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Escherichia coli infections

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Datasheet

Escherichia coli infections

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Escherichia coli infections
  • Overview
  • Escherichia coli is an important cause of disease worldwide and occurs in most mammalian species, including humans, and in birds. E. coli are classified into categories or pathotypes on the basis of produc...

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Pictures

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PictureTitleCaptionCopyright
The normal architecture in this pig lung is lost below a multitude of microabscesses caused by Escherichia coli.
TitleLung of the pig; chronic bacterial pleurisy and pneumonia
CaptionThe normal architecture in this pig lung is lost below a multitude of microabscesses caused by Escherichia coli.
CopyrightStan H. Done
The normal architecture in this pig lung is lost below a multitude of microabscesses caused by Escherichia coli.
Lung of the pig; chronic bacterial pleurisy and pneumoniaThe normal architecture in this pig lung is lost below a multitude of microabscesses caused by Escherichia coli.Stan H. Done
Liver of 4 weeks old broiler covered with gelatinous exudate and pericarditis caused by E. coli.
TitlePathology. E. coli infections of poultry.
CaptionLiver of 4 weeks old broiler covered with gelatinous exudate and pericarditis caused by E. coli.
CopyrightSri Poernomo
Liver of 4 weeks old broiler covered with gelatinous exudate and pericarditis caused by E. coli.
Pathology. E. coli infections of poultry.Liver of 4 weeks old broiler covered with gelatinous exudate and pericarditis caused by E. coli.Sri Poernomo
Liver of 4 weeks old broiler covered with gelatinous exudate and pericarditis caused by E. coli.
TitlePathology. E. coli infections of poultry.
CaptionLiver of 4 weeks old broiler covered with gelatinous exudate and pericarditis caused by E. coli.
CopyrightSri Poernomo
Liver of 4 weeks old broiler covered with gelatinous exudate and pericarditis caused by E. coli.
Pathology. E. coli infections of poultry.Liver of 4 weeks old broiler covered with gelatinous exudate and pericarditis caused by E. coli.Sri Poernomo

Identity

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Preferred Scientific Name

  • Escherichia coli infections

International Common Names

  • English: avian colibacillosis, coligranuloma, colisepticemia; bacterial endocarditis in ruminants; calf septicemia, bacteremia; cellulitis; colibacillosis, escherichia coli, in birds; coliform diarrhoea; coliform mastitis; coliform mastitis in goats; coliform mastitis in sows; coliform septicaemia; coliform urinary tract infections; coliform, escherichia coli, klebsiella, mastitis in cows; colisepticaemia; colisepticemia; diarrheic syndrome with ataxia in charolais calves; diarrhoea in pigs; diarrhoea in ruminants; E. coli infections; edema disease; edema disease in swine; enteric colibacillosis; enteric colibacillosis, calf or heifer scours; enteric colibacillosis, escherichia coli, in lambs and kids; enteric colibacillosis, escherichia coli, of suckling or weaned pigs; Escherichia coli enterotoxemia; gangrenous dermatitis of chickens and turkeys; hemorrhagic enteritis in calves and sheep; mastitis in ewes due to miscellaneous bacteria; mastitis in pigs; mastitis in ruminants; meningoencephalitis, meningitis, meningoventriculitis; oculofacial respiratory disease, swollen heads syndrome in birds; oedema disease; polyserositis due to escherichia coli in young pigs; rattle belly; rattle belly in lambs; septicaemia in pigs; septicaemia in ruminants; slavers; slavery mouth; urinary tract infections in pigs; watery mouth; watery mouth disease; watery mouth syndrome in lambs; weaning, postweaning diarrhea, colibacillosis, in swine; yolk sac, navel infection, omphalitis in young chicks

Pathogen/s

Top of page Bacillus cereus
Clostridium
Escherichia coli
Proteus
Proteus anguinus
Pseudomonas
Pseudomonas aeruginosa
Staphylococcus

Overview

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Escherichia coli is an important cause of disease worldwide and occurs in most mammalian species, including humans, and in birds. E. coli are classified into categories or pathotypes on the basis of production of virulence factors and on the clinical manifestations that they cause. The most important categories in farm animals are:

  • enterotoxigenic E. coli (ETEC)
  • enteropathogenic E. coli (EPEC)
  • verotoxigenic E. coli (VTEC)
  • septicaemic E. coli (SEPEC)
  • avian pathogenic E. coli (APEC)
  • non-septicaemic extra-intestinal E. coli

The most common clinical manifestations of E. coli in pigs are:

  • neonatal diarrhoea (ETEC)
  • postweaning diarrhoea (ETEC and EPEC)
  • oedema disease (VTEC)
  • septicaemia (SEPEC)

The most common clinical manifestations of E. coli infection in calves, lambs and kids are:

  • neonatal diarrhoea (ETEC)
  • haemorrhagic gastroenteritis (VTEC)
  • septicaemic (SEPEC).

In adult ruminants, the most common form is mastitis (non-septicaemic extra-intestinal E. coli).

Certain strains of VTEC, such as those belonging to serotype O157:H7, reside in the intestinal tract of, but are not pathogenic for, ruminants and cause haemorrhagic colitis and/or haemolytic uremic syndrome in humans following ingestion of foods contaminated with these bacteria. The most common clinical manifestations of E. coli infection in birds are colisepticaemia and cellulitis (APEC).

Host Animals

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Animal nameContextLife stageSystem
Alectoris rufa (red-legged partridge)Domesticated host, Wild host
Bos grunniens (yaks)Domesticated host
Bos indicus (zebu)Domesticated host, Wild hostCattle & Buffaloes: All Stages
Bos taurus (cattle)Domesticated host, Wild hostCattle & Buffaloes: All Stages
Camelus dromedarius (dromedary camel)Domesticated host
Capra hircus (goats)
Charolais cattle
Gallus gallus domesticus (chickens)Domesticated hostPoultry: All Stages
Lama glama (llamas)Domesticated host
Lama pacos (alpacas)Domesticated host
Meleagris gallopavo (turkey)
Numida meleagris (guineafowl)
Ovis aries (sheep)Domesticated host, Wild hostSheep & Goats: All Stages
Perdix perdix (grey partridge)Domesticated host, Wild host
Phasianus colchicus (common pheasant)Domesticated host, Wild host
Sus scrofa (pigs)Domesticated host, Wild hostPigs: All Stages

Hosts/Species Affected

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Pigs and ruminants


The clinical signs of the disease depend on the interaction of a number of factors such as virulence factors of the infecting strain of E. coli, environment, and age and immune status of the animal. Other host factors such as stress and over-eating (in the case of oedema disease in pigs) can also affect clinical signs.

Newborn diarrhoea and septicaemia are observed in the first few days after birth (from 0 to 4 days of age). This is particularly prevalent in animals with a deficiency in circulating immunoglobulin due to receiving insufficient colostral antibody from the mother. This can occur in newborns if they result from the mother's first gestation, if there is inadequate maternal vaccination, mastitis or if they are removed before receiving colostrum. In young animals kept at ambient temperatures of less than 25°C, a greater incidence and severity of diarrhoea is observed.

Postweaning diarrhoea and oedema disease occur in pigs following the alimentary and immune changes and stress related to weaning.

One host factor is very influential on the disease course in pigs; up to 50% of pigs lack the receptors for F4 (K88) adhesin. Genetic resistance is passed on by Mendelian inheritance. The allele for the receptor is dominant. Hence, three different genotypes. If the sow is the resistant parent, there is no specific anti-'ETEC' antibody in the colostrum, resulting in highly sensitive piglets.

Urogenital infections affect sows and sheep during the first two weeks postpartum (Riad et al., 1999).


Poultry


Respiratory tract infection complex is most frequent in birds of 4 to 9 weeks of age. Biological stress, such as viral or Mycoplasma infections, and environmental stress, such as exposure to ammonia or overcrowding, which results in deciliation of the epithelium of the respiratory tract, predispose birds to E. coli infections.

In laying birds, avian pathogenic E. coli (APEC) may infect the oviduct via the left abdominal airsac leading to salpingitis and loss of egg laying ability (Gross, 1994).

Embryonic mortality or death of young birds, observed for up to 3 weeks following hatching, results from faecal contamination of the surface of the eggs. The risk of infection is elevated when the shell is cracked or of poor quality (Gross, 1994).

Cellulitis, also referred to as necrotic dermatitis, causes an inflammatory exudate under the abdominal skin of broiler chickens (Messier et al., 1993; Gross, 1994). It has been suggested that cellulitis is associated with health problems in some flocks, since flocks with minimal health problems tend to have few condemnations due to cellulitis (Morris, 1994). In chickens, the lesions are generally located around the cloaca and between the thighs, whereas in turkeys, lesions are located over the breast muscle and may extend ventrally to the tail head (Martin and St.Hilaire, 2001).

