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?

Essential for tick survival. Signup and view all the answers

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

Asthma Signup and view all the answers

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

It mediates adhesion and immune evasion. Signup and view all the answers

Which immune evasion strategy is employed by Streptococcus pyogenes?

Molecular mimicry. Signup and view all the answers

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

By binding Factor H to evade complement recognition. Signup and view all the answers

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

It helps the bacteria avoid the immune response. Signup and view all the answers

What is the consequence of capsule loss in pyogenes?

Virulence loss. Signup and view all the answers

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

Exotoxin B (SpeB) Signup and view all the answers

What mechanism do efflux pumps contribute to in antibiotic resistance?

Transporting substances out of the cell. Signup and view all the answers

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

Paracellularly and through pili. Signup and view all the answers

Which characteristic of Streptococcus pneumoniae colonies indicates higher virulence?

Opaque colonies. Signup and view all the answers

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

To prevent IgA from binding to the bacteria. Signup and view all the answers

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

They cause cell membrane pore formation. Signup and view all the answers

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

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

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

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

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

Lockjaw Signup and view all the answers

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

It cleaves MEK, disrupting cell signaling Signup and view all the answers

What initiates spore formation in both Clostridium and Bacillus species?

The Spo0A response regulator Signup and view all the answers

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

Break down desmoglein-1 Signup and view all the answers

Which component of Staphylococcus aureus helps it resist phagocytosis?

Staphylothrombin Signup and view all the answers

What does the mecA gene encode in Staphylococcus aureus?

An alternate penicillin binding protein Signup and view all the answers

What is the most lethal form of Bacillus anthracis infection?

Inhalation anthrax Signup and view all the answers

Which of the following describes the role of staphyloxanthin?

Scavenges radicals from ROS Signup and view all the answers

Which Staphylococcus toxin is responsible for toxic shock syndrome symptoms?

Toxic shock syndrome toxin-1 Signup and view all the answers

How can Bacillus spores survive extreme environments?

By entering a dormant state Signup and view all the answers

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

Adhesion via MSCRAMMS Signup and view all the answers

Which pathogen is responsible for causing Yersiniosis?

Yersinia enterocolitica Signup and view all the answers

What is the primary mode of transmission for Yersinia pestis?

Transmission via fleas Signup and view all the answers

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

Enterocolitic Signup and view all the answers

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

Inhibits complement activation Signup and view all the answers

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

Erythema migrans Signup and view all the answers

Which virulence factor allows Yersinia pestis to survive inside fleas?

pMT1 Signup and view all the answers

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

Inhibits phagolysosomal fusion Signup and view all the answers

Which of the following diseases is caused by Borrelia burgdorferi?

Lyme disease 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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