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MICRO > Ch1: Skin > Flashcards

Ch1: Skin Flashcards

1
Q

Pathogens usually enter the lower layers of epidermis and dermis after what?

A

Damage

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2
Q

Pathogens can infect the follicle how?

A

Descending from surface of skin

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3
Q

Pathogens can also infect subcutaneous and dermis how?

A

Leaving the blood

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4
Q

Function of the skin is to do what? (6)

A
  1. Protect from environment
  2. Sensation
  3. Shape
  4. Temp regulation
  5. Blood pressure
  6. Synthesize Vitamin D
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5
Q

Normal skin flora inhabit what areas predominately?

A

Moist: groin, armpits

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6
Q

What are the most common genera of skin flora? 2

A
  1. Staph epidermidis (100% of pop)

2. Staph aureus (20% of pop)

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7
Q

Host defenses of the skin include?

A
  1. Stratum corneum: Sloughed cells carry microbes away
  2. Low moisture = fewer microbes
  3. Salty sweat = discourage growth
  4. Sebum = decreases pH –> discourage growth
  5. Hair follicles = Produce lysozyme
  6. Lower temperature = discourage growth
  7. Langerhans cells = APC’s of skin
  8. Innate immunity
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8
Q

What are the two steps for inflammation of the skin? (2)

A
  1. Recognition

2. Recruitment

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9
Q

What happens in recognition?

A

Bacterial components such as peptidoglycan, LPS, and other PAMP’s are recognize by Toll-like receptors that cause release of inflmmatory cytokines

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10
Q

What happens in recruitment?

A

Effector cells are recruited to the site of infection by cytokines

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11
Q

What is the effect of cytokines on blood capillaries?

A

Dilates them –>

  1. WBC’s recruited
  2. Leakage of plasma –> Redness
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12
Q

Why does an inflammation cause pain in the skin?

A

Due to high density of nerve endings in the skin, swelling causes pain

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13
Q

What is pus formed from? (2)

A
  1. Neutrophils

2. Lysis of foreign things

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14
Q

Viscosity of pus is due to what?

A

DNA

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15
Q

What does TLR-4 recognize?

A

LPS from gram-negative bacteria

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16
Q

Infections of the skin are of what 3 categories?

A

Breach in skin
Hematogenous infection
Toxin-mediated damage

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17
Q

What is a macule?

A

Circumscribed change in skin color that is NOT raised

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18
Q

What is a papule?

Does it have liquid?

A

Solid elevated lesion with raised edges

Yes and No.

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19
Q

What is a pustule?

A

Circumscribed raised cavity containing pus

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20
Q

What is a abscess/boil?

A

Localized inflammation with pus

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21
Q

What is a furuncle?

A

Acute, deep-seated red hot nodule or abscess

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22
Q

What is a carbuncle?

Where are they normally found?

A

Deeper-seated composed of interconnecting abscesses/boils in subcutaneous fat
Neck and upper back where skin is elastic

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23
Q

What two lesions of the skin have pus?

What is pus due to?

A

Pustule and Abscess/boil

Neutrophils

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24
Q

What is staphylococci’s shape?

A

Spheres in clusters (Grape-like)

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25
Q

What is the test for staphylococcus?

A

Coagulase test

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26
Q

Staph aureus secretes what enzyme?

A

Coagulase

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27
Q

What does coagulase do?

A

Converts fibrinogen to fibrin

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28
Q

How does the coagulase test work?

A

Bacteria sample is suspeneded in tube with rabbit plasma, if the bacteria has coagulase produced, a clot will form due to fibrin formation

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29
Q

What does the aureus mean in staph aureus?

A

Gold, which i the color of colonies

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30
Q

Is staph aureus gram positive or negative?

A

Positive

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31
Q

Size of staph aureus?

A

1.0 um in diameter

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32
Q

What is the habitat of staph aureus?

A
  1. Human skin
  2. Anterior nares
  3. Conjunctivitis
  4. hands and fingers
  5. Arms and groin
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33
Q

What percentage of human population is colonized with staph aureus?

A

25-35%

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34
Q

Transmission of staph aureus is through what?

A
  1. Direct contact
  2. Fomites
  3. Endogenous
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35
Q

What are fomites?

A

Objects that can transmit an organism

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36
Q

What does endogenous mean?

