Infectious Diseases and Dermatology Quiz
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Questions and Answers

Which of the following can result from a secondary infection in the context of a dermatological condition?

  • Allergic reaction to environmental factors
  • Auto-inoculation leading to further infection (correct)
  • Transmitted diseases from direct contact
  • Increased pain from muscle strain
  • What is the primary mode of transmission for measles?

  • Vector-borne via insect bites
  • Direct skin contact with infected surfaces
  • Ingestion of contaminated food
  • Airborne respiratory droplets (correct)
  • Which virus is responsible for rubella?

  • Enveloped positive-stranded RNA virus (correct)
  • Non-enveloped negative-stranded RNA virus
  • Double-stranded RNA virus
  • Single-stranded DNA virus
  • What severe complication can arise from measles infection?

    <p>Pneumonia (C)</p> Signup and view all the answers

    How long can an infant congenitally infected with rubella shed the virus?

    <p>Up to 12 months (A)</p> Signup and view all the answers

    Which types of HPV are associated with common warts?

    <p>HPV-2, HPV-27, HPV-57 (C)</p> Signup and view all the answers

    What is the role of the E6 and E7 proteins in high-risk HPV types?

    <p>They facilitate viral genome amplification (B)</p> Signup and view all the answers

    How does the initial invasion of HPV occur more easily?

    <p>By damage to the skin or impairment of barrier function (A)</p> Signup and view all the answers

    Which of the following describes the structure of the human papillomavirus (HPV)?

    <p>Nonenveloped double-stranded DNA virus (D)</p> Signup and view all the answers

    Which HPV type is commonly associated with butcher's warts?

    <p>HPV-7 (B)</p> Signup and view all the answers

    What is another name for Erythema Infectiosum caused by Parvovirus B19?

    <p>5th disease (A)</p> Signup and view all the answers

    Which symptom pair is associated with the Papular purpuric gloves-and-socks syndrome?

    <p>Erythema and edema (C)</p> Signup and view all the answers

    What type of virus is Parvovirus B19?

    <p>Single-stranded DNA virus (B)</p> Signup and view all the answers

    What is the primary mode of transmission for Erythema Infectiosum?

    <p>Close contact (C)</p> Signup and view all the answers

    What specific antigen must be present for Parvovirus B19 to infect a cell?

    <p>Group P antigen (B)</p> Signup and view all the answers

    Which condition is commonly associated with Human Herpesvirus 6 (HHV-6)?

    <p>Febrile seizures (B)</p> Signup and view all the answers

    What type of DNA does Human Herpesvirus 6 possess?

    <p>Double-stranded DNA (A)</p> Signup and view all the answers

    Which cells does HHV-6 notably infect?

    <p>CD4+ T-cells (D)</p> Signup and view all the answers

    Which of the following exotoxins released by Pseudomonas aeruginosa directly activates the TLR4 receptor?

    <p>LPS (A)</p> Signup and view all the answers

    Which of these is NOT a primary cutaneous infection caused by Pseudomonas aeruginosa?

    <p>Ecthyma gangrenosum (A)</p> Signup and view all the answers

    What is the main reason Pseudomonas aeruginosa typically requires an existing skin injury to cause infection?

    <p>It is unable to penetrate intact skin. (D)</p> Signup and view all the answers

    What is the primary mechanism by which Pseudomonas aeruginosa promotes the development of septic shock?

    <p>Direct activation of the TLR4 receptor by LPS. (A)</p> Signup and view all the answers

    Which of these exotoxins is responsible for interfering with protein synthesis and ultimately leading to cell death?

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

    Which of the following is a characteristic of Pseudomonas aeruginosa that helps it survive in environments like hospitals?

    <p>It can form biofilms. (B), It can survive in harsh conditions. (D)</p> Signup and view all the answers

    Which of the following is NOT a mechanism by which the immune system combats Staphylococcus aureus?

    <p>Production of interferon-gamma by T helper 1 cells. (A)</p> Signup and view all the answers

    How do exfoliative toxins (ETs) produced by certain strains of Staphylococcus aureus cause blistering skin disorders?

    <p>By disrupting cell-cell adhesion by cleaving desmoglein-1. (A)</p> Signup and view all the answers

    Which of the following is a characteristic of bullous impetigo caused by exfoliative toxin A (ET-A)?

    <p>It is a localized blistering skin disorder. (C)</p> Signup and view all the answers

    What role does IL-17 play in the immune response against Staphylococcus aureus?

    <p>It promotes the recruitment of neutrophils to the site of infection. (D)</p> Signup and view all the answers

    Which of the following is a pattern recognition receptor (PRR) involved in neutrophil recruitment during Staph aureus infection?

    <p>Toll-like receptor 2 (TLR-2) (A)</p> Signup and view all the answers

    What is the primary reason for the recurrent nature of Staphylococcus aureus infections?

    <p>The adaptive immune response's limited ability to stop Staph aureus. (B)</p> Signup and view all the answers

    Which of the following statements about Staphylococcus aureus's pore-forming toxins is TRUE?

