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MSK Week 2 > Microbiology Midterm > Flashcards

Microbiology Midterm Flashcards

1
Q

Types of skin and soft tissue damage that can occur with infection

A

Exogenous, endogenous or toxin-mediated

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2
Q

Most soft tissue and exogenous skin infections are due to what?

A

Staph A or Strep pyogenes (Group A Strep)

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3
Q

Similarities between strep A and Staph A

A
  1. Both are transient skin flora
  2. They are both spreading infections
  3. Both form abscesses
  4. Both cause necrotizing fasciitis
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4
Q

What do we mean by spreading infection?

A
  1. Pyoderma (produces pus)
  2. Impetigo - Spreading infection of the epidermis
  3. Erysipelas
  4. Cellulitis - Subcutaneous, more serious
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5
Q

What types of necrotizing infections do they cause?

A

Fasciitis, gas gangrene (myonecrosis)

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6
Q

Streptococci in general are recognized how?

A
  1. Gram positive
  2. Chains
  3. Catalase negative (cannot convert H2O2)
  4. Have capsules
  5. Obligate extracellular bacteria, meaning they avoid uptake by neutrophils and have many anti-phagocytic virulence factors
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7
Q

Main virulence factor for strep

A

M protein, which binds the epidermis and is antiphagocytic

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8
Q

What kind of hemolytic pattern do we see in Strep A?

A

Beta

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9
Q

How do we know we are working with Strep A?

A
  1. Beta hemolytic
  2. PYR positive
  3. Sensitive to Bacitracin
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10
Q

What kind of capsule does Strep A have?

A

Hyaluronic acid capsule, which is identical to normal tissue and is anti-phagocytic

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11
Q

What are the key extracellular virulence factors for strep A?

A
  1. Makes pyogenic exotoxins
  2. Makes streptolysin 0 which is hemolytic
  3. Makes DNAases to evade neutrophil traps
  4. Makes streptokinase to lyse blood clots
  5. Makes C5a peptidase to stop attraction of PMNs
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12
Q

What do pyrogenic exotoxins do?

A

superantigens stimulate cytokines storm, nonspecifically activate T cells.

These are encoded by bacteriophages and can cause scarlet fever and toxic shock syndrome

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13
Q

Two types of clinical presentations of Strep A?

A

Suppurative vs. Non suppurative

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14
Q

Suppurative presentations of Strep A?

A

Pharyngitis (Can lead to Scarlet Fever, a super antigen)

Toxic Shock-like syndrome

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15
Q

Nonsupprative presentations of Strep A?

A

Rheumatic fever
Acute glomerulonephritis

Both of these diseases happen after the bug is gone, known as “post suppurative sequelae”

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16
Q

Rheumatic fever

A

Ab to M type from throat infection attack heart/body, requires long term abx to prevent reinfection

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17
Q

Acute glomerulonephritis

A

antigen-Ab complexes deposited in glomeruli s/p throat or skin infection

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18
Q

How do we treat Strep A?

A

PCN G

Cephalosporins

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19
Q

How do we treat Strep A if the patient also has Staph A?

A

PCNase resistant antibiotic

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20
Q

What pediatric syndrome is associated with Strep A?

A

PANDAS

pediatric autoimmune neuropsychiatric disorder assoicated with group A Strep

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21
Q

How many more or less strains are there of staph A than strep A?

A

90 of Strep A

30 Staph A

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22
Q

How do we recognize staph A?

A
  1. Beta hemolytic
  2. Catalase positive
  3. Coagulase positive
  4. Gram positive cocci
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23
Q

Staph A characteristics

A

Facultative anaerobe
Forms clusters
Common in hospitals
Pus infections

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24
Q

Besides cellulitis and impetigo which we also see in Strep A, what skin infections do we see in Staph A?

A

Furuncles
Carbuncles
Mastitis
Styes

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25
Q

What type of invasive infections do we see with Staph A?

A

Deep lesions
Bacteremia
Septic Shock

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26
Q

What type of deep lesions do we see with staph A?

A

Osteomyelitis
Septic Arthritis
Meningitis
PNA

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27
Q

What type of bacteremias do we see with Staph A?

