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Module 2: MSK > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are the two most common causes of skin and soft tissue infections as they appear on a Gram stain?

A
  1. Staphylococci: Gram+ cocci in clusters
  2. Streptococci: Gram+ cocci in chains

–> Each have thick murein layers, thus the Gram+ stain

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2
Q

What are the 3 sources of skin and soft tissue infections?

A
  1. Exogenous: direct invasion of microbe from external environment
  2. Endogenous: invasion of microbe from an internal source, such as blood or infected organ
  3. Toxin: mediated manifestations from an infection at a distant site
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3
Q

What are the most frequent transient skin flora found on humans?

A
  1. Staphylococcus aureus
  2. Streptococcus pyogenes (Group A strep)
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4
Q

What are the most frequent resident skin flora found on humans?

A
  1. staphylococcus epidermidis
  2. propionibacterium acnes
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5
Q

What types of skin and soft tissue infections are often caused by staphylococci?

A

Folliculitis

Carbuncles, furuncles

Impetigo

Cellulitis

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6
Q

What types of skin and soft tissue infections are often caused by streptococci?

A

Impetigo

Erysipelas

Cellulitis

Synergistic cellulitis

necrotizing fasciitis

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7
Q

What are the characteristics of pyogenic cocci?

A

Streptococci are:

Invasive

Produce purulent lesions

obligate extracelluar bacteria

have anti-phagocytic virulence factors

Facultative anaerobes (live w/ or w/o oxygen)

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8
Q

What diagnostic criteria need to be met to confirm streptococci infection?

A
  1. Gram+ stain in pairs or chains
  2. Catalase negative
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9
Q

What diagnostic criteria is used to classify streptococci?

A
  1. Hemolytic pattern on blood agar
  2. Physiological traits and biochemical reaction
  3. antigenic composition
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10
Q

What are the three hemolytic patterns found around streptococcal blood agar colonies?

A
  1. alpha-hemolytic: greenish hemolysis
  2. beta-hemolytic:complete/clear hemolysis (bad)
  3. gamma-hemolytic: no hemolysis (good)
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11
Q

What kind of hemolytic pattern does Group A strep (S. pyogenes) have?

A

beta-hemolysis: complete hemolysis

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12
Q

What are diagnostic characteristics of Group A strep?

A

Group A strep = Strep. pyogenes:

  • Gram+ cocci in chains
  • beta-hemolytic
  • catalase negative
  • PYR positive
  • bacitracin sensitive (shown by bacitracin disk in blood culture plate)
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13
Q

Describe the rapid test used to detect Streptococci bacteria in a patient.

A

Control antigen and test capture antibody are fixed to test strip.

Gold-labeled (red) antibody is diffuse and not fixed to paper.

Paper is dipped in specipen w/suspect antigen and if capture antibody and control antigen show, test is positive

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14
Q

What are virulence factors for S. pyogenes (Group A Strep)?

A

M Protein
Hyaluronic acid capsule
Pyrogenic exotoxins
Streptolysin O
DNAases
Streptokinase
C5a peptidase

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15
Q

What are components of the streptococcal cell wall?

A
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16
Q

What is M protein?

A

A virulence factor of Group A Streptococci:
Involved in binding to epidermis and is anti-phagocytic.

  • Antibody to M protein is type specific; there are ~90 types
  • Share sequence homology with some mammalian proteins (i.e. tropomyosin, human heart)
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17
Q

Why are vaccines to M proteins dangerous?

A

If vaccine was not thoroughly screened, it could lead to autoimmunity to those vaccinated b/c of M proteins molecular mimicry of host components

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18
Q

What is a hyaluronic acid capsule?

A

Group A Strep virulence factor:

identical to component in normal tissue, anti-phagocytic, antibody to capsule not protective to host

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19
Q

What is pyrogenic exotoxins?

A

Virulence factor of Group A Strep:

  • Fever producing toxin
  • Super antigens stimulate production of cytokins
  • Involved in pathogenesis of scarlet fever and toxic shock-like syndrome
  • Depends on lysogeny of bacterium with temperate phage
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20
Q

How do superantigens work?

