4B - Strangles

Question 1

characteristics of microbe (Streptococcus equi spp. Equi)

Answer 1

Gram- positive 
cocci
capsule
has exotoxins
non-motile

Question 2

pathogenesis (Streptococcus equi spp. Equi)

Answer 2

how a pathogen enters (invades), multiplies, evades the immune system and causes harm

Question 3

entry (Streptococcus equi spp. Equi)

Answer 3

Inhalation or ingestion from fomites or body fluids contaminated with the bacterium
Bacterium is deposited on the mucous membranes of the nasal or oropharynx and is trapped in the mucous layer

Question 4

adhesion and invasion mechanisms (Streptococcus equi spp. Equi)

Answer 4

poorly understood
M proteins on the bacterial cell wall attach to receptors on cell membranes of mucosal and tonsillar epithelial cells
Leukocyte trafficking
bacteria spreads via lymphatics

Question 5

Leukocyte trafficking

Answer 5

macrophages and dendritic cells may phagocytose and then carry the bacteria from the mucosa to the lymph nodes
bacteria spreads via lymphatics

Question 6

harm (Streptococcus equi spp. Equi)

Answer 6

Bacterial virulence determinants
complement is activated by peptidoglycan cell wall complements which leads to chemotaxis (neutrophils are attracted to the site
bacterial cell wall protein (SeeH) causes neutrophils to release of pro-inflammatory cytokines which leads to increased vascular permeability and edema (increase in intracellular/tissue fluid)

Question 7

evades (Streptococcus equi spp. Equi)

Answer 7

the bacterium is coated in virulence proteins that disrupt phagocytosis and killing
Hyaluronic acid in the capsule blocks the action of neutrophils against the bacteria
Leukocidal toxin and streptolysin S cell membrane pore forming toxins kill leukocytes and disrupt phagocytosis leads to accumulation of large numbers of bacteria in abscesses found in lymphoid tissues
IgG binding proteins - deflect response

Question 8

fibrin (and breakdown) (Streptococcus equi spp. Equi)

Answer 8

Strep equi produces a virulence factor that causes the breakdown of fibrin allowing the bacteria to spread
(normally fibrin creates a capsule around an abscess to isolate bactera and dying neutrophils)
Strep equi streptokinase turns plasminogen (an inactive plasma protein found in the blood) into active plasmin (active plasmin hydrolyzes fibrin inhibits capsule formation)

Question 9

nasopharyngitis

Answer 9

swelling of the nasal passages and throat

Question 10

lymphadenitis

Answer 10

enlargement of the lymph nodes typically due to infection

Question 11

bacteremia

Answer 11

bacteria in the blood

Question 12

Clinical signs of strangles

Answer 12

Nasopharyngitis with lymphadenitis with formation of abscesses
Mandibular and retropharyngeal LN most frequently affected
The abscesses amy rupture and discharge pus through a sinus in the skin surface, may lead to bacteremia

Question 13

strangles as a contagious disease (how its spread)

Answer 13

Direct contact  (horse to horse) 
Fomite (feed, waterer's, clothes)
Incubation period (3-14d)

Question 14

bastard strangles

Answer 14

when bacteremia develops due to widespread distribution, abscesses develope in other parts of the body

Question 15

purpura hemorrahagica

Answer 15

blood vessels swell due to an improper immune response (response to strangles)
Ab-Ag complexes (IgG and streptococcal M-protein) deposit in the walls of small blood vessels leads to inflammaiton, clotting and hemorrhage

Question 16

purpura

Answer 16

little red or purple macules (patches) caused by hemorrhages in the skin or mucous membranes