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Microbio Block 1 > Enterobacteriaceae, Klebsiella, Pseudomonas > Flashcards

Enterobacteriaceae, Klebsiella, Pseudomonas Flashcards

1
Q

Where are enterobacteriaceae?

A

Widely distributed Gram neg bacilli: in soil, water, plants, GI of humans and animals
Majority of urinary isolates; large portion of blood, peritoneum, and resp cavity isolates

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2
Q

Morphology of enterobacter

A

Average size, non-spore-forming G- bacilli that may have motility (flagella) or not (Kleb, Shig, Yersinia)
Aerobic or facultative anaerobes

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3
Q

Enterobacter and Quellung reaction

A

Some positive (Kleb, Enterobacter, E. coli), some negative

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4
Q

Species with positive Quellung

A 
Encapsulated: SHiNSKSS
Strep pneumo
H. influenza
N. meningitidis
Salmonella
Klebsiella
group B Strep
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5
Q

GNR infections

A

Enteritis (E. coli, Salmon, Shig, Yers)
Non-enteric: UTI, cellulitis, soft-tissue abscess, intra-abd abscess, bacteremia, liver/spleen abscess, foreign body infxn, pneumonia, endocarditis
*External or from gut spillage/ transmigration

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6
Q

Morphology & diseases of Escherichia

A

G-, fac anaerobe; oxidase neg, lactose fermenter
Commonest bact in gut, commonest cause of UTI
Most infections E. coli; most endogenous, enteritis exogenous

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7
Q

E. coli virulence factors

A

Fimbrial adhesins, secretion systems to export proteins for pathogenesis and toxins

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8
Q

E. coli causes of enteritis

A

ETEC (enterotoxigenic), EHEC (enterohemorrhagic), EIEC, EPEC, EAggEC
*Uropathogenic E. coli (most likely to be encapsulated, produce P fimbriae, produce cytolytic hemolysin, multiple Fe-acquiring mechanisms)

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9
Q

ETEC diseases, spread, tx

A

Leading cause bact diarrhea in developing world (Traveler’s diarrhea)
9% diarrheal deaths, 1% deaths in kids 1-2 days = sec diarrhea, n/v
Tx: rehydrate +/- abx (pregnant, immunocompromised)

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10
Q

Pathogenesis of ETEC

A

Ingestion of contaminated food, water -> attach to small intestinal epithelial cells but don’t invade -> secrete heat labile and heat stable toxins

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11
Q

Heat labile and heat stable toxin mechanisms

A

Labile: similar to cholera toxin, A-B toxin -> ADP ribosylation of Gs -> activate AC -> inc cAMP
Stable: stimulates GC -> inc cGMP

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12
Q

EHEC alternative name

A

Shiga toxin producing E. coli (STEC)

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13
Q

EHEC epidemiology

A

Undercooked meats, contaminated drinking water, foods; few organisms needed for infection

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14
Q

E. coli O157:H7 virulence & mechanism

A

EHEC with O and H antigens, Shiga like toxins Stx-1,2 encoded by phage
A subunit internalized, stops protein synthesis; B subunit binds GB3 glycolipid-R in colon, kidney

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15
Q

E. coli O157:H7 diseases

A

Common cause diarrhea/ dysentery in dev’d world

Severe abd pain, bloody diarrhea, hemorrhagic colitis, HUS

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16
Q

HUS

A

After 2-7% E. coli O157:H7 infections; mostly kids, 5-10% mortality
Thrombotic microangiopathy; acute renal failure, anemia, thrombocytopenia; can lead to HTN, renal impairment
*NO ABX - can worsen it; supportive care

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17
Q

Characteristics of enteritis caused by EIEC, EPEC, EAggEC

A

EIEC: Shigella-like dysentery w blood, mucus
EPEC: Pediatric diarrhea, esp infants; watery or bloody diarrhea in infants, person-person spread
EAgg: childhood diarrhea, more than 14 days; watery w mucus

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18
Q

Non-enteritis E. coli infections

A

UTI (CA or nosocomial), blood stream infections, pneumonias (neonatal, nosocomial), meningitis (after surgery, VP shunts), peritonitis (peritoneal dialysis)
Tx based on abx-susceptibility

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19
Q

Salmonella enterica serotypes and transmission

A

S. typhi and paratyphi are serovars - adapted to humans
2500+ serotypes based on H and O Ags
Fecal-oral spread, person-person

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20
Q

Epidemiology: non-typhi Salmonella

A

Contaminated foods, fecal-oral spread at day care or food service personnel; animal reservoirs: poultry, reptiles (TUTTLES), livestock, birds, domestic animals, rodents

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21
Q

Clinical syndromes of Salmonella

A

Enteritis (6-48 hr for 3-7d, n/v, diarrhea, cramps, +/- fever, constipation first, no blood or pus in stool, stools pos ww-yy post illness)
Septicemia, osteomyelitis, aortitis
*Especially in immunosuppressed (HIV+, malignancy, certain drugs)

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22
Q

Virulence of Salmonella

A

Endotoxin, invasion genes (chromosomal, attachment and invasion)
Entry into host: ingest contam food/water, fecal-oral spread, moderate number of bacteria
*Susceptible to low pH, antacids increase susceptibility to dz

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23
Q

How is Salmonella infection established?