A

Part of normal flora, but can accumulate or go somewhere they shouldn’t

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37
Q

What is a virulence factor?

A

Something that can promote disease

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38
Q

What are the two cell-associated virulence factors of staph aureus? (2)

A
  1. Polysaccharide capsule

2. Protein A

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39
Q

Function of polysaccharide capsule?

A

Surrounds the bacteria and acts as an anti-phagocytic

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40
Q

Function of protein A?

A

binds the FC portion of IgG antibodies (including those directed towards itself) which inhibits antibody-mediated phagocytosis

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41
Q

Where is Protein A exactly?

A

On cell wall and linked to PTG

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42
Q

What are the two secreted virulence factors of staph aureus?

A

Exfoliatin

Superantigens

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43
Q

What is exfoliatin?

A

Protease that degrades desmosomes of tight junctions between cells in epidermis

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44
Q

What does exfoliatin cause? (2)

A
  1. Scalded skin syndrome

2. Bullous impetigo

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45
Q

Genes encoding S. aureus superantigens are located where?

What type of transfer does this allow for?

A

In mobile genetic elements such as bacteriophage and pathogenicity islands
Horizontal transfer

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46
Q

Do all staph aureus species have the same superantigens?

A

No, different isolates have different compositions

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47
Q

Superantigens bind to what? 2

A

Simultaneously to the MHC class II molecule on surface of APC’s and the T-cell receptor

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48
Q

Result of superantigens binding to APC and T cell?

A

Non-specific stimulation of T cells (2-20%) resulting in excessive cytokine release leading to to fever, hypotension, rash and a variety of other clinical manifestations

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49
Q

What is the most common and important superantigens?
What does it cause?
Symptoms? (3)

A

Toxic Shock Toxin-1 (TST-1)

Toxic Shock Syndrome

Fever, Hypotension, Shock

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50
Q

What are the two categories of staph infections?

A

Bacterial

Toxigenic

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51
Q

What does bacteria disease of staph do?

A

The bacteria invades and evokes clinical manifestations

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52
Q

What does toxigenic disease of staph mean?

A

Clinical manifestations are due to staph toxin only

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53
Q

Skin diseases of staph?

A
  1. Abscess
  2. Impetigo
  3. Folliculitis
  4. Style
  5. Carbuncles
  6. Furuncles
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54
Q

What is impetigo?

A

Infection of epidermis leading to bullous impetigo

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55
Q

What is foliculitis?

A

Infection of hair follicle

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56
Q

What is a stye?

A

Folliculitis in eye

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57
Q

What are the three main bacterial versions of staph infection?

A
  1. Skin diseases
  2. Wound Infection
  3. Bacteremia
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58
Q

What can cause bacteremia? (4)

A
  1. Ruptured abscess
  2. Injury
  3. Needle
  4. Surgery
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59
Q

What can staph cause once in the blood? 4

A

Osteomyelitis
Arthritis
Pneumonia
Endocarditis

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60
Q

Three forms of toxigenic disease from staph aureus?

A
  1. Scalded skin syndrome
  2. Bullouis impetigo
  3. Toxic shock syndrome
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61
Q

Scalded skin syndrome is due to what?

A

Exfoliatin toxin

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62
Q

What does the exfoliatin toxin do uppon reaching the blood?

A

Spreads out and degrades desmosomes of epidermis –> Top layer of epidermis to be released

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63
Q

Complications of SSS? 2

A
  1. Fluid loss

2. Secondary infections of skin

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64
Q

How does scalded skin syndrome appear?

What population gets it?

A

Burn or blister

Neonates and children

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65
Q

How do you diagnose SSS? 2

A
  1. Patient history

2. Biopsy

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66
Q

What is bullous impetigo?

What causes it?

A

Localized SSS

Exfoliatin toxin

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67
Q

Toxic shock syndrome is caused by what?

A

Superantigens that nonspecifically stimulate cytokine production.

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68
Q

Most potent superantigen of s. aureus?

What can it cross that other superantigens can’t?

A

TST-1

Cross mucal membrane

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69
Q

TSS is based on what 4 features?

A
  1. Fever greater than 102
  2. Hypotension less than 90 mmHg
  3. Rash
  4. Abnormalities in 3 organ systems
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70
Q

Two types of TSS?

A

Menstrual

Non-menstrual

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71
Q

Describe menstrual TSS.

