Bacterial Disease - Clinical and Pathological Changes Flashcards
Commensal
- 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
Pathogen
- 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
Pathogenicity
Ability of a microbe to damage a host
Virulence
Relative capacity of pathogen to damage a host
Virulence factors
Bacterial traits that confer pathogenicity
* Adhesins
* Toxins
* Capsules
When do clinical consequences of infection occur?
When pathogenicity exceeds host defences
How do bacteria cause tissue damage?
Bacterial toxins
* Locally
* Systemically
Inflammatory reponse
Immune response
Outcomes of infection
- infection is eliminated and cleared
- Clinical disease occurs
* Acute
* Subacute
* Chronic - Subclinical infections
* carrier for disease
What determines shedding of agent?
Severity of disease
Type of pathogen
Tissues affected
Carrier state
Intermittent shedding of agent
Latent infection
Shedding of agent if disease is reactivated
Clinical changes in bacterial infections
Pathognomonic clinical presentation
Inflammatory response (non-specific to bacteria)
Cardiovascular consequences (in advanced stages)
Pathognomonic clinical presentation Example
Erysipelas in pigs
* Specific skin lesions
Inflammatory response
Non-specific to bacteria
○ Systemic
E.g. Pyrexia (^HR, ^RR)
○ Local
E.g. pain, heat, swelling, erythema
○ Pus – neutrophils – acute
○ Granulomas – macrophages – chronic
Cardiovascular consequences
Septicaemia
○ Congested mucous membranes
“Brick” or dark red
○ Toxic line
Purple line in gums near teeth – horses
Clinical changes in blood during inflammation
Neutrophils
Acute phase proteins
Cardiovascular changes
Coagulopathy
Neutrophil changes in inflammation
Number - up or down
Left-shift
□ Younger - strong response
Toxic change
□ Dysmaturation
Toxic Change
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
Acute phase proteins
Fibrinogen
C Reactive Protein - dogs
Serum Amyloid A - horses/cats
Haptoglobin - cattle
Cardiovascular changes in inflammation
Metabolic acidosis
Increased lactate
Bacteraemia
Presence of bacteria in blood
Septicaemia
Presence and replication on bacteria in blood
Toxaemia
Toxins from bacterial infection present in blood
Sepsis
Body’s extreme response to infection
Can you identify bacterial infections by examining blood under microscope?
No
(unless anthrax post-mortem)
Clinical changes in tissue during inflammation
Number of neutrophils
Type of neutrophils
Macrophages - chronic or acute?
What is the regenerative capacity of neutrophils in dogs?
Rapid
What is the regenerative capacity of neutrophils in horses?
Intermediate
What is the regenerative capacity of neutrophils in cows?
Slow
What does neutropaenia indicate in dogs?
Very severe infection
Can’t keep up with demand
What does neutropaenia indicate in cows?
Common in inflammation regardless of severity
Common in early infections
Better to rely on haptoglobin concentration
What factors cause a shift from marginal to circulating pool?
- Epinephrine
- Glucocorticoids
- Infections
- Stress
Left shift
More immature neutrophils due to infection
* Bone marrow producing more new neutrophils
* Common in acute infections
Regenerative
More segmented than immature
Neutrophilia
Degenerative
More immature than segmented
Neutrophilia or neutropaenia
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”
Coagulopathy of sepsis
Factors stimulated by sepsis which make animals pro-coagulant
Microthrombi in vasculature
Lower platelet counts
Lower coagulation factors
Degernerate neutrophils
- Being broken down by body
Cell is large with distended vacuolated cytoplasm - Swollen enlarged nucleus