A

Bind TCR to MHC; no specific peptid required

  • leads to wide-spread Tcell activation:
    Fever
    Confusion
    Hypotension
    Headache and vomiting
    Diarrhea
    Abdominal pain/weakness
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21
Q

What is streptolysin O?

A

Virulence factor for Group A Strep (S. pyogenes):

  • O2 labile, antigenic, hemolytic, toxic to wide variety of cells
  • antibodies to toxin basis of anti-streptolysin O test
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22
Q

What are DNAases?

A

Strep. pyogenes (Group A strep) virulence factor:

  • depolymerizes cell-free DNA in purulent lesions
  • measure antibodies to these proteins as aid to diagnosis of recent disease
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23
Q

What is streptokinase?

A

Group A Strep (S. pyogenes) virulence factor:

  • lyses blood clots
  • helps bacteria spread
  • can be used commercially to clean wounds (surgical enzymatic debridgement)
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24
Q

What are clinical presentations of suppurative streptococcal disease?

A

-Pharyngitis (uncommonly w/Scarlet Fever)

  • Pyoderma: Impetigo
    Ersipelas
    Cellulitis
    Necrotizing faciitis
  • Streptococcal toxic shock syndrome
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25
Q

What is Scarlet fever?

A

Group A strep (S. pyogenes) infection characterized by:

  • strawberry tongue
  • circumoral pallor around lips
  • desquamation that follows rash of S.F.
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26
Q

How does Streptococcal Toxic Shock Syndrome usually occur?

A

Infecting strains produce pyrogenic toxins

  • clinically, like staphyloccocal toxic shock syndrome EXCEPT PATIENTS ARE BACTEREMIC and many have necrotizing faciitis
  • high fatality rate
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27
Q

What are clinical presentations of non-suppurative streptococcal infection?

A

Rheumatic Fever

Acute glomerulonephritis

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28
Q

What is rheumatic fever?

A
  • Presents after streptococcal throat infection of 6-15 year olds after infection with certain rheumatogenic M types of Group A strep
  • Autoimmune mehcanisms likely; cross reaction between anti-M protein Abs and heart tissue
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29
Q

What is acute glomerulonephritis?

A

After throat or skin infection with certain nephritogenic M types of Streptococci.

  • Renal injury due to deposition of antigen-antibody complexes on glomeruli (Type III hypersensitivity)
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30
Q

Why is it critical to always treat Group A Strep (S. pyogenes) infections?

A

In order to prevent nonsuppurative disease post-infection

  • The earlier the treatment, the less time the patient’s immune system has to produce autoimmune antibodies resultant from infection
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31
Q

What is PANDAS Syndrome?

A

Pediatric Autoimmune neuropsychiatric disorder associated with group a Strep (PANDAS) characteristic of:

  • Presence of OCD and/or tic disorder
  • Pediatric onset
  • Abrupt onset and episodic course of symptoms
  • association with GAS infections
  • Association with neurologic abnormalities (i.e. motoric hyperactivity, choreiform movements, tics)
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32
Q

What are characteristics of Staphylococci that can be determined by culture?

A

Gram+ cocci that form clusters

Facultatively anaerobic (can go w/ or w/o oxygen)

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33
Q

What factors are used to identify staphylococcus species?

A
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34
Q

What is the hallmark of staphylococcal infections?

A

pus (PMNs, dead tissue, bacteria)

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35
Q

What is hydradentis Suppurativa?

A

Staphylococcal infection infection of sweat glands

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36
Q

What is the primary treatment of cutaneous staphylococcal infections and why?

A

heat and drainage

  • use of antibiotics only if invades subcutaneous layer b/c of antibiotic resistance
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37
Q

Why are antibiotics given to patients before surgery?

A

prophylaxis for hospital-acquired staph infections

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38
Q

What are some invasive, deep lesion infections caused by Staphylococcus aureus?

A

Osteomyelitis

septic arthritis

meningitis

pneumonia

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39
Q

What are some invaseive, bacteremia infections caused by Staphylococcus aureous?

A

endocarditis

meningitis

pneumonia

pyelonephritis

septicemia, septic shock

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40
Q

What are some risk factors for boils, furnuncles, carbuncles infections?

