PID Exam 1

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nielemi
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PID Exam 1
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2013-09-27 06:56:26
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Carver College Medicine Medical School Infectious Diseases
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Flashcards for first principles of infectious diseases class
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  1. Gram positive cell walls have what characteristics?
    • Thick peptidoglycan with techoic acid and lipotechoic acid which bind calcium and magnesium to help provide structure
    • Also often have a negatively-charged polysaccharide capsule, except for Bacillus anthracis, which has a poly D-glutamic acid capsule
    • Can have O-acetylated peptidoglycan, fimbriae, or flagella
    • Spores: Can be formed; contain dipicolinic acid (from lysine) and calcium in the coat to confer resistence
    • Protoplast: A gram-positive bacterium following treatment with lysozyme; the cell wall is removed
    • Poly-beta-hydroxy-butyric acid energy granules can also be seen in some bacteria upon staining
  2. Gram-negative cell walls have what characteristics?
    • Thinner and less cross-linked peptidoglycan layer which is partially covalently bound to lipoproteins
    • Lipopolysaccharide (LPS): Forms outer membrane with phospholipids; aka endotoxin; O somatic antigen is the immunogenic part (different for each bacteria strain), which is linked to a core polysaccharide and then lipid A; lipid A is the toxic portion--causes fever, hypotension, and shock and kills 100,000 people in US each year
    • Molecules of 800 MW or greater are trapped in periplasm
    • Capsule: May be present outside of outer membrane
    • Other outer membrane proteins (OMPs) may be present: Can be immunogenic or covalently linked to peptidoglycan; ex. porins
    • Pili or flagella may be present
    • Spheroplast: A gram-negative bacterium that has little cell wall; created by treating with lysozyme plus EDTA; cell walls may regrow
  3. Endotoxins versus exotoxins
    • Endotoxin: LPS; part of gram-negative bacteria and is not variable; nonenzymatic
    • Lethal at 1ug
    • Exotoxin: Can be secreted outside of gram-positive or to the periplasm of gram-negative bacteria; can be enzymatic
    • More lethal--in ng to pg range
  4. Pathways to shock
    • LPS: Can bind to TLR-4 on macrophages; causes release of TNFa that causes hypotension
    • Lipoteichoic acid (LTA): Can bind to TLR-2/6; causes release of TNFa and IL1-beta (fever)
    • Superantigen: Crosslinks MHCII with TCR; causes release of IFN-gamma and IL-2 (rash/scarlet fever and other symptoms) without proper antigen presentation; macrophages get activated by IFN-gamma and phagocytose RBCs and host
  5. Structure of peptidoglycan
    • Made of GA and MA beta-1,4 linkages
    • MA: N-acetylmuramic acid, which is GA + lactyl; tetrapeptide chains are found on MA that are cross-linked to each other through peptide bonds
    • GA: N-acetylglucosamine
    • Crosslinked by L-lysine usually
    • 75% crosslinked in gram positive
    • 25% crosslinked in gram negative, but covalently bound to lipoproteins
  6. O-acetylated peptidoglycan
    • Found in streptococci and Neisseria
    • Highly inflammatory and difficult to degrade; collects in joints and causes arthritis
  7. Phosphonomycin
    • Inhibits attaching MA to UDP in cytoplasm for peptidoglycan synthesis
    • Not approved in US
  8. Cycloserine
    • Inhibits attachment of pentamer to UDP-MA for peptidoglycan synthesis in the cytoplasm
    • Effective for TB
  9. Vancomycin
    • Prevents transpeptidation/cross-linking of peptidoglycan
    • Only effective against gram-positive bacteria because they do not have an outer membrane
    • Enterococcus faecalis and faecium may be resistant and can transfer resistence to other gram-positive bacteria
  10. Bacitracin
    • Inhibits pyrophosphatase from regenerating UDP precursor for peptidoglycan synthesis
    • Group A streptococci are 10 more sensitive than other bacteria
  11. Beta-lactam antibiotics
    • Bind to penicillin-binding proteins (PBPs)
    • Have sulfur in them, making them reactive with host proteins; can cause anaphylaxis
    • PBPs are involved in cross-linking, and have a transpeptidase activity
    • Inhibition of this activity destabilizes the cell wall
    • PBP2a, encoded by SCCmec is resistant to all beta lactam antibiotics (common in Staphylococcus aureus)
    • Includes penicillins, carbapenems (broadest spectrum), monobactams (low chance of cross-sensitivity), and cephalosporins
    • Beta-lactamase inhibitors: These prevent the inactivation of beta-lactam antibiotics by binding the beta-lactamase; include clavulanic acid
  12. Clindamycin
    Protein synthesis inhibitor that stops Staphylococcus aureus exotoxin production
  13. Quinalone antibiotics
    • Prevent formation of phosphodiester bonds by DNA gyrase
    • Fluroquinolones: Include ciprofloxacin (good against gram-negative bacteria) and norfloxacin (good for UTIs)
    • High risk of enterocolitis due to poor effect upon Clostridium difficile
  14. Metronidazole
    • Aka Flagyl
    • Good for anaerobic bacteria and microaerophilic bacteria; good for Trichomonas vaginalis; intercalates into DNA and prevents replication
  15. Rifampin and rifamycin
    • Inhibitors of bacterial transcription
    • High mucosal surface penetrating antibiotics
    • Cause red urine and contact lenses to turn red
    • Microbes develop resistance easily
  16. Differences in human in bacterial ribosomes
    • Human: 40S and 60S to make 80S
    • Bacteria: 30S and 50S for 70S
  17. Protein synthesis inhibitors
    • 50S Inhibitors
    • Clindamycin: Used to prevent toxin production; may allow growth of Clostridiium difficile
    • Chloramphenicol: Penetrates CNS well; used only for a variety of gram negatives; causes aplastic anemia!
