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E3.MHD > Enterobacteriaceae I & II > Flashcards

Enterobacteriaceae I & II Flashcards

1
Q

What are the four UNVARYING characteristics of the family Enterobacteriaceae?

A
  1. Facultative G NEGATIVE rods
  2. ferment GLUCOSE
  3. Oxidase NEGATIVE
  4. Reduce nitrate to nitrite

( Indigenous flora of GI tract, colonize respiratory tract of hospitalized pts
–grow rapidly areobically/anerobically (simple growth requirements)

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2
Q

Structure of Enterobacteriaceae

A

A. LPS (endotoxin)
-3 components:
a. O-antigen: produces distinct serotypes
b. core oligosaccharide: attaches directly to
c. Lipid A: endotoxin component, released into circulation when bacteria cells are lysed; cause fever, diarrhea, and possible fatal endotoxic/septic shock (with AB will get WORSE before you get better)
B. H-antigen: peritrichous (all around) flagella
C. K or Vi-antigen: more than 80 serotypes in capsule (important in causing extraintestinal colonization, UTI, and invasive disease–prevents phagocytosis)

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3
Q

7 Enterobacteriaceae Virulence Factors

A
  1. Endotoxins
  2. Capsule: protects from phagocytosis
  3. Antigenic Phase variation: protects from antibody mediated cell death
  4. Type III secretion systems: facilitates secretion of bacterial virulence factors into host cells
  5. Sequestration of growth factors-eg. Iron scavengers
  6. resistance to serum killing
  7. Antimicrobial resistance
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4
Q

What is a MacConkey agar?

A

Selects for gram NEGATIVE has bile salts inhibitory to gram POSITIVE and crystal violet which also inhibits G+.

  • Non-lactose fermenters –> colorless
  • Lactose fermenter –> purple
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5
Q

List the 7 established genera/tribes

A
  1. Escherichieae
  2. Edwardsielleae
  3. Salmonelleae
  4. Citrobactereae
  5. Klebsielleae
  6. Proteeae
  7. Yersinieae
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6
Q

Tribe 1. Escherichieae

A

5 species, important champ: **E. coli

Habitat: intestines of humans/animals (usually self inflicted, gets into a place it doesnt belong)

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7
Q

E. coli Habitat

  • what does its presence indicate?
  • when do babies acquire it?
  • Its a free living organism, right?
A
  • in humans, infants acquire within hours of birth
  • its presence in water=indicator of fecal contamination
  • NOT considered as a free living organism in the environment
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8
Q

E coli Clinical Syndromes

A
  1. gram NEGATIVE sepsis
  2. UTI (80% of community acquired UTIs)
  3. wound infections
  4. pneumonia in IC hospitalized pts
  5. Meningitis in neonates
  6. Gastroenteritis
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9
Q

What are the strains of E. coli that cause gastroenteritis?

A
  1. Enterotoxigenic (ETEC)
  2. Enteropathogenic (EPEC)
  3. Enteroinvasive (EIEC)
  4. Enterohemorrhagic (EHEC)/Shiga toxin producing (STEC)
  5. Enteroaggreative (EAggEC)
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10
Q

Pathogenic Phenotype of ETEC

A

elaboration of secretory toxins (LT, ST) that do not damage the mucosal epithelium

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11
Q

Signs and Symptoms of ETEC

A
  • secretory diarrhea (traveler’s diarrhea) similar to V. cholerae (go to Mexico and drink the water)
  • ***profuse watery diarrhea is predominant symptom
  • often accompanied by mild abdominal cramps
  • dehydration and vomiting occur in some cases
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12
Q

Pathogenic Phenotype of EPEC

A

adhere to epithelial cells in localized micro-colonies and cause attaching and effacing lesions

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13
Q

Signs and Symptoms of EPEC

A
  • usually occurs in INFANTS
  • characterized by low-grade fever, malaise, vomiting, and diarrhea
  • prominent amount of mucus but with NO GROSS BLOOD
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14
Q

Pathogenic Phenotype of EIEC

A

invade epithelial cells and elicits immune resp

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15
Q

Signs and Symptoms of EIEC

A
  • inflammatory diarrhea (dysentery) similar to shigella
  • hallmarks: fever and colitis
  • symptoms: urgency and tenesmus (a continual or recurrent inclination to evacuate the bowels)
  • BLOOD, MUCUS, and MANY LEUKOCYTES in stool
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16
Q

Pathogenic Phenotype of EHEC/STEC

A
  • elaboration of cytotoxins (Shiga toxins, Stx1 and Stx2)

- primarily caused by E. coli O157:H7 (serotype)

