Section 3- Bacteriology Flashcards

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1
Q

Coagulase

A

Clumping factor enzyme made by bacteria
Virulence factor- helps bacteria wall itself off so immune cells cannot reach it
Takes fibrinogen (soluble) and along with thrombin, makes fibrin (insoluble) which helps blood clot
+ = s. aureus
Can test on a slide (surface coagulase) or in a tube (secreted coagulase)

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2
Q

Mannitol Salt Agar (MSA)

A

Selective
Mannitol sugar fermentation results in acid production and media turns yellow
+ = S. aureus
- = S. epidermidis, S. saprophyticus

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3
Q

Blood Agar

A

Standard medium
Almost everything grows on
NOT Neisseria gonorrhoeae

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4
Q

Sepsis

A

Signs= fever, elevated pulse, respiratory distress and kidney failure
Indicative of bacterial infection

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5
Q

Pleural effusion

A

Excess fluid between pleura layers

Evidence of infection

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6
Q

HAP

A

Hospital Acquired Pneumonia

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7
Q

Nosocomial pneumonia pathogens (7)

A
Pseudomas aeruginosa
Klebsiella
Escherichia coli
Acinetobacter
Haemophilus influenzae
Staphylococcus aureus
Streptococcus pneumoniae
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8
Q

Alpha toxin

A

Hemolysin

Causes hemolysis of RBCs

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9
Q

MRSA

A
Methicillin resistant S. aureus
Emerged as nosocomial infection in U.S. 
Community acquired
Current epidemic in U.S.
Necrotizing pneumonias
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10
Q

von Willebrand factor binding protein (vWbp)

A

Cell wall associated
Binds host vW factor
Facilitates adhesion in blood vessels

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11
Q

Protein A (SpA)

A

Cell wall associated
Binds to Fc region of IgG and binds to Fab region of BCR
Prevents immune cell recognition and complement activation

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12
Q

Leukocidins

A

Target WBCs to form pores

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13
Q

Hemolysins

A

Target RBCs to form pores

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14
Q

Toxic Shock Syndrome Toxin (TSST-1)

A

Superantigen
Causes TSS
Superantigens cross-link MHC class II molecules with TCRs, Polyclonal T cells activated, Massive pro inflammatory cytokine release, then toxic shock (cytokine storm) and organs fail

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15
Q

Staphylococcal Enterotoxin B (SEB)

A

Superantigen
Heat stable
Released when bacteria replicate in food and causes staphylococcal food poisoning

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16
Q

Epidermolytic/Exfoliative Toxins (ET-A and ET-B)

A

Cause scalded skin syndrome

Released by S. aureus during growth

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17
Q

Skin and Soft Tissue Infections (SSTIs)

A

Infection of hair follicles, spectrum
Can be superficial or deep
Folliculitis (surface)
Boil (into pore of hair)
Carbuncle (follicle infection)
Impetigo (young children, fluid filled blisters; bullous and nonbullous)
Stye (sebaceous gland of eyelashes infection)
Abscess (Collection of pus in a tissue in response to infection)
Cellulitis (rapid dissemination of bacteria under superficial skin layers; rash appearance)
Treated with surgical drainage (I&D-Incision and Drainage) if necessary and antibiotic therapy (not beta lactams)

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18
Q

Staphylococcal Scalded Skin Syndrome (SSSS)

A

Post infectious complication of soft tissue infections

Caused by exfoliative toxins

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19
Q

Staphylococcal food poisoning

A

Meat mixes (Mayonnaise), Cooked ham or sausage, Dairy
Bacteria replicate in food and release SEB
Vomiting, diarrhea, stomach cramps
Very quick onset and resolves on own

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20
Q

Toxic Shock Syndrome (TSS)

A

Very serious
Rare, life-threatening
Results from exposure to TSST-1
Most commonly associated with use of superabsorbent tampons, surgical dressings, and nasal packing
Symptoms= Hypotension, high fever, diffuse erythematous rash, desquamation of palms and feet, vomiting, diarrhea, liver damage, renal distress, Altered mental status, myalgia
Treat with Clindamycin** (kills bacteria and stops toxin production)

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21
Q

Catalase

A
(+) = Staph, N. gonorrhoeae
(-) = Strep
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22
Q

M protein

A

Binds to factor H and prevents opsonization by complement

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23
Q

Capsule virulence

A

Blocks phagocytosis by neutrophils
Antigenic
Vaccine component sometimes

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24
Q

Lipoteichoic acid (LTA)

A

Helps with cell attachment

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25
Q

Streptococcal pyrogenic exotoxins

A

Superantigens

Cytokine storm

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26
Q

Streptolysin S

A

Beta hemolysis

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27
Q

Hylurodinase, Streptokinase, Deoxyribonucleases

A

Assist with tissue invasion

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28
Q

Scarlet Fever

A

Caused by release of Streptococcal Pyrogenic Exotoxin A (SpeA)
Perioral rash
Strawberry tongue
Usually children

