MICR 470 Exam #2
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MICR 470 Exam #2

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Questions and Answers

What function do periplasmic flagella serve in Treponema pallidum?

  • They enhance immune response.
  • They provide protection from immune response and increase motility. (correct)
  • They facilitate nutrient absorption.
  • They assist in reproduction.
  • Which protein is associated with antigenic variation in Borrelia burgdorferi?

  • Fc portion
  • M protein
  • Vmp
  • VlsE (correct)
  • What type of hemolysis do most Lancefield streptococci exhibit?

  • No hemolysis
  • Alpha-hemolytic
  • Gamma-hemolytic
  • Beta-hemolytic (correct)
  • What is the role of the Hpk1-Rrp1 two-component system in Borrelia burgdorferi?

    <p>Essential for tick survival.</p> Signup and view all the answers

    Which of the following is NOT a symptom of Group A Strep infection?

    <p>Asthma</p> Signup and view all the answers

    What is a characteristic feature of the capsule of Streptococcus pyogenes?

    <p>It mediates adhesion and immune evasion.</p> Signup and view all the answers

    Which immune evasion strategy is employed by Streptococcus pyogenes?

    <p>Molecular mimicry.</p> Signup and view all the answers

    What is the mechanism by which Lyme and relapsing fevers evade the immune response?

    <p>By binding Factor H to evade complement recognition.</p> Signup and view all the answers

    What role does the hyaluronic acid capsule play in bacteria like pyogenes?

    <p>It helps the bacteria avoid the immune response.</p> Signup and view all the answers

    What is the consequence of capsule loss in pyogenes?

    <p>Virulence loss.</p> Signup and view all the answers

    Which of the following exotoxins is responsible for degradation of host serum proteins in pyogenes?

    <p>Exotoxin B (SpeB)</p> Signup and view all the answers

    What mechanism do efflux pumps contribute to in antibiotic resistance?

    <p>Transporting substances out of the cell.</p> Signup and view all the answers

    How does Group B Streptococcus (Streptococcus agalactiae) primarily cross the blood-brain barrier?

    <p>Paracellularly and through pili.</p> Signup and view all the answers

    Which characteristic of Streptococcus pneumoniae colonies indicates higher virulence?

    <p>Opaque colonies.</p> Signup and view all the answers

    What is the primary action of the IgA1 protease found in Streptococcus pneumoniae?

    <p>To prevent IgA from binding to the bacteria.</p> Signup and view all the answers

    What is a common feature among beta-hemolysin toxins SLO and SLS?

    <p>They cause cell membrane pore formation.</p> Signup and view all the answers

    What is the primary function of the protective antigen (PA) in the anthrax toxin?

    <p>Facilitate the entry of lethal factor (LF) into cells</p> Signup and view all the answers

    Which of the following describes the capsule found in certain bacteria?

    <p>Comprised of poly-gamma-D-glutamic acid (PDGA)</p> Signup and view all the answers

    What is the most common symptom of tetanus caused by Clostridium tetani?

    <p>Lockjaw</p> Signup and view all the answers

    How does the lethal factor (LF) of the anthrax toxin affect host cells?

    <p>It cleaves MEK, disrupting cell signaling</p> Signup and view all the answers

    What initiates spore formation in both Clostridium and Bacillus species?

    <p>The Spo0A response regulator</p> Signup and view all the answers

    What is the primary function of exfoliative toxins released by Staphylococcus aureus?

    <p>Break down desmoglein-1</p> Signup and view all the answers

    Which component of Staphylococcus aureus helps it resist phagocytosis?

    <p>Staphylothrombin</p> Signup and view all the answers

    What does the mecA gene encode in Staphylococcus aureus?

    <p>An alternate penicillin binding protein</p> Signup and view all the answers

    What is the most lethal form of Bacillus anthracis infection?

    <p>Inhalation anthrax</p> Signup and view all the answers

    Which of the following describes the role of staphyloxanthin?

    <p>Scavenges radicals from ROS</p> Signup and view all the answers

    Which Staphylococcus toxin is responsible for toxic shock syndrome symptoms?

    <p>Toxic shock syndrome toxin-1</p> Signup and view all the answers

    How can Bacillus spores survive extreme environments?

    <p>By entering a dormant state</p> Signup and view all the answers

    What leads to the formation of a biofilm by Staphylococcus aureus?

