Flashcards in Microbiology Midterm Deck (79)
Types of skin and soft tissue damage that can occur with infection
Exogenous, endogenous or toxin-mediated
Most soft tissue and exogenous skin infections are due to what?
Staph A or Strep pyogenes (Group A Strep)
Similarities between strep A and Staph A
1. Both are transient skin flora
2. They are both spreading infections
3. Both form abscesses
4. Both cause necrotizing fasciitis
What do we mean by spreading infection?
1. Pyoderma (produces pus)
2. Impetigo - Spreading infection of the epidermis
4. Cellulitis - Subcutaneous, more serious
What types of necrotizing infections do they cause?
Fasciitis, gas gangrene (myonecrosis)
Streptococci in general are recognized how?
1. Gram positive
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
Main virulence factor for strep
M protein, which binds the epidermis and is antiphagocytic
What kind of hemolytic pattern do we see in Strep A?
How do we know we are working with Strep A?
1. Beta hemolytic
2. PYR positive
3. Sensitive to Bacitracin
What kind of capsule does Strep A have?
Hyaluronic acid capsule, which is identical to normal tissue and is anti-phagocytic
What are the key extracellular virulence factors for strep 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
What do pyrogenic exotoxins do?
superantigens stimulate cytokines storm, nonspecifically activate T cells.
These are encoded by bacteriophages and can cause scarlet fever and toxic shock syndrome
Two types of clinical presentations of Strep A?
Suppurative vs. Non suppurative
Suppurative presentations of Strep A?
Pharyngitis (Can lead to Scarlet Fever, a super antigen)
Toxic Shock-like syndrome
Nonsupprative presentations of Strep A?
Both of these diseases happen after the bug is gone, known as "post suppurative sequelae"
Ab to M type from throat infection attack heart/body, requires long term abx to prevent reinfection
antigen-Ab complexes deposited in glomeruli s/p throat or skin infection
How do we treat Strep A?
How do we treat Strep A if the patient also has Staph A?
PCNase resistant antibiotic
What pediatric syndrome is associated with Strep A?
pediatric autoimmune neuropsychiatric disorder assoicated with group A Strep
How many more or less strains are there of staph A than strep A?
90 of Strep A
30 Staph A
How do we recognize staph A?
1. Beta hemolytic
2. Catalase positive
3. Coagulase positive
4. Gram positive cocci
Staph A characteristics
Common in hospitals
Besides cellulitis and impetigo which we also see in Strep A, what skin infections do we see in Staph A?
What type of invasive infections do we see with Staph A?
What type of deep lesions do we see with staph A?
What type of bacteremias do we see with Staph A?
(Meningitis and PNA technically fall into this as well)
How can we kill Staph A with our own defense mechanisms?
Opsonophagocytosis. It is not susceptible to lysis by MAC complex or the classical pathway
Staph A virulence factors
Pa Likes His Ribs Cooked 4 times
linked to peptidoglycan, binds Fc end of Ab, avoids uptake by neutrophils
defense against phagocytes- breaks down H2O2 during oxidative burst
pokes holes in granulocyes
Ribotechoic acid and techoic
binds ECM to set up shop, techoic acid induces toxic shock
Walls off abscesses
Can't target this with a vaccine because it has 8 types
Breaks down Hyaluronic Acid to spread deeper
Cytotoxins of Staph A and what they do
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)
Toxin diseases of Staph A
Scalded Skin Syndrome
Staph Scarlet Fever
Toxic Shock Syndrome
Bullous impetigo caused by what toxin from Staph A?
Exfoliatin A, B cause bullous impetigo
What is the Staph A toxin mediated condition scalded skin syndrome?
ridders disease, Exfolatin serine proteases cause splitting of desmosomes in stratum granulosum of epidermis
What causes food poisoning in Staph A?
Staph enterotoxin A, B, C, D, E
What tools do we use to identify Staph A?
• Identify by Pulsed Field Gel Electrophoresis, bacteriophage typing (most strains carry phages)
Gene for MRSA
mecA gene (encodes PBP2’- altered penicillin binding protein)
Types of Vancomycin resistance in Staph A?
VISA- vancomycin intermediate S. aureus
VRSA- vancomycin resistant S. aureus
When are we concerned about Staph Intermedius?
Identifying Staph Epidermidis?
Catalase positive, coagulase negative. These are the guys that make biofilms
Takeaway diseases of Staph Epidermidis?
UTI (the biggie)
Indwelling device infection
Structural observations of Alpha Herpes Virus
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)
Cells affected by Alpha Herpes Simplex
Infects epithelial cells, latency in sensory ganglia/ neurons
Life Cycle of Alpha Herpes Virus
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
4 Phases of lytic phase
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)
Treatment for Alpha Herpes Viruses
1. Herpes Thymidine Kinase
2. Phosphonoacetic acid/Phosphonoformate
Effect of Herpes Thymidine Kinase on Alpha Herpes viruses
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
What are the effects of Phosphonoacetic acid and phosphonoformate?
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
Herpes Simplex Virus types
HSV-1 Presents as what?
Oral cold sores, can cause blindness (keratitis) and encephalitis. Typically targets Trigeminal ganglia
HSV-2 Presents how?
Geneital, severe CNS disease in infants. IgG protection on reactivation but only have IgM on primary infection)
Herpes Zoster Virus presentation
Chicken pox on primary infection and shingles on secondary. Exists as varicella for pox and zoster as shignles. This spreads by the respiratory tract
How do we test for Herpes Zoster and what should we do to prevent it?
Use a Tzanck smear to find it, which will show synsitia/ multinucleated giant cells. And get the damn live attenuated vaccine for your kids.
What fungal types are there?
Yeast structure and reproductive traits?
Unicellular fungus that reproduces by budding or binary fission
Mold structure and reproduction?
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
Good targets on fungi?
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
Superficial pathogens. Malassezia yeast and trichosporon
Cutaneous typically. We have microsporum, trichophyton and Epidermophyton
How do we diagnose fungal infections?
1. Direct microscopy (KOH, calcoflour white)
2. Culture (Gold standard, use Sabouraud's ager which inhibits bacterial growth)
Types of antifungals?
Azoles, Polyenes, Echinocandins
What do azoles do?
Inhibit ergosterol snthesis. They can cause drug reactions and visual disturbances though.
What do Polyenes do?
Bind ergosterol and make pores for osmotic death (also called amphotericin). Danger for this is renal toxicity
What do echinocandins do?
Inhibit synthesis of B-glucan and block cell wall synthesis. These drugs end in "fungin" and are broad spectrum
What immune responses do we have to fungi?
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
How do we classify mycoses?
By their location
Describe superficial mycoses
outer keratinized skin, mostly yeast
What is Tinea Versicolor and how can we recognize it?
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
Describe cutaneous mycoses
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
Describe subcutaneous mycoses
invasion of subcutaneous tissue, may req surgery, rare, introduced traumatically, infection to dermis, subcutaneous tissue, bone
Common subcutaneous mycosis
Sporotrichosis (think stuck by a rosebush). Lives in soil, usually starts on hands, lesions and nodules track up lymphatics= "sporotrichoid spread"
Describe systemic mycoses
inhalation of spores, dimorphic fungi