    • Erythromycin: Used in penicillin-allergic patients; include azithromycin, macrolides, and clarithromycin
    • 30S Inhibitors
    • Aminoglycosides: Broad spectrum and good for many hard-to-kill gram negatives; cause hearing loss and kidney failure; include
    • Tetracyclines: Broad spectrum; may cause stomach upset; impairs bone development in children under 12; stains teeth cark in infants of mothers treated during pregnancy; binds calcium
    • Additional
    • Mupirocin: Topical that inhibits isoleucine tRNA
    • Linezolid: Used for MRSA, but resistance develops quickly
  18. Polymyxin B
    • Attacks membranes
    • Lots of human toxicity
  19. Daptomycin
    Membrane disrupter
  20. Sulfonamides and trimethoprim
    • Together, called Bactrim
    • Specific for bacterial folic acid metabolism
    • Broad spectrum: Aerobic and facultative bacteria; Pneumocystis carinii; NOT for anaerobes
  21. Antimycobacterials
    • Good for TB; take multiple at once
    • Isoniazid (cell wall synthesis), ciprofloxicin, cycloserine, and rifampin
  22. What are the bacilli-shaped bacteria and are they gram+ and gram-?
    • Gram Positive: Bacillus cereus (aerobe; spore former),
      Clostridium tetani (anaerobe; spore former), Corynebacterium 
      (aerobe), Listeria (aerobe), Propionibacterium (anaerobe), Lactobacillus (aerotolerant anaerobe; dominant mucosal normal flora), Bifidobacterium (anaerobe; normal flora of GI tract in breast-fed babies)
    • Gram Negative: Escherichia coli, Enterobacteriaceae (facultative anaerobes), Pseudomonadaceae (aerobes), Bactroides and Fusobacterium (anaerobes), Haemophilus, Bordetella, Legionella
  23. What are the cocci-shaped bacteria and are they gram+ and gram-?
    • Gram Positive: Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae
    • Gram Negative: Neisseria meningitidis, Acinetobacter
  24. What are the curvy-shaped bacteria and are they gram+ and gram-?
    • Gram-Negative Spirilli: Vibrio cholerae
    • Spirochete: Treponema pallidum (spirochetes do not gram stain well)
  25. Types of hemolysis
    • Beta: Complete lysis of RBCs in blood agar
    • Alpha: Blood agar turns green due to change in oxidation state of iron in blood from hydrogen peroxide and acids. [Viridans streptococci and Streptococcus pneumoniae]
    • Gamma: No lysis
  26. What bacteria are difficult to gram stain?
    • Mycobacteria, the causes of TB and leprosy, are best seen with hot fuchsin red stain because they have a lipid-dense cell wall, and the heat helps melt the lipids
    • Legionella pneumophila, which is tecnically gram negative, is best seen with a silver stain
    • Spirochetes are best seen with darkfield microscopy
    • Streptococcus pneumoniae can be stained with India Ink stain to visualize an unstained capsule contrasting with stained background (they do stain gram-positive)
  27. What is the lactose test useful for?
    • Determine if gram-negative rods are Enterobacteriaceae
    • Salmonella: Cannot use lactose; causes typhoid fever and gastroenteritis; found intracellularly
    • Shigella: Cannot use lactose; causes dysentery
    • Escherichia coli, Enterobacter, Klebsiella, Proteus, Arizona, Serrata are lactose positive, and appear pink instead of white on MacConkey agar