    <p>Adhesion via MSCRAMMS</p> Signup and view all the answers

    Which pathogen is responsible for causing Yersiniosis?

    <p>Yersinia enterocolitica</p> Signup and view all the answers

    What is the primary mode of transmission for Yersinia pestis?

    <p>Transmission via fleas</p> Signup and view all the answers

    Which of the following is NOT a type of plague caused by Yersinia pestis?

    <p>Enterocolitic</p> Signup and view all the answers

    What is a key function of the outer surface protein A (OspA) in Borrelia burgdorferi?

    <p>Inhibits complement activation</p> Signup and view all the answers

    Which symptom is commonly associated with the early stage of Lyme disease?

    <p>Erythema migrans</p> Signup and view all the answers

    Which virulence factor allows Yersinia pestis to survive inside fleas?

    <p>pMT1</p> Signup and view all the answers

    What role do Rab proteins play in the pathogenicity of Yersinia?

    <p>Inhibits phagolysosomal fusion</p> Signup and view all the answers

    Which of the following diseases is caused by Borrelia burgdorferi?

    <p>Lyme disease</p> Signup and view all the answers

    Study Notes

    Yersinia

    • Yersinia enterocolitica causes Yersiniosis
    • Yersinia pseudotuberculosis causes a rare form of foodborne illness
    • Yersinia pestis causes the Black Death
    • All Yersinia are facultative, intracellular pathogens
    • Yersinia species are transmitted through various means:
      • Y. pestis: Transmitted by fleas
      • Y. pestis: Pneumonic form transmitted person-to-person by droplets, deadliest form
    • Yersinia bacteria are protected by:
      • Biofilm, composed of N-acetyl-D-glucosamine (glucose derivative), produced by hms gene
        • Cyclic-di-GMP (c-di-GMP) regulates biofilm formation
        • c-di-GMP production is controlled by diguanylate cyclase, and degrades by phosphodiesterase
        • c-di-GMP binds to PilZ domains, inhibiting motility, virulence, and increasing biofilm formation
      • Rab proteins (4a and 1b) inhibit phagolysosomal fusion
      • Bacterial Secretion Systems:
        • All Yersinia species utilize Type III Secretion Systems, which possess injectosomes
        • T3SS effectors are known as Yops (B, D, E, T, A, H, J), collectively preventing phagocytosis
        • Yops and T3SS are encoded on plasmids
          • Plasmids are acquired through horizontal gene transfer
          • pCD1 plasmid contains both T3SS and Yop genes.
    • Yersinia virulence factors:
      • pMT1 plasmid: harbors genes essential for flea survival
      • pPla plasmid: encodes plasminogen, a protein that breaks down blood clots.

    Borrelia

    • Borrelia burgdorferi causes Lyme disease
    • Borrelia burgdorferi has a linear chromosome, unlike most bacteria which have circular chromosomes.
    • Lyme disease is transmitted by ticks.
    • Borrelia Outer Surface Proteins (OSPs):
      • OspA serves as an adhesin that blocks complement activation in the tick stage
      • OspC binds to SALP proteins, inhibiting the immune response
      • OspA expression is high in ticks and decreases upon transmission to the host, while OspC expression increases.
    • Lyme disease early symptoms:
      • Erythema migrans (bulls eye rash)
      • Flu-like symptoms
    • Lyme disease late stage:
      • Neuroborreliosis
      • Lyme Arthritis
    • Borrelia are spirochetes (spiral-shaped bacteria) and lack capsules.
    • Borrelia species and their diseases:
      • Lyme disease (Borrelia burgdorferi)
      • Relapsing fever (Borrelia hermsii)
      • Leptospirosis (Leptospira)
      • Syphilis (Treponema pallidum)
    • Borrelia virulence factors:
      • Periplasmic flagella (between inner and outer membranes), provide immune evasion and increased motility
      • Antigenic variation: changing surface proteins to evade immune response
        • B. burgdorferi: employs VlsE, a surface protein not expressed in ticks
        • B. hermsii: utilizes Vmp, a surface protein that switches between different cassettes
    • Borrelia immune evasion:
      • Borrelia species can bind to complement components, such as Factor H, to prevent the immune system from recognizing them.

