Set 2 Flashcards

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1
Q
A
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2
Q

What is Listeria monocytogenes, and where is it commonly found?

A
  • Gram-positive, facultative anaerobic bacillus.
  • Motile at 22-25°C with “rocket-like” tumbling motility.
  • Commonly found in soil, water, vegetables, and animal products.
  • Can survive and grow in refrigerated conditions.
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3
Q

What diseases are primarily caused by Listeria monocytogenes?

A
  • Listeriosis: Can manifest as:
    • Septicemia: Bloodstream infection.
    • Meningitis: Inflammation of the membranes surrounding the brain and spinal cord.
    • Fetal Infections: Including miscarriage, stillbirth, or neonatal sepsis.
  • Gastroenteritis: Mild infection with diarrhea and vomiting, mainly in immunocompromised individuals.
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4
Q

How is Listeria monocytogenes transmitted?

A
  • Foodborne Route: Consumption of contaminated foods such as:
    • Unpasteurized dairy products.
    • Soft cheeses.
    • Raw vegetables.
    • Processed meats (e.g., deli meats, hot dogs).
  • Vertical Transmission: From mother to fetus during pregnancy.
  • Person-to-Person: Rare, primarily via direct contact with infected individuals.
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5
Q

What are the clinical features of listeriosis?

A
  • Septicemia and Meningitis:
    • Fever, muscle aches, confusion.
    • Neck stiffness, headache, loss of balance.
  • Fetal Infections:
    • Miscarriage, stillbirth, or neonatal sepsis.
  • Gastroenteritis:
    • Diarrhea, abdominal pain, vomiting.
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6
Q

What are the risk factors for developing Listeria monocytogenes infection?

A
  • Pregnancy: Increased susceptibility; can affect the fetus.
  • Elderly Individuals: Weakened immune systems.
  • Immunocompromised Persons: Including those with HIV/AIDS, cancer, or on immunosuppressive therapy.
  • Newborns: Particularly premature or low birth weight infants.
  • Consumption of High-Risk Foods: Such as unpasteurized dairy products and processed meats.
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7
Q

How is Listeria monocytogenes infection diagnosed?

A
  • Clinical Evaluation: Based on symptoms and risk factors.
  • Laboratory Tests:
    • Blood Cultures: Positive in cases of septicemia.
    • Cerebrospinal Fluid (CSF) Analysis: For meningitis diagnosis.
    • Stool Culture: In cases of gastroenteritis.
  • Molecular Methods: PCR for rapid and specific identification.
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8
Q

What treatments are effective against Listeria monocytogenes infections?

A
  • Antibiotic Therapy:
    • Ampicillin: First-line treatment.
    • Gentamicin: Often combined with ampicillin for synergistic effect.
    • Vancomycin: Alternative for those allergic to beta-lactams.
  • Supportive Care: Includes hydration and management of symptoms.
  • Antibiotic Duration: Typically 2-3 weeks for invasive infections.
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9
Q

What are the prevention measures for Listeria monocytogenes infections?

A
  • Food Safety Practices:
    • Proper Cooking: Thoroughly cook meat and poultry.
    • Pasteurization: Use pasteurized dairy products.
    • Refrigeration: Maintain adequate cold storage to inhibit bacterial growth.
    • Avoid High-Risk Foods: Especially for pregnant women and immunocompromised individuals.
  • Hygiene:
    • Handwashing: After handling raw foods.
    • Cross-Contamination Prevention: Use separate utensils and surfaces for raw and cooked foods.
  • Public Health Measures:
    • Surveillance and Monitoring: To detect and control outbreaks.
    • Education: Informing high-risk populations about safe food practices.
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10
Q

What are the key virulence factors of Listeria monocytogenes?

A
  • Internalin Proteins (InlA and InlB): Facilitate entry into host cells.
  • ActA Protein: Promotes actin-based motility for cell-to-cell spread.
  • Listeriolysin O (LLO): Pore-forming toxin that allows escape from phagosomes.
  • Phospholipases: Aid in membrane disruption and spread within tissues.
  • Capsular Polysaccharides: Enhance immune evasion.
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11
Q

What are the public health implications of Listeria monocytogenes?

A
  • High-Risk Populations: Pregnant women, elderly, and immunocompromised individuals require special attention.
  • Food Industry Impact: Contaminated products can lead to recalls and economic losses.
  • Antibiotic Resistance Concerns: Although generally susceptible, monitoring for resistant strains is essential.
  • Bioterrorism Potential: Due to its ability to cause severe disease, though less common than other pathogens.
  • Surveillance Systems: Importance of monitoring and rapid response to outbreaks to minimize impact.
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12
Q

What is Corynebacterium diphtheriae, and where is it commonly found?

