Lecture 10: Infectious Diseases II

Question 1

Components of microbial transmission

Answer 1

1. Host defenses and microbial access
2. Spread and dissemination within body
3. Release and transmission to other hosts

Question 2

How microbes cause disease

Answer 2

1. Toxin/enzyme release that kills cells, degrades tissue, damages vessels, cause ischemia
2. Induce host immune responses that damage the body
3. Evade host immunity

Question 3

Tropism

Answer 3

Preference of a pathogen to infect a specific location

Question 4

Herpes simplex virus

Answer 4

• Transmission via lesion contact
• 80% asymptomatic; latent infection in proximal ganglia
• Lytic escape from cells during infection (lesions, meningoencephalitis)
• Triggers via stress, illness, immunosuppress.
• No cure/vaccine

Question 5

VZV, HHV-3

Answer 5

Aka varicella zoster virus
- Acute disease: chickenpox
- Latent reactivated: shingles

Question 6

Mechanisms of viral virulence and injury

Answer 6

1. Preferential site infection (tropism)
   - HIV and CD4 T cells
2. Receptor-ligand interaction -> invasion
   - HIV gp120 and host CD4, SARS-2 spike and host ACE-2
3. Exploitation of host cell machinery
   - Alter viral/host translation, transcription, apoptosis
4. Antiviral immune response
   - CTL attacks on host
5. Host cell transformation
   - Oncogenic viruses e.g. EBV, HPV
6. Direct cytopathic effects e.g. HSV cell lysis

Question 7

Viral persistence

Answer 7

Selection of cell subsets ideal for long-term viral genome maintenance
- Sanctuary sites (long-lived/terminally differentiated cells)
- Sites refractory to immune surveillance
E.g.:
HSV in neurons
EBV in memory B cells
HIV in resting T cells

Question 8

Mechanisms of bacterial virulence/injury

Answer 8

1. Receptor-ligand interactions/tropism (TB C3b opsonization -> mφ)
2. Survive/replicate in host cells (TB blocks mφ phagolysosome fusion)
3. Induce host immune/inflam. response (TB -> granulomatous inflam./necrosis)

Question 9

Bacterial toxin production

Answer 9

• Endotoxins (LPS): part of Gram negative bacterial cell wall; PAMP triggering cytokine cascade
• Exotoxins: bacterial enzymes that alter host cells

Question 10

Types of exotoxins

Answer 10

1. Neurotoxins (Clostridium tetani)
2. Enterotoxins (C. diff.)
3. Superantigens; T cell cytokine activation (S. aureus)
4. Enzymatic toxins (S. aureus, C. perfringens)
5. Binary toxins (Bacillus anthracis, Corynebacterium diptheriae)

Question 11

Immune evasion examples

Answer 11

• Strep. pneumoniae: avoid phagocytosis via capsule
• M. tuberculosis: resist IC killing
• CMV, EBV: express “fake” MHC homologues
• HIV: directly infect T cells

Question 12

Types of tissue injury/inflammation

Answer 12

1. Suppurative inflammation
2. Mononuclear-granulomatous inflammation
3. Cytopathic, cytoproliferative
4. Tissue necrosis
5. Chronic inflam./scarring

Question 13

Suppurative inflammation

Answer 13

Neutrophils + necrotic tissue generating pus (pyogenic bacteria e.g. Staph. aureus, group A strep)

Question 14

Granulomatous inflammation

Answer 14

Granuloma = mononuclear inflammation + giant cells; can have caseating necrosis
e.g. M. tuberculosis

Question 15

Cytopathic and cytoproliferative tissue injury

Answer 15

Cytopathic: herpesviruses, Hep B virus
Cytoproliferative: HPV
Neoplasia induction: EBV, HPV (warts)

Question 16

Necrotizing tissue injury

Answer 16

Rapid, severe necrosis; ulcers + abscesses

Question 17

Chronic inflammation + scarring

Answer 17

Common final pathway for many infections; scarring can lead to organ dysfunction