  28. What is the Kirby Bauer test useful for?
    • Used to determine Minimum Inhibitory Concentration, which prevents growth
    • A Minimum Bactericidal Concentration would be causing death
  29. Examples of oxygen usage by bacteria
    • Obligate aerobes: Bacillus, Mycobacterium
    • Facultative anaerobe: Staphylococcus, Excherichia
    • Aerotolerant anaerobes: Streptococcus
    • Obligate anaerobes: Clostridium
    • Microaerophiles: Neisseria, Borrelia (Lyme disease)
  30. Mesophile definition and exception
    • Pathogens that survie at body temperature
    • Mycobacterium leprae and dermatophytes (ringworm fungi) cannot grow at that temperature, so they are confined to the skin
  31. Invasive intracellular bacteria
    • Include Mycobacterium, Salmonella, and Listeria monocytogenes
    • Antibodies increase severity due to opsonization
    • Usually cause granuloma formation instead of inflammation
    • Vaccines are attenuated (weaked organisms)
    • Immunity: Neutralizing antibodies to exotoxins; direct T-cell killing or activation of macrophages (IFN-gamma) and CD8 T-cells (IL-2)
  32. Staphyloccocus aureus bacterial properties
    • Gram Stain: Positive
    • Morphology: Extracellular clustered cocci
    • Oxygen: Facultative aerobe/anaerobe, but only make TSS aerobically
    • Nonspore former, but is highly resistant to drying and is antibiotic resistant
    • Hemolysis: Usually gamma, but is beta for S. aureus
    • Catalase positive
    • Coagulase positive for S. aureus; coagulase negative for the other 15+ species of staphylococci
    • Can be normal flora or pathogens
    • Has a ribitol teichoic acid fuzz layer
  33. Staphylococcus
  34. Staphylococcus aureus clinical presentation
    • Primary Inflammatory of the Skin
    • Boils (furuncles)
    • Carbuncles (multiple boils)
    • Pimples (folliculitis)
    • Paronychia (infections of nail beds)
    • Impetigo
    • Soft tissue abscesses
    • Atopic dermatitis
    • All depend on walling off the organism by cell surface virulence factors and then spread by the secreted virulence factors
    • Primary Inflammatory of the Mucous Membranes
    • Sinusitis
    • Chronic otitis media
    • Bronchial pneumonia/necrotizing pneumonia
    • Urinary tract infections
    • Vaginal infections
    • Enterocolitis
    • These cause less inflammation than infection of the skin, and also produce less alpha-toxin
    • Primary Non-Inflammatory of Mucous Membranes
    • Scalded skin syndrome
    • Toxic shock syndrome
    • Staphylococcal Food Poisoning: Vomiting and diarrhea 2-8 hours after ingesting pre-formed SEs; lasts up to 48 hours)
    • Systemic Infections (Inflammatory & Non-Inflammatory)
    • Septicemia: Presents with high fever and disseminated intravascular coagulation (DIC)
    • Toxic shock syndrome
    • Endocarditis: Presents with fever, strokes, and metastatic abscesses
    • Osteomyelitis
    • Necrotizing fasciitis/myositis: Presents with fever and is often with TSS
  35. Treatment of Staphylococcus aureus infections (specific to location)
    • Mild Inflammatory and Non-Inflammatory Skin and Mucous Membranes
    • Antibiotics
    • Surgery to drain abscesses and furuncles
    • Remove infected ingrown hair/nail
    • Serious Infections
    • Hospitalization
    • Antibiotics (vancomycin, clindamycin, rifampin)
    • Blood pressure support
    • Surgery to drain abscesses or debride necrotic areas
    • IVIG if necessary
    • Activated protein C (to help break up clots)
    • Remove tampon, packing, or affected implants
    • Influenza vaccine to prevent future post-influenza TSS
  36. Staphylococcal Toxic Shock Syndrome
    • Localized or systemic Staphylococcus aureus releases the superantigens TSST-1, SE-B, or SE-C
    • This results in massive release of cytokines: IFN-gamma and IL-2 (rash/scarlet fever & activation of more macrophages by IFN-gamma), IL1-beta (fever), and TNF-alpha/beta (hypotension)
    • Associated with tampons--absorbency increases incidence
    • Common complication of influenza virus infection (35,000 deaths per year in US)
    • Diagnosis
    • Fever > 102F
    • Hypotension (systolic <90)
    • Rash (aka macular erythroderma)
    • Peeling of skin if patient survives
    • 3 multi-organ changes
    • Probable TSS is missing one criterion; toxin-mediated disease is missing more than one criterion
  37. Post-influenza toxic shock syndrome
    • Staphylococcus aureus, especially TSST-1+ strains, produce serine proteases that cleave influenza HA into active form
    • Influenza can infect epithelial cells and damage them, allowing sites for secondary S. aureus infection and additional TSST-1 production
  38. Menstrual toxic shock syndrome
    • 1/400 chance of TSS from tampons
    • 3.5/100,000
    • Symptoms: Sunburn rash, skin peeling, bloodshot eyes, low BP (can cause black extremities)
    • Remove tampon because Staph only make TSS aerobically
  39. 20th century influenza pandemics
    • 1918: Spanish flu (H1N1), 2 million American deaths
    • 1957: Asian flu (H2N2), 200,000 American deaths
    • 1968: Hong Kong flu (H3N2), 35,000 American deaths
  40. Influenza virus external proteins
    • HA: Hemagglutinin, which binds to sialic acid residues on epithelial cells to allow viral entry
    • The binding site on HA is exposed after a serine protease cleaves it
    • NA: Neuraminidase, which is necessary for the exit of virus from host cells
  41. Staphylococcus aureus epidemiology
    • 500,000 post-surgical infections
    • 45% of infectious endocarditis (100,000)
    • 3,000-35,000 post-influenza pneumonia
    • Most significant cause of serious infectious diseases & infectious disease deaths in US
    • Number 1 cause of infective endocarditis (20,000 deaths/year)
