PATHOGENESIS AND PATHOLOGY
The vast majority of E. coli that belong to the normal intestinal flora are non- pathogenic. Predisposing factors such as insufficient passive immunity in neonates, stress due to weaning and recent change in feed, a heavy grain diet and poor hygiene contribute to rapid growth and transmission of the pathogenic strains and onset of disease(20).
Pathogenicity is associated with virulence genes encoded by plasmids, bacteriophages or pathogenicity islands (PAI), including genes for enterotoxins, fimbriae or pili (plasmid-encoded), phage-encoded Shiga toxin genes, and PAI-encoded genes in EPEC and EHEC as well as UPEC(2). The main virulence factors of pathogenic E. coli are summarized in Table 30.1. Receptors for E. coli- adhesins are expressed for only the first week of life in calves and for the first 6 weeks of life in piglets(20). The relevance of E. coli as a pathogen in wild mammals is less clear. Escherichia albertii isolates from birds possessed virulence genes for intimin (eae) and cytolethal distending toxin (cdtB), suggesting that E. albertii is pathogenic to birds. However, the determinants of pathogenicity in birds remain to be clarified1-3’.In domestic animals, E. coli is a frequent cause of mastitis in cattle, pyometra and cystitis in dogs and cats, and oedema disease in swine. In poultry, respiratory or digestive exposure to large numbers of E. coli causes colisepti- caemia or colibacillosis, respectively — diseases of high economic impact. Young animals develop acute septicaemia or airsacculitis and fibrinopurulent polyserositis. Low colostral uptake predisposes neonates of some species to septicaemia. Few reports describe disease caused by E. coli in wild animals in Europe.
TABLE 30.1 Virulence factors of pathogenic E. coli and E. albertii (modified according to Amnise 2008(21); Gyles & Fairbrother, 2004(2); Oaks et al., 2010(3)).
| Organism | Virulence factors | Disease in animals |
| ETEC | Enterotoxins STI, STII | Neonatal diarrhoea, |
| (heat stable), LTI and | diarrhoea in young | |
| LTII (heat labile), fimbriae, AIDAa, EASTb 1 | animals | |
| STEC | Shiga toxin (Stx1 and/or | Diarrhoea, dysentery, |
| Stx2), intimin (eae), | oedema disease, | |
| LEEc, fimbriae, alpha | cutaneous and renal | |
| haemolysin, | glomerular | |
| extracellular serine | vasculopathy; zoonotic | |
| protease | potential | |
| EHEC | Haemolysin (HlyEHEo) | Of no significance |
| EPEC | LEE, intimin, bundle forming pili | Diarrhoea |
| EIEC | Ipad, Shigella-enterotoxin 2 | Of no significance |
| EAEC | EAST-1, plasmid encoded | Occurrence and relevance |
| protein, fimbriae | unknown | |
| DAEC | Fimbriae, AIDA-1, | Occurrence and relevance |
| intimin | unknown | |
| NTEC | Cytonecrotic factor | Enteritis, septicaemia, |
| (CNF1, CNF2), cytolethal distending toxin (CDT), fimbria, afimbrial adhesin | urinary tract infection | |
| APEC | Eerobactin, fimbriae, temperature-sensitive haemagglutinin | Septicaemia, cellulitis |
| UPEC | Eerobactin, CNF1, | Urogenital tract infection, |
| fimbriae, alpha haemolysin, iron- sequestering systems | pyometra | |
| E. albertii | Intimin, CDT | Diarrhoea |
aAIDA — adhesin involved in diffuse adherence
bEAST — heat stable enteroaggregative enterotoxin of EAEC cLEE — locus for enterocyte effacement
dIpa — Invasion plasmid associated proteins
Caseonecrotic, granulomatous lesions caused by E.
coli infection are called coligranulomas and are often found in wild birds. Preferred locations are air sacs, lungs, serosas, gastrointestinal tract and liver. Histopathologically the granulomas show central areas of caseous necrosis surrounded by a zone of cellular infiltration with macrophages, lymphocytes and abundant heterophils. A fibrous capsule surrounds the granulomas. This type of lesion, and additionally Gram- negative rods phagocytosed by giant cells, were described in a common buzzard (Buteo buteofl7'i.Escherichia albertii-associated gross lesions in a gyrfalcon (Falco rusticulos) and redpolls (Carduelis flammed) were inconsistent, but several redpolls had darkened intestines distended with excessive yellow to green digesta. Histologic findings in redpoll finches were consistent with acute, severe, fibrinous and necrotizing proventriculitis, multifocal heterophilic enteritis and small-crypt abscessation. Classic attaching-and- effacing lesions typically associated with eae-positive Escherichia were not detected. In the gyrfalcon, evidence of septicaemia was found(3).