A

S. aureus that normally colonizes the vagina grows to greater numbers during menstruation –> Produced superantigen (mainly TST-1) –> Crosses mucosa –> Enters blood –> Causes symptoms of TSS

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72
Q

Increased growth of s. aureus during menstruation is due to what? (3)

A
  1. Increase supply of nutrients in vagina
  2. Increase in pH of vagina
  3. Drying of vaginal mucosa by highly absorbent tampons leading to tears in epithelium
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73
Q

TST-1 production in menstrual TSS is enhanced by what?

A

Presence of synthetic fibers used in tampons

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74
Q

What is non-menstrual TSS? 2

A
  1. When superantigens produced by S. aureus colonizaiton of skin/wounds enters the bloodstream to cause systemic effects
  2. S. aureus is present in bloodstream and produces superantigens.
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75
Q

Non-menstrual TSS is associated with what? 4

A
  1. Post-operative
  2. Post partum
  3. Barrier contraceptives
  4. Cutaneous infections
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76
Q

What are the two tests to run when diagnosing potential staph aureus?

A
  1. Gram-stain = Positive

2. Coag test = Positive

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77
Q

S. aureus grows well on what medium?

A

Blood-agar

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78
Q

Mannitol salt agar is useful for what reasons in testing for staph aureus

A
  1. Selective: Selects ability of staph to grow in high salt environment
  2. Differential: S. aureus can ferment mannitol causing pH indicator to turn yellow
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79
Q

Why is culturing so important with staph aureus?

A

Have to determine degree the strain has resistance to different antibiotics

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80
Q

Treatment of skin lesions of staph aureus includes what?

A

Incision and drainage with or without mupirocin or additional antibiotics

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81
Q

What does antibiotic use against s. aureus depend on?

A
  1. Speed lesion is progressing
  2. Systemic symptoms
  3. extremes of age
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82
Q

What percentage of staph aureus is resistant to penicillin?

Why?

A

90%

Produce a penicillinase which degrades penicillin

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83
Q

MRSA is an isolate that is resistant to what?

A

All penicillinase-resistant Beta-lactam antibiotics: Methicillin, oxacillin, floxacillin

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84
Q

Resistance to methicillin-like antibiotics is associated with what?
What is this?

A

mecA gene

Mobile DNA element that encodes a penicillin binding protein that is NOT activated by methicillin like antibiotics

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85
Q

Due to the significance of MRSA how do we designate s. aureus?

A 
MRSA = Resistant
MSSA = Sensitive
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86
Q

Is hospital acquired MRSA different from community acquired?
Why?

A

Yes

They are different genetically, and HA-MRSA is more resistant to antibiotics

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87
Q

Which of the two, HA-MRSA and CA-MRSA is a recently emerged infectious agent?

A

CA-MRSA

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88
Q

CA-MRSA have what gene?

A

mecA

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89
Q

CA-MRSA can have what effects in addition to normal s. aureus? (3)

A
  1. Necrotizing fasciitis
  2. Purpura fulminans
  3. Necrotizing pneumonia
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90
Q

Treatment of CA-MRSA is most effective when?

A

If the antibiotic sensitivity of the organism is determined.

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91
Q

In severe cases in which MRSA is suspected, what antibiotics are used? 3

A

Vancomycin
Linezolid
Daptomycin

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92
Q

CA-MRSA requires what to be accurately treated?

A

Multiple sampling for > 90% sensitivity

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93
Q

Treatment of CA-MRSA depends on what? 2

A
  1. Severity of disease

2. Local susceptibility data

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94
Q

What is VISA?

A

Vancomycin-intermediate resistant staph aureus

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95
Q

VISA produces what anatomically?

A

Thicker cell wall of PTG that decreases vancomycin’s ability to weaken cell wall

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96
Q

What is VRSA?

A

Vancomycin-resistant staph aureus

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97
Q

VRSA has what genetic advantage?
What does this do?
Where did it get it from?

A

vanA gene

Modifies structure of PTG making it not susceptible to vancomycin

Vancomycin-resistant enterococci

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98
Q

VanA VRSA have what protein change?

A

D-ala D-lac in PTG crosslinking instead of D-ala, D-ala

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99
Q

What vaccine exists for staph aureus?

A

None

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100
Q

What does the word streptococci mean?

