Bacterial Colonization and in vivo Expression of F1 (Type 1) Fimbrial Antigens in Chickens Experimentally Infected with Pathogenic Escherichia coli

Abstract

Escherichia coli strains that cause septicemia of poultry often possess F1 (type 1) fimbriae (encoded by pil [fim] homologous gene clusters) and/or P fimbriae (encoded by pap homologous gene clusters). These fimbriae are thought to be involved in infection and colonization. To study the dynamics of infection due to E. coli with different virulence determinant profiles and to examine the expression of these fimbriae in vivo, three pathogenic E. coli isolates--O1 (pil+/pap+), O2 (pil+/pap), and O78 (pil+/pap+)--were administered intratracheally to 1.5-week-old chickens. Chickens were euthanatized from 3 to 144 hr after infection. The three isolates caused lesions in 30 to 55% of birds. Colonization rates of the trachea, lungs, internal organs, and pericardial fluid were similar for all three isolates, whereas significant differences among isolates were observed in colonization of the air sacs and blood. Bacteria appeared rapidly in the blood, liver, and spleen, whereas presence in the pericardial fluid generally occurred only after 24 hr postinoculation. The dynamics of colonization of the air sacs varied among isolates. Immunofluorescence of frozen tissue sections demonstrated F1 fimbriae (pil expressed) but not P fimbriae on all three isolates colonizing the trachea and on the O1 and O78 isolates colonizing the air sacs. Results suggest that F1 fimbriae are involved in the early stages of development of colisepticemia by promoting association of pathogenic E. coli with the trachea and air sacs of chickens.

Avian pathogenicEscherichia colitransmission from broiler breeders to their progeny in an integrated poultry production chain

“…Escherichia coli is present in the normal intestinal flora of birds. Only some strains with specific virulence attributes, designated as avian pathogenic E. coli (APEC), are able to cause disease such as acute colisepticaemia, fibrinopurulent polyserositis, aerosacculitis, pericarditis, salpingitis, synovitis, omphalitis, yolk sac infection, swollen head syndrome, coligranuloma, and cellulitis (Vidotto et al ., 1990;Dozois et al ., 1994;Gomis et al ., 1997;Pourbakhsh et al ., 1997;Dho-Moulin & Fairbrother, 1999). Among the virulence factors involved in the pathogenesis of colibacillosis, F1 (type 1) fimbriae have been shown to adhere to chicken respiratory epithelial cells of the pharynx and trachea (Dozois et al ., 1994;Dho-Moulin & Fairbrother, 1999), Temperature-sensitive haemagglutinin (Tsh) plays a role in the colonization of air sacs (Dozois et al ., 2000), the aerobactin ironsequestering system allows E. coli growth in a low concentration of free iron in physiological liquids such as blood (Dho-Moulin & Fairbrother, 1999) and P fimbriae are important in the later stages of infection for the adhesion to internal organs (Dho-Moulin & Fairbrother, 1999), giving resistance to phagocytosis (Pourbakhsh et al ., 1997).…”

Studies on avian pathogenic Escherichia coli in commercial broiler chicken in South East Queensland

“…Globally, the economic, public health and animal welfare significance of avian colibacillosis, has led to a number of studies from United States of America aiming to define APEC and to identify pathogenicity mechanisms (Jeffrey et al, 1999;Kariyawasam and Nolan, 2009;Norton et al, 2000). Studies have identified a large number of VGs in E. coli cultured from birds with avian colibacillosis (Antão et al, 2008;Dissanayake et al, 2014; and relevance of these VGs in the pathogenicity of avian colibacillosis is still poorly understood and the majority of studies on APEC and APEC-associated VGs are descriptive (Dozois et al, 1994;Jeffrey et al, 1999;Norton et al, 2000;Obeng et al, 2012;Zhao et al, 2009)…”

“…Both fimbriae types 1 and P adhere to tracheal epithelial cells of chickens (La Ragione et al, 2000;Yerushalmi et al, 1990). Type 1 fimbriae can be found on more than 70% of APEC cultured from the respiratory tract of birds with colibacillosis (Dho-Moulin and Fairbrother, 1999;Dozois et al, 1994;Janssen et al, 2001;Pourbakhsh et al, 1997). In contrast, P fimbriae were expressed by less than 30% of APEC strains that were colonising the respiratory system and internal organs (Pourbakhsh et al, 1997;Stordeur et al, 2004).…”

“…Dozois et al (1994) and Pourbakhsh et al (1997) reported that the expression of type 1 fimbriae only take place in the upper respiratory tract and not in any other internal organs, which suggests they have a role in initial colonisation. An early study of APEC infection by La Ragione et al (2000) was able to demonstrate the significant role of type 1 fimbriae for the adherence, colonisation and invasion of APEC into the host epithelial cells.…”

Some adhesins of avian pathogenic Escherichia coli (APEC) isolated from septicemic poultry in Brazil

“…The role of type 1 fimbriae in colibacillosis has been associated with mucus adherence and trachea and intestinal tract colonization (8,11,13,28,31,35). P fimbriae are mannose resistant hemagglutinating fimbriae present in E. coli strains causing urinary tract infections in humans and also may be expressed by some E. coli of avian origin.…”