MICR 470 Exam #2 Study Guide PDF

**Ch.9 Yersinia** Pathogen type - Facultative (with or without O2, unlike obligate), intracellular Names: - *Yersinia enterocolitica*: causes Yersiniosis - *Yersinia pseudotuberculosis:* rare form of foodborne illness - Yersinia pestis*:* the Black Death Transmission: - Pestis is t...

**Ch.9 Yersinia** Pathogen type - Facultative (with or without O2, unlike obligate), intracellular Names: - *Yersinia enterocolitica*: causes Yersiniosis - *Yersinia pseudotuberculosis:* rare form of foodborne illness - Yersinia pestis*:* the Black Death Transmission: - Pestis is transmitted by the flea Types: - Bubonic - Transmitted by fleas - Septicemic - Pneumonic - Transmitted p2p by droplets (Deadliest) Discovery - Alexandre Yersin - Kitasato Shibasaburo Protection - Biofilm - Main component: *N*-acetyl-*D-*glucosamine (glucose derivative) - Produced by *hms* gene - Biofilm regulation - Cyclic-di-GMP - Produced by diguanylate cyclase w/ GGDEF - Degraded by phosphodiesterase w/ EAL or HD-GYP - Binds to PilZ domains that inhibit: - Motility - Virulence - Increases biofilm formation - Rab proteins - 4a and 1b inhibit phagolysosomal fusion - Bacterial Secretion Systems - All Type 3 - Type 3 all have injectosomes - Effectors of T3SS = Yops - Work together to prevent phagocytosis - Examples: B,D,E,T,A,H,J (don't need to know) - Yops and T3SS are **plasmid encoded** - Plasmid encoded virulence factors are acquired through HGT - pCD1 plasmid contains T3SS and Yop Virulence Factors - pMT1: genes that allow flea survival - pPla: encodes plasminogen (protein that breaks down blood clots) **Ch. 10 Borrelia** Names/Diseases: *Borrelia burgdorferi*: Lyme disease - Has a linear chromosome (most bacteria have circular) Transmission: - Ticks - Outer Surface Proteins - A: adhesin that blocks complement activation - C: binds to SALP proteins which inhibt immune response - In tick: OspA = high - Transmission: OspA decreases and OspC increases Early Signs and Symptoms: - Erythema migrans (bulls eye rash) - Flu-like symptoms Late Stage - Neuroborreliosis - Lyme Arthritis Spirochetes (spiral noodle shape), do not have capsules 1. Lyme disease 2. Relapsing fever (***borrelia hermsii*)** 3. Leptospirosis (*Leptospira*) 4. Syphilis (*Treponema pallidum*) Virulence Factors - Periplasmic flagella (between inner and outer membranes) - Protect from immune response + more powerful - Antigenic variation (changing proteins on surface of bacteria) - Surface protein in burgdoferi: VlsE - Not expressed in ticks - Pieces of silent cassettes to generate new antigens - Not expressed in tick since ticks don't have adaptive immunity - Surface protein in hermsii: Vmp - Switches cassettes to express on surface Immune Evasion - Most species can bind to component of complement - Both Lyme and Relapsing can bind Factor H which is a way for complement to prevent the system from recognizing itself Two-component System Regulation - Comprised of Histidine Kinase and Response Regulator - Output for RR is transcription factor or enzymatic activity - Only 2 systems in burgdorferi - Hpk1-Rrp1 - Critical for tick survival - Hpk2-Rrp2 - Critical for host survival **Ch. 11 Streptococcus** Names: Lancefield groupings - Pyogenes: Group A Strep - Agalactiae: Group B Strep - Pneumoniae - No Lancefield carb antigen Hemolysis Test - Hemolysis = destruction of RBCs - Most Lancefield streptococci are **beta-hemolytic** w/ large zone of clearing around growth - Viridians streptococci are **alpha-hemolytic** which is a partial degradation of RBCs - **Gama-hemolytic:** do not lyse RBCs Group A Strep - Symptoms of strep throat - Impetigo (skin infection w/ sores and blisters) - Scarlet Fever - Rheumatic fever (immune response) Infections - Rheumatic heart disease - Glomerulonephritis (kidney inflammation) - Toxic shock syndrome (TSS) - Necrotizing fasciitis GAS Virulence Factors Adhesion: - Mediated by M proteins - Bind to fibronectin and plasminogen - Also bind to Fc portion of antibodies - S. pyogenes uses molecular mimicry to evade immune system - Capsule: - S. pyogenes hyaluronic acid capsule - Another mechanism of molecular mimicry since hyaluronic acid is in host cells - Also protects against complement - Capsule Loss = Virulence Loss - Lipoteichoic acid (LTA) is thought to facilitate weak attachment - S protein binds RBC membranes to protect against phagocytosis - Immunoglobulin: 3 IgG proteases that degrade IgG - Family of proteins that trigger excessive stimulation of T cells - All are exotoxins - Exotoxin B (SpeB) degrades host serum proteins (\*\*not a superantigen) Cytolytic Toxins - Streptolysin O (SLO) - Streptolysin S (SLS) - Both cause pore formation in host cell membranes - Are cause of beta-hemolysis of GAS (rupture RBCs) Antibiotic Resistance - Sensitive to beta-lactams - Fluoroquinolones (target DNA gyrase) - Tetracycline binds to ribosomes and block translation - Resistance comes from efflux pumps (transport substances out of cell) and proteins (TetM and TetO, which are obtained by HGT) - Macrolides (like erythromycin) bind bacterial ribosome and prevent translation - Resistance comes from efflux pumps No vaccine!!! - Due to cross-reactivity esp myosin proteins in human heart Group B Strep: Streptococcus