Systems Affected

Top of page blood and circulatory system diseases of large ruminants
blood and circulatory system diseases of poultry
blood and circulatory system diseases of small ruminants
bone, foot diseases and lameness in pigs
digestive diseases of large ruminants
digestive diseases of pigs
digestive diseases of poultry
digestive diseases of small ruminants
mammary gland diseases of large ruminants
mammary gland diseases of small ruminants
multisystemic diseases of large ruminants
multisystemic diseases of pigs
multisystemic diseases of poultry
multisystemic diseases of small ruminants
respiratory diseases of poultry
skin and ocular diseases of poultry
urinary tract and renal diseases of large ruminants
urinary tract and renal diseases of pigs
urinary tract and renal diseases of poultry
urinary tract and renal diseases of small ruminants

Distribution

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E. coli infections are widespread, occurring in all climatic, geographic and socioeconomic zones where livestock are farmed.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

BahrainAmin, 1988
ChinaCui, 1982
-JiangsuPresentWu et al., 1982; Yun et al., 1995; Hui et al., 1997; Yun et al., 1997
-JilinPresentCong PeiQing, 1997; Zhang, 1997
-ShaanxiPresentWang et al., 1996
IndiaPresentKapur et al., 1982; Tripathi and Soni, 1984; Arora et al., 1986; Sanjiv et al., 1996; Pal et al., 1999
-AssamPresentSaikia et al., 1995
-SikkimPresentMishra, 1995
IndonesiaPresentSupar, et al., 1990
-SumatraPresentSupar, 1995
IranPresentTadayon et al., 1980
IraqPresentHadad et al., 1995; Hassan and Al-Sanjary, 1999
IsraelPresentKornitzer and Tamarin, 1979; Sechter et al., 1983; Wolk et al., 1992; Brenner et al., 1993
JapanPresentNakazawa et al., 1981; Fujita et al., 1994; Ishii et al., 1997; Miyao et al., 1998
-HokkaidoPresentWada et al., 1994
JordanPresentLafi et al., 1998
Korea, Republic ofPresentCha and Kim, 1996b; Lee and Park, 1980; Chae et al., 1998
LebanonPresentBarbour et al., 1997
MalaysiaPresentBaloda et al., 1992
PakistanPresentKhan and Khan, 1997
PhilippinesPresentJoya et al., 1990
Saudi ArabiaPresentAl-Ghamdi et al., 1999
Sri LankaPresentMohammad et al., 1986; Tokhi et al., 1993
TaiwanPresentTsen et al., 1998; Chiueh et al., 1999
ThailandPresentSuthienkul et al., 1990
TurkeyPresentGenc, 1997
United Arab EmiratesPresentBailey et al., 1998

Africa

AlgeriaPresentMellata et al., 1998; Said et al., 1998
BotswanaPresentBinta et al., 1996
EgyptPresentAbdel Karim, 1978; Gab-Allah, 1995; Ibrahim et al., 1998; Sayed et al., 1998
EthiopiaPresentAbraham et al., 1992
KenyaPresentBebora et al., 1994; Kariuki et al., 1999
MoroccoPresentAmara et al., 1995
South AfricaPresentVorster et al., 1994
SudanPresentAbdelrahim et al., 1990; Obied et al., 1996
ZambiaPresentNgoma et al., 1993

North America

CanadaPresentSandhu et al., 1999
-ManitobaPresentJin et al., 2000
-OntarioPresentElfadil et al., 1996a; Elfadil et al., 1996b; Borman-Eby et al., 1993; Wilson et al., 1993; Johnson et al., 1994; Steele et al., 1997
GreenlandPresentClausen et al., 1980
MexicoPresentGonzález et al., 1990; Nevárez et al., 1997
USAPresentMorris, 1991
-IowaPresentJanke et al., 1989
-MichiganPresentHolland et al., 1999
-MinnesotaPresentJanke et al., 1989
-MontanaPresentTzipori et al., 1989; Pal et al., 1999
-NebraskaPresentJanke et al., 1989
-New YorkPresentShin et al., 1994; Lee et al., 1996
-North DakotaPresentAlstad et al., 1981
-OhioPresentLee et al., 1996
-South DakotaPresentJanke et al., 1989
-WashingtonPresentLee et al., 1996
-WisconsinPresentJanke et al., 1989

Central America and Caribbean

Costa RicaPresentPérez et al., 1998
Trinidad and TobagoPresentAdesiyun and Kaminjolo, 1992; Lambie et al., 2000

South America

ArgentinaPresentMagnasco and Odeon, 1984; Bellinzoni et al., 1990; Sanz et al., 1998; Parma et al., 2000
BrazilPresentCastro et al., 1984; Silva et al., 1994; Mores et al., 1998
-ParanaPresentSaridakis et al., 1997
-PernambucoPresentMendonÇa et al., 1996
-Rio de JaneiroPresentLázaro et al., 1994; Cerqueira et al., 1999
ChilePresentBorie et al., 1997a; Borie et al., 1997b; Pinochet et al., 1989; Zamora et al., 1999
ColombiaPresentMattar and Vasquez, 1998
VenezuelaPresentGarcía et al., 1987

Europe

AustriaPresentKöfer et al., 1992
BelgiumWieler et al., 1996a; Mainil et al., 1995; China et al., 1998; Contrepois et al., 1998; Van et al., 1999
BulgariaPresentSimeonov et al., 1981
CroatiaPresentHumski et al., 1998
Czech RepublicPresentAlexa et al., 1995a; Alexa et al., 1995b; Cízek et al., 1999
DenmarkPresentJorgensen, 1983
FinlandPresentRidell et al., 1996
FrancePresentContrepois et al., 1979; De et al., 1981; White et al., 1993; Contrepois et al., 1998; Lemoine, 1998
GermanyPresentWieler et al., 1996a; Baljer et al., 1990; Wieler et al., 1996; Karch et al., 1997; Gollnisch et al., 1999
HungaryPresentPesti and Semjen, 1976; Nagy et al., 1996
ItalyPresentCaprioli et al., 1993; Conedera et al., 1997; Mosso et al., 1998; Bonardi et al., 1999; Galiero et al., 1999
MacedoniaPresentKyriakis et al., 1997a; Kyriakis et al., 1997b
MoldovaPresentParaico and Paraico, 1994
NetherlandsPresentNabuurs et al., 1993; Heuvelink et al., 1996; Heuvelink, 1999; Heuvelink et al., 1999
NorwayPresentBinde et al., 1984
PolandPresentOsek, 1999a; Osek, 1999b; Osek, 1998
Russian FederationPresentBiswas et al., 1996
SpainPresentBlanco et al., 1993a; Blanco et al., 1993b; Blanco et al., 1996a; Blanco et al., 1996b; Blanco et al., 1996c; Blanco et al., 1997a; Blanco et al., 1997b; Blanco et al., 1997c; Blanco et al., 1997d; Blanco et al., 1998
SwedenPresentLindqvist et al., 1998
SwitzerlandPresentRutishauser et al., 1984; Busato et al., 1998; Stephan et al., 2000
UKPresentRichards et al., 1998
Yugoslavia (Serbia and Montenegro)PresentEmir, 1986

Oceania

AustraliaPresentFagan et al., 1999
-New South WalesFegan and Desmarchelier, 1999
-QueenslandPresentSidjabat-Tambunan and Bensink, 1997; Fegan and Desmarchelier, 1999; Bettelheim et al., 2000
New CaledoniaPresentCosta et al., 1990

Pathology

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Pigs


Diarrhoea


Neonatal colibacillosis often leads to death, the mortality rate can be up to 70%. If clinical signs develop, they appear rapidly and are mainly characterized by yellowish diarrhoea, commonly termed 'scouring' or 'scours'. It is clearly visible around the perineum, which becomes wet and discoloured yellowish due to faecal material. Animals are listless. Their haircoat becomes roughened and increased. Animals are dehydrated and gaunt before dying (Cooper, 2000). Gross lesions may include dehydration, dilation of the stomach with undigested milk curd, venous infarcts in the greater curvature of the stomach and dilation of the small intestine.

In postweaning colibacillosis, postmortem findings may include dehydration, dilation of the stomach, and thrombi in the mucosa of the stomach (responsible for the appearance of gastric infarcts that may cover more than the half of the fundic region), intestinal dilation caused by fluid, and congestion and hyperaemia of the small intestine. Intestinal contents vary from yellow to green, watery to mucoid with blood sometimes and a characteristic odour.

On histopathological examination, layers of E. coli are observed adhering to the mucosa of the jejunum and ileum. In many cases, there is no typical microscopic lesion (except occasionally, inflammation: infiltration of neutrophils and macrophages, congestion of the lamina propria, some haemorrhages in the intestinal lumen, and some villous atrophy) (Faubert and Drolet, 1992). ETEC bacteria colonize the crypts of Lieberkühn and cover the apex of the villi. In cases of enteric colibacillosis complicated by shock, typical microscopic lesions of haemorrhagic gastroenteritis, congestion, and microvascular fibrinous thrombi and villous necrosis may be observed in the mucosa of the stomach, small intestine, and colon.

For EPEC infections, histopathological lesions range from mild and scattered through the large and small intestine, too severe and involving mostly the caecum and colon. They include light to moderate inflammation of the lamina propria, enterocyte desquamation and some mild ulceration, and light to moderate villous atrophy in the small intestine. There is also extensive multifocal bacterial colonization of the surface epithelium by a thin layer of dark-stained coccobacilli, often oriented in a palisade pattern. Electron microscopy can show typical intimate attachment of bacteria to intestinal epithelial cells and effacement of microvilli.


Oedema Disease


In oedema disease associated with ETEC, oedema is observed at specific sites, in the region of the glandular cardia of the stomach, sometimes in the gallbladder. Oedema fluid is serogelatinous, sometimes containing blood. At times, fibrin is observed in pericardial, pleural and peritoneal cavities. There is a patchy, sublobular congestion in the lungs

In typical acute cases involving VTEC, the animals are in good condition and subcutaneous oedema is seen in the eyelids, in the frontal area, over the nasal bone, in the groin and over the belly. The subcutaneous lymph nodes are oedematous with a reddish, mottled cut surface. Variable oedema is present in the lungs and in the wall of the gall bladder. The stomach is often full of unusually dry, fresh-looking, crumbly feed. The stomach mucosa is pale and submucosal oedema of variable thickness may be observed in the cardiac region of the stomach. The small intestine may be almost completely empty, whereas the colon usually contains a moderate amount of solid material in the lumen. Submucosal oedema is occasionally observed in the wall of the caecum and the colon. The mesentery of the spiral coil of the colon and of the terminal colon is commonly oedematous, whereas the mesentery of the small intestine is often simply moist (Bertschinger, 1994).