A

Endocarditis
Pyelonephritis
Septicemia
(Meningitis and PNA technically fall into this as well)

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28
Q

How can we kill Staph A with our own defense mechanisms?

A

Opsonophagocytosis. It is not susceptible to lysis by MAC complex or the classical pathway

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29
Q

Staph A virulence factors

A

Pa Likes His Ribs Cooked 4 times

Protein A
Leukocidin
Ribotechoic Acid
Catalase
Coagulase
Capsule
Cytotoxins
Hyaluronidase
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30
Q

Protein A?

A

linked to peptidoglycan, binds Fc end of Ab, avoids uptake by neutrophils

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31
Q

Catalase

A

defense against phagocytes- breaks down H2O2 during oxidative burst

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32
Q

Leukocidin

A

pokes holes in granulocyes

33
Q

Ribotechoic acid and techoic

A

binds ECM to set up shop, techoic acid induces toxic shock

34
Q

Coagulase

A

Walls off abscesses

35
Q

Capsule

A

Can’t target this with a vaccine because it has 8 types

36
Q

Hyaluronidase

A

Breaks down Hyaluronic Acid to spread deeper

37
Q

Cytotoxins of Staph A and what they do

A 
Alpha Hemolysin (forms pores)
Beta Toxin (sphingomyelinase C - Hydrolyzes membrane lipids)
Delta Toxin (Cytolytic)
Gamma Toxin and Panton Valentine Leukocidin (Both of these form pores and lyse neutrophils and macrophages)
38
Q

Toxin diseases of Staph A

A 
Bullous Impetigo
Scalded Skin Syndrome
Staph Scarlet Fever
Toxic Shock Syndrome
Food poisoning
39
Q

Bullous impetigo caused by what toxin from Staph A?

A

Exfoliatin A, B cause bullous impetigo

40
Q

What is the Staph A toxin mediated condition scalded skin syndrome?

A

ridders disease, Exfolatin serine proteases cause splitting of desmosomes in stratum granulosum of epidermis

41
Q

What causes food poisoning in Staph A?

A

Staph enterotoxin A, B, C, D, E

42
Q

What tools do we use to identify Staph A?

A

• Identify by Pulsed Field Gel Electrophoresis, bacteriophage typing (most strains carry phages)

43
Q

Gene for MRSA

A

mecA gene (encodes PBP2’- altered penicillin binding protein)

44
Q

Types of Vancomycin resistance in Staph A?

A

VISA- vancomycin intermediate S. aureus

VRSA- vancomycin resistant S. aureus

45
Q

When are we concerned about Staph Intermedius?

A

Dog Bite

46
Q

Identifying Staph Epidermidis?

A

Catalase positive, coagulase negative. These are the guys that make biofilms

47
Q

Takeaway diseases of Staph Epidermidis?

A

UTI (the biggie)
Osteomyelitis
Bacteremia
Indwelling device infection

48
Q

Structural observations of Alpha Herpes Virus

A
  1. Lipid Bilayer envelope
  2. Large genome with double stranded DNA (They encode enzymes for DNA replication so they can survive in cells that don’t divide)
49
Q

Cells affected by Alpha Herpes Simplex

A

Infects epithelial cells, latency in sensory ganglia/ neurons

50
Q

Life Cycle of Alpha Herpes Virus

A
  1. Lytic Phase - Occurs in epithelial cells
  2. Latency phase - Occurs in neurons. Express LAT transcript, DNA remains in nucleus of neuron but no proteins are made.
  3. Reactivation - In epithelial regions innervated by a neuron and can be asymptomatic like in HSV-2
51
Q

4 Phases of lytic phase

A

4 phases of gene expression:

  1. immediate early (transcription factors)
  2. early (enzymes for DNA rep)
  3. DNA replication
  4. late (structural proteins/ viral assembly)
52
Q

Treatment for Alpha Herpes Viruses

A
  1. Herpes Thymidine Kinase

2. Phosphonoacetic acid/Phosphonoformate

53
Q

Effect of Herpes Thymidine Kinase on Alpha Herpes viruses

A

Drugs are converted from their prodrug form to active inhibitor of DNA replication by the Viral TKs themselves.

Examples are acyclovir and gancicyclovir which are used to treat CMV

54
Q

What are the effects of Phosphonoacetic acid and phosphonoformate?

