Bacterial Disease - Clinical and Pathological Changes Flashcards

(38 cards)

1
Q

Commensal

A
  • Stable polymicrobial communities present throughout life as part of ‘normal microflora’
  • Found on skin and hollow organs whose surfaces are exposed to environment
  • Acquired soon after birth
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2
Q

Pathogen

A
  • Microorganism which causes disease
  • Competes with normal microflora to gain foothold within niche
  • Evades or overcomes host defences
  • Expresses genes which encode factors which cause disease
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3
Q

Pathogenicity

A

Ability of a microbe to damage a host

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4
Q

Virulence

A

Relative capacity of pathogen to damage a host

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5
Q

Virulence factors

A

Bacterial traits that confer pathogenicity
* Adhesins
* Toxins
* Capsules

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6
Q

When do clinical consequences of infection occur?

A

When pathogenicity exceeds host defences

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7
Q

How do bacteria cause tissue damage?

A

Bacterial toxins
* Locally
* Systemically
Inflammatory reponse
Immune response

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8
Q

Outcomes of infection

A
  1. infection is eliminated and cleared
  2. Clinical disease occurs
    * Acute
    * Subacute
    * Chronic
  3. Subclinical infections
    * carrier for disease
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9
Q

What determines shedding of agent?

A

Severity of disease
Type of pathogen
Tissues affected

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10
Q

Carrier state

A

Intermittent shedding of agent

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11
Q

Latent infection

A

Shedding of agent if disease is reactivated

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12
Q

Clinical changes in bacterial infections

A

Pathognomonic clinical presentation
Inflammatory response (non-specific to bacteria)
Cardiovascular consequences (in advanced stages)

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13
Q

Pathognomonic clinical presentation Example

A

Erysipelas in pigs
* Specific skin lesions

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14
Q

Inflammatory response

A

Non-specific to bacteria
○ Systemic
E.g. Pyrexia (^HR, ^RR)
○ Local
E.g. pain, heat, swelling, erythema
○ Pus – neutrophils – acute
○ Granulomas – macrophages – chronic

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15
Q

Cardiovascular consequences

A

Septicaemia
○ Congested mucous membranes
“Brick” or dark red
○ Toxic line
Purple line in gums near teeth – horses

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16
Q

Clinical changes in blood during inflammation

A

Neutrophils
Acute phase proteins
Cardiovascular changes
Coagulopathy

17
Q

Neutrophil changes in inflammation

A

Number - up or down
Left-shift
□ Younger - strong response
Toxic change
□ Dysmaturation

18
Q

Toxic Change

A

Morphologic abnormalities acquired during maturation under conditions that intensely stimulate neutrophil production and shorten the maturation time in marrow
Refers to neutrophil in BLOOD
How well bone marrow is working

19
Q

Acute phase proteins

A

Fibrinogen
C Reactive Protein - dogs
Serum Amyloid A - horses/cats
Haptoglobin - cattle

20
Q

Cardiovascular changes in inflammation

A

Metabolic acidosis
Increased lactate

21
Q

Bacteraemia

A

Presence of bacteria in blood

22
Q

Septicaemia

A

Presence and replication on bacteria in blood

23
Q

Toxaemia

A

Toxins from bacterial infection present in blood

24
Q

Sepsis

A

Body’s extreme response to infection

25
Can you identify bacterial infections by examining blood under microscope?
No (unless anthrax post-mortem)
26
Clinical changes in tissue during inflammation
Number of neutrophils Type of neutrophils Macrophages - chronic or acute?
27
What is the regenerative capacity of neutrophils in dogs?
Rapid
28
What is the regenerative capacity of neutrophils in horses?
Intermediate
29
What is the regenerative capacity of neutrophils in cows?
Slow
30
What does neutropaenia indicate in dogs?
Very severe infection Can't keep up with demand
31
What does neutropaenia indicate in cows?
Common in inflammation regardless of severity Common in early infections Better to rely on haptoglobin concentration
32
What factors cause a shift from marginal to circulating pool?
* Epinephrine * Glucocorticoids * Infections * Stress
33
Left shift
More immature neutrophils due to infection * Bone marrow producing more new neutrophils * Common in acute infections
34
Regenerative
More segmented than immature Neutrophilia
35
Degenerative
More immature than segmented Neutrophilia or neutropaenia
36
Neutrophil toxic change
Sign of severe infection Rapid neutropoesis Not enough time to mature fully ○ Diffuse cytoplasmic basophilia Persistent of cytoplasmic RNA Incl segmented neutrophils ○ Döhle bodies Focal blue-grey cytoplasmic structures (RER/RNA) Foamy cytoplasm Dispersed organelles (not discrete –EDTA) Isolated finding in some healthy cats ○ Asynchronous nuclear maturation Finely granular nuclear chromatin but in “segments”
37
Coagulopathy of sepsis
Factors stimulated by sepsis which make animals pro-coagulant Microthrombi in vasculature Lower platelet counts Lower coagulation factors
38
Degernerate neutrophils
* Being broken down by body Cell is large with distended vacuolated cytoplasm * Swollen enlarged nucleus