On histopathological examination, patchy layers of adhering E. coli are typically found in the small intestines of pigs examined early in the disease. A degenerative angiopathy affecting small arteries and arterioles may be found in various organs. The mesocolon adjacent to the colic lymph nodes is frequently affected. Swelling of endothelial cells may be observed. Vascular lesions may be difficult to detect in acute cases, but are more apparent in subclinically affected and surviving pigs. In pigs surviving for several days following acute signs, lesions of focal encephalomalacia are observed in the brain stem.


Septicaemia


In acute, primary septicaemia, there may be no gross lesions, but congestion of the intestine, the mesenteric lymph nodes and the extraintestinal organs may be observed. In subacute cases, subserous or submucosal haemorrhages and fibrinous polyserositis with gross lesions of pneumonia are usually observed, and may be accompanied by fibrinopurulent arthritis and meningitis (Fairbrother and Ngeleka, 1994).

In pigs with shock and rapid death, typical histopathological lesions of septicaemia such as haemorrhagic gastro-enteritis, congestion, renal haemorrhage and thrombi in the mucosa of the stomach (leading to gastric infarcts) and small intestine are observed. These lesions probably result from the rapid release of bacterial polysaccharide from the intestine into the circulation.


Urinary tract infections


In urinary tract infection in sows, focal or diffuse mucosal hyperaemia is often present in the bladder, at times followed by ulceration with fibrinopurulent exudate. The bladder wall may then thicken. In pyelonephritis, the inflammatory process extends to the renal parenchyma with eventual fibrosis. Histopathological lesions include proliferation of goblet cells, infiltration of the epithelium by neutrophils, and of the lamina propria by mononuclear cells.


Ruminants


Diarrhoea


In cases of diarrhoea due to ETEC, extensive faecal soiling of the perineum and dehydration and generalized muscle wasting may be observed on postmortem. The small and large intestine are distended with fluid and gas and the intestinal mucosa may be shiny to the naked eye.

The intestinal mucosa usually appears normal on histopathological investigation. Lesions due to VTEC are often severe and are most common in the colon, extending to the small intestine in severe cases. Lesions include oedema, ulceration, and erosions in the large intestinal mucosa and subsequently localized and diffused haemorrhages can be observed in the intestinal lumen. There is extensive multifocal bacterial colonization of the surface epithelium by a thin layer of dark-stained coccobacilli, often oriented in a palisade pattern. Electron microscopy can show typical intimate attachment of bacteria to intestinal epithelial cells and effacement of microvilli.


Septicaemia


On postmortem examination, in peracute cases there are usually petechial haemorrhages on the epicardium and serosal surfaces and there may be enlargement of the spleen and pulmonary oedema and haemorrhage. Little dehydration is observed unless there is also enteric infection. Fibrinous polyarthritis and meningitis will be observed in chronic cases.


Mastitis


In mastitis of cows, lesions are often difficult to precisely localize because of the colour and heat of the skin, and the subcutaneous fat oedema. The exudate is creamy, sometimes like pus, with fibrin and blood. Bacteria are free or within phagocytes in the ductural and alveolar lumina. An inflammation with a massive accumulation of neutrophils in the lumina of affected glands is observed. Regional lymph nodes are often affected (Szazados and Kadas, 1974).

On histopathological investigation of animals that have died in peracute cases early in the lactation, extensive damage to the ductular and secretory systems involving most of the gland may be observed. Epithelia are denuded and large areas of interstitial tissue are haemorrhagic. Large numbers of bacteria are seen throughout the gland with evidence of bacterial phagocytosis by cells of the secretory epithelia.


Poultry


Colisepticaemia


Respiratory tract infection with APEC results in depression, fever and death (Gross, 1994; Dho-Moulin and Fairbrother, 1999). Air sacs of infected birds are thickened and often have a caseous exudate on the respiratory surface. On histopathology, oedema is the earliest change, and initial respiratory infections are characterized by aerosacculitis with serous to fibrinous exudates, an initial infiltration with heterophils and a subsequent predominance of macrophages, which is frequently followed by a general infection (perihepatitis, pericarditis). Septicaemia due to APEC may occur in adult birds. Lesions may be absent or include pericarditis, peritonitis and bile-staining and necrotic foci in the liver. APEC may infect the oviduct of laying birds via the left abdominal airsacs leading to salpingitis and loss of egg laying ability. APEC may sporadically invade the peritoneal cavity via the oviduct leading to peritonitis and death. APEC may also cause a specific syndrome called the swollen head syndrome characterized by a gelatinous oedema of the facial skin and periorbital tissues, and caseous exudate in the conjunctival sac, facial subcutaneous tissues and lacrymal gland.


Cellulitis


APEC are also associated with cellulitis or necrotic dermatitis of the lower abdomen and thighs that are not associated with clinical illness. Carcasses of affected birds are usually in good body condition. Gross lesions are mostly between 3 and 6 cm in diameter, in the skin of the postventral region, tend to be unilateral, and show moderate to severe thickening of the skin (Messier et al., 1993). The skin is discoloured and may be covered with brownish-yellow crusts. Plaques of yellowish fibrinocaseous exudate are found in the subcutaneous tissues underlying the skin lesions.

On histopathology, moderate hyperkeratosis and hyperplasia of the epidermis, fibrous thickening of the dermis with evidence of neovascularization, and diffuse infiltration of mononuclear cells and heterophils is observed in the skin lesions. There may be focal ulceration of the epidermis and coalescing granulomas, characterized by the accumulation of a fibrinocaseous exudate surrounded by a thin layer of epithelioid and multinucleated giant cells, in the subcutaneous tissues. The exudate in the subcutaneous tissues consists of cellular debris, fibrous tissue, inflammatory cells, and short Gram-negative rods. Feather follicules may be involved.

Diagnosis

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Pigs


Diarrhoea


Clinical diagnosis


Initial diagnosis is mostly based on the clinical picture which usually characterizes enteric colibacillosis, including age of the piglet, the circumstances of occurrence of the disease and manifestations such as faecal material around perineum, diarrhoea, dehydration and, potentially, death. A presumptive diagnosis may be made by the observation of an alkaline faecal pH due to the presence of secretory diarrhoeic fluid.


Lesions


Few specific pathological changes may be attributed to enteric colibacillosis. The characteristic smell of the small intestinal contents on postmortem examination is helpful in diagnosis of postweaning diarrhoea due to E. coli. It is preferable, if possible, to perform postmortem examination as soon as possible after killing a live, infected pig. On histological examination, the presence of Gram-negative bacteria usually closely adhering to the small intestinal mucosa is a strong indication of the presence of this disease.


Differential diagnosis


Enteric colibacillosis in young unweaned pigs must be differentiated from infection due to Clostridium perfringens, transmissible gastroenteritis virus, rotavirus, and coccidia. The differential diagnosis of postweaning diarrhoea and enteric colibacillosis complicated by shock, particularly when a high mortality rate is observed and at greater intervals following weaning, would include salmonellosis and transmissible gastroenteritis.


Laboratory diagnosis


Gram-staining of direct smears from rectal swabs or intestinal contents will often demonstrate a predominance of Gram-negative rods. As E. coli is part of the normal intestinal flora, of which only a small proportion are pathogenic, the diagnosis of enteric colibacillosis is strengthened by the isolation from rectal swabs or intestinal contents of pathogenic E. coli of the appropriate serogroup or, more importantly, belonging to one of the pathotypes. Rectal swabs or, preferably, samples of intestinal contents should be inoculated onto blood and MacConkey agar or other media which are selective for Enterobacteriaceae and allow differentiation of lactose-fermenting from lactose-nonfermenting, Gram-negative enteric bacilli. Use of transport medium such as alginate swabs or Stuart's medium should be considered if isolation cannot be done within 24 h.

Morphology, lactose-fermentation on MacConkey agar, and odour of colonies are a first indication of the identity of bacteria involved in the infection. Then, the species E. coli should be identified. An essential assay is to determine the capacity of colonies to transform indole, since 99% of E. coli strains are indole-positive. Identification can be completed by the citrate assay (E. coli are not able to use citrate as the only carbon source) and by the methyl red assay. Colonies of F4(K88)- and F18-positive enterotoxigenic strains are almost always haemolytic on blood agar. However, it should be remembered that F5(K99)-positive and other enterotoxigenic E. coli involved in enteric colibacillosis are usually not haemolytic.

Pathogenic E. coli may be identified by serotyping, since a small number of specific O groups have been associated with enteric disease. Hence, a diagnostic laboratory can use OK typing sera to obtain a presumptive diagnosis (Wray and Woodward, 1997). This may be carried out in most laboratories using a suspension of live bacteria as the antigen and pools of OK antiserum, in the slide agglutination test. O serotyping may be carried out by slide and tube agglutination using specific O typing sera and bacterial suspensions heated at 100?C or autoclaved for 2.5 h. Complete O and H serotyping can only be carried out in a few reference laboratories.

Pathotyping, or determination of the virulence factors, is a more definitive way of identifying pathogenic E. coli associated with enteric disease. See the pathogen datasheet on E. coli for a list of the pathotypes most commonly associated with diarrhoea in pigs. Until recently, detection of enterotoxins and cytotoxins has been based on tests for biological activity. STa activity may be determined in the infant mouse test, STb in pig and rat ligated gut loops and LT and Stx in cell culture assays. However, these tests require access to animal care facilities and equipment that are more likely to be found in research and reference laboratories. ELISA tests have been developed for the detection of Stx-producing cultures or for direct detection of the Stx-producing bacteria in the faeces and may be used more widely in diagnostic laboratories (Ball et al., 1994; Mainil, 1999).