    <p>They promote the recruitment of neutrophils by activating caspase-1 and IL-1beta. (A)</p> Signup and view all the answers

    What is the primary mechanism by which Group A Streptococcus (GAS) causes superficial purulent skin infections?

    <p>Production of enzymes that break down skin tissue. (B)</p> Signup and view all the answers

    Which of these pore-forming toxins produced by Streptococcus causes apoptosis in neutrophils, macrophages, and epithelial cells?

    <p>Streptolysin O (D)</p> Signup and view all the answers

    Which of the following is NOT a mechanism by which Streptococcus evades the immune response?

    <p>Inhibition of TLR-2 and NOD-2 signaling pathways (A)</p> Signup and view all the answers

    Which of the following is a characteristic of superantigens produced by both Staphylococcus aureus and Streptococcus?

    <p>They activate T cells non-specifically, bypassing normal antigen processing (C)</p> Signup and view all the answers

    How does Streptococcus contribute to vascular injury and tissue necrosis?

    <p>By inducing an excessive inflammatory response that damages tissues (D)</p> Signup and view all the answers

    Which of the following is a likely mechanism by which Streptococcus gains entry into host cells?

    <p>Binding to specific receptors on the cell surface (A)</p> Signup and view all the answers

    What is the effect of Streptococcal Pyrogenic Exotoxin A, C, G, and M on the immune system?

    <p>They non-specifically activate T cells, leading to an exaggerated immune response (A)</p> Signup and view all the answers

    Which of the following molecules produced by Streptococcus contributes to the breakdown of neutrophil extracellular traps?

    <p>Nuclease A (A)</p> Signup and view all the answers

    What is the role of TLR-2 and NOD-2 in the immune response to Streptococcus?

    <p>They facilitate neutrophil recruitment to the site of infection (D)</p> Signup and view all the answers

    Study Notes

    Microbiology of Skin Infections

    • This course covers the microbiology of skin infections, including viral, fungal, and bacterial infections.
    • Learning outcomes focus on understanding the pathophysiology, etiology, pathogenesis, and microbiology of various skin infections.
    • The skin microbiome is initially colonized by coagulase-negative Staphylococci (e.g., Staph epidermidis).
    • Other microbes, including fungi and viruses, contribute to the skin microbiome's development.

    Learning Outcomes

    • Understanding the pathophysiology and clinical features of skin, hair, and nail disorders caused by viruses like HSV, HPV, HZV, and fungi.
    • Knowing the basic etiology and pathogenesis of common fungal skin infections (e.g., tinea).
    • Understanding the basic etiology and pathogenesis of common viral skin infections (e.g., HSV, varicella, HPV).
    • Understanding the basic etiology and pathogenesis of exanthematous skin diseases (e.g., measles, rubella, erythema infectiosum).
    • Understanding the basic etiology and pathogenesis of gram-positive bacterial skin diseases associated with toxin production (e.g., Staph and Strep).
    • Differentiating between bacterial skin diseases caused by exfoliative and superantigenic toxins.
    • Understanding the basic etiology and pathogenesis of gram-negative bacterial skin diseases (e.g., Pseudomonas).

    Introduction

    • Normal skin (epidermis) is colonized by commensal bacteria after birth.
    • Coagulase-negative Staphylococci (Staph epidermidis) are common initial colonizers.
    • Fungi, bacteria, and viruses contribute to the skin microbiome.

    Staphylococcal Skin Infections

    • Staphylococcal infections are common superficial purulent skin infections (pyodermas).
    • Roughly 30% of healthy individuals are colonized with Staphylococcus aureus.
    • Factors contributing to skin infection include immunosuppression, diabetes, atopic dermatitis, and pre-existing tissue injury.
    • Staph epidermidis is mainly commensal, while Staph aureus can be both commensal and pathogenic.
    • Staphylococcus aureus produces toxins that damage tissues and evade immune defenses.
    • MRSA (methicillin-resistant Staphylococcus aureus) is a significant concern due to resistance to beta-lactam antibiotics.

    Strep Pathogenesis

    • Group A Streptococcus (GAS) is a common cause of superficial purulent skin infections, such as impetigo, ecthyma, intertrigo.
    • Invasive infections caused by GAS include erysipelas, cellulitis, and necrotizing fasciitis, potentially leading to sepsis and multiorgan failure.
    • Other GAS infections include lymphangitis, bacteremia, septic arthritis, osteomyelitis, pneumonia, meningitis, and streptococcal toxic shock syndrome.
    • Immunologic-mediated conditions like guttate psoriasis, acute rheumatic fever, rheumatic heart disease, and glomerulonephritis can be triggered or follow GAS infections.

    Staph Soft Tissue Infections (SSTI)

    • Risk factors for SSTI include compromised neutrophil function, cancer, chemotherapy, and genetics.
    • Pore-forming toxins (alpha-toxin, gamma-toxin) damage neutrophils and macrophages.
    • Phenol-soluble modulins destroy leukocytes and erythrocytes.
    • Exfoliative toxins (produced by certain strains or bacteriophages) target desmosomal cadherin and cause staphylococcal scalded-skin syndrome.