A
  • Gram-positive, non-spore-forming, club-shaped bacillus.
  • Facultative anaerobe.
  • Commonly found in the human respiratory tract as a colonizer.
  • Can survive on dry surfaces for weeks, facilitating transmission.
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13
Q

What disease is primarily caused by Corynebacterium diphtheriae?

A
  • Diphtheria: A respiratory and cutaneous disease characterized by the production of diphtheria toxin.
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14
Q

How is Corynebacterium diphtheriae transmitted?

A
  • Person-to-Person Contact: Through respiratory droplets from coughing or sneezing.
  • Contaminated Objects: Sharing personal items like towels or utensils.
  • Skin Lesions: Through direct contact with infected wounds in cutaneous diphtheria.
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15
Q

What are the clinical features of diphtheria?

A
  • Respiratory Diphtheria:
    • Pseudomembrane Formation: Greyish membrane on the tonsils, pharynx, or nasopharynx.
    • Sore Throat, Fever, Swollen Glands, Difficulty Breathing.
    • Systemic Effects: Myocarditis, neuropathy due to diphtheria toxin.
  • Cutaneous Diphtheria:
    • Ulcerative Lesions with gray membranes on the skin.
    • Common in tropical regions and among immunocompromised individuals.
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16
Q

What are the key virulence factors of Corynebacterium diphtheriae?

A
  • Diphtheria Toxin:
    • Exotoxin that inhibits protein synthesis in host cells by ADP-ribosylating EF-2, leading to cell death.
    • Responsible for systemic complications like myocarditis and neuropathy.
  • Pili and Adhesins: Facilitate attachment to host epithelial cells.
  • Cell Wall Components: Dimorphic properties aiding in immune evasion.
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17
Q

How is Corynebacterium diphtheriae infection diagnosed?

A
  • Clinical Evaluation: Presence of pseudomembrane, symptoms of diphtheria.
  • Laboratory Tests:
    • Culture: Grows on Loeffler’s medium or Tellurite agar (gray colonies).
    • PCR: Detection of tox gene encoding diphtheria toxin.
    • Elek’s Test: Immunodiffusion assay to confirm toxin production.
  • Serological Tests: Measurement of antitoxin antibodies.
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18
Q

What treatments are effective against Corynebacterium diphtheriae infections?

A
  • Antitoxin Administration:
    • Diphtheria antitoxin: Neutralizes free toxin; must be given early.
  • Antibiotic Therapy:
    • Penicillin G or Erythromycin: To eliminate bacterial carriage and prevent toxin production.
  • Supportive Care:
    • Airway Management: In cases of airway obstruction.
    • Cardiac Monitoring: For myocarditis.
  • Isolation: To prevent transmission to others.
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19
Q

What are the prevention measures for Corynebacterium diphtheriae infections?

A
  • Vaccination:
    • Diphtheria Vaccine: Part of the DTaP and Td vaccines; induces antitoxin antibodies.
  • Hygiene Practices:
    • Handwashing and respiratory etiquette to reduce spread.
  • Surveillance and Control:
    • Contact Tracing and prophylactic antibiotics for exposed individuals.
  • Public Health Measures:
    • Rapid Identification and isolation of cases to prevent outbreaks.
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20
Q

What are the risk factors for developing diphtheria?

A
  • Lack of Vaccination: Unvaccinated or incompletely vaccinated individuals.
  • Close Contact with Infected Persons: Living in crowded conditions.
  • Travel to Endemic Areas: Regions with low vaccination coverage.
  • Weakened Immune System: Immunocompromised individuals are more susceptible.
  • Poor Hygiene: Increases transmission likelihood.
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21
Q

What are the public health implications of Corynebacterium diphtheriae?

A
  • Outbreak Potential: Highly contagious with rapid spread in susceptible populations.
  • Vaccination Programs: Essential for prevention; resurgence possible if vaccination rates decline.
  • Bioterrorism Concern: Diphtheria toxin can be used as a biological weapon, necessitating preparedness.
  • Healthcare Burden: Requires prompt treatment and isolation measures to control transmission.
  • Global Health Disparities: Higher incidence in developing countries with limited vaccination infrastructure.
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22
Q

What is Mycobacterium tuberculosis, and where is it commonly found?