A 
Streptus = Pliant
Cocci = Berry
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101
Q

How does strep stain in a gram stain?

A

Gram positive

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102
Q

Two special shape characteristics of strep?

A
  1. Spherical

2. Cell division occurs in one plane –> Chain

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103
Q

How does strep react in a catalase test?

A

Catalase = Negative

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104
Q

Is strep an anaerobe or aerobe?

Do they tolerate O2?

A

Anaerobe

Yes

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105
Q

Two ways to classify strep?

A

Hemolysis

Lancefield

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106
Q

Describe the hemolysis classification of strep

A

Beta strep: Complete cleaning around colony
Alpha: Partial clearing (green)
Gamma: No hemolysis

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107
Q

What is hemolysis of strep performed on?

A

Agar plates with blood

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108
Q

What is lancefield classificaiton based on?

A

Presence of different carbohydrates in the cell walls of different strep species

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109
Q

How many species are in Group A and Group B strep?

A

Essentially one each

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110
Q

What is the Group A strep?

A

Streptococcus pyogenes

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111
Q

What is group A streps
Hemolysis classification?
Gram stain?
Appearance similar to?

A

Beta hemolytic
Gram positive
Similar to other beta-hemolytic

112
Q

Habitat of s. pyogenes?

Specifically? (4)

A

Human mucosal surfaces

Nasopharynx
Skin
Vagina,
Perianal

113
Q

What other organisms can s. pyogenes inhabit?

A

Only humans

114
Q

Transmission of s. pyogenes is how? 2

A

Droplets

Direct contact

115
Q

Cell associated Virulence factors of S. pyogenes? 2

A
  1. Polysaccharide capsule

2. M protein

116
Q

The polysaccharide capsule is comprised of what in s. pyogenes?
Is it antigenic?
Is it similar to hyaluronic acid in our bodies?
Function?

A

Hyaluronic acid
Not antigenic
Identical to hyaluronic acid in our bodies
Inhibits phagocytosis

117
Q

What is it called when s. pyogenes avoids detection by using the same hyaluronic acid as in humans?

A

Molecular mimicry

118
Q

The M protein of s. pyogenes is where?

A

Embedded in cell wall

119
Q

How many serotypes of M protein exist?

Does an antibody against one serotype protect against other serotypes?

A

Over 100

No

120
Q

What is the M protein’s 100 serotypes an example of?

A

Antigenic variation

121
Q

The M protein has what function? 2

A
  1. Inhibits phagocytosis

2. Allows GAS to adhere to human epithelial cells

122
Q

What is the most important virulence factor of GAS?

123
Q

What are the five secreted virulence factors of GAS?

A
  1. Streptolysin O
  2. DNAse’s
  3. Protease
  4. Streptokinase
  5. Superantigens
124
Q

What does streptolysin O do?

A

It is a pore-forming toxin that lyses eukaryotic cells

125
Q

How is streptolysin O seen diagnostically?

A

It is responsible for Beta-hemolysis

126
Q

What form is streptolysin O in?

127
Q

An elevated antibody titer to streptolysin O (ASO test) indicates what?

A
  1. Recent strep pyogenes pharyngeal infection, but not skin infection.
  2. Rheumatic fever
128
Q

How many types of DNAses does s. pyogenes release?

A

Four (A, B, C, D)

129
Q

DNAses are secreted into human host to do what?

A

Degrade nucleic acids present in Neutrophil Extracellular Traps, a part of innate immunity

130
Q

An elevated antibody titer to DNAse B suggests what? (2)

A
  1. S. pyogenes skin infection recently

2. Post-streptococcal glomerulonephritis

131
Q

What does protease do? (2)

What is it also known as?

A
  1. Degrades human proteins
  2. Promotes tissue invasion

Aggressin

132
Q

Streptokinase has what function?

A

Activates plasminogen to plasmin

133
Q

Plasmin can activate what? 3

A
  1. MMP’s
  2. Collagenases
  3. Proteins involved in tissue repair
134
Q

Human plasmin can also bind to the surface of bacterium to do what? (2)

A
  1. Degrade tissue

2. Promote dissemination

135
Q

What are the superantigens in strep pyogenes called?

A

Streptococcal pyrogenic exotoxins

136
Q

SPE’s are encoded by what?

A

Bacteriophage

137
Q

Streptococcal superantigens function how?