Slide agglutination is a simple and easy method for detecting fimbrial adhesins, which are expressed in culture media, and does not use any sophisticated equipment (Mosso et al., 1998). However, bacteria must be grown on the appropriate media. For instance, F5(K99) and F41 are only produced when the bacteria are grown in special minimal glucose media such as Minca, and F6 (987P) is often poorly produced in culture conditions. Reagents for latex slide agglutination assays are also available from some laboratories. ELISA is also used to determine the presence of adhesins (Nagy et al., 1996; Vazquez et al., 1996) or toxins. A diagnosis of enteric colibacillosis may also be confirmed by the detection of pathogenic E. coli adhering to the intestinal mucosa directly in infected pigs by examination of frozen sections using indirect immunofluorescence, or by examination of formalin-fixed, paraffin-embedded tissues by using immunohistochemistry.

Currently, genotypic analysis is more commonly used to identify the pathotypes involved in an infection. Techniques include colony or DNA hybridization (Mainil et al., 1998; Mellata et al., 1998), and polymerase chain reaction (PCR) (Bertin et al., 1996; Ascon et al., 1998; Meng et al., 1998; Nataro and Kaper, 1998; Tsen et al., 1998). These tests permit the detection of genes encoding for virulence factors such as toxins and adhesins. Primers recognizing different genes related to toxins (STa, STb, EAST-1 or LT) and adhesins (F4, F5, F18, F41...) for ETEC strains; attachment and effacement, such as eae; VT (Stx) for VTEC strains (China et al., 1998; Franck et al., 1998; Mainil, 1999) are readily available and can be used to perform PCR, or to prepare genetic probes for DNA hybridization. Gene probe techniques often involve the use of radioactivity and must therefore be performed in controlled laboratory conditions. Nonradioactive gene probes are being developed and could be used in kits for the detection of pathogenic E. coli directly in the faeces or intestinal contents. Multiplex PCR amplification may be used to detect the genes encoding for the virulence factors of pathogenic E. coli associated with diarrhoea in pigs, either in culture or directly in the faeces or intestinal contents. However, inhibitors may be present in clinical samples and even in certain culture media such as MacConkey. DNA purification kits are now commercially available and allow the successful preparation of DNA from clinical samples. As E. coli grow rapidly and easily in routine culture conditions, it may often be simpler and less costly to perform the PCR on DNA prepared from bacteria in broth culture or in individual colonies from agar plates. The former is more rapid, and indicates the presence of pathogenic E. coli, but does not permit the identification of specific pathotypes, as is possible when colonies are tested.

PCR may also be used to detect pathogenic E. coli directly in situ in formalin-fixed, paraffin-embedded tissues.


Oedema disease


Clinical diagnosis


Diagnosis of acute oedema disease is based on sudden appearance and neurological signs such as partial ataxia or a staggering gait in normal pigs 1-2 weeks after weaning. Subcutaneous oedema in the palpebrae and over the frontal bones is indicative of oedema disease, if present. There may be sudden death of pigs that were growing fast and in good body condition.


Lesions


Oedema helps to confirm the diagnosis, but is not always present. Hence, it may be helpful to examine more than one pig and to examine lesions on histopathology. Oedema can be most easily seen in the mesentery of the colon and the wall of the stomach.


Differential diagnosis


For sudden death, differential diagnosis includes dietetic microangiopathy and circulatory failure. For pigs showing nervous signs, differential diagnosis includes enteroviral polioencephalomyelitis, Aujeszky's disease (pseudorabies), meningoencephalitis due to Streptococcus suis or Haemophilus parasuis, or water deprivation.


Laboratory diagnosis


Isolation and identification of the E. coli from the small intestine and colon should be carried out as described for E. coli diarrhoea. In acute cases, bacteriological examination should demonstrate pure cultures of haemolytic E. coli on blood agar and identification of E. coli strains of the appropriate pathotypes and serotypes. However, in protracted cases, bacterial numbers decrease rapidly and the causative E. coli may not always be detected.


Septicaemia


Clinical diagnosis


Septicaemia due to E. coli is suspected with the appearance of the clinical signs described in the section on Disease Course.


Lesions


In most cases, postmortem lesions are useful in making a diagnosis.


Differential diagnosis


If lesions of polyserositis are present, the differential diagnosis includes Mycoplasma hyorhinis and Haemophilus parasuis. In the former, mortality is lower and lesions are detected later after infection. In the latter, exudates tend to be more serofibrinous and infection is observed rarely in the early suckling period but more often in pigs of 2-3 months of age. A differential diagnosis can be easily established after laboratory examination.


Laboratory diagnosis


Diagnosis is confirmed by the isolation in pure culture or in predominance of E. coli, particularly of one of the SEPEC serogroups or pathotypes, from the blood or extraintestinal organs of affected pigs. It should be remembered that SEPEC may be present in the intestinal contents of clinically normal as well as septicaemic pigs. Diagnosis of secondary septicaemia due to ETEC is confirmed by the isolation in pure culture or in predominance of E. coli belonging to one of the ETEC pathotypes, from the blood or extra-intestinal organs of affected pigs.


Urinary tract infections


Clinical diagnosis


Clinical diagnosis is mainly based on the presence of exudate in the urine.


Lesions


Cystitis or pyelonephritis may be seen in culled sows.


Differential diagnosis


This includes urinary tract infection (UTI), particularly pyelonephritis caused by Actinobaculum suis, and non-specific infection caused by a variety of bacterial species.


Laboratory diagnosis


In UTI, a bacteriological examination of urine is very important but is complicated by the presence of normal flora in the vagina and distal part of urethra. Thus, an E. coli infection is diagnosed if a viable count of higher than 105 is obtained. Urine pH becomes strongly alkaline in A. suis infections. Cytological analysis could complete the diagnosis by distinguishing bacteriuria, cystitis, and pyelonephritis.

Measuring the blood urea is also an indicator of UTI, rates of higher than 10 mmol/L being indicative of uraemia.

Care should be taken to avoid contact with urine when collecting samples, as Leptospira, which are pathogenic for humans may be present.


Ruminants


Diarrhoea


Clinical diagnosis


It is not possible to make a clinical diagnosis of enteric colibacillosis. Diarrhoea due to ETEC is mostly observed in calves up to 3 days of age. Diarrhoea or dysentery due to VTEC is usually observed in calves from 2 to 8 weeks of age.


Lesions


Distension of the small and large intestine with fluid and gas are observed in diarrhoea due to ETEC, but may also be observed in diarrhoea due to other causes. In diarrhoea due to ETEC, the intestinal mucosa is shiny and intact macroscopically and appears normal on histopathology. In diarrhoea or dysentery due to VTEC, hyperaemia of the distal small and large intestinal mucosa are usually observed macroscopically. On histopathology, focal and diffuse colonization of the distal small and large intestinal mucosa with Gram-negative rods and associated attaching and effacing lesions are observed. It is preferable, if possible, to perform a postmortem examination as soon as possible after killing a live calf with diarrhoea or dysentery.


Differential diagnosis


The differential diagnosis of diarrhoea due to ETEC includes diarrhoea due to rotavirus, coronavirus, and Cryptosporidium. Diarrhoea due to rotavirus and coronavirus is observed in calves from 3 days to 2 weeks of age, whereas diarrhoea due to Cryptosporidium is mostly observed in calves from 5 days to 6 weeks of age. The differential diagnosis may also include diarrhoea due to Salmonella spp. and coccidia.

The differential diagnosis of dysentery due to VTEC includes salmonellosis.


Laboratory diagnosis


As E. coli is part of the normal intestinal flora, of which only a small proportion are pathogenic, the diagnosis of enteric colibacillosis is strengthened by the isolation from rectal swabs or intestinal contents of pathogenic E. coli of the appropriate serogroup or, more importantly, belonging to one of the pathotypes. Rectal swabs or, preferably, samples of intestinal contents should be inoculated onto blood and MacConkey agar or other media which are selective for Enterobacteriaceae and allow differentiation of lactose-fermenting from lactose-nonfermenting Gram-negative enteric bacilli. Use of transport medium such as alginate swabs or Stuart's medium should be considered if isolation cannot be done within 24 hours.

Morphology, lactose-fermentation on MacConkey agar, and odour of colonies are a first indication of the identity of bacteria involved in the infection. Then, the species E. coli should be identified. An essential assay is to determine the capacity of colonies to transform indole, since 99% of E. coli strains are indole-positive. Identification can be completed by the citrate assay (E. coli are not able to use citrate as the only carbon source) and by the methyl red assay. F5(K99)-positive and other enterotoxigenic E. coli involved in enteric colibacillosis in calves are usually not haemolytic.

Pathogenic E. coli may be identified by serotyping, since a small number of specific O groups have been associated with enteric disease. Hence, a diagnostic laboratory can use OK typing sera to obtain a presumptive diagnosis (Wray and Woodward, 1997). This may be carried out in most laboratories using a suspension of live bacteria as the antigen and pools of OK antiserum, in the slide agglutination test. O serotyping may be carried out by slide and tube agglutination using specific O typing sera and bacterial suspensions heated at 100°C or autoclaved for 2.5 h. Complete O and H serotyping can only be carried out in a few reference laboratories.

Pathotyping, or determination of the virulence factors, is a more definitive way of identifying pathogenic E. coli associated with enteric disease. See datasheet on Escherichia coli for the pathotypes most commonly associated with diarrhoea in calves. Until recently, detection of enterotoxins and cytotoxins was based on tests for biological activity. STa activity may be determined in the infant mouse test, and Stx in cell culture assays. However, these tests require access to animal care facilities and equipment that are more likely to be found in research and reference laboratories. ELISA tests have been developed for the detection of Stx-producing cultures or for direct detection of the Stx-producing bacteria in the faeces and may be used more widely in diagnostic laboratories (Ball et al., 1994; Mainil, 1999).