A
  • Gram-positive, acid-fast, slow-growing bacillus.
  • Obligate Aerobe: Requires oxygen for growth.
  • Environmental Presence: Primarily found in the human respiratory tract.
  • Transmission: Spread through airborne droplets from infected individuals.
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23
Q

What disease is primarily caused by Mycobacterium tuberculosis?

A
  • Tuberculosis (TB): A chronic infectious disease affecting primarily the lungs (pulmonary TB) but can also affect other body parts (extrapulmonary TB).
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24
Q

What are the key virulence factors of Mycobacterium tuberculosis?

A
  • Mycolic Acids: Long-chain fatty acids in the cell wall that provide resistance to desiccation, chemicals, and immune responses.
  • Cord Factor (Trehalose Dimycolate): Facilitates intracellular survival and tissue necrosis.
  • ESAT-6 and CFP-10 Proteins: Involved in macrophage lysis and immune evasion.
  • Phthiocerol Dimycocerosate (PDIM): Affects membrane permeability and immune modulation.
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25
Q

How is Mycobacterium tuberculosis transmitted?

A
  • Airborne Transmission: Inhalation of droplet nuclei containing bacilli expelled when an infected person coughs, sneezes, or talks.
  • Close Contact: Higher risk among household members, healthcare workers, and individuals in crowded settings.
  • Latent Infection: Inhaled bacilli can remain dormant within granulomas without causing active disease.
26
Q

What are the clinical features of tuberculosis?

A
  • Pulmonary TB:
    • Chronic Cough: Lasting more than 3 weeks.
    • Hemoptysis: Coughing up blood.
    • Night Sweats, Fever, and Weight Loss.
    • Chest Pain and Fatigue.
  • Extrapulmonary TB:
    • Lymphadenitis: Swollen lymph nodes.
    • Meningitis: Inflammation of the meninges.
    • Spondylitis: Infection of the spine.
    • Pericarditis: Inflammation of the pericardium.
27
Q

How is Mycobacterium tuberculosis infection diagnosed?

A
  • Clinical Evaluation: Based on symptoms and exposure history.
  • Tuberculin Skin Test (Mantoux Test): Intradermal injection of PPD antigen to detect immune response.
  • Interferon-Gamma Release Assays (IGRAs): Blood tests measuring immune cell response to TB antigens.
  • Chest X-Ray: Identifies lung abnormalities such as cavities and infiltrates.
  • Sputum Smear Microscopy: Ziehl-Neelsen stain to detect acid-fast bacilli.
  • Culture: Growth on Lowenstein-Jensen medium is definitive but slow (weeks).
  • Molecular Tests: PCR-based assays for rapid DNA detection and drug resistance profiling.
28
Q

What treatments are effective against Mycobacterium tuberculosis infections?

A
  • First-Line Antibiotics:
    • Isoniazid
    • Rifampin
    • Ethambutol
    • Pyrazinamide
  • Treatment Regimen:
    • Initial Phase: Combination of Isoniazid, Rifampin, Ethambutol, and Pyrazinamide for 2 months.
    • Continuation Phase: Isoniazid and Rifampin for an additional 4-7 months.
  • Directly Observed Therapy (DOT): Ensures compliance and prevents resistance.
  • Second-Line Drugs: For drug-resistant TB, including Fluoroquinolones and Injectables like Amikacin.
29
Q

What are the prevention measures for Mycobacterium tuberculosis infections?

A
  • Vaccination:
    • BCG Vaccine (Bacillus Calmette-Guérin): Provides partial protection against severe forms of TB in children.
  • Infection Control in Healthcare Settings:
    • Isolation Rooms: For infected patients.
    • Respiratory Protection: Use of N95 respirators by healthcare workers.
    • Ventilation Systems: Ensure negative pressure rooms to prevent airborne spread.
  • Public Health Measures:
    • Contact Tracing: Identify and test individuals exposed to infected persons.
    • Screening Programs: Regular testing in high-risk populations.
  • Reducing Transmission:
    • Adequate Ventilation: In living and working spaces.
    • Mask-Wearing: In high-risk settings or during outbreaks.
  • Addressing Social Determinants:
    • Improving Living Conditions: Reducing overcrowding and malnutrition.
    • Access to Healthcare: Ensuring early diagnosis and treatment.
30
Q

What are the risk factors for developing tuberculosis?

