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Microbio Exam 1 > Tissue Responses to Infection > Flashcards

Tissue Responses to Infection Flashcards

1
Q

T/F:The response an individual shows to an organism is soley dependent upon the qualities of that organism.

A

False; depends on features of the host and the organism

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2
Q

List the 6 WBCs

A
  • neutrophil
  • basophil
  • eosinophil
  • B lymphocyte
  • T lymphocyte
  • Monocyte/macrophage
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3
Q

White blood cells can be grouped into granulocytes and mononuclear cells. Divide the WBCs into these categories.

A
  • Granulocytes: neutrophil (hypersegmented), eosinophil(bilobed), basophil
  • Mononuclear: macrophage/monocyte (kidneyshaped), lymphocytes/plasma cells
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4
Q

-itis means

A

-inflammation

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5
Q

T/F: If one sees inflammation, there must be an infection.

A

False; there are MANY causes of inflammation, and infection is just one of them!

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6
Q

5 categories of microbes

A
  1. bacteria
  2. viruses
  3. fungi
  4. parasites: protozoa and helminths
  5. prions
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7
Q

Where do microbes live: intra or extracellular

  1. bacteria
  2. viruses
  3. parasites
  4. fungi
  5. prions
A
  1. either
  2. intracellular
  3. either
  4. either
  5. intracellular
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8
Q

Acute vs. chronic infection

A

Acute: rapid onset, short duration, “days”
Chronic: slower onset, longer duration, weeks, months,years

subacute is in between

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9
Q

What are the 6 categories of tissue response to infection?

A
  1. acute inflammation
  2. chronic inflammation
  3. Granulomatous inflammation (subtype of chronic)
  4. Eosinophilia
  5. Cytopathic/cytoproliferative changes
  6. Tissue necrosis
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10
Q

What are the characteristics of inflammation

A
  • rubor (red)
  • calor (hot)
  • Tumor (swelling)
  • Dolor (pain)
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11
Q

What organisms cause acute inflammation?

A
  • extracellular/pyogenic bacteria: GPC and GNR

- some extracellular fungi

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12
Q

________________________ are the first line of defense against extracellular pathogens.

A

-neutrophils and macrophages

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13
Q

What is pus?

A
  • viable and dying WBCs

- primarily neutrophils, liquified tissue and cellular debris

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14
Q

Acute tonsilitis is an example of acute inflammation. What causes it?

A

-GAS

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15
Q

Edema

A

-excess, protein-rich fluid in the interstitial spaces

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16
Q

If you were to microscopically examine exudate (pus), what would you see?

A
  • neutrophils
  • macrophages
  • protein-rich edemic fluid
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17
Q

3 potential outcomes of acute inflammation

A
  1. normal healing (usual outcome!)
  2. tissue destruction
  3. progression to chronic inflammation
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18
Q

2 examples of tissue destruction due to acute infections

A
  • abscess formation

- scarring and fibrosis

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19
Q

What organisms are associated with rapid, extensive tissue destruction and abscess formation?

A
  • Staphylococcus

- Klebsiella

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20
Q

What is an abscess?

A
  • lesion consisting of a central area of tissue necrosis and neutrophils
  • where acute inflammatory response has resulted in local destruction and replacement with a collection of neutrophils (pus)
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21
Q

How can you tell if an acute infection and become chronic? What does this signify?

A
  • inflammatory cell infiltrate will change primarily from neutrophils and macrophages to lympocytes, plasma cells, and macrophages
  • signifies a switch from innate immunity to adaptive immunity
  • acute inflammatory cells may still persist and one may see a mix of inflammation
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22
Q

Abscesses with pus are usually due to __________.

A

-Staphylococcus aureus

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23
Q

Bacterial abscesses are most common, but ________ are often seen, especially in immunocompromised hosts with decreased neutrophilic activity.

A

-fungal abscesses

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24
Q

What eventually happens to an abscess that is not resolved?

A
  • becomes surrounded by a rim of blood vessels and fibrous tissue
  • fibrosis serves to “wall off” the area of infection and necrosis
  • blood vessels in wall serve as ongoing source of neutrophils for abscess
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25
Q

What is seen within a chronic abscess?

A

-neutrophils, macrophages, necrotic tissue

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26
Q

If you see an abscess, there are 2 types of organisms that may cause is, what are they?

A
  • bacteria

- fungi

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27
Q

Vascular changes associated with acute inflammation

A
  • increased blood flow

- edema

28
Q

What will be the pathology of acute infections due to intracellular microbes?

A
  • see lymphocytic infiltrate as NK cells are first line of defense for extracellular organisms
  • early response by NK cells, followed by cell-mediated immune reactions
  • NO PUS bc no neutrophils
29
Q

A patient presents with acute infection and microscopy shows a dense lymphocytic infiltrate, what can be ruled out?

A
  • extracellular bacteria/fungi
  • this is classic sign of intracellular infection
  • usually this is an acute viral infection
30
Q

Chronic inflammation is used to describe the pattern of inflammation seen in tissues in which ___________ predominate.

A
  • mononuclear cells: lymphocytes, macrophages, plasma cells

* note the lymphocyte overlap with acute viral infections

31
Q

What are the potential infection organisms of chronic inflammation?

A
  • viruses (intracellular)
  • intracellular bacteria
  • intracellular parasites
  • spirochetes
  • any persistent infection due to any organism
32
Q

On top of the mononuclear and lymphocytic cells involved in chronic inflammation, what else is a mediating factor?

