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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
Staphylococcus epidermis Basics?
* Normal **Skin flora.** Contaminants blood cultures * Opportunistic pathogen * Grows on **mannitol salt** but does **not ferment** mannitol ⇢ red. * **Capsule and biofilms.**
26
Staphylococcus epidermidis Infection
* **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.
27
Staphylococcus saprophyticus traits
* 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
S. saprophyticus common disorder?
* UTIs (uncomplicated cystitis/pyelonephritis) in adolescent females, often newly sexually active. Treated with UTI antibiotics.
29
What are common UTI antibiotics?
Fluoroquinolones, Bactrim, Nitrofurantoin
30
Streptococcus pneumoniae traits? Catalase, Hemolysis, shape, capsule, sensitivity, solubility, antigens, respiration and fermentation.
* 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
How to type Streptococcus pneumoniae?
Use capsular Abs = Quelling reaction
32
Where does S. pneumoniae colonize?
Throat and nasopharynx ⇢ resp. droplet (aerosol) spread.
33
How does *S. pneumoniae* inhibit phagocytosis?
Capsular polysaccharide (90 serotypes) inhibits phagocytosis unless specific Ab is present.
34
How does *S. pneumoniae* increase adherence to mucosal surfaces?
**IgA protease cleaves secretory IgA.**
35
Describe *S. pneumoniae*'s **membrane-disrupting toxin:**
* Pneumolysin O = Pore-forming hemolysin from autolyzed *S. pneumo.* Activates complement, damages resp. epithelium ⇢ productive cough + blood.
36
Most common cause of **sepsis in children with sickle cell disease and dysfunctional spleen?**
Streptococcus pneumoniae
37
Pneumococcal pneumonia results in what kind of pneumonia? and what are it's symptoms?
* **Lobar** pneumonia * **Blood-tinged, rusty sputum** * Major cause of death * Blood cultures often positive. * **Meningitis** * Preceded by Bacteremia * **Otitis media and sinusitis**
38
What are the two **vaccines** for Streptococcus pneumoniae?
1. **Pneumococcal conjugate vaccine or PCV13 (Prevnar13)** 1. Vax for kids 2. **Pneumococcal polysaccharide vaccine or PPSV23** 1. Adult vax
39
Treatments for *S. pneumoniae*
* Macrolides, cephalosporin, and fluoroquinolones are used as alternatives to penicillin for pneumonia, otitis media, and sinusitis. * Cefotaxime or ceftriaxone (3rd gen) for meningitis.
40
Streptococcus pyogenes traits? Catalase, Hemolysis, shape, capsule, sensitivity, grouping, reservoir, solubility, antigens, respiration and fermentation.
* 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
How do you differentiate *Streptococcus pyogenes* from other B-hemolytic *Strep.?*
* **Use Bacitracin to differentiate.** * *S. pyogenes* is **sensitive** to penicillin G.
42
Streptococcus pyogenes Pathogenesis for adhesion/colonization:
* **M proteins** = immunogenic fimbriae adhesins * Protein F - binds fibronectin
43
Streptococcus pyogenes Pathogenesis for Invasion:
* Hyaluronidase = hydrolyze hyaluronic acid. May help tissue spreading. * Streptokinase = breaks down fibrin clot by activating plasminogen.
44
Streptococcus pyogenes Pathogenesis to inhibit phagocytosis:
Hyaluronic acid capsule = antiphagocytic but nonimmunogenic polysaccharide.
45
Streptococcus pyogenes Pathogenesis - Immune interference:
* 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
Streptococcus pyogenes Pathogenesis - Membrane-disrupting toxins:
* 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
Streptococcus pyogenes Suppurative Infections:
* Erysipelas * **Impetigo (non-bullous) - honey-crusted skin lesions ( versus S. aureus bullous impetigo).** * **Strep throat** * **Cellulitis** * **Necrotizing Fasciitis** * **Osteomyelitis, puerperal sepsis.**
48
Streptococcus pyogenes Toxin-Mediated Diseases:
* **Scarlet fever**: Strep throat + sandpaper rash + “strawberry tongue”. * **Toxic shock syndrome** (with bacteremia).
49
Streptococcus pyogenes Poststreptococcal sequelae:
* **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
Streptococcus pyogenes Treatment:
* 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
Non-bullous impetigo (pyoderma, impetigo contagiosa)
* 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
Describe Erysipelas:
* 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
Streptococcal disease complication
* **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
Streptococcus agalactiae Group B Strep (GBS)
* Catalase: Positive * Diplococci in chains * **B-Hemolytic** * Incomplete hemolysin = CAMP factor (Positive) * **CAMP test** (\>zone of hemolysis with S. aureus + hydrolyze Hippurate = ID
55
Streptococcus agalactiae Infections in adults
Asymptomatic carriage, mild febrile illness or UTI that can lead to amnionitis or endometritis in **Pregnant** women.
56
Streptococcus agalactiae Infections in **Neonate:**
* **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
What are the three species of **Viridans Streptococci?**
* ***S. salivarius*** * ***S. mutans*** * ***S. sanguinis***
58
Viridans Streptococci normal environment?
Normally found in **oral, GI, GU** tract microbiota.
59
Viridans Streptococci can be responsible for what two issues?
* **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
**Streptococcus bovis** traits
* 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
Enterococcus species that I need to know.
**E. faecalis** and **E. faecium**
62
Enterococcus traits:
* 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
Define nosocomial
Originating in a hospital
64
Enterococcus infection
* 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
Enterococcus Treatment
* 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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