A
  • Immunocompromised States:
    • HIV/AIDS
    • Diabetes Mellitus
    • Organ Transplant Recipients
  • Close Contact: Living or working with TB-infected individuals.
  • Substance Abuse: Including smoking and injecting drugs.
  • Malnutrition: Weakens the immune system.
  • Geographical Location: Higher prevalence in low- and middle-income countries.
  • Age: Elderly and young children are more susceptible.
  • Socioeconomic Factors: Poverty, homelessness, and overcrowded living conditions.
31
Q

What are the public health implications of Mycobacterium tuberculosis?

A
  • Global Health Burden:
    • High Prevalence: Especially in developing countries.
    • Leading Cause of Death: Among infectious diseases globally.
  • Antibiotic Resistance:
    • Multidrug-Resistant TB (MDR-TB): Resistant to Isoniazid and Rifampin.
    • Extensively Drug-Resistant TB (XDR-TB): Resistant to first-line and some second-line drugs.
  • Economic Impact:
    • Healthcare Costs: Long treatment durations and resource-intensive management.
    • Lost Productivity: Due to illness and death.
  • Infection Control Challenges:
    • Ensuring Treatment Adherence: To prevent relapse and resistance.
    • Stigma: Associated with TB can hinder seeking treatment.
  • Bioterrorism Potential:
    • High Infectiousness: M. tuberculosis could be used as a biological weapon, requiring preparedness.
  • Public Health Strategies:
    • Vaccination Programs: Promoting BCG vaccination in high-risk areas.
    • Strengthening Healthcare Systems: Ensuring access to diagnosis and treatment.
    • Research and Development: Developing new diagnostics, vaccines, and therapeutics.
32
Q

What is Mycobacterium avium subspecies paratuberculosis (MAP), and where is it commonly found?

A
  • Gram-positive, acid-fast, slow-growing bacillus.
  • Facultative Aerobe with a complex cell wall rich in mycolic acids.
  • Commonly found in soil, water, and animal feces.
  • Reservoir Hosts: Primarily ruminants like cattle, sheep, and goats.
33
Q

What disease is primarily caused by MAP?

A
  • Paratuberculosis (Johne’s Disease):
    • Chronic, Progressive gastrointestinal disease.
    • Primarily affects the small intestine of ruminants.
    • Potential Association: Investigated link with Crohn’s Disease in humans (controversial).
34
Q

How is MAP transmitted?

A
  • Fecal-Oral Route: Ingestion of contaminated feed or water containing MAP spores.
  • Vertical Transmission: From dam to calf through colostrum or milk.
  • Environmental Persistence: MAP spores can survive in the environment for years due to their resistance.
35
Q

What are the clinical features of paratuberculosis in animals?

A
  • Progressive Weight Loss: Despite normal or increased appetite.
  • Diarrhea: Chronic, watery stools.
  • Reduced Milk Production: In dairy cattle.
  • Weakness and Depression: General signs of poor health.
  • Death: Often occurs in advanced stages due to severe malnutrition and dehydration.
36
Q

How is MAP infection diagnosed?

A
  • Clinical Signs: Based on symptoms like weight loss and diarrhea.
  • Laboratory Tests:
    • Culture: Growing MAP from feces, tissues, or blood; extremely slow (can take up to 16 weeks).
    • PCR: Detects MAP DNA; faster but may lack sensitivity.
    • Serological Tests: ELISA for antibodies against MAP.
    • Histopathology: Intestinal biopsies showing granulomatous enteritis.
37
Q

What treatments are effective against MAP infections?

A
  • Limited Treatment Options: No effective antibiotic treatment for paratuberculosis in animals.
  • Management Practices:
    • Culling Infected Animals: To prevent spread.
    • Improved Sanitation: Enhancing hygiene in animal housing.
    • Feed Management: Avoiding contaminated feed and ensuring clean water sources.
    • Vaccination: Developing vaccines is ongoing but not widely available.
38
Q

What are the prevention measures for MAP infections?

A
  • Herd Management:
    • Test-and-Cull Programs: Identifying and removing infected animals.
    • Minimize Calf Exposure: Preventing vertical transmission by controlling calf feeding practices.
  • Environmental Controls:
    • Clean Housing: Regularly cleaning and disinfecting barns and feeding equipment.
    • Pasture Rotation: Reducing soil contamination.
  • Biosecurity Measures:
    • Prevent Introduction: Screening new animals before introducing to the herd.
    • Isolation Practices: Separating infected from healthy animals.
39
Q

What are the key virulence factors of MAP?