A

Attach to epi cells, uptake, replication in endosome, penetrate into subepi tissue, inflam response contained -> spreads to blood = sepsis

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24
Q

Treating, preventing, controlling Salmonella

A

Sx: fluid replacement
Abx not for uncomplicated GI -> may prolong carrier state; abx for septicemia
Prev/control: sanitation, water and sewage treatment, proper food prep and storage

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25
Q

S. typhi epidemiology

A

Contaminated food or water; humans are only reservoir, but passive carriage by flies from feces to food
Chronic carriers: GB colonization, endemic reservoirs

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26
Q

Symptoms of S. typhi

A

Enteric fever; incubate 7-21 d, starts as diarrhea, bacteremia -> fever (3-4 w), malaise, anorexia, myalgia, HA, rose spots, relative bradycardia, hepatosplenomegaly, lymphocytosis
Complications: infxn of bone, heart valves, brain, Peyer’s patches bleeding (longitudinal ulcer)

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27
Q

Virulence factors & mechanisms of disease of S. typhi

A

Vi PS capsule, endotoxin
Invade M cells in PPatches, replicate and transport to subepi tissue, survive in MFs, enter blood and lymph -> replicate in liver, spleen with prolonged release of endotoxin -> GB colonization, shed in bile

28
Q

Treating, preventing, controlling S. typhi

A

Tx: abx if complicated and susceptible

Sanitation, carriers shouldn’t handle food, vaccines against Vi capsular PS (oral or IM)

29
Q

Epidemiology of Shigella

A

Fecal-oral spread, primarily dz of kids
Contaminated food or water
FEW organisms for infection (vs. Salmonella)

30
Q

Clinical symptoms of Shigella

A

Watery diarrhea -> in 1-3 days: abd cramps, fever, blood/ pus in stools, tenesmus
*Identical to EIEC
Can cause HUS (toxin)

31
Q

Morphology of Shigella

A

G- bacillus, non-motile, species classified by O Ag, n H Ag

Not a lactose fermenter, relatively biochemically inactive

32
Q

Virulence factors of Shigella

A

Shigatoxin (some spp), virulence plasmid (attachment, invasion, intracellular replication)

33
Q

Tx, prevention, control of Shigella

A

Tx: fluid replacement, abx to shorten duration and fecal excretion (cipro, TMP)
Prevent: wash hands, chlorinate water, sanitation

34
Q

Yersinia reservoirs

A

Y. enterocolitica: pigs, rodents, livestock

Y. pestis: rodents

35
Q

Y. entercolitica physiology, structure, epidemiology

A

G- bacillus, motile, flagella at low temp (22), growth at 4 C (inc metabolic activity at low temp)
Fecal-oral spread; milk, food, water
Common in Scandinavia, cold areas of N. America

36
Q

Clinical syndromes of Y. entercolitica

A

Diarrhea, fever, abd pain (“appendicitis”); similar to Salmonella, mesenteric lymphadenitis
Complications: septicemia, hepatic abscesses
Post-infxn: reactive arthritis (HLA B27)

37
Q

Pathogenesis and tx for Y. entercolitica

A

Invasive; heat-stable enterotoxin similar to E. coli ST

Tx: supportive care for non-complicated cases; FQs, ceph, tetras, etc. based on sensitivity

38
Q

Y. pestis epidemiology

A

Rat fleas from rat to human; common in Africa, Asia, SW USA
1000-2000 cases in world per year
Used as biological weapon

39
Q

Morphology of Y. pestis

A

Non-motile, non-spore forming, not lactose fermenter
Bipolar staining with Giemsa or Wright stain
Aerobic on most media, optimal at 28*

40
Q

Clinical symptoms of Y. pestis

A

Bubonic plague: fevers, chills, HA, firm buboes (groin) w edema; 50% fatal wo tx
Pneumonic plague: 1’ or 2’, pneumonia w watery or purulent sputum w bacteria; 50% mortality (100% wo tx)
Septicemic plague: bacteremia, no buboes, fever, sepsis, 33% fatal (100% wo tx)

41
Q

Tx of Y. pestis

A

Streptomycin, gentamicin, tetracyclines, chloramphenicol

*Many side effects

42
Q

Klebsiella pneumoniae infections

A

Aspiration pneumonia
Abscesses in lung, liver
especially in Alcoholics, diabetics
Can get MD-ResistAnce

43
Q

Klebsiella virulence & symptoms

A

PS capsule -> mucoid colonies
Currant jelly sputum in pneumonia (esp alcoholics)
MDR strains: ESBL, KPC

44
Q

Proteus morphology & clinical syndromes

A

P. mirabilis most common pathogen
G- bacillus, very motile
Causes UTIs, kidney stones (alkaline urine bc urease pos -> precipitation of Mg and Ca)

45
Q

Urease positive organisms

A 
PUNCHK
Proteus
Ureoplasma
Nocardia
Cryptococcus
Helicobacter
Klebsiella
46
Q

Enterobacter morphology & clinical syndromes

A

G-, lactose fermenter, fac anaerobe
Pathogens: E. cloacae, aerogenes
UTI, pneumonia, blood stream infxn, nosocomial infxn, etc.