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17
Q

Signs and Symptoms of EHEC/STEC

A
  • BLOODY DIARRHEA sans wbcs
  • often no fever
  • abdominal pain is common
  • may progress to hemolytic uremic syndrome (HUS)
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18
Q

Pathogenic Phenotype of EAggEC

A

adhere to epithelial cells in a pattern resembling a pile of stacked bricks

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19
Q

Signs and Symptoms of EAggEC

A

symptoms include:

  • WATERY DIARRHEA WITH BLOOD AND MUCUS
  • vomiting
  • dehydration
  • less commonly: abdominal pain
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20
Q

STEC-Shiga Toxin Producing E. Coli

A
  • produce 1 or more Shiga toxins (verocytotoxins)
  • produce attaching and effacing lesions
  • E coli O157 most commonly identified serotype
  • incidence and major serotypes of non-O157 strains causing diarrhea and HUS not determined
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21
Q

E. coli O157 Transmission

A
  • STEC is shed in feces of cattle, sheep, deer, other ruminants
  • human infection acquired via contaminated food/water OR via direct contact with an infected patient
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22
Q

E. coli O157 illness and modes of transmission

A
  • foodborne outbreaks most commonly associated with undercooked ground beef
  • reservoir: healthy dairy cattle
  • sporadic cases assoc. with unpasteurized milk, apple cider, lettuce and other produce, petting zoos, state fair show barns, contaminated water
  • largest US outbreak occurred in w. USA (‘93). Over 500 confirmed cases, 41 with HUS, 4 deaths. Jack-in-the-Box undercooked hamburgers.
  • causes both bloody and non-bloody diarrhea
  • ***HEMOLYTIC UREMIC SYNDROME (HUS), HEMORRHAGIC COLITIS
  • young children and elderly at increased risk for severe complications
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23
Q

STEC Incidence

A
  • an estimated 265,000 STEC infections occur/yr in the US

- STEC O157=36% of these infections + 60 deaths/yr

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24
Q

What are the physical manifestations of E. coli O157 HEMORRHAGIC COLITIS

A
  • abdominal cramps, watery diarrhea, bloody discharge
  • no significant fever
  • absence of WBC in stool
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25
Q

What are the physical manifestations of E. coli O157 HUS (hemolytic uremic syndrome)

A
  • HAT triad of symptoms for HUS:
    1. hemolytic anemia
    2. acute renal failure
    3. thrombocytopenia (no platelets)
  • preceded by bloody diarrhea
  • leading cause of acute renal failure in children
  • occurs in 20% of pediatric O157:H7 cases
  • 50% require dialysis, 3-5% die
  • usually diagnosed a wk after diarrhea onset
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26
Q

EHEC (Enterohemorrhagic)-Clinical symptoms

A

-3-4 days non-bloody diarrhea with abdominal pain
-onset of bloody diarrhea and severe abdominal pain
-resolution in 4-10 days
OR
-HUS–> death or sequelae (renal impairment [not urinating], HTN, or CNS dysfunction)

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27
Q

E. coli O157:H7 histology

A
  • schistocytes=fragmented RBC–> microangipathic
  • hemolytic anemia–>lethargy
  • hyperchromic cells (white centers)
  • white cell surrounded by red cells, but no platelets (thrombocytopenia)
  • already in reanl faillure, not urinating–>One of the HUS-HAT triad
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28
Q

Actions of the toxins (1/2)

A
  • organism never invade bloodstream, produce shiga toxins which invade, attach to receptors on endothelial cells in blood vessel lining (largest [ ] of receptors for shigatoxin are in the renal epithelial area-around the kidneys)
  • toxin adherence–>damage to vessel wall
  • body response by forming a scab+consuming plateley
  • small narrow vessle with fibrin deposits on inside of vessel wall narrow lumen, RBC stat shearing on rough surface
  • oxygen supply to kidney starts to get affected, pt goes into renal failure
  • infarction of mucosa–>bleeding into bowel and bloody diarrhea
  • inhibition of protein synthesis targets:
    1. commensal bacteria
    2. host cells
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29
Q

Action of the toxins (2/2)

A
  • toxins also trigger many signaling cascade influencing cellular functions such as cytokine secretion and the induction of cell death by apoptosis
  • many endothelial and epithelial cells in the kidney and the CNS are sensitive to cytotoxicity induced by Shiga toxins
30
Q

E. coli O157:H7 Complications of HUS

A
  • 3-5% die acutely
  • 14% develop sever in-hospital complications i.e. stroke, blindness, bowel resection
  • 39% develop chronic kidney abnormalities years later
31
Q

What are the two settings in which E. coli O157:H7 can occur?