    • Number 1 cause of osteomyelitits
    • Number 2 cause of pneumonia
  42. Staphylococcus aureus can cause what symptoms?
    • Toxic Shock Syndrome (TSS)
    • UTIs
    • 90% of bone infections (osteomyelitis from orthopedic surgery)
    • Scalded Skin Syndrome in neonates
  43. MRSA comes from where?
    • MRSA makes up 50% of hospital-acquired infections and 30% of community-acquired infections
    • SCCmec encodes PBP2a for methicillin resistance
    • SCCmec II usually found in hospital-acquired, while community-acquired usually have SCCmec II or IV
  44. Strains of MRSA
    • USA 300 PFGE type
    • SCCmec IV encodes methicillin resistance
    • Common on skin; causes serious necrotizing pneumonia in children; and soft tissue infections in all ages; most common
    • USA 400
    • SCCmec IV encodes methicillin resistance
    • Have SE-B or SE-C
    • Causes serious necrotizing pneumonia and toxic shock syndrome in children, and soft tissue infections in all ages
    • USA 200
    • SCCmec II or IV encodes methicillin resistance
    • Has TSST-1
    • Most common on mucosal surfaces; causes serious necrotizing pneumonia and toxic shock syndrome in all ages; rare to cause skin infections
    • USA 100
    • Is found mostly in hospital-associated infections
    • Common
  45. Staphylococcus aureus cell surface virulence factors
    • All are attached to Staphylococcus aureus using LPXTG anchors
    • Coagulase protein (clumping factor): Converts fibrinogen to fibrin, allowing for clotting and walling-off of the microbe [is an MSCRAMM]
    • Fibronectin binding proteins: Bind to integrins
    • Collagen binding proteins
    • Laminin binding proteins
    • Vitronectin binding proteins
    • Protein A: Binds to the Fc of IgG to turn them backwards as an antiphagocytic defense
  46. Staphylococcus aureus secreted virulence factors
    • Coagulase protein: In addition to the cell surface coagulase protein, this is secreted to activate the clotting cascade and wall off the microbe
    • Hemolysins
    • Alpha: Forms a pore as a heptamer to lyse rabbit RBCs (not human ones though); also causes necrosis of the skin and blocks nerve repolarization; most/all S. aureus make
    • Beta: The "hot-cold" hemolysin (made at hot, lyses at cold) and is a sphingomyelinase; toxic to lymphocytes
    • Gamma: Causes RBC hemolysis in humans; can also assemble as a heptamer to make the Panton-Valentine Leukocidin (PVL), which kills leukocytes
    • Delta: Acts as a surfactant to solublize host membranes or forms small pores; related to phenol-soluble modulins
    • These toxins are redundant, so it's difficult to determine their role in disease
    • Spreading Factors
    • Hyaluronidase: Cleaves hyaluronic acid in ground substance, making it easier to spread
    • Staphylokinase: Breaks clots that have formed in walling off the organism
    • Other
    • Lipase: Necessary for survival on skin; breaks down fatty acids, which are toxic to the organism
    • DNAses, RNAses, Proteases (including serine and cysteine), beta-lactamases
    • TSST-1
    • Staphylococcal Enterotoxins and Staphylococcal Enterotoxin-Like
    • Staphylococcal Exfoliative Toxins
  47. TSST-1
    • Toxic Shock Syndrome Toxin-1
    • Superantigen that crosslinks MHCII alpha-chain to the variable part of the beta-chain of the T-cell receptor (TCR)
    • This crosslinking results in massive cytokine release from macrophages and T cells
    • Causes menstrual staphylococcal TSS and half of non-menstrual staphylococcal TSS
  48. Staphylococcal enterotoxins (SEs) and Staphylococcal enterotoxin-like (SE-like) toxins
    • Staphylococcal enterotoxins: A through E, I
    • Staphylococcal enterotoxin-like toxins: G, H, J-X
    • These are also superantigens that crosslink MHCII and variable regions of the beta-chain of the T-cell receptor (TCR)
    • Oral ingestion causes vomiting/diarrhea  2-8 hours after ingestion
    • Intravenous injection or inhalation all cause TSS
    • SE-B and SE-C are systemic causes of shock--superantigens
  49. Staphylococcal exfoliative toxins
    • Types A and B
    • Scalded Skin Syndrome: These are serine proteases that cleave desmoglein 1 in the neonatal epidermis, causing separation of the layers of skin
    • Affects adults little because skin has mainly desmoglein 3 instead of 1
  50. Other Staphylococcus aureus virulence factors
    • Capsules: Small antiphagocytic capsules (types 5 and 8) are more virulent than the larger ones
    • Slime: Aka polysaccharide intercellular adhesin (PIA)
    • Iron-Surface Proteins (ISPs): Siderophores and related iron uptake systems