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29
Q

Necrotizing Fasciitis

A

Severe infection of subcutaneous tissues and fascia
Very rapid dissemination of bacteria
Must debride dead, damaged, and infectious tissues
May have to amputate
Give large dose penicillin and/or clindamycin

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30
Q

Acute Rheumatic Fever (ARF)

A

Anti-M protein antibodies cross-react with epitopes on heart, joint, skin, and brain leading to tissue damage
Type II Hypersensitivity
Can lead to Carditis and congestive heart failure and also subcutaneous nodules (painless, not severe)

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31
Q

Acute Glomerulonephritis (AGN)

A

Antibody-antigen complexes deposit in glomerular membrane, which recruits complement and neutrophils
Kidney failure
Type III Hypersensitivity

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32
Q

Pneumolysin

A

Partial hemolysis (alpha)

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33
Q

Thayer Martin Agar

A

Contains vancomycin and colistin to control growth of other species
Grows Neisseria gonorrhoeae and Neisseria meningitidis ONLY

34
Q

Gonorrhea

A

Dysuria and urethral discharge

WBCs in discharge containing gram (-) diplococci

35
Q

Type IV Pilus

A

Hair-like projections; allow bacteria to adhere to epithelial tissues in urinary tract
Can be assembled or retracted for motility (grappling hook)
Under antigenic variation to evade immune response

36
Q

Lipo-oligosaccharide (LOS, Endotoxin)

A

Very similar to LPS
Resistance to serum killing, complement can’t bind
Fever, cytokine storm
Diffuse intravascular coagulopathy (DIC), rash, low BP, Organ damage

37
Q

IgA protease

A

Cleaves mucosal IgA antibodies

Immune evasion

38
Q

Epididymitis

A

Inflammation of testicles

Sterile if untreated

39
Q

Disseminated Gonococcal infection (DGI)

A

Necrotic pustules on an erythmatous base

Anywhere on body

40
Q

Meningitis symptoms

A

Still neck, severe headache, delirium, *****non-blanching petechial rash = hallmark

41
Q

Waterhouse-Friderichsen Syndrome

A

Most severe form of meningococcemia
Diffuse intravascular coagulopathy causes massive hemorrhage within adrenal glands
Hormonal imbalance
Almost always fatal

42
Q

2 types of H. influenzae

A

Serotypable (capsule)
vs.
Non-typable (no capsule)
*Serotype B is most important

43
Q

Otitis media

A

Middle ear infection
Caused by S. pneumoniae and H. influenzae
Swelling of eustachian tubes prevents mucus drainage and provides bacterial breeding grounds
Anatomical differences between kids and adults explain why infection rates increased for infants
Pressure placed on tympanic membrane creates pain

44
Q

Satellite test

A

Some bacteria can’t grow on blood agar and need another way to get nutrients
S. aureus plated and has B hemolysis to release nutrients
Stimulates growth of bacteria that could not grow before only in the hemolytic zone
EX: H. influenzae

45
Q

Pertactin and hemagglutinin

A

Adhesins

Promote attachment to cilia in lungs

46
Q

Adenylate cyclase toxin and pertussis toxin (PTx)

A

Alter intracellular CAMP concentrations

47
Q

Tracheal cytotoxin

A

Suppresses cilia activity and promotes coughing fits

48
Q

Acellular Pertussis vaccine

A

Contains all virulence factors

49
Q

3 stages of Pertussis

A

1) Catarrhal (low fever and mild, occassional cough)
2) Paroxysmal (severe paroxysmal cough (whoop), vomiting, exhaustion, paroxysmal attacks, death)
3) Convalescent (gradual recovery)
Death often due to secondary pneumonia infection

50
Q

Bordet- Gengou Agar and Regan-Lowe medium

A

Selective for Bordatella species (pertussis)

51
Q

DaPT vaccine

A

Diphtheria, acellular Pertussis, and Tetanus vaccine

Booster required as a teenager

52
Q

MacConkey Agar

A

Selective for gram (-) ONLY
Gram (+) will not grow
Contains lactose, bile, and crystal violet

53
Q

Medusa-head colonies

A

Comma-shaped protrusions from colony edge under magnification
Bacillus anthracis

54
Q

Bacillus anthracis Tissue vs BAP culture

A

Tissue- short chains in capsules

BAP- long chains with endospores

55
Q

Anthrax spores

A

Infectious form
Sporulation requires poor nutrient conditions and exposure to oxygen
Very resistant to heat, cold, pH, dessication, and chemicals
Can survive for decades
Taken up by host and germinate

56
Q

Anthrax toxin

A
3 components
Lethal factor ( inactivates key signaling proteins and leads to cell death)
Edema factor (generates cyclic nucleotides to increase vascular permeability and edema)
Protective antigen (mediates entry of LF and EF into cell)
57
Q

Cutaneous anthrax

A

Spores enter skin through wound
Papule to vesicle to necrotic ulcer (eschar)
Infection typically more contained to entry site
Low fatality rate

58
Q

Inhalational anthrax

A

**Meningitis is a complication of INHALATIONAL ANTHRAX
Need a lot of spores to be infected
Spores rapidly engulged by macrophages in alveoli and transported to lymph nodes
Spores can germinate, lyse macrophages, and rapidly replicate in lymph node
Release of toxin results in mediastinal widening and pleural effusion
Bacteria enters bloodstream and causes toxemia and septic shock
High fatality

59
Q

Gastrointestinal anthrax

A

Consumption of undercooked contaminated meat
Bloody diarrhea, abdominal pain, toxemia and sepsis
High fatality rate
Not documented in U.S.