A

Diabetes mellitus, acne, occupational (wet conditions), poor hygiene

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41
Q

What are some risk factors for wound infections?

A

Diabetes mellitus, steroid therapy, obesity, malnutrition, prolonged surgery, foreign body

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42
Q

What is the #1 host defense against S. aureous?

A

Opsonophagocytosis –> granulocytopenic or C3b subunit deficient individuals are at high risk of infection

  • Staph is resistant to PMN NETs because they are Gram+; so complement is best response
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43
Q

What are virulence factors of S. aureus?

A
  • Protein A
  • Catalase
  • leukocidin
  • Ribotechoic and techoic acid
  • Coagulase
  • Capsule
  • Hyaluronidase
  • Cytotoxins
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44
Q

What virulence factors of S. aureus defend against phagocytes?

A
  • Protein A
  • Catalase
  • Leukocidin
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45
Q

What is Protein A?

A

Virulence factor for S. aureus

  • binds to Fc receptors to prevent phagocytosis
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46
Q

What is catalase?

A

virulence factor for S. aureus

  • prevents breakdown in phagosome
  • converts H2O2 to H2O and O2
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47
Q

What is leukocidin?

A

Virulence factor of S. aureus:

  • Punches holes in PMN to prevent phagocytosis and release bacteria
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48
Q

What is ribotechoic and techoic acid?

A

Virulence factors for S. aureus:

  • bind fibronectin
  • techoic acid induces shock that is similar to endotoxin-mediated shock
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49
Q

What is Coagulase?

A

Virulence factor for S. aureus:

  • extracellular and suface-bound
  • initiates conversion of fibrinogen to fibrin
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50
Q

How is a capsule useful to S. aureus?

A

A virulence factor, it is a polysccharide that prevents complement binding

  • 8 different serological types
  • maximum expression in vivo
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51
Q

How is hyaluronidase useful to S. aureus?

A

A virulence factor, it:
- actos on hyaluronic acids in connective tissue, which facilitates dissemination through subcutaneous tissues

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52
Q

What cytotoxins are used by S. aureus?

A

Alpha hemolysin: potent pore-former, toxic to many cell types

Beta toxin: AKA sphingomyelinase C; kills cells via hydrolysis of membrane phospholipids

Delta toxin: cytolitic for many cells; nonspecific detergent-like action

Gamma toxin: pore-forming toxin; lysis of neutrophils and macrophages

Panton-Valentine leukocidin: same as gamma toxin

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53
Q

What in S. aureus causes:
Bullous impetigo
scalded skin syndrome
staphylococcal scarlet fever

A

Exfoliatin A, B

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54
Q

Why are S. epidermidis infections common with indwelling foreing devices such as:

  • catheters
  • peritoneal dialysis shunts
  • CSF and hemolialysis shunts
    etc. .
A

Because the coagulase(-) bacteria is good at making biofilms

55
Q

What are common infections of S. epidermidis?

A

Urinary tract infections (hospital acquired)

Osteomyelitis

Endocarditis (native or prosthetic valve)

Bacteremia (immuneosuppressed patients)

Endophthalmitis (after ocular surgery)

Infections of indwelling foreign devices (due to biofilm)

56
Q

What is S. intermedius?

A
  • Coagulase(+) bacteria, differs from S. aureus
  • invasive, zoonotic pathogen for humans:
    Suspect if dog bite is source of wound
    common oral, nasal, and skin flora in healthy dogs
57
Q

What are toxin-mediated disease of S. aureus?

A
  • bullous impetigo
  • scalded skin syndrome
  • staphylococcal scarlet fever
  • toxic shock syndrome
  • food poisoning
58
Q

What is toxic shock syndrome?

A

Caused by Toxic Shock Syndrome Toxin-1 in S. aureus:

  • Sudden onset: fever, chills, vomiting, diarrhea, muscle pains, rash
  • Later: hypotension, involvement of mucous membranes and multiple systems, desquamation

Fatality rate: 5%

Risk Groups:

  • menstruating women
  • women w/barrier contraceptive devices
  • persons who have undergone nasal surgery
59
Q

What is scalded skin syndrome?