  51. Staphylococcus aureus vaccine approaches
    • Vaccines have been made against capsules and the polysaccharide intercellular adhesin (PIA) slime, but trials have failed
    • The only vaccines that have shown complete protection in animals are toxoids of endotoxins, and the immunity is serotype-specific
  52. Staphylococcus aureus pathogenicity islands (SaPI)
    • Phages that became permanently trapped in the chromosome
    • They are all variable genetic traits, meaning that some strains express these toxins and others do not
    • TSST-1
    • SE-B, SE-C, SE-E to SE-like-X
  53. Where in the genome are other Staphylococcal virulence factors encoded?
    • Pathogenicity Islands: TSST-1, SE-B, SE-C, and SE-E to SE-like-X
    • Bacteriophages: SE-A, Exfoliative toxin A, PVL (gamma hemolysin)
    • Plasmids: SE-D, Exfoliative toxin B
    • The above are all variable genetic traits; some strains express and others do not
    • Chromosome: The rest of the virulence factors
  54. Global regulators of Staphylococcal enterotoxins
    • Agr C: Accessory gene regulator that turns on production of exotoxin when a quorum of bacteria are reached; this is determined by accumulation of an octapeptide
    • Oxygen sensor: Shuts off exotoxin production when no oxygen present
  55. Other Staphylococcus Infections
    • Coagulase-negative, unlike Staphylococcus aureus
    • These are all opportunists
    • Staphylococcus epidermidis
    • Number one cause of septicemia
    • Forms biofilms on heart catheters and causes endocarditis; also forms biofilms on urinary catheters and causes UTIs
    • Toxins: Has PIA and cytolysins, but rarely superantigens
    • Staphylococcus saprophyticus
    • UTIs
    • Staphylococcus lugdunensis
    • Causes endocarditis
  56. MSCRAMMs
    • Microbial Surface Components Recognizing Adhesive Matrix Molecules
    • Includes Staphylococcus aureus coagulase protein
    • Group A strep Streptococcus pyogenes M protein is also included; helps adhere to host
  57. Examples of exotoxins encoded on bacteriophages
    • Scarlet Fever Toxins: Streptococcal pyrogenic exotoxin superantigens
    • Staphylococcal Enterotoxin A: Superantigen and agent of food poisoning
    • Cholera Toxin
    • Shiga-Like Toxin: Hemolytic uremic syndrome
    • Diphteria Toxin
  58. Corynebacterium diptheriae bacterial properties
    • Gram Stain: Positive
    • Morphology: Rod
    • Is normal flora and is transmitted by aerosols and direct contact
  59. Corynebacterium diptheriae clinical presentation
    • Colonizes pharynx, larynx, and nose while making exotoxin
    • Coughing and sneezing
    • Pseudomembrane: The exotoxin kills epithelial cells and infiltrating PMNs, creating an ulcer, which is covered with a necrotic exudate, forming a false membrane that becomes foul smelling and dark
    • Bull-Neck Appearance: Inflammation and swelling occurs, with lymphadenepathy of the cervical lymph glands
    • Respiratory obstruction and asphyxiation can occur
    • Systemic disease
    • Exotoxin is absorbed into lymphatics and the blood
    • Causes fever, vomiting, diarrhea, exhaustion
    • Myocarditis with heart failure may occur
    • Polyneuritis: Demyelination leading to paralysis of the soft palate and regurgitation of fluids
    • Really is an intoxication illness
  60. Diptheria toxin
    • Exotoxin
    • Made from a single protein strand that is cleaved into A and B
    • A: Active enzyme; inhibits protein synthesis
    • B: Binding protein; allows for internalization of A
    • Encoded on bacteriophage
    • High iron levels repress exotoxin production; low iron levels allow exotoxin to be made
  61. Diptheria diagnosis, management, and prevention
    • Diagnosis: Pseudomembrane, culture, and exotoxin production
    • Treatment: Antitoxin; make sure patient is not in contact with other non-vaccinated individuals; penicillin/erythromycin; tracheotomy and other supportive care
    • Prevention: Vaccination with diptheria toxoid (diptheria still causes 100,000 cases worldwide)
  62. Listeria monocytogenes bacterial properties
    • Gram Stain: Positive
    • Facultative intracellular (in the cytoplasm), as it can escape phagosomes
    • Morphology: Motile rod (flagella present)
    • Oxygen:
    • Spore:
    • Hemolysis: Beta
    • Often acquired from contaminated cheeses, other dairy products, and meats; however, can also colonize the intestinal tract of women for transport across the placenta to the fetus
  63. Listeria monocytogenes clinical presentation and management
    • Granulomas: Formed when Listeria escape phagosomes using listeriolysin O (an oxygen labile hemolysin), and cause CD4 T cells to activate macrophages