    Two-component systems in B. burgdorferi

    • Consist of a histidine kinase (HK) and a response regulator (RR)
    • HK phosphorylates the RR, which then acts as a transcription factor or enzyme
    • B. burgdorferi has two critical two-component systems:
      • Hpk1-Rrp1: crucial for tick survival
      • Hpk2-Rrp2: vital for host survival

    Streptococcus

    • Lancefield grouping is a classification based on surface carbohydrate antigens:
      • Group A Strep: Streptococcus pyogenes
      • Group B Strep: Streptococcus agalactiae
      • Streptococcus pneumoniae: No Lancefield group
    • Hemolysis test:
      • Hemolysis refers to the destruction of red blood cells (RBCs).
      • Many Lancefield streptococci are beta-hemolytic, showing a clear zone around their growth on agar plates.
      • Viridans streptococci exhibit alpha-hemolysis (partial RBC degradation).
      • Gamma-hemolytic streptococci do not lyse RBCs.

    Group A Strep (S. pyogenes)

    • Causes various infections, including:
      • Strep throat
      • Impetigo
      • Scarlet fever
      • Rheumatic fever (an immune response)
    • S. pyogenes are responsible for:
      • Rheumatic heart disease
      • Glomerulonephritis
      • Toxic shock syndrome (TSS)
      • Necrotizing fasciitis
    • S. pyogenes virulence factors:
      • Adhesion:
        • M proteins mediate adhesion, binding to fibronectin, plasminogen, and the Fc portion of antibodies
        • Molecular mimicry helps evade the immune system
        • Hyaluronic acid capsule (another molecular mimicry mechanism), protecting against complement
        • Capsule loss = Virulence loss
        • Lipoteichoic acid (LTA) facilitates weak attachment
        • S protein binds to RBC membranes to protect against phagocytosis
      • Immunoglobulin:
        • Three IgG proteases degrade IgG antibodies.
      • Exotoxins:
        • Several proteins trigger excessive stimulation of T cells.
        • Exotoxin B (SpeB) degrades host serum proteins (not a superantigen).

    Cytolytic Toxins in S. pyogenes

    • Streptolysin O (SLO)
    • Streptolysin S (SLS)
    • Both form pores in host cell membranes and are responsible for beta-hemolysis of GAS.

    Antibiotic Resistance in S. pyogenes

    • Susceptible to beta-lactams
    • Susceptible to fluoroquinolones (target DNA gyrase)
    • Resistance to tetracycline: efflux pumps and proteins (TetM and TetO) obtained from HGT
    • Resistance to macrolides (e.g., erythromycin): efflux pumps
    • No vaccine due to cross-reactivity, especially with myosin proteins found in the human heart.

    Group B Strep (S. agalactiae)

    • All capsule types contain sialic acid linked to various sugars.
    • Most common cause of meningitis in infants.
    • S. agalactiae virulence factors:
      • Adhesins: Bind fibrinogen or laminin
      • Pili promote GBS colonization
      • Hemolytic pigment:
        • Protects GBS from immune elimination
        • Contributes to beta-hemolysis on agar plates
        • Cell death aids in crossing the blood-brain barrier (BBB)
      • BBB crossing:
        • Paracellularly and transcellularly
        • Alpha C protein (ACP) binds glycosaminoglycans
        • GBS infection induces Snail 1 expression, blocking transcription of host cell junction genes.
    • S. agalactiae is the second most common cause of sepsis in infants.

    Streptococcus pneumoniae

    • Most common cause of meningitis.
    • S. pneumoniae virulence factors:
      • Capsule:
        • Polysaccharide capsule prevents phagocytosis and reduces complement
        • Opaque colonies: more virulent
        • Transparent colonies: better adapted to the nasopharynx
        • Inverted repeats cause phase variation, altering protein expression
      • IgA1 protease:
        • Found in the nasopharynx, inhibiting IgA binding to bacteria.
        • NanA cleaves sialic acid from host cells.
        • Pneumolysin: pore-forming toxin, triggers ROS release by immune cells, causing host tissue damage.
      • BBB crossing:
        • Transcellularly (aided by S. pneumoniae binding to endothelial cells)
        • Paracellularly (mediated by pneumolysin).