A

Same as superantigens in staph

138
Q

What is impetigo?

A

Infection of epidermis caused by S. pyogenes, S. aureus, or both

139
Q

What is erysipelas?

A

Infection of dermis

140
Q

What is cellulitis?

What typically causes it?

A

Infection of dermis and/or cutaneous tissue

  1. S. pyogenes
  2. S. aureus
141
Q

What are some Characteristics of cellulitis?

A
  1. Might be able to culture the bacteria
  2. Lymph nodes are swollen
  3. Fever, chills, malaise
  4. Infection can progress rapidly –> Sepsis
142
Q

Which has a more clear demarcation, erysipelas or cellulitis?

A

Erysipelas

143
Q

what is necrotizing fasciitis?

A

Infection of subcutaneous CT and fascia with myonecrosis

144
Q

What can cause necrotizing fasciitis? 4

A
  1. S. pyogenes
  2. MRSA
  3. Clostridium perfringens
  4. Aeromonas hydrophila
145
Q

Where does necrotizing fasciitis typically begin?

A

Site of trauma

146
Q

Symptoms of necrotizing fasciitis?

A

Intense pain

147
Q

What antibiotic works well against necrotizing fasciitis?

A

Penicillin

148
Q

Foot/limb infections in diabetic patients are typically caused by what?

A

Mixed infections of s. aureus, s. pyogenes, pseudomonas, enterobacteriaceae

149
Q

Diabetic neuropathy is due to what?

A

Tissue hypoxia

150
Q

What is post infection sequelae?

A

Disease that occurs after primary infection

151
Q

Can post-infection sequelae occur even if the microbe has been eliminated?

152
Q

Post-infection sequelae is caused by what?

A

Misdirected immune response to microbe

153
Q

S. pyogenes infection precedes what three post-infection sequelae?
What type of infection does each follow?

A
  1. Post-streptococcal acute glomerulonephritis (PSAGN): Skin
  2. Acute rheumatic fever/heart disease: Pharyngeal
  3. Pediatric autoimmune neuropsychiatric disorders: (Pharyngeal)
154
Q

What happens in PSAGN

A

Antibody-antigen complexes are deposited in glomerula of kidney causing inflammation and damage

155
Q

Laboratory diagnosis of s. pyogenes shows what in

  1. Gram stain
  2. Blood-agar culture
  3. Catalase
  4. Lancefield:
A
  1. Gram positive
  2. Beta-hemolytic
  3. Catalase negative
  4. Group A
156
Q

To obtain evidence of a recent s. pyogenes skin infection determine what?

A

Levels of antibody titer against streptococcal DNAseB

157
Q

What is drug of choice for s. pyogenes?

What else works? (3)

A

Penicillin

Amoxicillin, Erythromycin, Cephalosporins

158
Q

Why is erythromycin used sometimes instead of penicillin?

A

Avoid allergic responses to penicillin

159
Q

Is there a vaccine for s. pyogenes?

160
Q

what are the two most important gram positive spore formers?

A

Clostridia

Bacillus

161
Q

What does clostridium perfringens cause?

A

Gas gangrene

162
Q

4 main features of gas gangrene?

A
  1. Gram positive
  2. Bacillus shape
  3. Forms endospores
  4. Anerobic
163
Q

Habitat of clostridium perfringens? (4)

A
  1. GI tract of animals
  2. Soil
  3. Water
  4. Sewage
164
Q

How does one make sure to be rid of clostridium perfringens on fomites?

165
Q

How is c. perfringens transmitted?

A

Exogenously or endogenously

166
Q

Two clinical infections of c. perfringens?

A

Traumatic gas gangrene

Spontaneous/Nontraumatic gas gangrene

167
Q

Traumatic gas gangrene results from what?

A

Contamination at site of trauma (cut, gun shot, puncture wound) with spores that germinate to initiate infections.

168
Q

How does trauma facilitate better growth of c. perfringens?

A

Trauma –> Decreased tissue oxygenation

169
Q

Spontaneous/nontraumatic gas gangrene occurs in patients with what?
Why?
Specifically what?

A

Vascular diseases

Tissues lack adequate oxygen

Diabetes, colon cancer, atherosclerosis

170
Q

Since c. perfringens is an anaerobe, it ferments, thus producing what?

