Pathogenesis Flashcards
ETEC virulence factors and function
clinical signs
fimbriae - attachment
F4 (K88) swine
F5 (K99) calves, swine, lambs
enterotoxins
Sta & LT - Cl- secretions
Stb - secretion of serotonin & vasoactive intestinal peptide
diarrhea, no inflammation
STEC virulence factor
Stx toxins - Stx2e - shigatoxin in piglets that causes edema
Locus of Enterocyte Effacement (LEE)/intimin - attachment, T3SS
Hemolysin
Acid resistance
why are Abx controversial with STEC
Abx can activate SOS response which increases transcription of stx genes
EPEC virulence factors
clinical sign
LEE/intimin
cytoskeletal changes in enterocytes
diarrhea, mild inflammation
ExPEC virulence factors
pathogenesis
clinical signs
nonspecific virulence factors:
-LPS
-mucoid capsule production
-hemolysins
-siderophores
translocation across GI mucosa to access to the circulation
septicemia in neonates
all gram negatives have which endotoxin?
LPS
salmonella virulence factors
pathogenesis
capsule
LPS
siderophores
virulence plasmids with spv (salmonella plasmid virulence) genes
pathogenicity islands (secretion system)
bacterial-mediated endocytosis (BME) by M cells –> T3SS
Campylobacter pathogenesis
clinical signs
translocation through epithelium into lamina propria “zipper” & “trigger” mechanisms & causes cytoskeletal modulation
suppurative inflammation/IL/cytokines cause blood diarrhea
Yersinia pathogenesis
clinical signs
invasion of M cells initially
invade macrophages using T3SS
express yersinia outer proteins (YOPS) to evade phagocytosis
acute gastroenteritis/diarrhea
Brachyspira virulence factors
pathogenesis
hemolysin/cytotoxin
LPS
penetrates mucous layer of LI → coagulative necrosis of epithelium and more neutrophil influx → diarrhea
Lawsonia pathogenesis
- organisms attach to enterocytes and internalized into a vacuole
- escape vacuole and replicate in the cytoplasm
- passed on via mitosis in enterocytes
- extend along crypts
- replace goblet cells/mature enterocytes causing malabsorption
Helicobacter pathogenesis
colonization in the mucous layer of gastric mucosa results in a strong inflammatory response (GALT proliferation & neutrophils/lymphocytes)
Mycobacterium avium paratuberculosis
Johne’s Disease
excessive pro-inflammatory cytokines → macrophage infiltration
chronic, cell-mediated, minimal Ab response, gut function disturbed
C.perfringens virulence factors
pathogenesis
fibronectin-binding proteins
capsule (deters phagocytosis)
toxins (alpha, beta, epsilon, iota, E, beta-2)
pseudomembrane formation, villi necrosis, mixed inflammation & hemorrhage
C. perfringens Type A
hemorrhagic enteritis in horses