    Staphylococcus

    • Staphylococcus aureus (Staph) causes staphylococcal scalded skin syndrome (SSSS)
    • S. aureus virulence:
      • Two exotoxins related to SSSS:
        • Exfoliative toxins: bind to desmosomes in the epidermis, breaking down desmoglein-1.
      • Staphylococcal Enterotoxins (SEs) (class of exotoxins):
        • Superantigens that induce vomiting.
        • Superantigens bind to both MHC class II and TCR, excessively activating T cells.
        • Serotonin stimulation of the vagus nerve induces vomiting
      • Toxic shock syndrome toxin-1 (TSST-1):
        • A superantigen
        • Responsible for most toxic shock symptoms
      • Mobile genetic elements:
        • Pieces of DNA that can move within genomes or between organisms
        • SCCmec (cassette chromosome mec):
          • Contains mecA gene responsible for methicillin resistance in S. aureus.
          • MecA encodes an alternate penicillin-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 the epithelial barrier
        • Particularly prevalent in pneumonia.
      • Leukotoxins:
        • Create pores in membranes (alpha toxin is a type of leukotoxin)
        • Most common in sepsis

    Biofilm in S. aureus

    • S. aureus uses various adhesins to initiate biofilm formation, many of which are MSCRAMMs (microbial surface components recognizing adhesive matrix molecules)
    • Biofilm components:
      • Proteins
      • Sugars
      • DNA
    • Staphylothrombin:
      • S. aureus binds fibrin, leading to molecular mimicry and inhibition of neutrophil phagocytosis
    • SpA (surface protein A): binds to the Fc portion of immunoglobulins (Igs), reducing opsonization and phagocytosis.

    ROS protection in S. aureus

    • S. aureus produces staphyloxanthin, an orange pigment that scavenges reactive oxygen species (ROS)
    • S. aureus also has enzymes that protect against ROS:
      • Superoxide dismutase: converts superoxide to H2O2
      • Catalase: detoxifies H2O2 to O2 and H2O

    Bacillus

    • Bacillus anthracis causes anthrax
    • The Sterne strain is a widely used animal vaccine, lacking a capsule.
    • Anthrax types:
      • Cutaneous: most common and least dangerous, spores enter the skin.
      • Inhalation: inhalation anthrax is deadliest (55% death rate without treatment)
      • Gastrointestinal: rare in the US, acquired through undercooked food.
      • Injection: spores injected, often during IV drug use.
    • Bacillus species are spore-forming bacteria.
      • Spores: dormant forms of bacteria
      • Endospores: form inside bacterial cells of Clostridium and Bacillus
    • Bacillus spores can withstand extreme environmental conditions.

    Spore formation

    • Bacillus spore formation steps:
      • Polar septum formation, creating a mother cell (MC) and a forespore (FS)
      • MC engulfs the FS
      • A cortex layer forms between the two membranes
      • A coat assembles around the cortex, providing resistance.
    • Stress is thought to trigger spore formation.

    Capsule in B. anthracis

    • The capsule is composed of poly-gamma-D-glutamic acid (PDGA)

    Plasmids in B. anthracis

    • pX01 plasmid: encodes for toxins
    • pX02 plasmid: encodes for the capsule

    Anthrax toxin

    • Anthrax toxin: a tripartite A2B toxin
      • A subunits:
        • LF (lethal factor)
        • EF (edema factor)
      • B subunit:
        • PA (protective antigen)
      • LF + PA = LT (lethal toxin), disrupts cell signaling through MEK cleavage, leading to cell death.
      • EF + PA = ET (edema toxin):
        • EF is an adenylyl cyclase, converting ATP to cAMP, which activates protein kinase A (PKA).
      • LF and EF are thought to maintain a balance between host cell killing and bacterial dissemination.

    Clostridium

    • Clostridium species are obligate anaerobic bacteria and spore-forming.
    • Clostridium species:
      • Clostridium tetani: tetanus.
      • Clostridium botulinum: botulism.
      • Clostridium perfringens: gas gangrene.
      • Clostridium difficile: colitis.
    • Clostridium spores: refer to spore characteristics described for Bacillus

    Activation of spore formation in Clostridium()

    • Both Clostridium and Bacillus use the Spo0A response regulator to initiate spore formation.
    • The Spo0A response regulator is activated by phosphorylation by orphan histidine kinases.

    Two-component systems in Clostridium()

    • Clostridium two-component systems have a HK and RR (genes often co-transcribed in one operon).

    C. tetani and C. botulinum (tetanus and botulism)

    • Tetanus symptoms:
      • Lockjaw is the most common symptom.
      • All symptoms are caused by tetanus toxin (TeNT, a single type).

    Botulism types

    • Foodborne botulism: comes from improperly preserved food.
    • Wound botulism: commonly seen in IV drug users.
    • Infant botulism: caused by feeding honey to an infant.

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