A

Toxin-mediated disease of S. aureus:

Exfoliatins (serine proteases) cause splitting of desmosomes in s.granulosum epidermis

60
Q

What makes an antibiotic bactericidal?

A

They kill microorganisms rapidly

61
Q

What makes an antibiotic bacteriostatic?

A

They inhibit growth reversibly (prevents further replication)

62
Q

When do bactericidal drugs have a higher efficacy than bacteriostatic?

A

When the body’s defenses are insufficient to clear the invading agents.

i.e. bacterial endocarditis, bacterial meningitis, and infections in patients with low circulating neutrophils (agranulocytopenia)

63
Q

Explain the tenants of selective toxicity

A

Characteristics of antibiotics that reduce side-effects:

  • Absence of target from host
  • permeability differences (effective [antibiotic] is too low to cause side effects in humans)
  • structural differences in target
64
Q

How do many antibiotics specifically target bacteria, and not humans?

A

They target bacterial ribosomes and inhibit protein synthesis

65
Q

What are the main steps of bacterial protein synthesis?

A
  1. Amino acid activation: “Charging” of tRNA; tRNA are attached to target AA and become activated
  2. Formation of initiation complexes: 30S initiation complex comprised of charged fMet tRNA, mRNA and 30Sribosomal subunit+IFs+GTP;
    50S complex then enters and creates the 70S complex
  3. Polypeptide chain synthesis: recognition, peptidyl transfer, translocation and release
66
Q

What antibiotics target the amino acid activation of bacteria?

A

None

  • there are NO clinically significant inhibitors of AA activation

(possibly due to the fact that prokaryotic and eukaryotic processes are so similar)

67
Q

What antibiotics target Formation of initiation complexes in bacteria?

A
  1. Linezolid
68
Q

What are the 4 steps of peptide chain synthesisn and which antibiotics target each step?

A
  1. Recognition:
    - Aminoglycosides
    - Spectinomycin
    - Tetracyclines
  2. Peptidyl Transfer:
    - Chloramphenicol
    - Lincomycin
    - Clindamycin
  3. Translocation:
    - Macrolides
    - Ketolides
    - Streptogramins
  4. Release:
    - None
69
Q

What are the characteristics of Linezolid?

A
  • Only clinically significant drug taht inhibits formation of 70S complex
  • First of new class of antibiotics called oxazolidinones
  • prevents formation of N-formylmethionyl-tRNA-mRNA-70S ribosomal ternary complex

Activity: Bacteriostatic for Staphylococci and enterococci
Bactocidal for Streptococci

NOT approved for catheter-related blood stream, catheter-site, or gram(-) infections

70
Q

What antibiotics are included in the family of Aminoglycosides?

A

Streptomycin

Kanamycin

Tobramycin

Gentamycin

Neomycin

Amikacin

Paramomycin

71
Q

What are the characteristics of Aminoglycosides?

A

Inhibitors of activated tRNA recognition:

Broad Spectrum (G+/-)
Bactericidal
Target specific proteins in the 30S ribosomal subunit

Selective Toxicity: 1. 30S vs 40S subunit
2. actively transported into bacteria, not euks.

72
Q

What are the 3 mechanisms of action of Streptomycin?

A
  1. Misreading: at low concentrations, or in case of ribosomes engaged in elongation, we see insertion of incorrect AA
  2. Cyclic Polysomal Blockade: 70S complex forms but is unstable and falls apart; results in cell death due to inability to make proteins
  3. Faulty outer Membrane Proteins: Translational misreading results in mutant membrane proteins that cause bacterial membrane to be leaky, thus more drug is taken into cell and acts at 30S subunit
73
Q

What are Positive and Negative aspects of aminoglycoside therapy?

A

Positive: Rapid bactericidal effect
Broad spectrum
effective against Pseudomonas (notoriously antibiotic resistance)

Negative: Resistance
Ototoxicity and nephrotoxicity
Antagonized by anaerobiasis
low pH
ineffective against intracellular bacteria
induce biofilm production

74
Q

How do bacteria become resistant to Aminoglycosides?

