase negative
  5. All except klebsiella, shigella and yersinia are motile
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5
Q

Enterobacteriaceae virulence and antigenic factors

A

Endotoxin, capsule, antigenic phase variation, sequestration of growth factors (any nutrient it can’t make itself), resistance to serum killing, antimicrobial resistance

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6
Q

Watery diarrhea

A

3 or more liquid stools within 24 hours; liquid stool with no inflammatory cells (PMN)

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7
Q

Inflammatory diarrhea

A

3 or more liquid stools within 24 hours, with PMN cells, mucus and possibly small amounts of blood

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8
Q

Dysentery

A

Inflammatory diarrhea with blood, mucus, and tissue in stool (extreme form of inflammatory diarrhea)

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9
Q

Bloody diarrhea

A

Brick red. Implies the presence of whole blood in the stool, without evidence of inflammation (no PMN)

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10
Q

Enterobacteriaceae diarrhea diagnosis

A

Look for fecal leukocytes
(20+ per high power field, 80% PMN)= inflammatory (Shigella)
Few fecal leukocytes with watery diarrhea= bacterial OR viral

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11
Q

Enterobacteriaceae diarrhea treatment

A

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

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12
Q

Escherichia Coli fermenting ability

A

Ferments lactose, glucose, and xylose (by-products include acid and CO2)

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13
Q

Escherichia Coli motility

A

Motile

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14
Q

Escherichia Coli diseases

A

Wide range, but major cause of neonatal meningitis and septicemia, gastroenteritis, urinary tract infections and wound infections

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15
Q

5 types of Escherichia Coli GI infections

A
  1. Enteropathogenic (EPEC)
  2. Enterotoxigenic (ETEC)
  3. Enteroinvasive (EIEC)
  4. Enterohemorrhagic (EHEC)
  5. Enteroaggregative (EaggEC)
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16
Q

Enteropathogenic Escherichia Coli infection

Symptoms:

A

usually in hospital nurseries/ daycare
Watery diarrhea with mucous (no blood)
Fever and vomiting

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17
Q

Enteropathogenic Escherichia Coli infection

Diagnosis and treatment

A 
Serotyping
Rehydration therapy (no antibiotic intervention)
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18
Q

Enteropathogenic Escherichia Coli infection

Disease mechanism/ virulence factors

A

Virulence factor: bundle forming pili and intimin
- bacteria bind to cells with bundle forming pili, intimin allows tighter adherence. Results in effacement of enterocytes

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19
Q

Enterotoxigenic Escherichia Coli infection (ETEC)

Symptoms

A

Traveler’s diarrhea, diarrhea in malnourished infants (montezuma’s revenge)
Watery diarrhea, nausea, abdominal cramps, low-grade fever

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20
Q

Enterotoxigenic Escherichia Coli infection (ETEC)

Virulence factors

A

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

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21
Q

Enterotoxigenic Escherichia Coli infection (ETEC)

Treatment

A

TMP (trimethoprim) or SMX (sulfamethoxazole) and rehydration. Clam stomach with rice water!
Prophylaxis with doxycycline or high-dose peptobismol

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22
Q

Enteroinvasive Escherichia Coli infection (EIEC)

Symptoms

A

Found mostly in 3rd world in contaminated food and water
mild diarrhea to dysentery: watery, mucous, blood
Fever, abdominal cramps, malaise and toxemia

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23
Q

Enteroinvasive Escherichia Coli infection (EIEC)

Virulence

A

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)

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24
Q

Enteroinvasive Escherichia Coli infection (EIEC)

Treatment

A

TMP (trimethoprim) or SMX (sulfamethoxazole) and rehydration. Clam stomach with rice water!
Prophylaxis with doxycycline or high-dose peptobismol

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25
Q

Enteroaggregative E. Coli (EaggEC) infection

Symptoms

A

Persistent watery diarrhea, low grade fever, vomiting, dehydration if no fluid replacement

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26
Q

Enteroaggregative E. Coli (EaggEC) infection

Virulence

A

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

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27
Q

Enteroaggregative E. Coli (EaggEC) infection

Treatment

A

Treat the same as for ETEC and EIEC

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28
Q

Enterohemorrhagic E. Coli (EaggEC) infection

Symptoms

A

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

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29
Q

Enteroaggregative E. Coli (EaggEC) infection

Virulence factors

A

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
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30
Q

Enteroaggregative E. Coli (EaggEC) infection

treatment

A

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)

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31
Q

Hemolytic uremic syndrome (HUS)

A

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%

32
Q

Uropathogenic E. Coli

A

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)

33
Q

Klebsiella

A

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)

34
Q

Enterobacter

A

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

35
Q

Proteus

A

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

36
Q

Common characteristics of Salmonella, shigella, and yersinia

A

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

37
Q

Salmonella general characteristics

A

Resistant to bile salts and produce H2S!
Motile gram negative facultative anaerobes
DO NOT ferment lactose

38
Q

Salmonella transmission

A

Animals main reservoir
Ingestion of contaminated food (eggs and poultry)
Fecal-oral route (especially in children)
Disease of consumption

39
Q

Clinical syndromes of salmonealla

A 
Generic= salmonellosis
Enteritis= acute gastroenteritis 
Enteric fever= severe form is typhoid fever
Septicemia 
Asymptomatic carriage
40
Q