    • CD8 T cells are important for immunity
    • CNS Infections: Has a trophism for CNS and affects fetus and immunosuppressed patients
    • Meningitis with granulomas present
    • Management: Treat with antibiotics and supportive care
  64. Listeria monocytogenes virulence factors
    • Can survive in macrophages, PMNs, dendritic cells, B cells
    • Internalin: A surface protein that helps with the invasion of cells
    • Listeriolysin O: Allows Listeria to escape phagosomes; reason for CD8 T cell involvement
    • Actin polymerization: These organisms are propelled by formation of an actin-polymerizing tail of ActA and gelsolin
  65. Koch's postulates
    • 1: Associate an organism with disease
    • 2: Isolate the organism in pure culture
    • 3: Produce the illness in experimental animals
    • 4: Re-isolate the organism from the animal
    • 5: Repeat until it is obvious the organism causes illness
    • Bacillus anthracis was one of the first organisms shown to cause disease
  66. Bacillus anthracis bacterial characteristics
    • Gram Stain: Positive
    • Morphology: Medusa head colony appearance; non-motile
    • Oxygen: Obligate anaerobes
    • Spore-forming
    • Hemolysis: Gamma
    • These are very large (10umx2um) and stick together end-to-end
    • Capsule can stain white in an India Ink Stain
  67. Bacillus anthracis transmission, pathogenesis, and clinical presentation
    • Transmission: Weaponized (silicone) spores or ingestion from an infected animal from endemic areas such as MN, ND, or TX; can be ingestion, inhalation, or direct contact with skin
    • Pathogenesis: Spores grow vegetatively and incubate for 2-10 days before clinical signs show
    • For aerosol transmission, the spores are carried to the mediastinum by phagocytic cells where they germinate and proliferate. Capsule production prevents further phagocytosis, and the organism produces lethal and edema toxins. Leads to death (80% untreated, 20-40% treated).
    • Clinical presentation
    • Skin Infection: Pustule develops that looks like an eschar (floor burn), which progresses to a dark/black scab-like lesion in days
    • Aerosol Infection: Causes massive edema of neck, chest, and mediastinum with a
    • nonproductive cough, fever, and repiratory failure; septicemia/gram-positive shock
    • Death can occur from respiratory failure, anoxia, or significant edema
  68. Bacillus anthracis virulence factors
    • Capsule: Anti-phagocytic poly d-glutamic acid capsule, encoded by a plasmid
    • Lethal Toxin: Encoded by a plasmid; lethal factor proteins (A) combine with protective antigen (B) heptamers; two of these complexes combine to form lethal toxin
    • Edema Toxin: Encoded by a plasmid; edema factor (A) combines with protective antigen (B) heptamers to form edema toxin
    • Remember that these A:B-type toxins are referring to active enzyme and a host-binding protein
  69. Bacillus cereus bacterial characteristics
    • Gram Stain: Positive
    • Morphology: Non-motile rods
    • Oxygen:
    • Spore-forming
    • Hemolysis: Yes
    • These are very large (10umx2um) and stick together end-to-end
  70. Bacillus cereus transmission and clinical presentation
    • Transmission: Accidental intrduction of spores into wounds, or growth in starchy foods and enterotoxin production causing food poisoning
    • Their enterotoxins are not destroyed by re-heating; food poisoning happens for 2-8 hours; ingestion of spores results in food poisoning for up to two days
    • Can cause necrotizing fasciitis or myositis occasionally
  71. Clostridium tetani
    • Gram Stain: Positive
    • Morphology: Tennis racket-shaped rods
    • Oxygen:
    • Spore-former
    • Hemolysis:
    • Secretes tetanus toxin
  72. Neisseria meningitidis bacterial characteristics
    • Gram Stain: Negative
    • Morphology: Diplococcus; has pili for attachment to host cells
    • Oxygen:
    • Spore:
    • Hemolysis:
    • Capsule: Types A, B, C, H, I, K, L, X, Y, Z, 29E, and W135 exist (vaccine available for A, C, W135, and Y); Group B capsule is non-immunogenic, so vaccine is unavailable
    • Endotoxin: Causes fever and hypotension/shock
  73. Neisseria meningitidis clinical presentation, transmission, treatment and prevention
    • Pus
    • Sepsis: Petechia, tissue necrosis (purpura fulminans), hypotension
    • Gram-negative shock, which is severe and rapidly progressing
    • Transmission: Kissing/sharing pop cans
    • Treatment: Fluid & electrolytes to restore BP, corticosteroids to prevent inflammatory processes, and cephalosporin (ceftriaxone) or penicillin (?)