A

H2S that stinks and you can see the gas

171
Q

Laboratory diagnosis of c. perfringens? (2)

A
  1. Gram positive rods in fluid from infected area

2. Nagler’s reaction

172
Q

How does Nagler’s reaction work to test for c. perfringens?

A

Since c. perfringens secretes a lecithinase, when it is grown on agar plate with lecithin (egg yolk), it will degrade the lecithin and form a zone of opacity.

173
Q

Treatment of c. perfringens? (3)

A
  1. Prompt surgical remova of dead, damaged, infected tissue
  2. Amputation if necessary
  3. Antibiotics (penicillin)
174
Q

IV drug users can insert drugs how? 3

A
  1. Using contaminated needles
  2. Not disinfecting skin
  3. Injecting drugs contaminated with microbes
175
Q

Is propionibacterium acnes part of normal flora?

176
Q

What type of bacteria is propionibacterium acnes?

177
Q

Habitat of propionibacterium acnes?

A

Sebaceous glands of skin because there is not much oxygen and sebum provides nutrients

178
Q

End product of propionibacterium acnes eating sebum? (3)

A
  1. Fatty acids
  2. Inflammation
  3. Pus
179
Q

Transmission of propionibacterium acnes?

A

Endogenously

180
Q

Inflammatory acne is due to what?

A

Bacterial infection, and mainly propionibacterium acnes

181
Q

What are the sebum channels called?

A

Pilosebaceous ducts

182
Q

What must happen to pilosebaceous ducts for propionibacterium acnes to grow well?

A

Duct has to get clogged so that bacteria are not washed out to surface of skin.

183
Q

Hormonal changes associated with puberty may result in acne why? (2)

A
  1. Increased sebum production

2. Increased keratinizaiton

184
Q

Treatment of propionibacterium acnes? (4)

A
  1. Benzoyl Peroxide
  2. Tetracycline
  3. Erythromycin
  4. Retoinoids
185
Q

What does benzoyl peroxide do?

A

Generates O2 as it breaks down in skin –> Inhibits propionibacterium acnes growth

186
Q

What do retinoids do?

A

Inhibit sebum production

187
Q

Burns have what two main effects on skin?

A
  1. Damage physical barrier of skin

2. Diminish neutrophil function

188
Q

Minimizing colonization of burn involves what?

A

Topical antimicrobials like silver nitrate

189
Q

Most important pathogens involved in burn wounds? (3)

A
  1. Pseudomonas aeruginosa
  2. Staph aureus
  3. Strep pyogenes
190
Q

Physical treatment of burn? (2)

A
  1. Surgical debridement to decrease bacterial numbers

2. Different forms of silver to inhibit microbes

191
Q

Antibiotic treatment of burns?

A

Whatever antibiotic is best for the specific agent

192
Q

Pediatric burn patients are more susceptible to what? 2

A
  1. Bacteremia
  2. Toxic shock syndrome

S. aureus and x. pyogenes

193
Q

Pseudomonas aeruginosa is seen in what clinical infection setting?

194
Q

Pseudomonas aeruginosa can cause what? (3)

A
  1. Pyoderma
  2. External otitis
  3. Hot tub rash/itch
195
Q

What is pyoderma?

A

Infection of epidermis

196
Q

What is external otitis?

A

Infection of external auditory canal

197
Q

Pseudomonas aeruginosa is diagnosed how in the lab?

A
  1. Using Woods lamp with UV light to see fluorescein which is produced by Pseudomonas aeruginosa
  2. Culture from blood or skin
198
Q

Treatment of vaccine for Pseudomonas aeruginosa?

A

Treatment: Ceftazidime
Vaccine: none

199
Q

Is Pseudomonas aeruginosa very resistant to antibiotics?

A

Yes to many common ones

200
Q

Leprosy is called by what?

A

Mycobacterium leprae

201
Q

Characteristics of Mycobacterium leprae? 5

A
  1. Acid fast positive
  2. Aerobe
  3. Grows best at 30 degrees Celsius
  4. Can not culture on solid media
  5. grows on armadillo
202
Q

Habitat of Mycobacterium leprae? (3)

A
  1. humans
  2. armadillos
  3. monkeys
203
Q

Is Mycobacterium leprae a zoonotic disease?

A

No, have to get from another human

204
Q

How is Mycobacterium leprae transmitted?

A

Nasal secretions

205
Q

Mycobacterium leprae has a predilection for what type of cell?