A

a. diarrheal related-classical HUS, vast majority of cases
b. non-diarrheal HUS-much less common can occur in association with:
- pneumococcal infection
- chemotherapy
- transplant immunosuppression

32
Q

What are risk factors for HUS following O157 infection?

A
  1. Host factors
    - very young or old
    - mental retardation
    - P antigen expression by RBCs (carried by 50%, also on other tissue including endothelial cells, attachment site for Shiga)
  2. Clinical Factors
    - bloody diarrhea
    - fever
    - increase WBCs
  3. Treatment Factors
    - use of anti-motility agents
    - use of certain antimicrobials
  4. Other factors
    - produce STII instead o both I and II
33
Q

Emergence of EHEC/STEC NON-O157 disease

A
  • more than 150 serotypes identified

- most freq in N. America: O26, 45, 103, 111, 121

34
Q

Laboratory Diagnosis-collection and transport of specimens

A
  • Timing: collect in early stages of any enteric illness (first 4 days of onset) when organism load is higher and before antibiotic tx is initiated
  • Type: whole stool, multiple specimens
  • Transport: ASAP, refrigerate at 4C if >1-2hrs
35
Q

What are the three main modalities to detect antigen?

A
  1. direct fecal specimen detection
  2. enriched broth culture detection (more sensitive)
  3. FilmArray GI panel-multiplex PCR
36
Q

How is STEC Diarrhea treated?

A

(treat symptoms)

  1. oral rehydration (Gatorade, Pedialyte), supportive care and careful monitoring of kidney function
  2. HUS and renal failure: can be managed by dialysis
  3. ***Antibiotics are NOT given in STEC!!! (it would kill all the E coli, release all the shigatoxin and endotoxin at once, endo would enter bloodstream and upregulate shiga activity)
  4. ***No antimotility agents!!!
  5. ***Chemoprophylaxis with SXT or ciprofloxacin for travelers’ diarrhea NOT recommended
37
Q

Tribe I: Escherichieae

A
  • Genus Shigella-4 species: Shigella (dysenteriae, flexneri, boydii, sonnei)
  • key ID: MacConkey is flat-dry, NON-lactose fermenter, indoel NEGATIVE, NOT motile, no CO2 (unlike E. coli)
  • Habitat: human intestines (20-30k cases/yr in US)
38
Q

How is Shigella Transmitted? 5Fs + what kind of kids?

A
  • person to person via fecal route
  • contaminated water +5 F’s (food, flies, fingers, fomites, feces)
  • highest risk: young children in day care center, nurseries, custodial institutions
    • siblings and parents of ^ kids
    • MSM (fecal oral sans vector)
39
Q

What is the pathogenesis of Shigella?

A
  • virulent strains carry plasmid for attachment and entry
  • enters cells by phagocytic vacuole
  • organism escapes in cytoplasm
  • intracellular replication
  • actin “tail” drives organism in cytoplasm
  • organism enter adjacent cells
  • Shigella phagocytosed into new cell and released into cytoplasm
  • shigella can kill phagocytic macrophages
  • infection does not extend into lamina propria
  • some strains prodcue shiga toxin–>more severe disease
40
Q

What are the clinical syndromes of Shigella?

A

**Bacillary dysentery
-abdominal cramps, tenesmus (urge to stool), pus and blood in stool
-tissue invasion limited to epithelial cells and submucosa
-fecal leukocytes present
-incubation 1-3 days lasting 48hrs
-humans=natural host
-most communicable of bacterial diarrheas
-

41
Q

Tribe II: EdwardsiellEAE

A

-*Edwardseilla tarda

Habitat: cold blooded vertebrates (snakes), fresh water, catfish

42
Q

What are the clinical syndromes of E. tarda?

A
  • primarily causes gastroenteritis, rare cases of septicemia
  • GI dz include:
    • acute, self-limiting gastroenteritis with watery diarrhea
    • typhoid-like illness with bloody diarrhea and possible fever, nausea, vomiting, colonic ulcerations and terminal ileum nodularity
  • has been mistaken for salmonellosis and inflammatory bowel dz (Crohn’s dz)
43
Q

Tribe III: SalmonellEAE

A
  • Salmonella, all serotypes are considered a single species
  • it takes a LOT to cause infection
    habitat: lower animals (poultry, chickens, turkeys, cows, pigs, pets) for NONtyphoid strains (Humans for S. typhi)
44
Q

What are the 5 main characteristics of Salmonella?