A
  1. Altered target in 30s ribosomal subunit
  2. Decreased cellular uptake
  3. Enzymatic modifications of the aminoglycoside (typically by enzymes coded on transposons or plasmids)

Gentamicin specifically has:
Potential sites for acetylation
Potential sites of adenylylation or phosphorylation
- both of which alter the antibiotic activity, rendering it useless

75
Q

What are characteristics of Spectinomycin?

A

Inhibitor of Recognition:

Bacteriostatic

Causes formation of unstable 70S initiation complexes (does not cause misreading or inhibit polysomal ribosomes)

Exclusively for treatment of gonorrhea caused by beta-lactamase-producing gonococci or to treat gonorrhea in patients allergic to penicillins

76
Q

What are characteristics of Tetracyclines?

A

Inhibitors of recognition:

Broad Spectrum

Bacteriostatic

Hydrophobic

Used to Treat:
Chlamydia, Mycoplasma, Rickettsia (intracellular pathogens)
and certain G+ and G- bacterial infections

Selective Toxicity: high affinity uptake of drugs by acterial cells and increased targeting of 70S

77
Q

What is the mechanism of action for tetracyclines?

A

Tetrcyclines bind to 30S ribosomal subunit and inhibit bindign of aa-tRNA to the A site

78
Q

How do bacteria become resistant to tetracyclines?

A
  1. Decreased uptake (often due to mutations in the OmpF porin)
  2. Efflux from the bacterial cell; actively pump drug out of cell before it’s able to bind to 30S ribosomal subunit
  3. Elongation factor-like proteins that protect 30S subunit
79
Q

What are characteristics of Chloramphenicol?

A

An inhibitor of Peptidyl transfer:

Broad Spectrum

Bacteriostatic

Mechanism:
Binds reversibly to 50S ribosomal subunit and alters the tRNA structure blocking peptidyl transfer

Selective Toxicity:
Cannot enter mitochondria
Does not bind to host 60S subunit

Resistance:
plasmid-encoded acetyltransferase that catalyze the acetylation of -OH groups; preventing 50S binding

80
Q

What are characteristics of Lincomycin and Clindamycin?

A

Inhibitors of Peptidyl Transferase:
Narrow Spectrum

Bacteriostatic

Mechanism:
Similar to chloramphenicol

Selective Toxicity:
Very effective for treatment of G+ bacterial infections
Clindamycin: Very effective for staphylococcal and anaerobic G- infections

Resistance:
Methylation of 23S ribosomal RNA which prevents drug binding to 50S subunit

81
Q

What are characteristics of Macrolides?

A

Inhibitors of Translocation:

Characterized by macrocyclic lactone structure

Medium Spectrum

Bacteriostatic

Treatment:
infections caused by Mycoplasma, Legionella, Chlamydia, and Campylobacter
and G+ bacteria in patients allergic to penicillins

Azithromycin and Clarithromyin: certain Mycobacteria

82
Q

What are two common antibiotics in the Macrolide family?

A

Azithromycin and Clarithromycin

(modified forms of erythromycin)

83
Q

What is the mechanism of Macrolides?

A

Not entirely clear, but likely to:

  1. Prevent elongation
  2. prevent release of empty tRNA
  3. blockage of transpeptidation
84
Q

What contributes to Macrolide resistance?

A
  1. Methylation of 23S RNA of teh 50S subunit; which prevents binding of drug
  2. Hydrolysis of lactone ring by and esterase
  3. Efflux of drug
85
Q

What are characteristics of Ketolides?

A

Inhibitors of Translocation

First ketolide approved by FDA: Telithromycin

New family of antimicrobials structurally related to macrolides

Mechanism:
binding within exit tunnel of 50S subunit, thus blocking exit of nascent polypeptides
Strongly binds simultaneously to two domains of subunit (macrolides only bind to one)

Bactericidal or bacteriostatic depending on bacterium

86
Q

What are characteristics of Streptogramins?

A

Inhibitors of Translocation:
Class of natural cyclic peptide antibiotics produced by certain subspecies of Streptomyces

Mechanisms:

Dalfopristin: binds to 50S subunit; prevents elongation and facilitates binding of quinupristin to 50S

Quinupristin: premature release of peptide chains from ribosome

Synercid (quinupristin+dalfopristin)
Alone = bacteriostatic
Together = bactericidal

87
Q

What bacteria are treated with Streptogramins?