Slide agglutination is a simple and easy method to determine the presence of fimbrial adhesins that are expressed in culture media (Mosso et al., 1998). However, bacteria must be grown on the appropriate media. For instance, F5(K99) and F41 are only produced when the bacteria are grown in special minimal glucose media such as Minca. Reagents for latex slide agglutination assays are also available from some laboratories. ELISA is also used to determine the presence of adhesins (Nagy et al., 1996; Vazquez et al., 1996) or toxins. A diagnosis of enteric colibacillosis may also be confirmed by the detection of pathogenic E. coli adhering to the intestinal mucosa directly in infected calves by examination of frozen sections using indirect immunofluorescence or by examination of formalin-fixed, paraffin-embedded tissues using immunohistochemistry.

Currently, genotypic analysis is more commonly used to define the pathotypes involved in an infection. Techniques include colony or DNA hybridization (Mainil et al., 1998; Mellata et al., 1998), and polymerase chain reaction (PCR) (Bertin et al., 1996; Ascon et al., 1998; Meng et al., 1998; Nataro and Kaper, 1998; Tsen et al., 1998). These tests permit the detection of genes encoding for virulence factors such as toxins and adhesins. Primers recognising different genes related to toxins (STa) and adhesins (F5, F41) for ETEC strains; attachment and effacement, such as eae; VT (Stx) for VTEC strains (China et al., 1998; Franck et al., 1998; Mainil, 1999) are readily available and can be used to perform PCR, or to prepare genetic probes for DNA hybridization. Gene probe techniques often involve the use of radioactivity and thus must be performed in controlled laboratory conditions. Nonradioactive gene probes are being developed and could be used in kits for the detection of pathogenic E. coli directly in the faeces or intestinal contents. Multiplex PCR amplification may be used to detect the genes encoding for the virulence factors of pathogenic E. coli associated with diarrhoea in calves, either in culture or directly in the faeces or intestinal contents. However, inhibitors may be present in clinical samples and even in certain culture media such as MacConkey. DNA purification kits are now commercially available and allow the successful preparation of DNA from clinical samples. As E. coli grow rapidly and easily in routine culture conditions, it may often be simpler and less costly to perform the PCR on DNA prepared from bacteria in broth culture or in individual colonies from agar plates. The former is more rapid, and indicates the presence of pathogenic E. coli, but does not permit the identification of specific pathotypes, as is possible when colonies are tested.

PCR may also be used to detect pathogenic E. coli directly in situ in formalin-fixed, paraffin-embedded tissues.


Septicaemia


Clinical diagnosis


Septicaemia is a common problem in debilitated newborn ruminants. Blood culture studies of debilitated calves indicate that Gram-negative bacteria account for approximately 80% of bacterial isolates, E. coli being the most frequently isolated bacteria. The spectrum of clinical signs associated with septicaemia depends on the integrity of the host immune system, the duration of illness, the severity and route of infection, the target organs, and are not exclusive to E. coli septicaemia. Early in the clinical course of disease, clinical signs are usually non-existent or vague, non-specific, and easily attributed to other diseases.


Lesions


Septicaemia in newborn ruminants commonly involves multiple organs, with the respiratory and gastrointestinal systems most commonly affected (Smith, 2001). As fever is inconsistently present in septicaemic animals; the possibility of septicaemia should never be ruled out because of the absence of fever.


Differential diagnosis


The differential diagnosis of E. coli septicaemia in calves includes septicaemia due to other bacteria such as other Enterobacteriaceae, Streptococcus sp and Pasteurella sp. Septicaemia due to these organisms tends to be more sporadic than that due to E. coli.


Laboratory diagnosis


Positive blood culture results are essential to make the diagnosis of septicaemia. However, it is clear that treatment cannot be delayed until the results of blood cultures are obtained. Blood cultures are easy to perform but must be done carefully for accurate results. Blood must be withdrawn from the vein aseptically and deposited into both the aerobic and anaerobic blood culture bottles. A liquid or solid blood culture medium can be used. Popular culture media are Columbia Broth Medium with sodium polyanetholsulfonate as anticoagulant for aerobic cultures (Septi-Chek, Roche Laboratories, USA) and a brain-heart infusion media for anaerobic cultures. Further tests should be performed on each positive culture for standard E. coli identification (see Laboratory Diagnosis of diarrhoeic ruminants). Diagnosis is confirmed by the isolation in pure culture or in predominance of E. coli, particularly of one of the SEPEC serogroups or pathotypes, from the blood or extraintestinal organs of affected calves. SEPEC may be present in the intestinal contents of clinically normal as well as septicaemic calves.


Mastitis


Clinical diagnosis


Acute mastitis is often characterized by a swollen, painful gland that may be oedematous or very hard, making if difficult for the animal to walk normally. Systemic signs may be slight or severe, with a sudden onset. Anorexia, depression, and elevated rectal temperature are often associated with this clinical event. Severe, toxic cases may have low serum calcium and paraplegia resembling milk fever (Smith, 2001).


Lesions


Acute mastitis is often characterized by a swollen, painful gland that may be oedematous or very hard (Smith, 2001).


Differential diagnosis


Mastitis must be distinguished from other mammary abnormalities, such as periparturient udder oedema, passive congestion of udder, rupture of suspensory ligament and haematomas. Blood may be found in the milk of recently-calved cows (Radostits et al., 2000). Peracute E. coli mastitis can appear similar to parturient hypocalcaemia. The differential diagnosis of E. coli mastitis includes mastitis due to other coliforms such as Enterobacter aerogenes and Klebsiella spp. or to other pathogenic bacteria.


Laboratory diagnosis


Culture of mammary gland secretions or suspected milk should be carried out when E. coli mastitis is suspected. A somatic cell count can be performed both on milk samples from individual cows and on bulk tank milk. Indirect testing for subclinical mastitis can be performed using the California Mastitis Test, or the Hymast diagnostic kit in order to differentiate between Gram-positive and Gram-negative pathogens in the case of clinical mastitis (Radostits et al., 2000). Identification of E. coli isolates can be performed using standard techniques. No predominant pathotypes or O-serotypes are found in E. coli isolates from mastitis, although serum-resistance is a consistent characteristic of these isolates.


Poultry


Colisepticaemia


Clinical diagnosis


The symptoms observed may vary greatly. Birds in apparently good condition may die without any apparent morbidity. However, in most cases birds are listless with ruffled feathers and indications of fever. Symptoms including laboured breathing, occasional coughing and rales may be apparent.


Lesions


Acute septicaemic infection may result in sudden death with few or no lesions apparent. Common lesions include dehydration, swelling and congestion of the liver and spleen and kidneys and pinpoint haemorrhages in the viscera. Infected air sacs are thickened and often have caseous exudates on the respiratory surface. Females may develop chronic salpingitis characterized by a large caseous mass in a dilated, thin-walled oviduct.


Differential diagnosis


Many other organisms (viruses, mycoplasmas, staphylococci, salmonellae, Streptobacillus moniliformis, Chlamydia, Bacillus spp.) can cause the same lesions as those caused by E. coli.


Laboratory diagnosis


Laboratory diagnosis is necessary since coliform infection in its various forms may resemble and be easily confused with many other diseases. Pathogenic organisms may be isolated and identified. Cultures should be taken from affected tissues such as the liver, spleen, pericardial sac and marrow, taking great care to avoid contamination from intestinal contents. Material should be streaked on appropriate media (eosin methylene blue (EMB), MacConkey, or tergitol-7 agar). Care must be taken to avoid faecal contamination of samples. Biochemical and serological tests should be used to confirm the presence of E. coli. The presence of virulence factors (aerobactin, serum resistance, P fimbriae, K1 capsule or TSH) may help to confirm the identification of the isolates as APEC (Dho-Moulin and Fairbrother, 1999).


Cellulitis


Clinical diagnosis


Birds with cellulitis are in apparently good condition. It is difficult to detect cellulitis before processing without closely examining the breast area of affected birds. The lesions are generally noted on postmortem inspection.


Lesions


Avian cellulitis, recognized as an inflammatory process, is characterized by lesions located in the skin between the thigh and midline. Lesions are sheets of caseated, heterophilic exudate in subcutaneous tissues.


Differential diagnosis


Cellulitis lesions result from secondary bacterial infection of skin wounds (Messier et al., 1993). E. coli is the commonest isolated organism from lesions in chickens (Messier et al., 1993). However, other bacteria including Enterobacter agglomerans, Pasteurella multocida, Proteus vulgaris and Pseudomonas aeruginosa may be isolated from cellulitis lesions (Vaillancourt et al., 1992).

According to Martin and St-Hilaire (2001) one quarter of the cellulitis lesions from turkeys contained no bacterial pathogens, one fifth yielded E. coli only, one fifth yielded E. coli in combination with other organisms and approximately one third yielded other bacteria including Staphylococcus, Streptococcus, Proteus, Pseudomonas, Arcanobacterium and Corynebacterium.


Laboratory diagnosis


Swabs from cellulitis lesions should be streaked on appropriate media (eosin methylene blue (EMB), MacConkey, or tergitol-7 agar). Care must be taken to avoid faecal contamination of samples. Biochemical and serological tests should be used to confirm the presence of E. coli. The presence of virulence factors (aerobactin, serum resistance, P fimbriae, K1 capsule, TSH) may help to confirm the identification of the isolates as APEC (Dho-Moulin and Fairbrother, 1999).

