Pathology of Infectious Diseases Flashcards

1
Q

infection is established if (2 factors)

A
  1. virulence factors overcome normal host defenses
    OR
  2. host defenses are compromised
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2
Q

infections can get in by various methods, including

A

-breaching epithelial surfaces
-inhalation
-sexual transmission
-vertical transmission (mother to fetus, birth, postnatal maternal milk)

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3
Q

dissemination of pathogens

A

-may remain at localized site
OR
-spread to other sites via:
*direct extension (following tissues planes of least resistance)
*lymphatics
*bloodstream
*nerves
*tissue tropism (specific tissue involvement/characteristic disease patterns)

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4
Q

evasion of defenses by pathogens

A

-antigenic variation (looking different to the immune system: expressing different surface antigens, etc)
-avoiding phagocytosis (capsule, protein A, etc)
-inactivation of complement
-suppressing adaptive immunity
-latency phase genes

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5
Q

damage mechanisms of pathogens

A
  1. direct cytotoxicity (infect a cell and kill it or transform it)
  2. indirect cytotoxicity (release toxins, killing distant cells)
  3. collateral cytotoxicity (induce host immune responses, causing tissue damage)
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6
Q

endotoxins

A

LPS in outer membrane of gram - organisms stimulates host immune responses and injury

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7
Q

exotoxins

A

secreted bacterial proteins that cause cellular injury and disease

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8
Q

spectrum of inflammatory responses to infection

A
  1. suppurative acute inflammation
  2. non-suppurative inflammation
  3. granulomatous inflammation
  4. cytopathic / cytoproliferative change
  5. necrotizing inflammation
  6. chronic inflammation
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9
Q

suppurative acute inflammation

A

neutrophilic infiltration
*response to acute infection from extracellular bacteria
*results in formation of EXUDATE (pus = neutrophils + liquefactive necrosis)

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10
Q

non-suppurative inflammation

A

**NON-neutrophilic infiltrates (eosinophils, lymphocytes, monocytes, etc)
*response to acute infections from viruses, intracellular bacteria, or parasites

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11
Q

granulomatous inflammation

A

*defined aggregates of macrophages, some combining into multi-nucleated giant cells
*T-cell mediated immune response
*response to SLOWLY DIVIDING organisms (mycobacteria, fungi)

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12
Q

cytopathic / cytoproliferative change

A

*virus-mediated cellular damage
*ABSENT host inflammatory response
1. polykaryons (cells induced to fuse, forming a blister)
2. inclusion bodies (visible viral replication within cell)
3. neoplastic cellular proliferation (b/c of oncogene expression)

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13
Q

necrotizing inflammation

A

*toxin-mediated severe tissue damage and cell death
*typically only few inflammatory cells involved
-viruses may cause necrotic inflammation when host cell damage is widespread and severe

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14
Q

what are the most relevant pathogens for necrotizing inflammation

A

*Clostridium perfringens
*group A strep

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15
Q

chronic inflammation / scarring

A

*lymphocytes/plasma cells with associated fibrosis
*final common pathway of many infections
*progressive shift in cell type at site of inflammation
*simultaneous destruction and healing

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16
Q

exit strategies for pathogens

A

release from body for transmission to other individuals:
-person to person (direct contact)
-respiratory aerosolization
-direct ingestion
-fecal-oral
-parenteral direct inoculation
-sexual
-childbirth
-zoonotic exposures

17
Q

gold standard for identifying pathogens in lab

A

culture (from a biopsy/tissue)