A

Staphylococci

Streptococci

Enterococcus faecium
(Restricted for treating vancomycin-resistant forms)

88
Q

What are the functions of bacterial cell wall?

A
  • Protects bacterium from osmotic shock (from inside and outside)
  • Maintains shape of the bacterium
  • Assists in cell division
  • Mediates bacterial-host interactions
89
Q

What is peptidoglycan?

A
  • heteropolymer of glycan chains cross-linked by AA
  • Unique chemistry of bacterial cell walls; makes enzymes in their synthesis ideal targets for antibiotics
  • not found in mycoplasma
90
Q

What are the steps in assembly of peptidoglycan?

A
  • *Cytoplasmic:**
    1. Synthesis of amino acids (GlcNAc and MurNAc)
    2. Synthesis of D-amino acids (relatively rare in nature)
    3. Assembly of pentapeptide component (Park nucleotide)
  • *Membrane-associated:**
    1. Addition of glycosyl carrier lipid
    2. Addition of GlcNAc
    3. Flippase to flip PG to outer cell wall
    4. Transglycosylation resulting in linked dissacharides of the PG sugar backbone w/side chain

Post-Translocation

91
Q

How do bacteria become resistant to beta-lactam antibiotics?

A
  • Inactivation through beta-lactamases
  • Altered PBP (mecA-PBP2a)
92
Q

What do you think of when you see spaghetti and meatballs?

A

Pityriasis Versicolor
(AKA tinea versicolor)

93
Q

What are the clinical categorizations of mycoses?

A

Superficial

cutaneous

subcutaneous

systemic

opportunistic

94
Q

Describe a superficial mycoses (with example)

A

-colonization of outer keratinized surface of skin
Skin
Hair
Nails

  • little to no immune response
  • mostly caused by yeasts
  • easily treated

Example: tinea/pityriasis versicolor, +/- dandruff

95
Q

Describe a cutaneous mycoses (with examples)

A
  • invasion of epidermis with inflammatory response
  • primarily caused by dermatophytes

Example: Athlete’s foot, jock itch, ring worm

96
Q

Describe a subcutaneous mycoses

A
  • invasion of subcutaneous tissue
  • often slowly progressive, may require surgery
97
Q

Describe a systemic mycoses (with example)

A
  • systemic response
  • most acquired by inhalation of spores
  • typically caused by dimorphic fungi
98
Q

Describe opportunistic mycoses

A

fungal infections that predominantly occur in immune compromised hosts

99
Q

What is the clinical presentation of pityriasis versicolor?
How is it diagnosed?
How is it treated?

A
  • *Superficial Mycoses**:
  • causes hypo- or hyper-pigmented macules on chest, neck, back
  • Wood’s lamp exam may show yellow-green fluorescence

Diagnosis:
direct visualization of yeastlike cells and short, infrequently branched pseudohyphae
(spaghetti and meatballs)
Note: culture growth is enhanced by adding olive oil

  • *Treatment:**
  • Course: persistent, rarely self-cures
  • topical therapy (azoles, selenium sulfide shampoo)
  • short course/single dose oral azoles if widespread
100
Q

What do dermatophytic fungy cause?

A

Cutaneous mycoses

Often: Trichophyton species
Epidermophyton species
Microsporum species

Cause: breakdown of keratin
invade skin, hair, nails
invade outermost layer of epidermis (s. corneum)

101
Q

What is the clinical presentation of a dermatophytic fungi?
How is it diagnosed?
How is it treated?

A

Cutaneous Mycoses

  • *Clinical:**
  • Causes “ringworm” or “tinea infections”
  • inflammatory scaling, often in the pattern of a ring
  • frequent hair loss

Transmitted by: indirect contact (infective elements remain viable in desquamated scales and hair for long periods of time) and direct contact

  • *Diagnosis:**
  • often clinical
  • microscopy or culture for definitive result
  • *Treatment:**
  • Skin only = topical agents (azole or terbinafine)
  • hair or nail = oral therapy (azole, terbinafine, griseofulvin)
102
Q

What are the common subcutaneous mycoses?