List of Symptoms/Signs

Top of page
SignLife StagesType
Acoustic Signs / Purulent, mucoid discharge, excess wax, foul odour, ears Sign
Cardiovascular Signs / Absent p waves Sign
Cardiovascular Signs / Arrhythmia, irregular heart rate, pulse Sign
Cardiovascular Signs / Arrhythmia, irregular heart rate, pulse Sign
Cardiovascular Signs / Atrial fibrillation Sign
Cardiovascular Signs / Atrial fibrillation Sign
Cardiovascular Signs / Heart murmur Sign
Cardiovascular Signs / Jugular pulse Sign
Cardiovascular Signs / Palpable precordial thrill Sign
Cardiovascular Signs / Peripheral venous distention, jugular distention Sign
Cardiovascular Signs / Prolonged capillary refill time Sign
Cardiovascular Signs / Sinus tachycardia Sign
Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate Cattle & Buffaloes:Calf Sign
Cardiovascular Signs / Ventricular premature beat, multifocal or unifocal Sign
Cardiovascular Signs / Weak pulse, small pulse Cattle & Buffaloes:Calf Sign
Digestive Signs / Abdominal distention Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Cattle & Buffaloes:Calf,Pigs:Gilt,Pigs:Sow Sign
Digestive Signs / Ascites, fluid abdomen Sign
Digestive Signs / Bilateral ping, auscultable gas filled viscus both sides Sign
Digestive Signs / Bloat in ruminants, tympany Sign
Digestive Signs / Bloody stools, faeces, haematochezia Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
Digestive Signs / Decreased amount of stools, absent faeces, constipation Sign
Digestive Signs / Decreased amount of stools, absent faeces, constipation Sign
Digestive Signs / Decreased amount of stools, absent faeces, constipation Sign
Digestive Signs / Diarrhoea Cattle & Buffaloes:Calf,Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
Digestive Signs / Dysphagia, difficulty swallowing Sign
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism Sign
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism Sign
Digestive Signs / Grinding teeth, bruxism, odontoprisis Sign
Digestive Signs / Grinding teeth, bruxism, odontoprisis Sign
Digestive Signs / Grinding teeth, bruxism, odontoprisis Sign
Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly Sign
Digestive Signs / Melena or occult blood in faeces, stools Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
Digestive Signs / Mucous, mucoid stools, faeces Sign
Digestive Signs / Mucous, mucoid stools, faeces Sign
Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears Sign
Digestive Signs / Ping left side, auscultable gas filled viscus Sign
Digestive Signs / Ping right side, auscultable gas filled viscus Sign
Digestive Signs / Rumen hypomotility or atony, decreased rate, motility, strength Cattle & Buffaloes:Calf Sign
Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears Sign
Digestive Signs / Unusual or foul odor, stools, faeces Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
Digestive Signs / Vomiting or regurgitation, emesis Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Diagnosis
General Signs / Abnormal proprioceptive positioning, knuckling Sign
General Signs / Abnormal proprioceptive positioning, knuckling Sign
General Signs / Ataxia, incoordination, staggering, falling Cattle & Buffaloes:Calf Sign
General Signs / Cyanosis, blue skin or membranes Cattle & Buffaloes:Calf,Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
General Signs / Decreased, absent thirst, hypodipsia, adipsia Sign
General Signs / Dehydration Cattle & Buffaloes:Calf,Pigs:Piglet,Pigs:Weaner Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Fever, pyrexia, hyperthermia Cattle & Buffaloes:Calf Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Generalized weakness, paresis, paralysis Cattle & Buffaloes:Calf,Cattle & Buffaloes:Cow Sign
General Signs / Haemorrhage of any body part or clotting failure, bleeding Sign
General Signs / Head, face, ears, jaw weakness, droop, paresis, paralysis Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area Sign
General Signs / Hypothermia, low temperature Cattle & Buffaloes:Calf,Pigs:Piglet,Pigs:Weaner Sign
General Signs / Inability to stand, downer, prostration Cattle & Buffaloes:Calf,Cattle & Buffaloes:Cow,Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
General Signs / Increased mortality in flocks of birds Poultry:All Stages Sign
General Signs / Kyphosis, arched back Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
General Signs / Lack of growth or weight gain, retarded, stunted growth Poultry:Young poultry,Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes Sign
General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia Cattle & Buffaloes:Calf Sign
General Signs / Opisthotonus Sign
General Signs / Opisthotonus Sign
General Signs / Opisthotonus Sign
General Signs / Opisthotonus Sign
General Signs / Opisthotonus Sign
General Signs / Oral cavity, tongue swelling, mass in mouth Sign
General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass Sign
General Signs / Pale mucous membranes or skin, anemia Sign
General Signs / Pale mucous membranes or skin, anemia Sign
General Signs / Pale mucous membranes or skin, anemia Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Sign
General Signs / Petechiae or ecchymoses, bruises, ecchymosis Cattle & Buffaloes:Calf Sign
General Signs / Polydipsia, excessive fluid consumption, excessive thirst Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Stiffness or extended neck Sign
General Signs / Sudden death, found dead Pigs:All Stages Sign
General Signs / Swelling mass vagina Sign
General Signs / Swelling of the limbs, legs, foot, feet, in birds Sign
General Signs / Swelling, mass, prolapse, cloaca Sign
General Signs / Tenesmus, straining, dyschezia Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
General Signs / Tetraparesis, weakness, paralysis all four limbs Sign
General Signs / Tetraparesis, weakness, paralysis all four limbs Sign
General Signs / Tetraparesis, weakness, paralysis all four limbs Sign
General Signs / Torticollis, twisted neck Sign
General Signs / Torticollis, twisted neck Sign
General Signs / Trembling, shivering, fasciculations, chilling Cattle & Buffaloes:Calf,Pigs:Piglet,Pigs:Weaner Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Cattle & Buffaloes:Calf,Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
General Signs / Weight loss Cattle & Buffaloes:Calf,Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
Musculoskeletal Signs / Forelimb spasms, myoclonus Sign
Musculoskeletal Signs / Hindlimb spasms, myoclonus Sign
Nervous Signs / Abnormal behavior, aggression, changing habits Sign
Nervous Signs / Abnormal behavior, aggression, changing habits Sign
Nervous Signs / Circling Sign
Nervous Signs / Coma, stupor Sign
Nervous Signs / Coma, stupor Sign
Nervous Signs / Coma, stupor Sign
Nervous Signs / Coma, stupor Sign
Nervous Signs / Coma, stupor Sign
Nervous Signs / Constant or increased vocalization Sign
Nervous Signs / Constant or increased vocalization Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Cattle & Buffaloes:Calf,Cattle & Buffaloes:Cow,Poultry:All Stages,Pigs:All Stages Sign
Nervous Signs / Excitement, delirium, mania Sign
Nervous Signs / Head pressing Sign
Nervous Signs / Head tilt Sign
Nervous Signs / Head tilt Sign
Nervous Signs / Head tilt Sign
Nervous Signs / Head, face, neck, tongue hypoesthesia, anesthesia Sign
Nervous Signs / Hyperesthesia, irritable, hyperactive Sign
Nervous Signs / Propulsion, aimless wandering Sign
Nervous Signs / Propulsion, aimless wandering Sign
Nervous Signs / Seizures or syncope, convulsions, fits, collapse Sign
Nervous Signs / Seizures or syncope, convulsions, fits, collapse Sign
Nervous Signs / Seizures or syncope, convulsions, fits, collapse Sign
Nervous Signs / Seizures or syncope, convulsions, fits, collapse Sign
Nervous Signs / Tetany Sign
Nervous Signs / Tremor Sign
Nervous Signs / Tremor Sign
Nervous Signs / Tremor Sign
Nervous Signs / Tremor Sign
Ophthalmology Signs / Abnormal pupillary response to light Cattle & Buffaloes:All Stages Sign
Ophthalmology Signs / Anisocoria Sign
Ophthalmology Signs / Blepharospasm Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling Sign
Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling Sign
Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling Sign
Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature Cattle & Buffaloes:All Stages Sign
Ophthalmology Signs / Conjunctival, scleral, redness Cattle & Buffaloes:All Stages Sign
Ophthalmology Signs / Corneal edema, opacity Sign
Ophthalmology Signs / Enophthalmos, sunken eyes Sign
Ophthalmology Signs / Exophthalmos, eyes protruding, proptosis Sign
Ophthalmology Signs / Exophthalmos, eyes protruding, proptosis Sign
Ophthalmology Signs / Hypopyon, lipid, or fibrin, flare, of anterior chamber Sign
Ophthalmology Signs / Hypopyon, lipid, or fibrin, flare, of anterior chamber Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Sign
Ophthalmology Signs / Miosis, meiosis, constricted pupil Sign
Ophthalmology Signs / Miosis, meiosis, constricted pupil Sign
Ophthalmology Signs / Mydriasis, dilated pupil Cattle & Buffaloes:All Stages Sign
Ophthalmology Signs / Nystagmus Sign
Ophthalmology Signs / Nystagmus Sign
Ophthalmology Signs / Papilledema, increased size optic nerve Sign
Ophthalmology Signs / Prolapsed third eyelid, protrusion nictitating membrane Sign
Ophthalmology Signs / Purulent discharge from eye Sign
Ophthalmology Signs / Strabismus Sign
Pain / Discomfort Signs / Ocular pain, eye Sign
Pain / Discomfort Signs / Pain mammary gland, udder Cattle & Buffaloes:Cow,Pigs:Sow Sign
Pain / Discomfort Signs / Pain on external abdominal pressure Sign
Pain / Discomfort Signs / Pain on external abdominal pressure Sign
Pain / Discomfort Signs / Pain, neck, cervical, throat Sign
Reproductive Signs / Abnormal length estrus cycle, long, short, irregular interestrus period Cattle & Buffaloes:Cow Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow Sign
Reproductive Signs / Agalactia, decreased, absent milk production Pigs:Sow Sign
Reproductive Signs / Bloody milk, red, pink, brown milk Cattle & Buffaloes:Cow Sign
Reproductive Signs / Cold mammary gland, cool udder Cattle & Buffaloes:Cow Sign
Reproductive Signs / Decreased hatchability of eggs Poultry:Embryo Sign
Reproductive Signs / Decreased, dropping, egg production Sign
Reproductive Signs / Edema of mammary gland, udder Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow Sign
Reproductive Signs / Firm mammary gland, hard udder Cattle & Buffaloes:Cow,Pigs:Sow Sign
Reproductive Signs / Mastitis, abnormal milk Cattle & Buffaloes:Cow Sign
Reproductive Signs / Slough of mammary gland, udder Sign
Reproductive Signs / Slough of mammary gland, udder Sign
Reproductive Signs / Warm mammary gland, hot, heat, udder Cattle & Buffaloes:Cow,Pigs:Sow Sign
Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign
Respiratory Signs / Change in voice, vocal strength Sign
Respiratory Signs / Change in voice, vocal strength Sign
Respiratory Signs / Coughing, coughs Sign
Respiratory Signs / Coughing, coughs Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Cattle & Buffaloes:Calf,Poultry:Young poultry,Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Cattle & Buffaloes:Calf,Poultry:Young poultry,Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Sign
Respiratory Signs / Purulent nasal discharge Sign
Respiratory Signs / Purulent nasal discharge Sign
Respiratory Signs / Sneezing, sneeze Sign
Skin / Integumentary Signs / Broken, damaged feathers Sign
Skin / Integumentary Signs / Cold skin, cool ears, extremities Cattle & Buffaloes:Calf,Cattle & Buffaloes:Cow Sign
Skin / Integumentary Signs / Loss of feathers, loose feathers Sign
Skin / Integumentary Signs / Moist skin, hair or feathers Sign
Skin / Integumentary Signs / Pruritus, itching skin Sign
Skin / Integumentary Signs / Rough hair coat, dull, standing on end Pigs:All Stages Sign
Skin / Integumentary Signs / Ruffled, ruffling of the feathers Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin erythema, inflammation, redness Sign
Skin / Integumentary Signs / Skin erythema, inflammation, redness Sign
Skin / Integumentary Signs / Skin fistula, sinus Sign
Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene Cattle & Buffaloes:Cow Sign
Skin / Integumentary Signs / Soiling of the feathers, vent feathers Sign
Skin / Integumentary Signs / Soiling of the feathers, vent feathers Sign
Skin / Integumentary Signs / Subcutaneous crepitation, skin emphysema Sign
Urinary Signs / Haematuria, blood in urine Sign
Urinary Signs / Polyuria, increased urine output Sign
Urinary Signs / Proteinuria, protein in urine Sign
Urinary Signs / Urinary incontinence, dribbling urine Sign