A

Treat CMV by inhibiting the replication of herpes. These are analogs of triphosphate, and thus competitively bind active sites of DNA polymerase, making them useless. The only problem is that this must be given continuously via IV

55
Q

Herpes Simplex Virus types

A

HSV-1

HSV-2

56
Q

HSV-1 Presents as what?

A

Oral cold sores, can cause blindness (keratitis) and encephalitis. Typically targets Trigeminal ganglia

57
Q

HSV-2 Presents how?

A

Geneital, severe CNS disease in infants. IgG protection on reactivation but only have IgM on primary infection)

58
Q

Herpes Zoster Virus presentation

A

Chicken pox on primary infection and shingles on secondary. Exists as varicella for pox and zoster as shignles. This spreads by the respiratory tract

59
Q

How do we test for Herpes Zoster and what should we do to prevent it?

A

Use a Tzanck smear to find it, which will show synsitia/ multinucleated giant cells. And get the damn live attenuated vaccine for your kids.

60
Q

What fungal types are there?

A

Yeast
Mold
Dimorphic

61
Q

Yeast structure and reproductive traits?

A

Unicellular fungus that reproduces by budding or binary fission

62
Q

Mold structure and reproduction?

A

Multicellular fungus that has networks of hyphae (mycelium, apical growth) septa (walls) and can have pores. It reproduces by making spores which are dormant dispersal units

63
Q

Good targets on fungi?

A

Cell Wall - Has Chitin-B (1,6) Glucan and B-(1,3) glucan which are not found in humans.
Cell Membrane - Ergosterol, also not in humans

64
Q

Yeast pathogens

A

Superficial pathogens. Malassezia yeast and trichosporon

65
Q

Mold pathogens

A

Cutaneous typically. We have microsporum, trichophyton and Epidermophyton

66
Q

How do we diagnose fungal infections?

A
  1. Direct microscopy (KOH, calcoflour white)

2. Culture (Gold standard, use Sabouraud’s ager which inhibits bacterial growth)

67
Q

Types of antifungals?

A

Azoles, Polyenes, Echinocandins

68
Q

What do azoles do?

A

Inhibit ergosterol snthesis. They can cause drug reactions and visual disturbances though.

69
Q

What do Polyenes do?

A

Bind ergosterol and make pores for osmotic death (also called amphotericin). Danger for this is renal toxicity

70
Q

What do echinocandins do?

A

Inhibit synthesis of B-glucan and block cell wall synthesis. These drugs end in “fungin” and are broad spectrum

71
Q

What immune responses do we have to fungi?

A

Endothelial cells - Have Dectin-1 receptor to recognize B-glucans. Release defensins
Neutrophils target extracellular molds like aspergillus
Th1 targets intracellular fungi like histoplasmosis
Th17 targets mucosal fungal infections

72
Q

How do we classify mycoses?

A

By their location

  1. Superficial
  2. Cutaneous
  3. Subcutaneous
  4. Systemic
  5. Opportunistic
73
Q

Describe superficial mycoses

A

outer keratinized skin, mostly yeast

74
Q

What is Tinea Versicolor and how can we recognize it?

A

Tinea versicolor - dandruff, hypo or hyperpigmented macules- caused by overgrowth of malassezia furfur.

Culture growth is enhanced by lipids (it is a lipophilic yeast) Looks like spaghetti in stain

75
Q

Describe cutaneous mycoses

A

invasion of epidermis with inflammatory response. Can cause athlete’s foot, ringworm and is caused by dermatophytes, the most common being trichophyton, epidermophyton, and microsporum

76
Q

Describe subcutaneous mycoses

A

invasion of subcutaneous tissue, may req surgery, rare, introduced traumatically, infection to dermis, subcutaneous tissue, bone

77
Q

Common subcutaneous mycosis

A

Sporotrichosis (think stuck by a rosebush). Lives in soil, usually starts on hands, lesions and nodules track up lymphatics= “sporotrichoid spread”

78
Q

Describe systemic mycoses

A

inhalation of spores, dimorphic fungi

79
Q

Opportunistic Mycoses

A

Occur in immune compromised hosts

MSK Week 2 (28 decks)

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