A

Sporotrichosis

Chromoblastomycosis

Eumycotic mycetoma

  • all rare
  • introduced traumatically
  • infection into dermis, subcu tissue, and bone
  • rarely spread to distant organs
  • VERY difficult to treat
103
Q

What is the clinical presentation of a Sporotrichosis?
How is it diagnosed?
How is it treated?

A
  • *Subcutaneous mycoses:**
  • Dimorphic
  • ubiquitous in soil and decaying vegetation
  • rose gardener’s get this
  • *Clinical:**
  • Primary lesion at site of inoculation
  • nodule grows, ulcerates, and becomes painful
  • very little systemic illness
  • 2-3 weeks later, secondary lesions along lymphatics
  • lesions progress proximally
  • *Diagnosed**:
  • H&E shows eosinophilic granulomatous structure with starburst pattern
  • culture is best tool
  • *Treatment:**
  • several weeks minimum
  • itracanazol
  • classic therapy = oral potassium iodide
104
Q

What is the clinical presentation of a Chromomycosis?
How is it diagnosed?
How is it treated?

A
  • Subcutaneous mycoses*:
  • chronic local fungal infection of skin
  • caused by many fungal agents
  • *Clinical:**
  • Causes warty and/or nodular outgrowths
  • slowly progressive
  • disease is mostly in tropis, on feet and legs
  • Granulomatous inflammation
  • *Diagnosis:**
  • H&E shows muriform cells: brown cells, divided by internal septation (Medlar bodies)
  • *Treatment**:
  • Very difficult
  • itraconazole or terbinafine
  • local heat or cryotherapy to help shrink lesions
  • surgery contraindicated (risk recurrence)
105
Q

What is the clinical presentation of Eumycotic mycetoma?
How is it diagnosed?
How is it treated?

A
  • Subcut*aneous mycoses:
  • Deep, subcu fungal infection
  • caused by soil organisms entering wounds
  • *Clinical:**
  • grossly see localized swelling with underlying sinus tracts
  • granulomas develop with granule formation (aggregates of hyphae)
  • pus and ranules can drain through skin
  • *Diagnosis:**
  • detection of granules by gross visualization or microscopy
  • H&E shows black grain mycetoma (not req’d for diagnosis)
  • *Treatment:**
  • antifungal agents and local surgery can be tried, but often not effective
  • frequently cure is by amputation
106
Q

What are the different presentations of cutaneous mycoses?

A

Head: Tinea capitis (often ringworm)

Trunk: tinea corporis

Face: tinea barbae

Groin: tinea cruris (jock itch)

Foot: tinea pedis (“athlete’s foot)

Nails: tinea unguium

107
Q

What is the common immune response cycle for HSV and VZV?

A

Productive infection, controlled, virus enters latency

immune suppression or other stimulation leads to reactivation

immune deficiency due to old age, AIDS, organ transplantation, or chemotherapy can lead to virus reactivation

108
Q

What is the structure of Herpesvirus?

A

Nucleocapsid surrounded by ttegumen

enveloped virus

linear dsDNA

icosahedral capsid

infects mucousal epithelial cells

replicates in nucleus

viral perticles bud through nuclear membranes and into membrane of exocytic vesicles during egress

109
Q

What are possible presentations of HSV-1?

A

labial lesions (cold sores)

fever blisters

keratitis

and possibly encephalitis

110
Q

What are possible presentations of HSV-2?

A

genital lesions

severe CNS disease in neonates (congenital herpes infection)

111
Q

What are presentations of VSV?

A

Chicken pox

shingles

112
Q

How are herpesvirsuses transmitted?

A

Most by: close contact
sex
transplants

VSV: transmitted by respiratory droplets

113
Q

What is the herpesvirus life cycle?

A
  1. Lytic replication
  2. latency
  3. reactivation
114
Q

What happens in the lytic replication of herpesvirus?