60
Q

Life cycle of Listeria

A

Bacteria actively invade intestinal epithelium
Become trapped in endocytic vacuole
Use Listeriolysin O (LLO) to escape from endocytic vacuole–pores made
Rapidly divide in cytoplasm
Form comet tails
Propel into cell wall and pentrate adjacent cell
Trapped in vacuole and escape again
Cycle repeats

61
Q

Diphtheria toxin (DTx)***

A

Only virulence factor for C. dipheriae
Single gene
Inactivates elongation factor 2
Prevents protein synthesis which leads to cell death

62
Q

Tinsdale Agar

A

Selective and differential

C. diphtheriae is black with brown halo

63
Q

Enterobacteriaceae family

A
Small gram (-) rods
Require selective media
4 major features:
1. Ferment glucose
2. Reduce nitrates to nitrites
3. Oxidase (-)
4. Motile (except Klebsiella and Shigella)
64
Q

4 major groups of Shigella

A

**S. dysenteriae (SD1)
S. flexneri
S. boydii
S. sonnei

65
Q

Dysentery

A

Diarrhea with blood and mucus in stool

66
Q

Hemolytic Uremic Syndrome (HUS)

A

Lysis of RBCs
Thrombocytopenia
Renal failure
Treat with Ciprofloxacin

67
Q

Reiter’s Syndrome

A

Conjunctivitis, urethritis, and arthritis

Only in people with HLA-B27 type

68
Q

Shiga toxin (STx)

A

Produced by S. dysenteriae only
Cleaves adenine residue from rRNA subunit which inhibits protein synthesis
Damages endothelial cells lining blood vessels–leads to HUS and kidney failure

69
Q

E coli serotypes

A
MANY
H antigen (flagella)
O antigen (LPS)
K antigen (capsule)
70
Q

Pathogenic E. coli

A
Divided into 6 pathovars
ETEC
EPEC
EHEC
EIEC
EAEC
UPEC
71
Q

Pyuria

A

WBCs in urine

72
Q

UPEC

A

Uropathogenic E. coli
Major cause of lower and upper UTIs in US
*****Expression of multiple pili (Type I pilus allows colonization of bladder) (P-type pilus allows colonization of ureters and kidneys)

73
Q

ETEC

A

Enterotoxigenic E. coli
Traveler’s diarrhea and childhood diarrhea (contaminated water)
Adhere to intestinal mucosa by fimbriae
Produce enterotoxins (heat-labile and heat-stable toxins)
Toxins cause water and electrolyte loss and rapid dehydration
Large volume watery diarrhea
Must rehydrate

74
Q

EPEC

A

Enteropathogenic E. coli
Persistent diarrheal disease in cihldren
High infant mortality in developing countries
Causes attaching and effacing lesions (loss of microvilli)
Large volume watery diarrhea

75
Q

EHEC

A

Enterohemorrhagic E. coli
Can cause hemorrhagic colitis, HUS (produces Shiga toxin)
Bloody diarrhea
Can be found in undercooked hamburger because cattle can be colonizers (O157:H7 serotype)

76
Q

If large volume watery diarrhea, suspect which two E. coli?

A

ETEC or EPEC

77
Q

If bloody stools suspect which 4 bacteria?

A

EHEC
Shigella
EIEC (maybe)
EAEC (maybe)

78
Q

Guillain Barre Syndrome

A

Peripheral neuropathy
Affects nerves in feet causing debilitating paralysis and neuro complications (spreads up)
Usually effects are temporary as nerves regenerate
Patients develop antibodies that are similar to self and attack nerve cells

79
Q

Pathogenesis of H. pylori

A

Invade mucus layer with polar flagella to reach underlying gastric epithelial cells
Release mucinase to degrade mucin layer
Release VacA to disrupt epithelial cell layer and T cell functions
Lamina propria exposed to stomach acid and cells death occurs
Peptic ulcer forms

80
Q

Halotolerant

A

Can grow at high salt concentrations

81
Q

Pathogenesis of Vibrio cholerae

A

Adhere to mucosal cell layer
Cholera toxin upregulates activity of CFTR chloride ion channel, leads to Cl- efflux and ionic imbalance
Leads to profuse, watery diarrhea
Little to no abdominal pain or vomiting

82
Q

Legionnaire’s disease

A

Immunocompromised, smokers, Chronic lung disease patients
Myalgia, headache, fever, chills, dry cough that leads to productive cough
Chest pain, vomiting, diarrhea, confusion, delirium
Septic shock
high mortality