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BMR 605 TEST 2 > TEST 2 Bugs 1 Part 1/2 > Flashcards

TEST 2 Bugs 1 Part 1/2 Flashcards

1
Q

Staphylococcus aureus
Catalase?
Coagulase?
Hemolytic? (Details)
Colony description
Salt?

A
  • Catalase: Positive
  • Coagulase: Positive
  • B-Hemolytic (Pale/Clear area surrounding colonies on blood agar)
  • Golden yellow colonies
    • Grape-like clusters
    • Polysaccharide capsule
  • Ferments Mannitol salt (yellow)
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2
Q

Staphylococcus aureus

Pathogenesis for colonization:

A
  • Adhesins = attach to collagen
  • Fibronectin-binding protein = bind to clots and
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3
Q

Staphylococcus aureus

Pathogenesis for Invasion:

A
  • Staphylokinase = lyse fibrin clot
  • Hyaluronidase = hydrolyze hyaluronic acid. Tissue Spreading.
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4
Q

Staphylococcus aureus

Pathogenesis for inhibit phagocytosis:

A
  • Polysaccharide capsule
  • Protein A - bind IgG Fc.
  • Coagulase - activates prothrombin to form a clot.
  • Clumping factor = bound coagulase - bind fibrin to wall off abscess
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5
Q

Staphylococcus aureus

Pathogenesis to enhance survival:

A
  • Catalase - Removes H2O2
  • B-lactamase - cleaves penicillin
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6
Q

Staphylococcus aureus

Pathogenesis

Membrane-disrupting toxins:

A
  • Cytolytic/hemolysins - alpha, beta, sigma, gamma.
    • Cause eukaryotic cell pores.
  • Panton-Valentine Leukocidin (PVL) - pore forming toxin encoded on plasmids in CA-MRSA strains.
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7
Q

Staphylococcus aureus

Pathogenesis

Exotoxins:

A
  • TSST-1 - Superantigen that binds MHC-II without processing antigen ⇢ activated T cells ⇢ massive cytokine release (Toxic shock syndrome, TSS).
  • Enterotoxins A (SEA), B(SEB), C, D, etc. Heat-Stable superantigens.
  • Cause vomiting and diarrhea (food poisoning) and TSS.
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8
Q

Staphylococcus aureus

Infections

Pyogenic Infections

A
  • Impetigo (bullous and non-bullous), folliculitis, styes, furuncles/boils, carbuncles, mastitis, wound infections, otitis externa.
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9
Q

Staphylococcus aureus

Infections

Systemic Infections

A
  • Pneumonia (often after influenza virus infection), empyema, septicemia, septic arthritis, osteomyelitis, endocarditis.
    • Endocarditis: Acute endocarditis, rapid onset of symptoms, very ill patient, often no pre-existing valve disease (i.e. NO mitral valve prolapse).
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10
Q

Staphylococcus aureus

Infections

Toxigenic Infections:

A
  • Food poisoning, toxic shock syndrome, Staph. scalded skin syndrome.
    • Food poisoning
      • Common in Mayonnaise
      • Preformed toxins: Rapid (3-6hr) onset of nausea, vomiting, abdominal cramps and diarrhea (rare). Over in <24hr.
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11
Q

Staphylococcus aureus

Toxic Shock Syndrome (TSS)

A
  • Found commonly in Surgical Packing or hyper-absorbent tampons.
  • S. aureus produces TSST-1 or SEB/C
    • Results in: High fever, rash (diffuse, red erythroderma), hypotension, vomiting, diarrhea, desquamation of palms and soles, possible multi-organ failure.
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12
Q

Staphylococcus aureus

Staphylococcal scalded skin syndrome (SSSS)

A
  • Infection of umbilicus or face in < 5 year-olds.
  • Exfoliative toxins ⇢ large bullae (blisters) and epithelial desquamation (intra-epidermal, stratum granulosum).
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13
Q

Staphylococcus aureus

Anti-staph antibiotics

A
  • Most strains of Staph resistant to penicillin by producing penicilinase (B-lactamase), treated with anti-staphylococcal penicillins:
    • Dicloxacillin, Nafcillin, oxacilin, or methicillin.
  • First generation cephalosporins:
    • Cephalexin
    • B-lactam plus inhibitor.
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14
Q

What is another name for penicillinase?

A

B-Lactamase

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15
Q

What does MRSA mean?