Disease Course

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Pigs


Diarrhoea


ETEC strains produce fimbriae (or pili) which mediate bacterial attachment to the small intestinal mucosa, and enterotoxins that stimulate the secretion of water and electrolytes into the intestinal lumen. ETEC cause severe watery diarrhoea, followed by dehydration, listlessness, metabolic acidosis, and death. In some cases, the infection may progress so rapidly that death occurs before the development of diarrhoea. One or more animals in a group are affected. Diarrhoea is mostly observed in the first few days after birth. Less watery diarrhoea may also be observed in the first one to two weeks of age, or as early as 2 days postweaning, with low mortality and, often, decreased weight gain. F4 (K88)-producing isolates occasionally proliferate rapidly in the small intestine of young pigs and induce symptoms of shock and rapid death. Enteric colibacillosis complicated by shock occurs in unweaned and recently weaned pigs and manifests as rapid death with some cutaneous cyanosis of the extremities, or less acutely with hyperthermia, diarrhoea, and anorexia. In farms where husbandry measures at weaning such as addition of higher levels of protein of animal source, plasma, acidifying agents, and zinc oxide are being used, peaks of diarrhoea and enteric colibacillosis complicated by shock may be observed often at 3 weeks after weaning, or even at 6 to 8 weeks after weaning, at the time when the pigs enter the growing barns.

EPEC attaches to and effaces the microvilli of the small and large intestinal mucosa and has been associated with diarrhoea in postweaning pigs. At the present time, EPEC only represent a small proportion of diarrhoeagenic porcine E. coli (Bosse et al., 1992). The exact mechanisms by which they cause diarrhoea are not yet known. However, the similarity to human EPEC both in terms of the pattern of intestinal colonization, the type of lesion produced and the presence of eae on bacteria strongly suggest that porcine and human EPEC share similar pathogenic mechanisms.


Oedema Disease


VTEC strains adhere to the small intestinal mucosa by means of the fimbrial adhesin F18, proliferate in the small intestine, and produce VT2e, which enters the circulation and causes lesions associated with endothelial cell damage. Affected pigs usually die suddenly without previous signs of illness. Pigs with early symptoms eat sparingly, and tend to manifest hind or forelimb paralysis within a few hours. In other cases, pigs can have attacks of convulsive running movements. Some slight reddening of the skin and eyelid oedema may also be observed. Forced respiratory movements occur shortly before death. Constipation is a marked feature of VTEC infection in pigs and diarrhoea is often a terminal event and is sometimes haemorrhagic (Bertschinger, 1994).

In weaned piglets, ETEC strains are also responsible for oedema disease that is characterized by a subcutaneous oedema accompanied by pruritus and sometimes dyspnoea. Watery diarrhoea with blood occurs at the terminal stage of the disease.


Septicaemia


ExPEC are found in the normal intestinal microflora and in certain circumstances, such as in young animals which have received low levels of colostral antibodies, these strains are able to traverse the intestinal epithelial barrier by pinocytosis or transepithelial migration to mesenteric lymph nodes. They persist and multiply in the blood and other extraintestinal sites, due to their ability to resist the bactericidal effects of complement and phagocytosis. E. coli septicaemia occurs in newborn pigs and is observed less frequently in suckling pigs. It is characterized by an acute, generalized infection, sometimes with diarrhoea at the terminal stage (loose, mucoid faeces), with signs of shock (listlessness, loss of interest then depression, poor response to external stimuli, tachycardia, prolonged capillary fill time, cardiovascular collapse, coma) often followed by death (in 3-8 h with fatality of up to 100%). Some biological signs may be observed if animals are examined at an early stage: leucocytosis followed by leucopenia, and hypoproteinaemia. In some animals, the infection becomes localized, causing polyarthritis (often fibrinous), pneumonia, metritis, abortion (Burns et al., 1996; Pohl et al., 1992; Pohl et al., 1993; Bilkei et al., 1994) and meningitis (with signs such as tremor, hyperaesthesia, opisthotonos, convulsion and coma).

Bacteria are excreted in nasal and oral secretions, urine, and faeces of affected animals.


Urinary tract infections


Urinary tract infections are more often sporadic and manifest as cystitis or pyelonephritis. Cystitis is rarely accompanied by any typical clinical signs and is therefore not often observed by the farmers. However, thorough observation shows that sows urinate with pain, from an abnormal dog-sitting position and produce small quantities of urine. Sometimes this is accompanied by vulvitis with mucoid, mucohaemorrhagic to purulent discharge (Bilkei et al., 1994). It seems that this pathology affects reproduction, with smaller litters and increased intervals between litters. In contrast, when females are affected by pyelonephritis, body temperature decreases, and heart rate increases. Polypnoea, cyanosis, and ataxia are also observed.


Mastitis


In sows, clinical signs are detected on the first or second day after farrowing. Changes are quite similar to those described in sows with lactation failure. They include increased temperature of the udder, listlessness, weakness, fever, mammary hardening and tenderness, and loss of interest in the piglets. Sows remain in sternal recumbency. Their respiratory and heart rates are increased. Consumption of feed and water is reduced.


Ruminants


Diarrhoea


As in pigs, ETEC strains produce fimbriae (or pili) which mediate bacterial attachment to the small intestinal mucosa, and enterotoxins that stimulate the secretion of water and electrolytes into the intestinal lumen. ETEC cause severe, watery diarrhoea, followed by dehydration, listlessness, metabolic acidosis and death. In some cases, the infection may progress so rapidly that death occurs before the development of diarrhoea. One or more animals in a group are affected. In calves and lambs, diarrhoea is mostly observed in the first few days after birth. Calves produce large amounts of foul-smelling pasty to watery faeces varying from pale yellow to white in colour and occasionally containing flecks of blood. In acute cases, extensive loss of body water leads to a great decrease in body weight within 6-8 h of the onset of diarrhoea. In more chronic cases, a combination of body weight loss and generalized muscle wasting led to body weight loss.

VTEC attach to the intestinal mucosa in a similar manner to EPEC and cause dysentery or mucoid or bloody diarrhoea in young calves of between 1 and 8 weeks of age, with a peak between 4 and 5 weeks of age (China et al., 1998). Diarrhoea does not result in death of the calves very often but is recurrent, even after treatment (Mainil, 1999). Symptoms in calves may include dysentery, pyrexia, depression, dehydration, and poor growth, and tend to be more chronic or recurrent with less dehydration than observed in ETEC diarrhoea.


Septicaemia


As in pigs, ExPEC are found in the normal intestinal microflora and in certain circumstances, such as in young animals which have received low levels of colostral antibodies, these strains are able to traverse the intestinal epithelial barrier by pinocytosis or transepithelial migration to mesenteric lymph nodes. They persist and multiply in the blood and other extraintestinal sites by resisting the bactericidal effects of complement and phagocytosis. E. coli septicaemia occurs in calves in the first few days of life and in lambs at 2 to 3 weeks of age. It is characterized by an acute, generalized infection, sometimes with diarrhoea at the terminal stage (loose, mucoid faeces), with signs of shock (listlessness, loss of interest, then depression, poor response to external stimuli, tachycardia, prolonged capillary fill time, cardiovascular collapse, coma) often followed by death (in 3-8 hours with fatality of up to 100%). Some biological signs may be observed if animals are examined at an early stage: leucocytosis followed by leucopenia, and hypoproteinaemia. During the early hyperdynamic phase of sepsis, clinical signs may include lethargy, hypotonia, more time spent sleeping, decreased nursing frequency followed by complete loss of the suckling reflex, hyperaemic mucous membrane with rapid capillary refill time associated with peripheral vasodilation. Other signs include increased cardiac output, tachycardia, bounding peripheral pulses, extremities that are still warm, tachypnoea, and variable body temperature. Capillary leakiness contributes to the early appearance of petechiae on the gums and sclera, inside the ears, and on the coronary bands. Mental disturbance can be present, associated with other signs (Smith, 2001). In some animals, the infection becomes localized, causing polyarthritis (often fibrinous), pneumonia, metritis, abortion (Burns et al., 1996; Pohl et al., 1992; Pohl et al., 1993; Bilkei et al., 1994) and meningitis (with symptoms such as tremor, hyperaesthesia, opisthotonos, convulsion and coma). Bacteria are excreted in nasal and oral secretions, urine, and faeces in affected animals.