A
  1. NON-lactose fermenter
  2. produces hydrogen sulfide (black)
  3. transmission via improper food handling
  4. found in humans (S. typhi) and livestock
  5. secondary transmission person-to-person
45
Q

What is the incidence and mode of transmission of Salmonella?

A
  • ~1.4 million cases/yr in US, 16k hospitalizations and 600 deaths
  • ~35k typed by PH labs
  • ~1/2 Salmonela epidemics are result of contaminated poultry and poultry products
  • also associated with reptiles (lizards, snakes, turtles)
46
Q

5 Salmonella Clinical Syndromes

A
  1. Asymptomatic (carrier) stat
  2. Febrile Gastroenteritis
  3. Enteric Fever
  4. Septicemia
  5. Focal Infections
47
Q

Asymptomatic (carrier) state-Salmonella

A
  • relatively limited with non-S. typhi, occasionally prolonged over a year.
  • chronic or decades long with S. typhi
48
Q

Febrile Gastroenteritis-Salmonella

A
  • most common presentation in man
  • fond in 2/3 of pts with culture confirmed Salmonella infections
  • incubation: 12-48 hrs
  • Symptoms: malaise, nausea, sometimes with vomiting, followed by abdominal pain and diarrhea
  • self-limited, duration 3-5 days
  • dont want to treat because dont want to destroy food flora, its needed to re-establish intestinal health and dont want to cause AB resistance
49
Q

Enteric Fever-Salmonella

A
  • prolonged, serious illness, best known example: Typhoid fever
  • caused by S. typhi and S. paratyphi A and B, rare with other serotypes
  • incubation: 1-2 weeks
  • illness duration: 4 weeks characterized by increasing fever for 2 wees (bactermic stage) followed by GI symptoms for 1-2 wks
  • only known reservoir of S. typhi is man
  • usally in aread with poor sanitation (India, Indonesia)
50
Q

Septicemia-Salmonella

A
  • without major GI involvement-characteristically found in pts with underlying leukemia, lymphoma, AIDS, SLE, sickle cell crisis, and alcoholic hepatitis
  • found frequently in infections due to S. choleraesuis, S. dublin, and S. oranienburg
  • relapses are common
51
Q

Focal Infections-Salmonella

A
  • Osteomyelitis
  • Meningitis
  • Brain Ascess
  • Endocarditis
  • gets in the blood then disseminated to some distant site
52
Q

Pathogenesis of Enteric Fever-Salmonella

A
  • bacteria bind to M cells
  • infection kills cell, bacteria go to Peyer’s patches
  • organisms invade macrophages where they multiply
  • inhibition of oxidative metabolic burst allows organism to survive intracellularly
  • bacteria spread drom Peyer’s patches–>RE (reticular endothelium)–>bloodstream
  • LPS acts as a major virulence factor causing septic shock
  • immunity is humoral and cell-mediated
  • S. typhi occurs only in humans
  • transmission person-to-person
  • *always get blood and stook if unsure what stage theyre in (it is BI-MODAL)
53
Q

Path of Gastroenteritis-Salmonella

A
  • Salmonella produces an adhesion–>stimulates rearrangement of plasma cell membrane to form ruffles
  • bacteria enter cell by pinocytosis associated with ruffles
  • organism invade large and small bowel and lamina propria
  • large inflammatory response induced
54
Q

Clinical Manifestations of Enteric Fever-Salmonella

A

-presents with fever, headache, rose spots, constipation
-rose spots; pink macules or prupuric lesions
-fever; temperature-pulse dissociation (refers to relative bradycardia with a pulse rate less than expected at a given body temp. associated with specific infection, including intracellular organisms such as salmonella, legionella, and chlamydia)
-neuropyschiatric manifestations
-Complications:
»GI bleeding
» Perforation of ileal ulcers
»circulatory collapse
»relapse following treatment
»asymptomatic long term carriage

55
Q

Clinical Manifestations of Bacteremia-Salmonella

A

-increased risk in peds, geriatric, AIDS pts
-clinically similar to other gram NEG bacteremias
-10% localized suppurative infections
»osetomyelitis, endocarditis, arthritis
-diagnosed by positive blood cultures
-Rx: 3rd generation cephalosporin

56
Q

Tribe IV-CitrobacterEAE

A

Genus Citrobater: C. freundii, C. koseri

Habitat: intestinal tract humans/animals

57
Q

What are the clinical syndromes of Citrobacter?