A

In epithelial cells:

viruses take over cellular machineries for replication
macromolecular synthesis and virus assembly
evenutally leads to cell death

4 phases of gene expression:

  1. Immediate early
  2. Early
  3. DNA Replication
  4. Late

can produce proteins to prevent apoptosis

115
Q

What happens in the latency step of herpesvirus life cycle?

A

circular viral genome (episome) maintained in neurons without replication

expresses LAT transcript whihc plays role in latency establishment

116
Q

What happens in the reactivation step of herpesvirus?

A

involves limited viral replication in neurons

transport of viral capsid to axonal terminals

egress to regions innervated by specific neurons

asymptomatic reactivation facilitates virus spread

117
Q

What can cause HSV reactivation?

A

Stress

sun light

trauma

menstruation

118
Q

What can be unique about HSV-2 reactivation?

A

often asymptomatic

Primary HSV-2 infection preceding child birht poses great risk to neonates

119
Q

What can lead to Varicella Zoster virus reactivation?

A

immune-suppresion
depressed cell-mediated immunity (age)

120
Q

What are clinical features of HSV?

A

Primary Infection: accompanied by systemic symptoms such as fever and malaise

Reactivation: accompanied by prodromal symptoms such as pain, numbness, itchiness, tingling sensation

  • *Acute Infection:** direct destruction of tissues or induction of immunopathologic response
  • characteristic skin lesions are vesicles on an erythematous base
  • usually grouped as single anatomic site

Subclinical virus shedding: commona nd key to transmission, poses risk for neonates

121
Q

What are immune responses to Herpesvirus infection?

A
  • Antibodies play minor role in recover from primary HSV or VZV
  • cell-mediated immune mechanisms are most important for prevention or control of recurrent disease
  • AIDS patients; transplant recipients; patients under chemotherapy; patients with leukemia are susceptible to reactivation and prolonged infection
122
Q

What is used for the diagnosis of herpes?

A

Viral culture w/ or w/o immunostaining

Tzanch smear

serology

PCR

123
Q

What are two anti-herpes therapy targets?

A

Herpes Thymidine Kinase:
(acyclovir, ganciclovir)

Herpes DNA Polymerase:
(Phosphonoacetic Acid (PAA))

124
Q

What is acyclovir used for?

A

Treatment of HSV-2

  • DNA chain terminator, specifically activated by viral TK
  • incorporation into viral DNA and terminates DNA replication
125
Q

What is ganciclovir used for?

A

HSV-2 treatment

-a viral protein kinase homologue involved is involved in activating ganciclovir

126
Q

What is forscarnet used for?

A

A pyrophosphat analog, it is used to treat HSV and CMV retinitis in AIDS patients

Binds directly to the pyrophosphate binding sites of RNA or DNA polymerases

Does not need to be activated by cellular or viral kinasees

must be given continuously intravenously via infusion pump

renal side effects

127
Q

What are the recommendations for the Varicella Zoster Virus vaccine?

A

Recommended For:
susceptible children entering school or daycare
susceptible persons over 13
susceptible nonpregnant women of child-bearing age
susceptible persons with humoral deficiencies
HIV+ children with age-specific CD4+ counts greater than or equal to 25%

Not recommended for:
pregnant women
HIV+ persons, or personsn with other cellular immunodeficiencies
persons receiving immunosuppressive therapy

128
Q

What is the action of the Botulinum toxin.

A

7 toxin types.

Zn metal protease cleaves SNARE proteins inhibiting membrane fusion and Acetylcholine release.

Causes flaccid paralysis

129
Q

What types of Clostridia make neurotoxin?

A

C. Botulinum

C. Tentani

130
Q

Characterics of Clostridia

A

G+

Obligate Anaerobes

Spore Formers

131
Q

Mechanism of Tetnus toxin:

A

Zn metal protease that inhibits release of glycene from inhibitory interneurons.

Causes Spastic paralysis

132
Q

Treatment of Botulism

A

Antitoxin- heptavalent

prepared in horses

Infants treated with divalent babyBOT which is human derived.

133
Q

Treatment of tetnus

A

Vaccine before or after. Not effective if already symptomatic.

Antitoxin

Muscle relaxants

Ventilation

Module 2: MSK (11 decks)

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