A

Schwann cells

206
Q

What does Mycobacterium leprae do upon entering body?

A

Invades schwann cells, tissue macrophages, and endothelial cells –> Granuloma formation

207
Q

What special distinction does Mycobacterium leprae have?

A

Only bacteirum known to damage the peripheral nervous system

208
Q

Two states of leprosy?

A

Tuberculoid

Lepromatous

209
Q

Symptoms of tuberculoid leprosy?

A

Regions of skin lose sensation due to nerve damage from immune response –> injury and secondary skin infection

210
Q

What limits the infection in tuberculoid leprosy?
What gets activated?
How much bacteria is in skin and nose?

A

Cell mediated immunity

Macrophages

Very little, due to CMI response

211
Q

What does the tubercle mean in tuberculoid leprosy?

A

Granuloma containing M. tuberculosis has formed which indicates an effective immune response

212
Q

Is the person very infectious in tuberculoid leprosy?

213
Q

Lepromatous leprosy refers to a disease state of what?

A

When CMI response is ineffective.

214
Q

Are you safe if lepromatous leprosy skin test comes back negative?

215
Q

Bacteria in lepromatous leprosy grow where?

A

Skin and peripheral nerves –> Not contained by immune system

216
Q

which form of leprosy is most contagious?

A

Lepromatous

217
Q

Diagnosis of Mycobacterium leprae? (2)

A
  1. Acid fast test on nose, lesion, and earlobe biopsies

2. Lepromin test

218
Q

What is lepromin test?

A

Extract of Mycobacterium leprae

219
Q

Antibiotics for Mycobacterium leprae? 3

A

Dapsone (folic acid synthesis)
Rifampin
Clofazimine

220
Q

Mycobacterium marinum is endemic where?

221
Q

How is mycobacterium marinum commonly called?

A

Fish tank or swiming pool granuloma

222
Q

Initially where does M. marinum infect?
Visibly looks how to start?
Progresses to what?

A

Skin at sites of minor trauma
After 2-8 weeks looks like papule
Becomes suppurative ulcer

223
Q

Mycobacterium ulcerans is endemic where?
Infections occur where?
Sign of disease?

A

Africa and australia
Sites of trauma
Painless ulcerative lesions

224
Q

Mycobacterium tuberculosis colonizes skin how? (2)

A
  1. Usually hematogenous dissemination

2. Direct inoculation can occur

225
Q

How does m. tuberculosis look clinically?

A

Papule –> Painless ulcer

226
Q

Superficial mycoses include what?

A

Pityriasis versicolor or tinea versicolor

227
Q

What causes pityriasis versicolor/tinea versicolor?

A

Malassezia furfur

228
Q

Is malassezia furfur a normal flora of skin?
How does its lesion appear?
Why?
Is it contagious?

A

Yes

Well-demarcated with scaling patches of different color

Melanin synthesis disrupted

No

229
Q

KOH wet mount of a malassezia furfur appears how?

A

Spaghetti and meatball yeast forms

230
Q

Dermatophyte infections involve organisms that do what?

A

Eat keratin

231
Q

Dermatophyte infections are spread by what?

232
Q

What are the three dermatopyte species?

A
  1. Trichophyton
  2. Microsporum
  3. Epidermophyton
233
Q

Dermatophytes invade what structures? 3

A
  1. Skin
  2. hair
  3. nails
234
Q

How can dermatophytes be clinically diagnosed? (2)

A
  1. Fluoresce under UV light

2. Grow on sabouraud’s agar

235
Q

Symptom of dermatophytes?

236
Q

Dermatophyte infections are treated how?

Do they disseminate?

A

Topically

No

237
Q

Tinea means what?

What causes it?

A

Ringworm

Fungi

238
Q

What is tinea capitis?

A

Ringworm of scalp and hair

239
Q

Is tinea capitis infectious?

What is important for transmission?

A

Yes very

Fomites

240
Q

Most common causes of tinea capitis?

A

Trichophytan

Microsporum (most likely)

241
Q

What is tinea cruris?

What is common cause? 2

A

Jock itch

Tricophyton
Epidermophyton

242
Q

What is tinia pedis?

What is common cause?

A

Athletes foot

Tricophyton

243
Q

Candida species cause what two skin manifestations?