A

-cytokines

33
Q

Compare acute to chronic inflammation microscopic pathology

A

Acute: neutrophils, macrophages, edema
Chronic: lymphocytes, plasma cells, macrophages, but primarily lymphocytes

34
Q

Compare microorganism causes of acute and chronic inflammation

A
  • acute: extracellular organisms (bacteria and fungi)

- Chronic: intracellular organisms (viruses, some bacteria and fungi)

35
Q

If a patient presents with a microscopically “chronic”-looking illness, what are the potential causes?

A
  • chronic persistent infection with intracellular organisms or any hard to eradicate organisms
  • acute infection with intracellular organisms
  • *can be acute or chronic**
36
Q

Acute and chronic inflammation may co-exist when?

A

-in chronic, hard to eradicate infections of any cause

37
Q

What is the hallmark of a granuloma?

A

-a collection of activate macrophages (epithelioid cells or epithelioid histiocyte” which are large cells with abundant pink cytoplasm

38
Q

Epithelioid cells often fuse to form _______.

A

-giant cells

39
Q

What may or may not accompany granulomas in a granulomatous inflammation?

A
  • with or without a rim of lymphocytes, fibroblasts

- with or without central necrosis (caseous necrosis)

40
Q

What 2 things are involved in granuloma formation?

A
  • CD4+ T cells

- cell mediated immunity

41
Q

Steps of granuloma formation

A
  • APC present intracellular organism to CD4+ TH1 cell
  • T cell is activate and produces cytokines which recruit monocytes/macrophages from circulation to the tissue where they are needed
  • macrophages are also activated by these cytokines to increase their phagocytic activity
  • on going interactions between T cells and macrophages maintain the granuloma
42
Q

When you identify a granuloma, it indicates what? Main examples?

A

-that there has been a cell mediated response against a poorly degradable intracellular microbe

43
Q

What organisms elicit granulomatous inflammation?

A
  • intra cellular
  • poorly digestible, poorly soluble
  • resistant to eradication
  • Mycobacterium: TB!!!!!
  • Some fungi (Histoplama)
  • Some worms (Schistosoma)
44
Q

If you see granulomatous inflammation in the lungs, what should you be thinking?

A

-TB!!!

45
Q

__________ is a characteristic of TB

A

-caseous necrosis that accompanies granulomatous inflammation

46
Q

Pathology of granulomatous inflammation

A
  • epithelioid histiocytes (activated macrophages)
  • giant cells
  • lymphocytes
  • plasma cells
47
Q

Clinical presentation of granulomatous inflammation

A

-chronic infections due to a limited number of organisms (TB!!!!!, some fungi and worms)

48
Q

How to tell an abscess and caseating necrosis apart?

A
  • Microscopically: abscess have neutrophils and pus in it, while caseating necrosis doesnt have cells despite them both have necrosis tissue
  • Cultures
49
Q

Eosinophils defend against __________. How?

A
  • helminthic (worm) infections

- IgE abs bind to helminthic parasites and the Fc regions recognized by eosinophils which activates release of granules

50
Q

Why do eosinophils rely moreso on granule release that phagocytosis?

A
  • worms are extracellular organisms and are too large to be ingested
  • they are also resistant to most of the phagocytic enzymes and antimicrobial products
51
Q

Eosinophilic granules contain _________. What is good and bad about this compound?

A
  • Major basic protein

- it is toxic to helminths, but also causes extensive host tissue damage

52
Q

When we see eosinophils in the inflammatory infiltrate, we look for _______ as a potential cause.

A

-worms

53
Q

Granulomas often form in response to foreign materials, and as such may else be present with _______ infections due to eggs.

A
  • worm

* *remember granulomas can also signify hard to digest tissues, like foreign objects and eggs or parasites

54
Q

Cytopathic changes are ______ induced. What are some common features?

A
  • virus induced
  • nuclear inclusions, cytoplasmic inclusions (both due to viral aggregates) and multinucleated cells due to cell fusion, cell enlargement
  • amount of inflammation is variable
55
Q

Viruses can cause observable changes in the morphology of the cells. These changes are called ___________.

A

-cytopathic effects

56
Q

Cytomegalovirus cytopathic effects

A

-intranuclear and cytoplasmic inclusions

57
Q

Cytopathic changes see with herpes simplex virus

A

-multinucleated cells (cell fusion)

58
Q

HPV cytopathic changes

A
  • enlarged nucleus
  • binucleated
  • perinuclear halo
59
Q

Adenovirus cytopathic changes

A

-intranuclear inclusion

60
Q

T/F: Not all viruses cause cytopathic changes.

A

-True; but when they do, they give us insight into their identification

61
Q

Cytoproliferative changes are _____ mediated. What are they a mechanism for?

A
  • virus-mediated

- mechanism to transform cells into benign or malignant cells

62
Q

HPV as an example of benign and malignant cytoproliferative changes

A
  • Benign proliferative=warts; viral proteins free in cytoplasm, NOT DNA
  • Cervical cancer: viral proteins integrated into host DNA
63
Q

T/F: HPV infection alone is sufficient for the development of cancer.

A

-false; many other co-factors must be involved as well

64
Q

Characteristics of tissue necrosis

A
  • tissue damage due to toxins
  • little inflammation
  • widespread necrosis
65
Q

What can cause tissue necrosis?

A
  • toxin mediated via bacteria, parasites

- viruses

Microbio Exam 1 (13 decks)

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