A
  • Cell Wall Components: Rich in mycolic acids providing resistance to host defenses.
  • Secreted Proteins: Facilitate macrophage invasion and immune evasion.
  • Adhesins: Enable attachment to intestinal epithelial cells.
  • Slow Growth Rate: Allows persistent infection within the host.
  • Spore Formation: Ensures environmental survival and transmission.
40
Q

What are the risk factors for developing paratuberculosis?

A
  • Age: Young animals are more susceptible to infection.
  • Herd Size: Larger herds have higher transmission rates.
  • Management Practices: Poor hygiene, overcrowding, and inadequate sanitation increase risk.
  • Genetic Susceptibility: Some breeds may be more vulnerable.
  • Environmental Contamination: Presence of MAP spores in soil and water.
41
Q

What are the public health implications of MAP infections?

A
  • Zoonotic Potential:
    • Controversial Link: Investigated association with Crohn’s Disease in humans, though not definitively proven.
  • Food Safety:
    • Contaminated Milk: Pasteurization is crucial to eliminate MAP spores.
    • Meat Processing: Ensuring proper cooking and hygiene to prevent foodborne transmission.
  • Economic Impact:
    • Livestock Losses: Reduced productivity, culling costs, and impact on dairy and meat industries.
  • Research and Development:
    • Vaccine Development: Ongoing efforts to create effective vaccines for herd immunity.
    • Diagnostic Improvements: Enhancing rapid and accurate testing methods.
  • Environmental Persistence:
    • Long-Term Contamination: MAP spores remain in the environment, posing ongoing transmission risks.
42
Q

What is Mycobacterium ulcerans, and where is it commonly found?

A

Gram-positive, acid-fast, slow-growing bacillus.
Environmental Reservoirs: Found in water bodies, soil, and associated with aquatic environments.
Geographical Distribution: Predominantly in West and Central Africa, Australia, and parts of Asia.

43
Q

What disease is primarily caused by Mycobacterium ulcerans?

A

Buruli Ulcer: A chronic, necrotizing skin disease characterized by large ulcers typically on the limbs.

44
Q

How is Mycobacterium ulcerans transmitted?

A

Environmental Contact: Through skin abrasions exposed to contaminated water or soil.
Vector Transmission: Possible role of insects (e.g., water bugs) as vectors.
Direct Contact: With infected individuals is rarely reported.

45
Q

What are the clinical features of Buruli Ulcer?

A

Early Stage: Painless nodules or plaques on the skin.
Advanced Stage: Progression to necrotic ulcers with undermined edges.
Minimal Inflammation: Often lack of pain and inflammatory response.
Complications: Bone involvement, disfigurement, and functional impairment.

46
Q

How is Mycobacterium ulcerans infection diagnosed?

A

Clinical Evaluation: Based on skin lesions appearance and epidemiological history.
Laboratory Tests:
* PCR: Detection of IS2404 gene specific to M. ulcerans.
* Culture: Growing on Lowenstein-Jensen medium; slow (can take several weeks).
* Histopathology: Presence of necrosis and acid-fast bacilli.
Imaging: Ultrasound or MRI for assessing extent of tissue involvement.

47
Q

What treatments are effective against Mycobacterium ulcerans infections?

A

Antibiotic Therapy:
* Combination of Rifampicin and Clarithromycin: Standard regimen for 8 weeks.
* Alternative Regimens: May include streptomycin or amikacin in severe cases.
Surgical Intervention:
* Debridement: Removal of necrotic tissue if necessary.
Supportive Care:
* Wound Care: Proper dressings and infection prevention.
* Reconstruction: In cases of disfigurement or functional loss.

48
Q

What are the prevention measures for Mycobacterium ulcerans infections?

A

Environmental Management:
* Avoiding Contact: Limiting exposure to contaminated water and soil, especially in endemic areas.
Protective Measures:
* Wearing Protective Clothing: When in high-risk environments.
Public Health Initiatives:
* Awareness Campaigns: Educating communities about risk factors and early signs.
Vector Control:
* Insect Management: Reducing insect vectors that may transmit the bacteria.

49
Q

What are the key virulence factors of Mycobacterium ulcerans?

A

Mycolactone: A polyketide-derived toxin responsible for tissue necrosis and immune suppression.
Biofilm Formation: Enhances environmental survival and transmission.
Iron Acquisition Systems: Essential for bacterial growth in host tissues.
Surface Proteins: Facilitate adherence to host cells and immune evasion.

50
Q

What are the risk factors for developing Buruli Ulcer?