A
  1. Thrush

2. Diaper rash

244
Q

Candida albicans require what for growth?

245
Q

Subcutaneous mycoses is caused the most by what in the US?

A

Sporotrichosis

246
Q

Sporotrichosis is a noedular condition caused by what?

A

Sporothrix schenckii

247
Q

Sporothrix schenckii is seen where? (3)

A
  1. Soil
  2. Thorned plants (gardeners)
  3. Sphagum moss
248
Q

Sporotrichosis enters body how?

A

Skin breaks and then follows lymphatics

249
Q

Systemic mycoses that can manifest in the skin include? (4)

A

blastomycosis, coccidioidomycosis,

histoplasmosis, and cryptococcosis.

250
Q

The systemic mycoses are initiated how?

A

Inhaled and then disseminate in blood

251
Q

Reactive arthritis is also known as what?
What happens in this disease?
Additional symptoms? (2)

A

Reiters’ syndrome
Microbe –> Autoimmune response –> Inflamed joints
Conjunctivitis and urethritis

252
Q

Common bacterial causes of reactive arthritis? 5

A 
Campylobacter spp., 
Yersinia spp., 
Salmonella spp., 
Shigella spp., 
Chlamydia trachomatis
253
Q

Septic arthritis is caused how?

Symptoms? (3)

A

Circulating bacteria in the blood localizes in a joint or bacteria gains access to join through skin.

Fever, pain, swelling

254
Q

How do you diagnose septic arthritis?

A

Culture synovial fluid and blood

255
Q

Common ways to pick up septic arthritis? 2

A

Surgery

Hematogeneously

256
Q

Common bacterial causes of septic arthritis?

A

S. aureus
S. pyogenes
S. agalactiae

257
Q

Treatment of bacterial arthritis? 2

A

Antibiotics and Drainage

258
Q

Osteomyelitis is what? 3

A

Bone infection by an adjacent infection (direct), orthopedic surgery, hematogenously

259
Q

Symptoms of osteomyelitis? (2)

A
  1. Pain at site

2. Fever

260
Q

Diagnosing osteomyelitis? (2)

A
  1. Radiology

2. Culturing

261
Q

Osteomyelitis is treated how? 2

A
  1. Surgery

Antibiotics

262
Q

Common bacterial causes of osteomyelitis?
Which type is common in newborns?
Which type is common in sickle cell?

A

S. aureus: newborns
Coag negative staph
Strep
Salmonella: Sickle Cell

263
Q

Treatment of osteomyelitis?

A
  1. Identify bacteria and resistance through needle aspiration and culture
264
Q

Antibiotic therapy lasts how long for osteomyelitis?

265
Q

Transmission of infective endocarditis?

A

Hematogenous: Circulating microbes bind to valves

266
Q

Guaranteed symptoms of infective endocarditis? (2)

A
  1. Fever
  2. Fatigue
  3. Heart murmur
267
Q

Endocarditis is categorized in what two ways?

What type of bacteria

A

Acute: Virulent bacteria like Staph Aureus
Chronic: Less virulent: Strep viridans

268
Q

Viridans strep describes what group?

A

Strep that lives in oral cavity normally

269
Q

Viridans strep regularly enter bloodstream when? 3

A
  1. Tooth brushing
  2. Flossing
  3. Dental procedures
270
Q

What type of heart do the less virulent strep viridans infect?

A

Previously damaged

271
Q

What is the mortality of infective endocarditis with treatment?
With no treatment?

A

20-50%

Fatal

272
Q

What is the diagnosis criteria for infectious endocarditis?

What is required? (3)

A

Duke criteria

2 Major
1 major and 3 minor
5 minor

273
Q

Major criteria for infectious endocarditis? 2

A
  1. More than one positive blood culture

2. Evidence of myocardial involvement

274
Q

Minor criteria for infectious endocarditis? (6)

A
  1. Predisposition (Rheumatic fever, IV drug use)
  2. Fever
  3. Vascular problems (Emboli, bleeding)
  4. Immunological problem (glomerulonephritis)
  5. One positive blood culture
  6. Echocardiographs consistent with endocarditis
275
Q

What is most important test for diagnosing infective endocarditis?

A

Blood culture

276
Q

Treatment for infective endocarditis? (2)

A
  1. 2-6 weeks of IV antibiotics

2. Surgical replacement

MICRO (22 decks)

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