A
  • nosocomial infections of urinary and respiratory tracts of debilitated, hospitalized pts, endocarditis, and hospital acquired bacteremias
  • C. freundii=rare cause of diarrhea
  • C. koseri=rare cause of meningitis and brain abscess in neonates
58
Q

Tribe 5-KlebsiellEAE-Genus Klebsiella

A

*K. pneumoniae, K. oxytoca, (K. ozaenae, K. rhinoscleromatic)
Habitat: intestines and upper respiratory tract of humans and animals

59
Q

Klebsiella Clinical Syndromes: K. pneuoniae and K. oxytoca

A

oxy: POSITIVE indol, penumoniae: NEG indol
- primary lobar penumoni characterized by destructive changes, necrosis, and hemorrhage (“currant jelly” sputum), bronchopneumonia, bronchitis, accounts for 9% of UTIs and 14% of bacteremias in hospitalized pts

60
Q

What are the 5 organisms responsible for NEONATAL MENINGITIS??

A 
1.
2. C. koseri
3.
4.
5.
61
Q

Klebsiella Clinical Syndromes: K ozaenae and K. rhinoscleromatis

A

K. ozaenae-atrophic rhinitis (ozena), destruction of mucosa and fetid mucopurulent discharge from nose

K. rhinoscelromatis-rhinoscleroma, chronic granulomatous dz involving mucosa of upper respiratory tract

62
Q

Tribe 5-KlebsiellEAE-Genus Enterobacter

A

*E. aerogenes, E. cloacae

Habitat: widely distributed in the environment and GI tract of humans

63
Q

What are the clinical syndromes of Enterobacter?

A
  • frequent colonizers of hospital patients (**nosocomial infections), cause opportunistic infections involving urinary tract, respiratory tract, cutaneous wounds, occasional cause of septicemia and meningitis
  • antibiotic therapy can be ineffective, because the organism are frequently resistant to multi antibiotics
64
Q

Tribe 5-Klebsielleae-Genus Serratia

A

*S. marcescens
Habitat: widely distributed in the environment
on MacConkey, show RED-pigmented colonies

65
Q

What are the clinical syndromes of Serratia?

A
  • nosocomial infections, pneumoniae, septicemia, UTI, surgical wound and cutaneous infections
  • also reported as a cause of endocarditis and osteomyelitis in IV drug addicts
66
Q

Tribe 6-ProeEAE-Genus Proteus

A

*P. mirabilis (indol NEGATIVE), P. vulgaris (indol POSITIVE)
Key ID features: **swarming observed on blood agar, lactose NEG on MacConkey, STRONGLY urease POSITIVE
Habitat: soil, water and intestinal tract of humans and animals

67
Q

What are the clinical syndromes of Proteus?

A
  • second to E. coli in frequency of isolation in the clinical lab
  • P. mirabilis is most frequently isolated species, cause of UTIs and wound infections
    • strongly urease POSITIVE produces highly alkaline urea which can lead to renal calculi (renal stones)
    • composed of struvite (Mg ammonium PO4)
  • P. vulgaris is most commonly recovered from infected sites of immunocompromised pts
68
Q

How many species are there of Genus Yersinia?

A

There are 11 species, the most important of which are Y. pesits–>responsible for the bubonic plague and Y. enterocolitica

69
Q

What are the key Identifying Features in Y. enterocolitica

A
  • pinpoint colonies on MacConkey blood agar plate at 24hrs
  • biochemical tests should be incubated at 25 C (grow better at cool temperature)
  • urease POSITIVE
  • lactose NEGATIVE, G (-)
70
Q

What is the epidemiology of Y. enterocolitica?

A
  • most common spp in clinical specimens
  • widely distributed in lakes and reservoirs (adapted to environments with cooler temps)
  • epizootic outbreaks of diarrhea, lymph-adenopathy, pneumonia, and spontaneous abortions occur in various animals
  • over 50 serogroups, O:3** serotype infecting humans
  • pigs=major reservoir for infection in humans
  • diarrheal illness assoc with household prep of chitlins
  • portal of entry: oral digestive route
71
Q

What are the clinical syndromes of Y. enterocolitica?

A
  • orgs adhere to and penetrate the ileum, causing terminal ileitis, lymphadenitis, and acute enterocolitis.
  • mimics appendicitis and most common in children
  • enterocolitis accounts for 2/3 of infection. Diarrhea, fever, abdominal pain lasting 1-2 weeks.
  • chronic form can persist months to >1yr.
  • also associated with blood transfusios related sepsis, arthritis, intra-abdo abscess, hepatitis, osteomyelitis
  • blood contamination occurs due to asymptomatic Y. enterocolitica bactermemia at time of blood donation
  • Y. enterocolitica can proliferate in blood stored at 4 C after 2-3 weeks

E3.MHD (6 decks)

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