A

Methicillin Resistant Staph Aureus

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16
Q

MRSA contain Xsomal mecA gene, what is it?

A

Modified penicillin-binding proteins (PBSs, transpeptidase).

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17
Q

What is HA-MRSA treated with?

(Hospital Acquired)

A

Treated with Vancomycin, linezolid, daptomycin, or ceftaroline.

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18
Q

Describe CA-MRSA

A
  • Less antibiotic resistance than HA-MRSA.
  • More virulent and more invasive (PVL).
  • Treated with trimethoprim-sulfamethoxazole (Bactrim).
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19
Q

Where did Methicillin- and vancomycin-resistant S. aureus acquire this trait from?

A

Enterococcus plasmid

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20
Q

Describe B-Lactamases?

A
  • Major mechanism of antibiotic resistance in Gram-negative pathogens.
  • Synthesized in cytoplasm and secreted into periplasm.
  • Gram-positives synthesize in cytoplasm and secrete them extracellularly.
  • Most are on plasmids.
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21
Q

What are the Three types of B-Lactamases?

A
  1. Penicillinases inactivate penicillins
  2. Extended-spectrum B-Lactamases (ESBLs) inactivate most B-lactams except for carbapenems.
  3. Carbapenemases (e.g., OXA, KPC, metallo-B-lactamase) inactivate carbapenems.
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22
Q

Define Bacteriostatic

A

Agents inhibit bacterial growth while the agent is present. Rely on the immune system (of an immunocompetent person) to aid the bacteriostatic agent and clear the infection.

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23
Q

Define Bactericidal?

A

Agents kill bacteria but are bacteriostatic under some conditions, e.g., in biofilms.

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24
Q

Staphylococcus epidermidis
Catalase?
Coagulase?
Urease?
Hemolytic? (Details)
Colony description
Capsule type
Notable Sensitivity?

A
  • Catalase: Positive
  • Coagulase: Positive
  • Urease: Positive
  • Hemolytic? Non-Hemolytic (gamma-hemolysis) salt tolerant.
  • White Colonies, arranged in grape-like clusters.
  • Polysaccharide Capsule
  • Novobiocin sensitive
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25
Q

Staphylococcus epidermis Basics?

A
  • Normal Skin flora. Contaminants blood cultures
  • Opportunistic pathogen
  • Grows on mannitol salt but does not ferment mannitol ⇢ red.
  • Capsule and biofilms.
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26
Q

Staphylococcus epidermidis Infection

A
  • Catheter or prosthetic device infections (hip implant, heart valve). Endocarditis of artificial valves.
  • Endocarditis in people with indwelling IV catheters or IV drug users.
  • Vancomycin is the drug of choice.
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27
Q

Staphylococcus saprophyticus traits

A
  • Catalase: Positive
  • Coagulase: Negative
  • Novobiocin resistant
    • Differentiate from S. epidermidis with novobiocin.
  • Nitrite negative on urine dipstick
  • Opportunistic pathogen.
  • Sexual activity (honeymooner’s cystitis)
  • Normal Vaginal and GIT flora
28
Q

S. saprophyticus common disorder?

A
  • UTIs (uncomplicated cystitis/pyelonephritis) in adolescent females, often newly sexually active. Treated with UTI antibiotics.
29
Q

What are common UTI antibiotics?

A

Fluoroquinolones, Bactrim, Nitrofurantoin

30
Q

Streptococcus pneumoniae traits?

Catalase, Hemolysis, shape, capsule, sensitivity, solubility, antigens, respiration and fermentation.

A
  • AKA, Pneumococcus
  • Catalase: Negative
  • A-Hemolytic (green colony on blood agar under room air)
  • Lancet-shaped diplococcus
  • Polysaccharide capsule
  • Optochin sensitive (P disk)
    • Used to differentiate S. pneumoniae from a-hemolytic Viridans Strep.
  • Bile Soluble (cellular autolysin is activated by bile salts).
  • No Lancefield antigens
  • Facultative anaerobe, but ferments in the presence of O2.
31
Q

How to type Streptococcus pneumoniae?

A

Use capsular Abs = Quelling reaction

32
Q

Where does S. pneumoniae colonize?

A

Throat and nasopharynx ⇢ resp. droplet (aerosol) spread.

33
Q

How does S. pneumoniae inhibit phagocytosis?

A

Capsular polysaccharide (90 serotypes) inhibits phagocytosis unless specific Ab is present.