Salmonella enteritis

A

Most common form of salmonellosis
High infectious dose
6-48hr incubation period
Nausea, vomiting, non-bloody diarrhea, fever, cramps, myalgia (tiredness), headache common

41
Q

Salmonella enteritis virulence factors

A

Due to invasive ness, intracellular survival and multiplication in macrophages, and endotoxin lipid A

42
Q

Events in salmonellosis (non-typhoid)

A
  1. Penetrate mucus,
  2. Internalized into GI M-cells, and multiply
  3. PMN’s take up, to confine infection to GI, but travel in macrophages to other areas
  4. Inflammatory response (and cAMP) causes diarrheal symptoms
43
Q

Salmonella enteric fevers

A

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)

44
Q

Asymptomatic carriers

A

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)

45
Q

Salmonella syndromes treatment

A

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

46
Q

Shigella strains

A

Shigella Sonnei: most common in industrial world
Shigella flexneri: most common in developing world
Shigella boydiii
Shigella dysenteriae: greatest clinical impact/ most dangerous

47
Q

Shigella diagnostic characteristics

A 
Non-lactose fermenting
Gram-negative facultative anaerobe
Resistant to bile salts
Low infectious dose (10-100 organisms!)
Humans only reservoir
48
Q

Shigella transmission

A

Person to person, fecal-oral route
At-risk people: children, daycares, nurseries; male homosexuals;
Incubation period: 1-3 days

49
Q

Shigella clinical presentation

A 
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
50
Q

Shigella invasion

A
  1. Shigella attaches to M cell. Endocytosis
  2. Bacteria lyses phagosome and replicates in the cell
  3. Develops actin tails to move cell to cell- cell to cell engulfment
  4. Causes apoptosis of PMN’s to reinfect
  5. Loss of epithelial cells destroys the integrity of the mucosal surface
  6. Red blood cells leak into the lumen, resulting in bloody diarrhea
51
Q

Shigella virulence factors

A

-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

52
Q

Yersinia gram stain

A

Gram negative

53
Q

Yersinia oxygen requirements

A

Facultative anaerobe

54
Q

Yersinia oxidase usage

A

Oxidase negative

55
Q

3 most important Yersinia species

A 
Yersinia pestis (plague)
Yersinia enterocolitica (enteropathogenic)
Yersinia pseudotuberculosis (enteropathogenic)
56
Q

Yersinia enterocolitica and Yersinia pseudotuberculosis acquisition

A

Ingestion of contaminated food

57
Q

Yersinia enterocolitica and Yersinia pseudotuberculosis reservoirs

A

Rodents and domestic animals

58
Q

Yersinia enterocolitica and Yersinia pseudotuberculosis diseases

A

Yersinia enterocolitica commonly causes a disease in humans, Yersinia pseudotuberculosis commonly is a disease of other animals

59
Q

Yersinia enterocolitica and Yersinia pseudotuberculosis disease symptoms

A

Both cause fever and abdominal pain, but ENTEROCOLITICA causes bloody diarrhea

60
Q

Yersinia enterocolitica and Yersinia pseudotuberculosis disease process

A

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)

61
Q

Yersinia enterocolitica and Yersinia pseudotuberculosis serological identification

A

Side agglutination to identify cultures with specific antibodies based on the “O”-antigen

62
Q

Yersinia enterocolitica and Yersinia pseudotuberculosis treatment

A

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)

63
Q

Yersinia enterocolitica and Yersinia pseudotuberculosis prevention

A

No preventative measures available beyond general hygiene

64
Q

Yersinia pestis Cell morphology

A

Tiny, gram-negative bacilli (unusual bipolar staining)

65
Q

Yersinia pestis virulence factors

A
  1. Capsule and envelope proteins (protect against phagocytosis and foster intracellular growth)
  2. Coagulase- clots plasma
  3. Endotoxin- responsible for many of the damaging symptoms
  4. Murine toxin- causes edema and necrosis in mice and rats (has not been shown to play a role in human disease)
66
Q

Yersinia pestis epidemiology/ history

A

Zoonotic infection- humans accidental hosts

Very very contagious and with a very short treatment window

67
Q

Three epidemiological cycles of Yersinia pestis

A

Sylvatic (wild) plague
Urban (domestic) cycle of plague
Human cycle of plague

68
Q

Sylvatic plague cycle

A

Wild rodents serve as the reservoir (prairie dogs, mice, rabbits etc.) with a wild rodent flea as the vector

69
Q

urban cycle of plague

A

Reservoir: domestic (urban) black rat
Vector: oriental rat flea (xenopsylla Cheopis)

70
Q

Human cycle of plague

A

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

71
Q

Bubonic plague (Yersinia pestis)

A

Swollen, painful lymph nodes, fever, septic shock in later stages (transmission= from vector to host through bite)

72
Q

Pneumonic plague (Yersinia pestis)

A

Host-to-host transmission via inhaled bacterial material (cough)
Flu-like illness progressing to mucous, bloody sputum, dyspnea, cyanosis and is rapidly fatal

73
Q

Bubonic plague pathology

A
  • 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)
74
Q

Pneumonic plague pathology

A

Infection localized to the lungs, highly contagious, toxin permeates rapidly and is almost always fatal without treatment. Bacteria grows within macrophages.

75
Q

Yersinia pestis treatment and prevention

A

Streptomycin, tetracycline, or chloramphenicol (and quarantine)
Vaccine not widely available but exists, and given in rare occasions

Medical Microbiology (11 decks)

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