agalactiae - All capsule types have sialic acid linked to many dif sugars - Most common cause of meningitis in babies Virulence Factors Adhesins - Bind fibrinogen or laminin - Pili increases colonization of GBS Hemolytic Pigment - Responsible for resistance to elimination by immune system - Also responsible for beta-hemolysis on agar plates - Cell death also aids in crossing BBB Crossing the BBB - Paracellularly - Alpha C protein (ACP) binds glycosaminoglycans - Hypervirulent GBS adhesin (HvgA) contributes to BBB crossing - GBS infection induces expression of Snail 1 that blocks transcription of host cell junction genes Streptococcus pneumoniae - Most common cause of meningitis Virulence factors Capsule - Polysaccharide capsule: antiphaygocytic and reduces complement - Opaque colonies = more virulent - Transparent colonies = more adapted to nasopharynx - Inverted repeats cause phase variation (variation of protein expression, frequently in an on-off fashion) IgA1 protease - Found at nasopharynx - Prevents IgA from binding bacteria - NanA cleaves sialic acid from hsot cells - Pore-forming toxin that triggers immune cells to release ROS to damage host tissues - Transcellularly: aided by S. pneumoniae binding endothelial cells - Paracellularly: mediated by pneumolysin **Ch. 12 Staphylococcus** Names/Disease: - Staphylococcus aureus: staph - Staphylococcal scalded skin syndrome (SSSS) Virulence - S. aureus releases 2 exotoxins related to SSSS - Exfoliative toxins - Bind to a desmosome in epidermis - Breaks down desmoglein-1 - Staphylococcal Enterotoxins (SEs) (type of exotoxin) - Superantigens that induce vomiting - Superantigens bind both MCH class II and TCR and excessively activate T cells - Serotonin stimulation of vagus nerve induces vomiting - Toxic shock syndrome toxin-1 (TSST-1) - Also a superantigen - Responsible for majority of toxic shock symptoms - Mobile genetic elements - Pieces of DNA that can move to other parts of genome/other organisms - SCCmec (cassette chromosome mec) - Mobile genetic element that has *mecA* gene, responsible for methicillin resistance in S. aureus - *MecA* encodes for an alternate pencicillin binding protein (PBP2a) which is not susceptible to beta-lactam antibiotics - Staphylococcal Pathogenicity Islands (SaPIs) - Carry many virulence toxins - Alpha toxin - Promotes invasion by disrupting epithelial barrier - More common in pneumonia - Leukotoxins - Make pores in membrane (alpha toxin is type of leukotoxin) - Most common in sepsis Biofilm Adhesion - Uses many adhesins to begin formation of biofilm, many are MSCRAMMS (microbial surface components recognizing adhesive matrix molecules) - Components: - Proteins sugars and DNAs Staphylothrombin - Binds fibrin, which leads to molecular mimicry and blockage of neutrophil phagocytosis - SpA (surface protein A) binds Fc portion of Igs = less opsonization and phagocytosis ROS protection - Staphyloxanthin = orange pigment which scavenge radicals from ROS - Superoxide dismutase converts superoxide to H2O2 - Catalase: detoxifies H2O2 to O2 and H2O **Ch. 13 Bacillus** Names/Disease: - Bacillus anthracis: anthrax - Sterne strain = annimal vaccine - Still used today - Has no capsule Types Cutaneous: spores enter skin, most common and least dangerous Inhalation: inhalation = it sucks, deadliest form (55% death rate w/out treatment) Gastrointestinal: rare in the US, from undercooked food Injection: spores injected during IV drug use Spores - Bacillus is spore-forming - Spore: dormant form of bacteria - Endospores: form inside bacterial cells of Clostridium and Bacillus - Can withstand extreme environemnts Spore Formation 1. Polar septum formation which creates mother cell (MC) and forespore (FS) 2. MC engulfs FS 3. Cortex layer forms btwn the 2 membranes 4. Coat assembles around this cortex, resistant to many things - Stress is thought to trigger spore formation Capsule - Comprised of polymer of poly-gamma-D-glutamic acid (PDGA) Plasmids - pX01: encodes for toxin - pX02: encodes for capsule Toxin - Anthrax toxin = A2B toxin - A subunits: - LF (lethal factor) - EF (edema factor) - B subunit: - PA (protective antigen) - LF + PA = LT (lethal toxin) - LF cleaves MEK, which disrupts cell signaling and causes cell death - EF+PA = ET (edema toxin) - EF is an adenylyl cyclase (enzyme that converts ATP to cAMP) - cAMP activates PKA - LF and EF are thought to balance host cell killing w/ bacterial dissemination **Ch. 14 Clostridium** - Obligate and spore-forming Names: 1. Clostridium tetani 2. Clostridium botulinum 3. Clostridium perfringens 4. Clostridium difficile Spores: - Refer to spores for Bacillus Activation - Both Clostridium and Bacillus use Spo0A response regulator (opposite to HK) to initiate spore formation - Orphan histidine kinsases have been found that are thought to phosphorylate and activate Spo0A Two-Component Systems - Consists of HK and RR, genes are often co-transcribed as part of 1 operon C. tetani and botulinum (Tetanus and botulism) Tetanus Symptoms - Most common symptom is lockjaw - All symptoms occur because of tetanus toxin (TeNT, 1 type) Botulism Types 1. Foodborne a. Comes from improperly preserved food 2. Wound b. Commonly seen in IV drug users 3. Infant c. Feeding honey to a \