Set 2 Flashcards
1
Q
A
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
13
Q
What disease is primarily caused by Corynebacterium diphtheriae?
A
- Diphtheria: A respiratory and cutaneous disease characterized by the production of diphtheria toxin.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
25
How is Mycobacterium tuberculosis transmitted?
* 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
What are the clinical features of tuberculosis?
* 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
How is Mycobacterium tuberculosis infection diagnosed?
* 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
What treatments are effective against Mycobacterium tuberculosis infections?
* 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
What are the prevention measures for Mycobacterium tuberculosis infections?
* 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
What are the risk factors for developing tuberculosis?
* 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
What are the public health implications of Mycobacterium tuberculosis?
* 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
What is Mycobacterium avium subspecies paratuberculosis (MAP), and where is it commonly found?
* 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
What disease is primarily caused by MAP?
* 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
How is MAP transmitted?
* 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
What are the clinical features of paratuberculosis in animals?
* 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
How is MAP infection diagnosed?
* 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
What treatments are effective against MAP infections?
* 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
What are the prevention measures for MAP infections?
* 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
What are the key virulence factors of MAP?
* 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
What are the risk factors for developing paratuberculosis?
* 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
What are the public health implications of MAP infections?
* 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
What is Mycobacterium ulcerans, and where is it commonly found?
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
What disease is primarily caused by Mycobacterium ulcerans?
Buruli Ulcer: A chronic, necrotizing skin disease characterized by large ulcers typically on the limbs.
44
How is Mycobacterium ulcerans transmitted?
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
What are the clinical features of Buruli Ulcer?
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
How is Mycobacterium ulcerans infection diagnosed?
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
What treatments are effective against Mycobacterium ulcerans infections?
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
What are the prevention measures for Mycobacterium ulcerans infections?
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
What are the key virulence factors of Mycobacterium ulcerans?
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
What are the risk factors for developing Buruli Ulcer?
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
What are the public health implications of Mycobacterium ulcerans infections?
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
What is Mycobacterium leprae, and where is it commonly found?
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
What disease is primarily caused by Mycobacterium leprae?
Leprosy (Hansen’s Disease): A chronic infectious disease affecting the skin, nerves, eyes, and respiratory tract.
54
How is Mycobacterium leprae transmitted?
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
What are the clinical features of leprosy?
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
What are the risk factors for developing leprosy?
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
How is Mycobacterium leprae infection diagnosed?
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
What treatments are effective against leprosy?
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
What are the prevention measures for Mycobacterium leprae infections?
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
What are the key virulence factors of Mycobacterium leprae?
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
What are the public health implications of Mycobacterium leprae infections?
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.