34
Q

How does S. pneumoniae increase adherence to mucosal surfaces?

A

IgA protease cleaves secretory IgA.

35
Q

Describe S. pneumoniae’s membrane-disrupting toxin:

A
  • Pneumolysin O = Pore-forming hemolysin from autolyzed S. pneumo. Activates complement, damages resp. epithelium ⇢ productive cough + blood.
36
Q

Most common cause of sepsis in children with sickle cell disease and dysfunctional spleen?

A

Streptococcus pneumoniae

37
Q

Pneumococcal pneumonia results in what kind of pneumonia? and what are it’s symptoms?

A
  • Lobar pneumonia
    • Blood-tinged, rusty sputum
    • Major cause of death
    • Blood cultures often positive.
  • Meningitis
    • Preceded by Bacteremia
    • Otitis media and sinusitis
38
Q

What are the two vaccines for Streptococcus pneumoniae?

A
  1. Pneumococcal conjugate vaccine or PCV13 (Prevnar13)
    1. Vax for kids
  2. Pneumococcal polysaccharide vaccine or PPSV23
    1. Adult vax
39
Q

Treatments for S. pneumoniae

A
  • Macrolides, cephalosporin, and fluoroquinolones are used as alternatives to penicillin for pneumonia, otitis media, and sinusitis.
  • Cefotaxime or ceftriaxone (3rd gen) for meningitis.
40
Q

Streptococcus pyogenes traits?

Catalase, Hemolysis, shape, capsule, sensitivity, grouping, reservoir, solubility, antigens, respiration and fermentation.

A
  • Catalase: negative
  • B-Hemolytic
  • Arranged in chains
  • Hyaluronic acid capsule (aids in cellulitis)
  • Bacitracin sensitive (A disk)
  • Lancefield Group A
  • Reservoir: Human oropharynx
  • Facultative anaerobe, but ferments in the presence of O2.
41
Q

How do you differentiate Streptococcus pyogenes from other B-hemolytic Strep.?

A
  • Use Bacitracin to differentiate.
    • S. pyogenes is sensitive to penicillin G.
42
Q

Streptococcus pyogenes

Pathogenesis for adhesion/colonization:

A
  • M proteins = immunogenic fimbriae adhesins
  • Protein F - binds fibronectin
43
Q

Streptococcus pyogenes

Pathogenesis for Invasion:

A
  • Hyaluronidase = hydrolyze hyaluronic acid. May help tissue spreading.
  • Streptokinase = breaks down fibrin clot by activating plasminogen.
44
Q

Streptococcus pyogenes

Pathogenesis to inhibit phagocytosis:

A

Hyaluronic acid capsule = antiphagocytic but nonimmunogenic polysaccharide.

45
Q

Streptococcus pyogenes

Pathogenesis - Immune interference:

A
  • C5a peptidase - interferes with PMN attraction (reduce inflammation)
  • M Proteins - draw factor H to inhibit the alternative complement pathway (inhibiting C3b formation) and opsonization.
46
Q

Streptococcus pyogenes

Pathogenesis - Membrane-disrupting toxins:

A
  • Streptolysin O = a hemolysin that stimulates anti-streptolysin O (ASO) titer.
  • Erythrogenic toxins A and C (SPE-A and SPE-C) = pyrogenic superantigens ⇢ fever, rash, T cell proliferation and B cell suppression. Phage encoded. TSS.
47
Q

Streptococcus pyogenes

Suppurative Infections:

A
  • Erysipelas
  • Impetigo (non-bullous) - honey-crusted skin lesions ( versus S. aureus bullous impetigo).
  • Strep throat
  • Cellulitis
  • Necrotizing Fasciitis
  • Osteomyelitis, puerperal sepsis.
48
Q

Streptococcus pyogenes

Toxin-Mediated Diseases:

A
  • Scarlet fever: Strep throat + sandpaper rash + “strawberry tongue”.
  • Toxic shock syndrome (with bacteremia).
49
Q

Streptococcus pyogenes

Poststreptococcal sequelae:

A
  • Acute glomerulonephritis
    • Pharyngitis or impetigo
  • Rheumatic fever
    • Sequela to untreated GAS pharyngitis only (not impetigo). Abs cross-react between M protein and heart muscle or joint antigens ⇢ damage (autoimmune, molecular mimicry).
50
Q

Streptococcus pyogenes

Treatment:

