Intro to Infectious DIsease and Bacterial Skin Infections Flashcards

1
Q

What are the three lines of defense against bacterial infections?

A

innate intracellular defense

innate cellular defense

adaptive cellular defense

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2
Q

What did Fredrick Griffith’s Experiment in 1928 tell us?

A

Two types of bacteria: S (smooth) and R (rough) - only the S are infectious to mice

Inject S = mice dies

Inject heat-killed S = mice lives

Inject R = mice lives

Inject R and heat-killed S = mide dies!!!!!!!!

Showed us that DNA was the mode of genetic info transfer and showed that virulence factors can be shared among bacteria

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3
Q

what is a virulence factor?

A

any molecule of a microorganism that aides in its ability to establish and maintain a pathogenic infection

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4
Q

What are the steps of the pathway to infection?

A
  1. exposure to pathogens
  2. adherence to skin or mucosa
  3. invasion through epithelium
  4. colonization and growth (production of virulence factors)
  5. Toxicity (toxic effects are local or systemic) and invasiveness (further growth)
  6. Tissue damage = disease
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5
Q

What are the three general ways damage (leading to disease) comes from in bacterial infections?

A
  1. the growht of the organism itself - leading to direct cell lysis, apoptosis, and autophagy
  2. toxins produced by the microorganism
  3. immune system collateral damage or malfunction
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6
Q

WHat are some of the ways we can classify bacteria?

A
  1. gram positive or negative
  2. morphology: shape and organization
  3. biochemical characteristics
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7
Q

What makes skin such a good barrier against bacteria?

A

it’s dry

sweat has organic acids that block colonization

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8
Q

What are some common types of skin bacterial infections?

A

folliculitis
- furuncles and carbuncles form after folliculitis

impetigo

erysipelas

cellulitis

abscess

gangrene

necrotizing fasciitis

arthropod borne infections

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9
Q

what is folliculitis?

A

infection of the hair follicles = small, erythematous, often puritic lesions. Local therapy is typically sufficient treatment.

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10
Q

What are furuncles and carbuncles?

A

Furuncles and carbuncles usually develop from folliculitis. Carbuncles involve deeper tissues and may have systemic symptoms but rarely involve bacteremia. Antibiotic therapy and sometimes surgery are needed.

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11
Q

What is impetigo?

A

superficial infection involving the epidermis usually due to group A streptococcus infection. Presents as a purulent discharge with crusting and is highly contagious

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12
Q

What is erysipelas?

A

cute inflammation of the dermis involving lymphatic vessels. Usually caused by group A strep. Fever and leukocytosis may occur. Butterfly wing rash on face.

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13
Q

What is cellulitis?

A

involves all layers of skin to the subcutaneous tissue. Causes fever and leukocytosis and sometimes bacteremia. Group A strep and Staphylococcus aureus most common.

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14
Q

What is an abscess?

A

localized collection of purulent material (pus), formation is caused by host defenses trying to wall off the infection.

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15
Q

What is gangrene?

A

advanced stage of cellulitis that has lead to significant tissue necrosis and gas in the soft tissues. Typical organisms are streptococci, mixed infection with anaerobes, and clostridial infection (classic gas gangrene)

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16
Q

What is necrotizing fasciitis?

A

rare but life-threatening infection of subcutaneous tissues. Commonly caused by group A strep.

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17
Q

WHat is the most common infectious agent of the skin?

A

staphylococcus aureus

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18
Q

What sorts of skin infections will staph aureus cause?

A

impetigo, cellulitis, folliculitis, furuncles and carbuncles

it’s a common infectious agent of surgical wounds

19
Q

what are the general characteristics of staph auerus?

gram?

shape?

biochemical characteristics? (2)

A

it’s a gram positive bacteria

cocci in clusters

catalase positive

coagulase positive

20
Q

What three virulence factors allow staph aureus to evade the host defenses?

A

protein A - it binds the Fc portion of IgG

coagulase - forms fibrin coat to protect the organism

hemolysins and leukocidins to destroy RBCs and WBCs

21
Q

What three virulence factors allow staph aureus to invade the deep tissue?

A

hyaluronidase - breaks down connective tissue

staphylokinase - lises formed clots

lipase - breaks down fat

22
Q

What two syndromes can staph aureus cause through toxin production?

A

toxic shock syndrome

scalded skin syndrome

23
Q

WHat happens in toxic shock syndrome?

A

the toxic shock syndrome toxin -1 (TSST-1) diffuses systematically.

it’s a superantigen, so it grabs onto the MHC class 2 and forces it to interact with a naive T cell even if that T cell isn’t specific for the antigen.