    Superantigens

    • Superantigens trigger a massive immune response, resulting in high fever, hypotension, scarlet fever-like rash, desquamation of skin, and multiorgan dysfunction.
    • Examples include toxic shock syndrome toxin 1 (TSST-1), enterotoxins (A, B, C,...), and SE-like superantigens.

    Staph – Neutrophil Evasion

    • Staphylococcal proteins (e.g., CHIPS, staphopain A) inhibit chemotaxis and block complement receptors.
    • Staph superantigen-like 5 and 11 block neutrophil adherence.
    • Catalase and other enzymes inhibit reactive oxygen species (ROS) mediated killing.
    • Staphylococcal nuclease destroys neutrophil extracellular traps (NETs).

    Immune Response Against Staph

    • Antimicrobial peptides (e.g., beta-defensins, cathelicidins) produced by skin cells inhibit bacterial growth.
    • Neutrophil recruitment by pattern recognition receptors (PRRs) is crucial in controlling infection.
    • TLR-2 recognizes peptidoglycan and lipoproteins, NOD-2 recognizes muramyl dipeptide.
    • Staph pore-forming toxins activate caspase-1, causing IL-1Beta production, thus promoting neutrophil recruitment.

    Exfoliative Toxins

    • Exfoliative toxins (ETs) are serine proteases that target cell-adhesion molecule desmoglein-1.
    • Loss of cell-cell adhesion leads to skin blistering, characterized by bullous impetigo and staphylococcal scalded-skin syndrome (SSSS).

    Pseudomonas Aeruginosa - Intro

    • Ubiquitous Gram-negative rod, commonly found in aqueous environments.
    • Characterized by a sweet, grape-like odor and blue-green color.
    • Often found in warm environments (preferring temperatures above 42 degrees Celsius).
    • Can cause skin infections, including green nail syndrome and ecthyma gangrenosum in hospitalized patients.
    • Often found in nosocomial or cystic fibrosis settings.

    Pseudomonas Aeruginosa - Pathogenesis

    • Bacteria use various enzymes to degrade skin structures.
    • Exoenzymes like ExoS, ExoT, ExoU, and ExoY disrupt cell membranes, cellular processes, and protein synthesis.
    • Exotoxin A interferes with protein synthesis, contributing to cell death.
    • Procyanins influence inflammatory reactions and oxidative effects; LPS activates TLR4, potentially leading to septic shock.
    • Quorum sensing coordinates gene transcription and biofilm formation.

    Pseudomonas Aeruginosa - Pathogenic Features

    • Prolonged colonization promotes alginate overproduction, hindering phagocytosis and complement activation.
    • Biofilm formation provides protection against antibiotics and antimicrobial peptides.
    • Multidrug efflux pumps and beta-lactamases contribute to antibiotic resistance.

    Viral Skin Infections (Measles, Rubella, Erythema Infectiosum)

    • Measles (rubeola): highly contagious, enveloped RNA virus.
    • Rubella (German measles): enveloped RNA virus, lifelong immunity typical.
    • Erythema infectiosum (fifth disease): single-stranded DNA virus from Parvoviridae family, causes a rash.

    Human Herpesvirus 6 (HHV-6)

    • Part of Herpesviridae family.
    • HHV-6 infects a wide range of cells (monocytes, macrophages, NK cells, neuronal cells, CD4+ T-cells).
    • The virus integrates its DNA with the host.
    • Reactivates during immunosuppression (e.g., after stem cell transplantation).

    Herpes Simplex Virus (HSV)

    • DNA virus, Herpesviridae family.
    • Usually causes intermittent reactivation.
    • HSV-1 (oral) or HSV-2 (genital) can infect body parts.
    • Most primary infections are asymptomatic.
    • Transmission frequently occurs during asymptomatic shedding

    Varicella-Zoster Virus (VZV)

    • From Herpesviridae family, causes chicken pox and shingles.

    • Highly contagious viral infection.

    • Chickenpox: rash begins on face, spreads to trunk, and may involves extremities.

    • Shingles: reactivation of the virus that cause chickenpox, usually in a one side of the body. Causes severe neuropathic pain.

    Human Papillomavirus (HPV)

    • DNA virus.
    • Over 150 types, some with low and some with high risk for malignancy.
    • Infections of keratinocytes are common.
    • Causes warts, and plays an important role in malignancies.

    Dermatophytes

    • Fungal keratin infections (e.g., tinea barbae, tinea corporis, tinea cruris, tinea pedis, tinea mannum).
    • Transmission common through fomites, autoinoculation, or contact with infected individuals, animals, or the environment.
    • Immune response is essential in clearing fungal infection.
    • Inflammatory skin reactions at site of the infection are common.

    Onychomycosis

    • Fungal infection of the nail.
    • 90% of cases are caused by Trichophyton rubrum and Trichophyton interdigitale.

    Other information

    • Pictures and case studies are often included for clinical applications, which are not included in these notes.

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    Description

    Test your knowledge on infectious diseases and their dermatological implications. This quiz includes questions about viruses such as measles, rubella, HPV, and Parvovirus B19, along with their transmission modes and complications. Perfect for students studying dermatology or infectious diseases.

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