47
Q

Treatment of enterobacter & resistance mechanism

A

“Inducible AmpC” -> tx failure w use of routine abx

Consider FQs, carbapenems

48
Q

Serratia morphology and clinical syndromes

A

G- enterobacteriaceae

Any infection, commonly nosocomial infections

49
Q

Resistance mechanism of Serratia

A

Inducible AmpC -> tx failure w use of routine abx

50
Q

Pseudomonas aeruginosa morphology

A

Aerobic, G- bacilli (single or pairs), oxidase+, non-lactose fermenter, motile with monotrichous polar flagellum, multiple cell surface pili/fimbriae
Can use wide range of carbon/energy sources

51
Q

Pigmentation and hemolysis of P. aeruginosa

A

Blue-green phenazine (pyocyanin), red (pyorubin), or black (pyomelanin)
Colonies have metallic sheen, sometimes slimy
B-hemolysis
Grape-like odor

52
Q

What is alginate?

A

“Mucoid exopolysaccharide”, leading to mucoid appearance of strains from CF patients and occasionally other patients w chronic P. aeruginosa infxns
Most strains of P. aeruginosa can produce it

53
Q

Pseudomonas virulence factors

A

Adhesins, alginate, exotoxin A, exoenzyme S, elastolytic activit, phospholipase C, pyocyanin, abx resistance

54
Q

What are exotoxin A, exoenzyme S, and pyocyanin of Pseudomonas?

A

A: inhibits protein synthesis, causes tissue damage (eye infxn, burn)
S: inhibits protein synthesis, interferes with phagocytosis
Pyo: makes ROS -> tissue damage

55
Q

Where is Pseudomonas found?

A

Ubiquitous in water, soil, plants; can colonize anywhere in body and cause any infection

56
Q

Pseudomonas infections

A

Wound infxn, hot tub dermatitis; chronic or malignant otitis externa; burn wound infxn, endocarditis (IVDU); bacteremia, sepsis, ecthyma gangrenosum; nosocomial, UTI, pneumonia, meningitis
PSEUDO: Pneumonia, Sepsis, External otitis, UTI, Drug use/Diabetic, Osteomyelitis

57
Q

Transmission of Pseudomonas & at risk populations

A

Moist reservoirs
Can be normal GI flora in hospitalized pts
Contact and endogenous spread
Immunocompromised, drug users, burn patients

58
Q

Pseudomonas tx and prevention

A

Resistant to: FQ, B-lactam, AGs; easily MDR
Endocarditis: double coverage
Good aseptic technique, avoid unnecessary use of broad-spectrum abx, remove indwelling lines asap
Isolate pts with MDR strain

59
Q

Campylobacter epidemiology

A

Most common cause bacterial gastroenteritis
Transmitted by chickens, cattle, swine, cat/dog
Contaminated meat, fish, milk, mushrooms, raw seafood
Contaminated water (animal feces)

60
Q

Campylobacter jejuni morphology

A

G- bacillus, very small, comma- or S-shaped
Motile: single polar flagella or darting corkscrew
Growth: reduced O2, increased CO2, elevated temp

61
Q

Clinical syndromes Campylobacter

A

Gastroenteritis (1-7d post): watery diarrhea or dysentery (fever, and pain, bloody stool) for 1-2 w
Septicemia rarely

62
Q

Autoimmune responses to Campylobacter

A

? IBS; reactive arthritis; Guillain-Barre syndrome (may cause 20-40% GB cases; 2-3 post febrile illness) d/t Ab to core sugars of LPS cross-rx w gangliosides

63
Q

Tx and prevention Campylobacter

A

Self-limiting; fluid- and electrolyte replacement; multiple abx-res plasmids
Erythromycin (enteritis) or AGs (septicemia)
Prevention: proper food prep, good sanitation, pasteurize milk

64
Q

H. pylori morphology

A

G- spiral-shaped bacillus w corkscrew motility

65
Q

Epidemiology and clinical syndromes H. pylori

A

In 70-100% pts with gastritis, gastric ulcer, duodenal ulcer
Infxn increases with age
? also gastric adenocarcinoma?

66
Q

Virulence and transmission of H. pylori

A

Urease, motility, mucinase, adherence factors, endotoxin, cytotoxin
No animal reservoir, likely fecal-oral spread

67
Q

Dx and tx of H. pylori

A

Gastric biopsy or culture; serology or urea breath test (monitor tx this way)
Tx: combo abx (amox, tetra, metro); PPI, bismuth (anti-inflam)

Microbio Block 1 (14 decks)

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