    • Prevention: Rifampin is given due to its great mucosal surface penetrating ability
  74. Streptococci of medical importance
    • Group A S. pyogenes (90%)
    • Group B S. agalectiae
    • Group C S. equisimilis
    • Group D Enterococcus and S. bovis
    • Group G S. dysgalactiae
    • Viridans S. mutans, S. sanguinis, and others
    • S. pneumoniae
    • The grouping is based upon Carbohydrate C, which is found in the cell wall
  75. Streptococcus pneumoniae bacterial properties
    • Gram Stain: Positive
    • Has O-acetylated peptidoglycan, which can cause rheumatic fever or arthritis
    • Morphology: Round strings/diplococci (used to be called Diplococcus pneumoniae)
    • Oxygen:
    • Spore:
    • Hemolysis: Alpha
    • Catalase: Negative
    • Virulence Factors: O-acetylated peptidoglycan in antiphagocytic polysaccharide capsule; pneumolysin; IgA1 protease
    • Is a primary pathogen
    • Sensitive to optochin disks
    • Has an anti-phagocytic, negatively-charged capsule
  76. Streptococcus pneumoniae clinical presentation
    • Transmitted by droplet infection
    • Green-cap meningitis: Myeloperoxidase (MPO), a human protective enzyme, is released, causing a greenish color due to the oxidation state of iron in the enzyme
    • Pneumonia: Most common cause
    • Rhematic fever: Arthritis, carditis, and neurologic autoimmune disease; occurs due to O-acetylated peptidoglycan
    • Post-gonococcal arthritis: Also due to O-acetylated peptidoglycan
  77. Streptococcus pneumoniae treatment and management
    • Corticosteroids are given to reduce inflammation from O-acetylated peptidoglycan and to increase patient survival (case:fatality rate changes from 55% to <30%)
    • Antibiotics and supportive theraphy
  78. Most common causes of bloodstream infections
    • 1: Staphylococcus epidermidis
    • 2: Staphylococcus aureus
  79. Most common causes of infectious endocarditis
    • 1: Staphylococcus aureus (45%)
    • 2: Viridans streptococci (35%)
    • 3: Enterococcus facaelis and E. faecium (15%). These used to be called Group D streptococci; they are often highly antibiotic resistant and may be vancomycin resistant; can transfer resistance to other gram-positive bacteria
    • Management: Antibiotics, supportive care, valve replacement, and management of complications such as strokes
  80. Most common causes of pneumonia
    • 1: Streptococcus pneumoniae
    • 2: Staphylococcus aureus
  81. Most common cause of osteomyelitis
    Staphylococcus aureus
  82. Most common causes of meningitis
    • 1: Streptococcus pneumoniae
    • 2: Neisseria meningitidis
    • Children: Haemophilus influenzae type b
    • 40% of Neonates: Streptococcus agalactiae (Group B)
    • 10% of Neonates: Escherichia coli
    • 10% of Neonates: Listeria monocytogenes
  83. Most common causes of purpura fulminans
    • 1: Staphylococcus aureus
    • Common: Streptococcus pyogenes
    • Common: Neisseria meningitidis
    • Bacillus cereus
    • Group G strep can occasionally cause this
  84. Group A streptococcus (Streptococcus pyogenes) bacterial characteristics
    • Gram Stain: Positive
    • Morphology: Cocci
    • Oxygen: Aerotolerant anaerobe
    • Hemolysis: Beta, due to streptolysins O (anaerobically) and S (aerobic/anaerobically)
    • Catalase: Negative, like all streptococci and enterococci
    • Have an anti-phagocytic, negatively-charged hyaluronic capsule that mimics self
    • M protein: Creates a fuzz layer on the surface, allowing for adhesion to host tissues; this is how Group A are further typed--over 150 different M types; antiphagocytic due to prevention of proper complement deposition
    • Makes streptococcal pyrogenic exotoxins (SPEs)
  85. Group A streptococcus (Streptococcus pyogenes) virulence factors
    • Cell-Surface Virulence Factors
    • M Protein: Prevents proper complement deposition
    • C5a Peptidase: Cleaves C5a, which is the chemotactic part of complement, at its PMN binding site to prevent PMN influx
    • Hyaluronic Acid Capsule: Negatively charged to prevent phagocytosis
    • Fibronectin Binding Proteins: Bind to integrins
    • IgG and IgA Fc Binding Proteins
