What are the three lines of defense against bacterial infections?
innate intracellular defense
innate cellular defense
adaptive cellular defense
What did Fredrick Griffith’s Experiment in 1928 tell us?
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
what is a virulence factor?
any molecule of a microorganism that aides in its ability to establish and maintain a pathogenic infection
What are the steps of the pathway to infection?
- exposure to pathogens
- adherence to skin or mucosa
- invasion through epithelium
- colonization and growth (production of virulence factors)
- Toxicity (toxic effects are local or systemic) and invasiveness (further growth)
- Tissue damage = disease
What are the three general ways damage (leading to disease) comes from in bacterial infections?
- the growht of the organism itself - leading to direct cell lysis, apoptosis, and autophagy
- toxins produced by the microorganism
- immune system collateral damage or malfunction
WHat are some of the ways we can classify bacteria?
- gram positive or negative
- morphology: shape and organization
- biochemical characteristics
What makes skin such a good barrier against bacteria?
it’s dry
sweat has organic acids that block colonization
What are some common types of skin bacterial infections?
folliculitis
- furuncles and carbuncles form after folliculitis
impetigo
erysipelas
cellulitis
abscess
gangrene
necrotizing fasciitis
arthropod borne infections
what is folliculitis?
infection of the hair follicles = small, erythematous, often puritic lesions. Local therapy is typically sufficient treatment.
What are furuncles and carbuncles?
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.
What is impetigo?
superficial infection involving the epidermis usually due to group A streptococcus infection. Presents as a purulent discharge with crusting and is highly contagious
What is erysipelas?
cute inflammation of the dermis involving lymphatic vessels. Usually caused by group A strep. Fever and leukocytosis may occur. Butterfly wing rash on face.
What is cellulitis?
involves all layers of skin to the subcutaneous tissue. Causes fever and leukocytosis and sometimes bacteremia. Group A strep and Staphylococcus aureus most common.
What is an abscess?
localized collection of purulent material (pus), formation is caused by host defenses trying to wall off the infection.
What is gangrene?
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)
What is necrotizing fasciitis?
rare but life-threatening infection of subcutaneous tissues. Commonly caused by group A strep.
WHat is the most common infectious agent of the skin?
staphylococcus aureus
What sorts of skin infections will staph aureus cause?
impetigo, cellulitis, folliculitis, furuncles and carbuncles
it’s a common infectious agent of surgical wounds
what are the general characteristics of staph auerus?
gram?
shape?
biochemical characteristics? (2)
it’s a gram positive bacteria
cocci in clusters
catalase positive
coagulase positive
What three virulence factors allow staph aureus to evade the host defenses?
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
What three virulence factors allow staph aureus to invade the deep tissue?
hyaluronidase - breaks down connective tissue
staphylokinase - lises formed clots
lipase - breaks down fat
What two syndromes can staph aureus cause through toxin production?
toxic shock syndrome
scalded skin syndrome
WHat happens in toxic shock syndrome?
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
Describe scalded skin syndrom
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
what types of skin infections are caused by strep pyogenes?
impetigo
erysipelas
cellulitis
what are the two tosin mediated syndromes that can occur in streptococcus pyogenes infections?
toxic shock syndrome
necrotizing fasciitis
What is the general pathology of strep pyogenes skin infections?
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.
Will strep pyogenes skin infections lead to rheumatic fever of glomerulonephritis?
glomerulonephritis
What are the general characteristics of strep pyogenes?
gram?
shape?
biochemical? (2)
sensitivities?
gram positive bacteria
cocci - in chains
catalase negative! but still an aerobe!
beta hymolysis
bacitracin sensitive
What are 6 important virulence factors for the spread and inflammation of strep pyogenes infections?
- streptokinase (converts plasminogen to plasmin)
- M protein (resists phagocytosis)
hyaluronidase (breaks down connective tissue)
DNAse (digests DNA)
Streptolysin O (destroys RBCs)
Streptolysin S (destroys WBCs)
Where are the streptokinase and hyaluronidase of strep pyogenes encoded?
a lysogenized prophage
Describe the necrotizing fasciitis that occurs in streptodoccus pyogenes infections
trauma allows for deep seated infection release of exotoxin B (protease) rapid necrosis along fascial planes with no damage to muscles
What is bullous impetigo? What is the normal pattern of an impetigo rash?
bullous impetigo involves pustules in the very superficial layers of the epidermis
the normal impetigo rash is a vasicular rash with a honeycomb pattern
What are the two situations in which pseudomonas aeruginosa skin infections can occur?
burn wound infection (cellulitis)
and hot tub infections (folliculitis)
What is the preferred environment of pseudomonas aeruginosa?
inhabits many environments such as the soil, water, and large intestine - typically warm areas
What are the general characteristics of pseudomonas aeruginosa?
gram?
shape?
biochemical characteristics? (3)
gram negative bacteria
bacilli
lactose non-fermenter
oxidase positive
glucose non-fermenter
What is hte most common vector-borne disease in the US?
Lyme disease
followed by rocky mountain spotted fever
What are the 3 stages of lyme disease?
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
What is the causative microorganism of lyme disease?
what are its characteristics?
shape? staining?
Borelia Burgdorferi
it’s a spirochete bacteria
stain with giemsa and silver stains
microaerophilic
What is the carrier for B. burgdorferi?
the Ixodes tick
it will transmit the bacteria from mice to humans
What is the causative agent of rocky mountain spotted fever?
How does this microorganism get its energy?
rickettsia rickettsii
it’s an obligate intracellular bacteria because it can’t synthesize its own ATP
What is the clinical presentation of RMSF?
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