A

Living in Endemic Areas: Such as West Africa, Australia, and parts of Asia.
Environmental Exposure: Frequent contact with water bodies and soil.
Age: Primarily affects children and young adults.
Immune Status: Immunocompromised individuals may be at higher risk.
Insect Bites: Possible association with insect vectors.

51
Q

What are the public health implications of Mycobacterium ulcerans infections?

A

Burden in Endemic Regions: Causes significant healthcare challenges and economic impact.
Bioterrorism Potential: Mycolactone toxin’s potent effects raise concerns for biological weapon use.
Need for Research: Ongoing studies on transmission mechanisms, vaccine development, and better diagnostics.
Healthcare Infrastructure: Requires adequate resources for diagnosis, treatment, and prevention in affected areas.
Community Education: Essential for early detection and reducing transmission through behavioral changes.

52
Q

What is Mycobacterium leprae, and where is it commonly found?

A

Gram-positive, acid-fast, slow-growing bacillus.
* Obligate Intracellular Pathogen: Primarily infects skin and nervous tissue.
* Environmental Presence: Not commonly found in the environment; primarily transmitted person-to-person.
* Low Reproduction Rate: Long generation time (~14 days).

53
Q

What disease is primarily caused by Mycobacterium leprae?

A

Leprosy (Hansen’s Disease): A chronic infectious disease affecting the skin, nerves, eyes, and respiratory tract.

54
Q

How is Mycobacterium leprae transmitted?

A

Respiratory Droplets: Inhalation of infectious droplets from an infected person.
* Prolonged Close Contact: Higher risk among household members.
* Possible Transmission: Through skin contact, though less common.

55
Q

What are the clinical features of leprosy?

A

Skin Lesions: Hypopigmented or reddish patches with reduced sensation.
* Nerve Damage: Leads to loss of sensation, muscle weakness, and deformities.
* Types of Leprosy:
* Tuberculoid: Few, well-defined lesions; low bacterial load.
* Lepromatous: Numerous lesions; high bacterial load.
* Borderline: Intermediate features between tuberculoid and lepromatous.

56
Q

What are the risk factors for developing leprosy?

A

Genetic Susceptibility: Certain genetic factors increase risk.
* Close Contact: Living with an infected individual.
* Immunocompromised States: Weakened immune system may increase susceptibility.
* Geographical Location: Higher prevalence in tropical and subtropical regions.

57
Q

How is Mycobacterium leprae infection diagnosed?

A

Clinical Evaluation: Based on skin lesions and nerve involvement.
* Skin Smear or Biopsy: Detection of acid-fast bacilli using Ziehl-Neelsen stain.
* PCR: Molecular detection of M. leprae DNA for higher sensitivity.
* Skin Patch Test: Assessing sensory loss in lesions.

58
Q

What treatments are effective against leprosy?

A

Multi-Drug Therapy (MDT): Combines multiple antibiotics to prevent resistance.
* For Tuberculoid and Borderline Leprosy:
* Rifampicin
* Dapsone
* For Lepromatous Leprosy:
* Rifampicin
* Dapsone
* Clofazimine
* Duration: Typically 6-12 months depending on the type.
* Supportive Care: Managing nerve damage and deformities.

59
Q

What are the prevention measures for Mycobacterium leprae infections?

A

Early Diagnosis and Treatment: Reduces contagiousness and prevents complications.
* Public Health Programs: Screening and contact tracing in endemic areas.
* Vaccination: BCG vaccine offers partial protection against leprosy.
* Hygiene Practices: Maintaining good personal hygiene and sanitation to reduce transmission.
* Awareness and Education: Informing communities about leprosy signs and reducing stigma.

60
Q

What are the key virulence factors of Mycobacterium leprae?

A

Phenolic Glycolipid-I (PGL-I): Facilitates adhesion to host cells.
* Mycolic Acids: Component of the cell wall providing resistance to host defenses.
* Lipoarabinomannan (LAM): Modulates immune responses and immune evasion.
* Toxin Complexes: Inhibit phagosome-lysosome fusion, allowing intracellular survival.

61
Q

What are the public health implications of Mycobacterium leprae infections?

A

Stigma and Discrimination: Persistent social stigma affecting patients’ quality of life.
* Economic Impact: Loss of productivity and healthcare costs associated with long-term treatment and disabilities.
* Global Health Challenge: Requires continued surveillance and resource allocation in endemic regions.
* Potential for Elimination: WHO aims to reduce global burden, but challenges remain in access to healthcare and early detection.
* Biotechnological Research: Ongoing efforts to develop effective vaccines and new diagnostic tools.