A
  • Penicillin G
  • Penicillin V
  • Erythromycin
  • Penicillinase-resistant penicillin: in skin infections where Staph could be the responsible organism.
  • After Rheumatic fever:
    • continuous prophylactic antibiotics to prevent repeat strep throat.
  • Clindamycin when:
    • Necrotizing fasciitis
    • Streptococcal toxic shock syndrome
51
Q

Non-bullous impetigo (pyoderma, impetigo contagiosa)

A
  • Most commonly caused by S. aureus, second most common S. pyogenes.
  • Contagious, superficial infection
  • Primarily young children
    • Poor personal hygiene
  • “honey colored” crusted lesions
  • Be careful: Nephrogenic GAS can lead to post-streptococcal glomerulonephritis.
52
Q

Describe Erysipelas:

A
  • Type of Cellulitis
    • Superficial erythematous and edematous lesions.
      • Fiery red (salmon red) advancing erythema.
  • Mainly caused by GAS
  • Be careful: Sometimes, erysipelas cannot be reliably distinguished from cellulitis. Patients that have systemic manifestations (fever/chills) should be treated with parenteral therapy to cover S. aureus.
53
Q

Streptococcal disease complication

A
  • Pharyngitis: “Strep throat” exudates (suppurative) on tonsils (children 5-15 yrs).
  • Scarlet fever: Complication of strep pharyngitis that occurs when the infecting strain is lysogenized by a bacteriophage that produces a pyrogenic exotoxin.
54
Q

Streptococcus agalactiae

Group B Strep (GBS)

A
  • Catalase: Positive
  • Diplococci in chains
  • B-Hemolytic
    • Incomplete hemolysin = CAMP factor (Positive)
      • CAMP test (>zone of hemolysis with S. aureus + hydrolyze Hippurate = ID
55
Q

Streptococcus agalactiae Infections in adults

A

Asymptomatic carriage, mild febrile illness or UTI that can lead to amnionitis or endometritis in Pregnant women.

56
Q

Streptococcus agalactiae Infections in Neonate:

A
  • Early onset (1-6 days) = Resp. problems, sepsis, pneumonia, meningitis.
    • Acquired in utero or at delivery.
    • Most common in premature infants
  • Late onset (≥7 days) = septicemia and meningitis.
    • Acquired postpartum
    • Low mortality rate (<20%)
57
Q

What are the three species of Viridans Streptococci?

A
  • S. salivarius
  • S. mutans
  • S. sanguinis
58
Q

Viridans Streptococci normal environment?

A

Normally found in oral, GI, GU tract microbiota.

59
Q

Viridans Streptococci can be responsible for what two issues?

A
  • SUBACUTE Endocarditis: May follow Dental trauma if have damaged heart valves.
    • Caused by S. sanguinis
  • Dental caries, tooth abscesses and periodontitis.
    • S. mutans causes dental plaque and dental caries through production of dextran biofilm.
60
Q

Streptococcus bovis traits

A
  • a or no Hemolysis
  • Lancefield group D
  • Important members:
    • S. gallolyticus
    • S. Infantarius
  • Colonizes the GI tract. Normal.
  • No growth in 6.5% NaCl
  • Strongly associated with Colorectal cancer
61
Q

Enterococcus species that I need to know.

A

E. faecalis and E. faecium

62
Q

Enterococcus traits:

A
  • Catalase: Negative
  • a, B, or no hemolysis
  • Normal in GI tract and vaginal microbiota.
  • Vancomycin resistance = modification of cell wall peptidoglycan pentapeptide precursor from -D-Ala-D-Ala to -D-Lactate-D-Lactate.
  • Grows in bile, and is bacitracin resistant.
63
Q

Define nosocomial

A

Originating in a hospital

64
Q

Enterococcus infection

A
  • Significant nosocomial agents.
    • Cause septicemia, wound infections, and UTI.
      • Esp. in patients with urinary or intravascular catheters.
  • Subacute endocarditis in patients with previously damaged hearts following urinary or GI tract manipulations.
65
Q

Enterococcus Treatment

A
  • Relatively resistant to cell wall agents.
    • Penicillin & vancomycin
  • Bacteremia: Often use synergistic therapy
    • Vancomycin/gentamycin
    • Ampicillin/gentamycin
  • Vancomycin-resistant enterococcus (VRE)
    • Dangerous hospital acquired infection
    • Linezolid, Daptomycin.

BMR 605 TEST 2 (10 decks)

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