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Questions and Answers
What function do periplasmic flagella serve in Treponema pallidum?
Which protein is associated with antigenic variation in Borrelia burgdorferi?
What type of hemolysis do most Lancefield streptococci exhibit?
What is the role of the Hpk1-Rrp1 two-component system in Borrelia burgdorferi?
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Which of the following is NOT a symptom of Group A Strep infection?
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What is a characteristic feature of the capsule of Streptococcus pyogenes?
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Which immune evasion strategy is employed by Streptococcus pyogenes?
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What is the mechanism by which Lyme and relapsing fevers evade the immune response?
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What role does the hyaluronic acid capsule play in bacteria like pyogenes?
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What is the consequence of capsule loss in pyogenes?
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Which of the following exotoxins is responsible for degradation of host serum proteins in pyogenes?
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What mechanism do efflux pumps contribute to in antibiotic resistance?
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How does Group B Streptococcus (Streptococcus agalactiae) primarily cross the blood-brain barrier?
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Which characteristic of Streptococcus pneumoniae colonies indicates higher virulence?
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What is the primary action of the IgA1 protease found in Streptococcus pneumoniae?
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What is a common feature among beta-hemolysin toxins SLO and SLS?
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What is the primary function of the protective antigen (PA) in the anthrax toxin?
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Which of the following describes the capsule found in certain bacteria?
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What is the most common symptom of tetanus caused by Clostridium tetani?
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How does the lethal factor (LF) of the anthrax toxin affect host cells?
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What initiates spore formation in both Clostridium and Bacillus species?
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What is the primary function of exfoliative toxins released by Staphylococcus aureus?
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Which component of Staphylococcus aureus helps it resist phagocytosis?
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What does the mecA gene encode in Staphylococcus aureus?
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What is the most lethal form of Bacillus anthracis infection?
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Which of the following describes the role of staphyloxanthin?
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Which Staphylococcus toxin is responsible for toxic shock syndrome symptoms?
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How can Bacillus spores survive extreme environments?
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What leads to the formation of a biofilm by Staphylococcus aureus?
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Which pathogen is responsible for causing Yersiniosis?
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What is the primary mode of transmission for Yersinia pestis?
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Which of the following is NOT a type of plague caused by Yersinia pestis?
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What is a key function of the outer surface protein A (OspA) in Borrelia burgdorferi?
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Which symptom is commonly associated with the early stage of Lyme disease?
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Which virulence factor allows Yersinia pestis to survive inside fleas?
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What role do Rab proteins play in the pathogenicity of Yersinia?
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Which of the following diseases is caused by Borrelia burgdorferi?
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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
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Yersinia species are transmitted through various means:
- Y. pestis: Transmitted by fleas
- Y. pestis: Pneumonic form transmitted person-to-person by droplets, deadliest form
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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.
- Biofilm, composed of N-acetyl-D-glucosamine (glucose derivative), produced by hms gene
-
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)
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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
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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
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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)
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S. pyogenes are responsible for:
- Rheumatic heart disease
- Glomerulonephritis
- Toxic shock syndrome (TSS)
- Necrotizing fasciitis
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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).
- Adhesion:
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).
- Capsule:
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
- Two exotoxins related to SSSS:
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)
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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.
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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.
- A subunits:
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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