    • Secreted Virulence Factors
    • Hemolysins/Cytolysins: Streptolysin S (oxygen stabile) causes necrotizing tissue damage; Streptolysin O forms pores (anti-Streptolysin O antibody titers can help diagnose rheumatic fever)
    • Streptokinase: Breaks clots; helps cause necrotizing tissue damage
    • Streptococcal Pyrogenic Exotoxins (SPEs): Superantigens; cross-bridge variable beta chain of TCR to MHCII on APCs to cause massive cytokine production and TSS; encoded by bacteriophages
    • Cysteine Protease: Important in necrotizing tissue damage
  86. Group A streptococcus (Streptococcus pyogenes) clinical presentation and treatment
    • Pharyngitis is most common; transmitted by droplet or direct contact
    • Impetigo transmitted by direct contact
    • Erysipelas are subcutaneous, highly inflammatory infections
    • Menstrual TSS: Independent of tampon use because they are aerotolerant anaerobes; 1/100 women are colonized vaginally
    • Puerperal Sepsis: If colonized with Group A during delivery, case:fatality rate of 60% untreated, 30% when treated with IVIG
    • Delayed Sequelae
    • Scarlet Fever: SPEs (aka scarlet fever toxins), specifically SPEA, cause a hypersensitivity reaction due to amplification of delayed hypersensitivity reaction (TH1 activation of macrophages); strawberry tongue present
    • Rheumatic Fever: Antibodies to M protein (specifically M18) cross-react with heart protein; Aschof bodies (granulomas) can form; repeated pharyngitis infections need to be treated with antibiotics to prevent this cross-reactivity; shaking palsy, mitral valve stenosis, and arthritis present
    • Acute Gomerulonephritis: Immune complex disease can occur after one infection; more common with skin infections of high M types; hypertension, decreased complement, and proteinura/hematuria seen
    • Guttate Psoriasis: Rose-petal shaped lesions in genetically susceptible people
    • Erythema Nodosum: Immune complex disease with painful nodular lesions, especially on arms and legs
    • PANDAS: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococci; M18 and SPEC have an association with OCD
    • Treatment
    • Augmentin (amoxacillin and clavulanic acid), penicillin, or azithromycin
    • Clindamycin to stop exotoxin production in serious invasive disease
    • IVIG for TSS
    • Activated protein C for purpura fulminans
    • Tissue debridement for necrosis and supportive care for hypotension
    • 10x more sensitive to bacitracin than other bacteria
  87. Peptostreptococcus
    Oxygen: Obligate anaerobe
  88. Viridans streptococci (S. mutans)
    • Gram Stain: Positive
    • Morphology: Cocci
    • Oxygen: Aerotolerant anaerobe
    • Hemolysis: Alpha
    • Normal flora of the throat; causes dental caries
  89. Group B strep (Streptococcus agalactiae)
    • Gram Stain: Positive
    • Morphology: Cocci in chains
    • Oxygen:
    • Catalase: Negative
    • Hemolysis: Beta
    • Nonimmunogenic capsule present, and 9 serotypes exist
    • 20-40% of women are colonized vaginally and can be treated before delivery with penicillin
    • Diseases: TSS can occur; otherwise, early-onset sepsis can happen quickly after birth (fever may not be present); late-onset meningitis in neonates can occur also (40% of neonatal meningitis)
    • Virulence Factors: Capsule, C5a peptidase, surface proteins alpha and beta (function unknown), cytolysins, superantigens (not yet isolated)
  90. Group D strep (Streptococcus bovis)
    • Gram Stain: Positive
    • Morphology: Cocci
    • Oxygen:
    • Hemolysis: Gamma
    • PYR: Negative (versus PYR positive being Enterococcus)
    • Can be normal flora in GI tract
    • Associated with gastrointestinal malignancy/polyps, endocarditis, UTIs, and sepsis
    • When patients have endocarditis due to Group D strep, test them for colon cancer!
  91. Group G strep (Streptococcus dysgalactiae)
    • Colonizes nose and throats; can cause pharyngitis
    • Can cause TSS and purpura fulminans via SPEA or SPEC
    • Our patient got T-cell malignancy following this infection
    • Group C is just like this

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