This activates the T cell inappropriatly and you get massive amounts of activated T cells and massive amounts of cytokines being released

This results in actue fever, rash, desquamation on palms and soles, hypotensive shock, organ dysfunction, and possible death

24
Q

Describe scalded skin syndrom

A

this is mostly in children

exfoliative toxins ET-A and ET-B diffuse systemically

the epidermis separates and the skin sloughs off

you get associated fluid loss, secondary infections, and possible death - 50% mortality rate in adults

RItter’s syndrome is severe in neonates - it’s an umbilical cord infection

25
Q

what types of skin infections are caused by strep pyogenes?

A

impetigo

erysipelas

cellulitis

26
Q

what are the two tosin mediated syndromes that can occur in streptococcus pyogenes infections?

A

toxic shock syndrome

necrotizing fasciitis

27
Q

What is the general pathology of strep pyogenes skin infections?

A

May be normal flora of the skin.

Can colonize in the skin (following trauma) leads to colonization  inflammation  pustular lesions and honeycomb-like crusts (impetigo) at the site of inoculation. Deeper infections lead to erysipelas and cellulitis.

28
Q

Will strep pyogenes skin infections lead to rheumatic fever of glomerulonephritis?

A

glomerulonephritis

29
Q

What are the general characteristics of strep pyogenes?

gram?

shape?

biochemical? (2)

sensitivities?

A

gram positive bacteria

cocci - in chains

catalase negative! but still an aerobe!

beta hymolysis

bacitracin sensitive

30
Q

What are 6 important virulence factors for the spread and inflammation of strep pyogenes infections?

A
  1. streptokinase (converts plasminogen to plasmin)
  2. M protein (resists phagocytosis)

hyaluronidase (breaks down connective tissue)

DNAse (digests DNA)

Streptolysin O (destroys RBCs)

Streptolysin S (destroys WBCs)

31
Q

Where are the streptokinase and hyaluronidase of strep pyogenes encoded?

A

a lysogenized prophage

32
Q

Describe the necrotizing fasciitis that occurs in streptodoccus pyogenes infections

A

trauma allows for deep seated infection  release of exotoxin B (protease)  rapid necrosis along fascial planes with no damage to muscles

33
Q

What is bullous impetigo? What is the normal pattern of an impetigo rash?

A

bullous impetigo involves pustules in the very superficial layers of the epidermis

the normal impetigo rash is a vasicular rash with a honeycomb pattern

34
Q

What are the two situations in which pseudomonas aeruginosa skin infections can occur?

A

burn wound infection (cellulitis)

and hot tub infections (folliculitis)

35
Q

What is the preferred environment of pseudomonas aeruginosa?

A

inhabits many environments such as the soil, water, and large intestine - typically warm areas

36
Q

What are the general characteristics of pseudomonas aeruginosa?

gram?

shape?

biochemical characteristics? (3)

A

gram negative bacteria

bacilli

lactose non-fermenter

oxidase positive

glucose non-fermenter

37
Q

What is hte most common vector-borne disease in the US?

A

Lyme disease

followed by rocky mountain spotted fever

38
Q

What are the 3 stages of lyme disease?

A

stage 1: 10 days after bite - erythema migrans

stage 2: weeks later - CNS involvement, CV involvement (carditis, AV nodal block), skin involvment (secondary annular lesions), joint involvement (migratory myalgias, transient arthritis)

stage 3: months to years later: chromic arthritis, encephalopathy, acrodermatitis chronicum atrophicans

39
Q

What is the causative microorganism of lyme disease?

what are its characteristics?

shape? staining?

A

Borelia Burgdorferi

it’s a spirochete bacteria

stain with giemsa and silver stains

microaerophilic

40
Q

What is the carrier for B. burgdorferi?

A

the Ixodes tick

it will transmit the bacteria from mice to humans

41
Q

What is the causative agent of rocky mountain spotted fever?

How does this microorganism get its energy?

A

rickettsia rickettsii

it’s an obligate intracellular bacteria because it can’t synthesize its own ATP

42
Q

What is the clinical presentation of RMSF?

A

you get fever, headache, maculopapular rash on palsm and soles that spreads to the trunk over time

the bacteria infects and proliferates in endothelial cells, so you get inflammation of the endothelial lining of small blood vessles (this causes the rash).

then you get widespread vasculitis, headache, CNS changes, and possibly renal damage

cam be fatal if untreated

43
Q
A