Mastitis


Mastitis in cattle is caused by wide range of serogroups (Pillai et al., 1979; Thebault, 1979; Hakogi et al., 1980; Burns et al., 1996; Pohl et al., 1992; Pohl et al., 1993) similar to those present in the intestinal flora of adult cattle. Most of these strains are able to resist the bactericidal effects of serum. Following faecal contamination from the immediate environment of the cow, E. coli enters the teat and remains in the teat canal and lactiferous sinuses. The E. coli is either rapidly eliminated by infiltrating neutrophils with mild damage to the epithelial cells of the teat sinus or proliferates rapidly and causes more extensive epithelial damage in the secretory areas of the mammary gland due to diffusion of endotoxin. E. coli mastitis affects lactating cows and varies from very mild with some milk clotting and swelling of the gland to a very acute reaction with widespread damage to the udder, bloody milk, signs of toxaemia and possibly death. E. coli mastitis may also be chronic-, recurrent-clinical or subclinical.


Poultry


Colisepticaemia


APEC respiratory tract infection occurs via the inhalation of faeces-contaminated dust. APEC adhere to epithelium of the respiratory tract of the chicken by means of their fimbriae (Dho and Lafont, 1984) and enter the blood stream via the lungs (Cheville and Arp, 1978; Rosenberger et al., 1985; Ackermann and Cheville, 1991; Pourbakhsh et al., 1997) and airsacs (Pourbakhsh et al., 1997) to reach internal organs. The involvement of other virulence factors in the disease course has not been elucidated yet (Dho-Moulin and Fairbrother, 1999).

In acute infections, birds are in good physical condition and become depressed, often having yellowish or greenish watery droppings. Body temperature increases and may reach 44°C immediately before death. Peritonitis causes a sudden sporadic mortality among laying hens.


Cellulitis


Cellulitis is not associated with clinical illness and does not seem to affect the growth of the bird (Elfadil et al., 1996). It is characterized by a diffuse inflammatory reaction in the subcutaneous tissue that results in the complete or partial condemnation of the carcass at processing (Messier et al., 1993). The lesion is initiated by a break in the integument, in some cases due to a scratch from another bird, followed by bacterial contamination. Cellulitis has been reported to be characterized by seasonal variation (Vaillancourt et al., 1992; Morris, 1994), and some climatic conditions may be predisposing factors (Gomis et al., 2000).

Epidemiology

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The most important reservoir of E. coli is the intestinal tract of all animal species. E. coli is part of the normal intestinal flora, of which only a small proportion possesses virulence factors and are pathogenic. Healthy individuals may carry pathogenic E. coli. Faeces, and in the case of poultry houses, dust, are important sources of pathogenic E. coli. These bacteria may remain viable for long periods in dry dust or litter in the immediate environment of the animals. Other potential sources of infection are contaminated feed ingredients or drinking water, and faeces of wild rodents or birds in contact with farm animals.


Epidemiology in pigs


Diarrhoea


Death in newborn piglets with diarrhoea often occurs 12 to 24 h after onset. Mortality can reach 70% in affected litters (Cooper, 2000). Neonatal E. coli diarrhoea represents approximately 11% of all preweaning mortality of affected cases (Alexander, 1994). In postweaning diarrhoea, mortality is often 1.5 to 2% of pigs and can reach 25% if no treatment is given (Hampson, 1994).


Oedema disease


Oedema disease is most often manifested as sporadic cases or small outbreaks limited to a specific age group (recently weaned pigs). One epidemiological study demonstrated a morbidity of 16% and a case mortality rate of 64% (Bertschinger, 1994).


Epidemiology in ruminants


Diarrhoea


Morbidity due to ETEC strains can reach 50% in beef calves and 75% in confined dairy calves. Five to 50% of sick animals usually die (Butler and Clarke, 1994).

In an epidemiological study of 20 veal calves, a morbidity rate of 100% and a mortality rate of 20% were observed for VTEC infections (Butler and Clarke, 1994). Another study demonstrated that VTEC could be isolated in 28% of calves with diarrhoea (China et al., 1998).


Septicaemia


In all studies conducted in the USA, Europe and Australia in the past 15 years, Gram-negative bacteria have been the predominant cause of infection in newborn large-animals, and E. coli has been by far the most common bacterium isolated. Polymicrobial infections are common in septicaemic calves (28%) (Smith, 2001).


Mastitis


Mastitis is the single most common disease syndrome in adult dairy cows, accounting for 38% of all morbidity. On an annual basis, 3 out of every 10 dairy cows have clinically apparent inflammation of the mammary gland. Of the affected cattle, 7% are culled and 1% will die as a consequence of the disease. A recent survey suggests that more than 25% of all disease-related economic losses of dairy cattle can be directly attributed to mastitis (Smith, 2001). It has been estimated that 10% of cows that develop peracute mastitis die, 70% became agalactic and 20% return to milking (Hill, 1994). An epidemiological study in UK in 1985 indicated that mastitis incidence can be up to 77% (Hill, 1994). In recent years, more widespread teat disinfection and antibiotic therapy at drying off have resulted in a much lower incidence of mastitis due to contagious pathogens, and mastitis due to E. coli has become one of the most common forms of the disease in cattle in early lactation (Hill, 1994).

Faeces are one of the most common sources of E. coli in the environment. It is probable that E. coli is not very contagious and that new infections result from environmental contamination. The more confined conditions of modern intensive farming methods have contributed to the increasing incidence of infections due to environmental contamination. Poor drainage and certain types of bedding, such as sawdust and woodshavings, permit a greater build-up of bacterial numbers in the environment, leading to greater bacterial contamination of teat ends and incidence of mastitis.


Epidemiology in poultry


Colisepticaemia


Chickens reared under intensive conditions such as often observed in the poultry industry are susceptible to opportunistic E. coli. This is especially critical when the shell of the eggs is cracked and during the first weeks of life, a time at which the immune system is not yet fully mature. Economic losses depend on the stage of infection. Yolk sac infection occurs late in incubation causes many affected embryos to die. Only a few virulent E. coli may result in the death of all embryos. Typically, losses continue during hatching and for an additional 3 weeks. Some chickens that live longer than 4 days also tend to have pericarditis, whereas some chicks seem to be able to control the infection. Some serogroups of E. coli of low virulence are associated with a 20% decrease in bodyweight, but with no mortality or decreased hatchability. Respiratory disease usually occurs between 2 and 12 weeks of age, with most losses occurring between ages of 4 and 9 weeks (20% mortality).


Cellulitis


Cellulitis does not result in mortality or clinical signs, but the presence of fibrinous plaques under the skin results in substantial losses through condemnation or downgrading of carcasses (Gross, 1994; Dho-Moulin and Fairbrother, 1999).

Impact: Economic

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Economic impact on pig production


E. coli diarrhoea may result in significant economic losses due to morbidity, mortality, decreased weight gain, and cost of treatment, vaccinations and food supplements. Up to 70% of an affected litter can die (Cooper, 2000). A study in Australia in 1980 showed a loss of production estimated at $A 80 per year for every sow, in cases of postweaning diarrhoea (Hampson, 1994).


Economic impact on cattle production


E. coli diarrhoea may result in significant economic losses due to morbidity, mortality, decreased weight gain, and cost of treatment, vaccinations and food supplements.

E. coli mastitis may result in economic losses due to decreased milk production and loss of milk following antibiotic treatment.

Septicaemic E. coli strains can provoke abortion, induce infection and often lead to death.


Poultry


Cellulitis and airsacculitis are two important avian diseases caused by E. coli and are responsible for extensive economic losses due to condemnation of broiler chickens with lesions associated with these diseases (Morris, 1991; Elfadil et al., 1996; Caya et al., 1999). In the USA in 1981 and in Japan in 1990, losses due to colibacillosis were estimated at more than US$ 100 million (Nakamura et al., 1994). Colibacillosis is responsible for 4 to 45% of condemnation of broiler chickens with lesions (Barnes and Gross, 1997). In France it constitutes a major bacterial pathology in avian production (Arné, 1999). The morbidity may be between 20% and 50% with a mortality that does not exceed 5% of livestock (Gross, 1994; Wray et al., 1996).

Zoonoses and Food Safety

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Pigs and ruminants


Zoonosis due to E. coli is usually associated with EHEC since ETEC and EPEC strains isolated from farm animals are usually not considered zoonotic (Aiello, 1998). Nevertheless, a clinical case of a ETEC food-borne outbreak in 4 elementary schools was reported in Japan in 1998 (Mitsuda et al., 1998). More than 800 people were contaminated. The outbreak was due to tuna paste served for lunch at these schools. All ETEC isolates were of the O25:NM serotype and possessed an Stb gene suggesting an animal origin for the outbreak.

The most common EHEC serotype associated with zoonosis is O157:H7, although other serotypes such as O26:H11, O111:H8, O111:H- (Henning et al., 1998), O104:H21, and O48:H21 have also implicated. EHEC zoonoses are widespread, since cases have been reported in North and South America, Europe, South Africa, Japan and Australia. The principal sources of contamination are ruminants, particularly bovines. Disease usually occurs after ingestion of uncooked or undercooked ground beef, or food or water contaminated with bovine faeces (Aiello, 1998). These strains are non-pathogenic in animals (Eriksson and Aspan, 2000). Moreover VTEC strains causing disease in cattle are generally different from those causing disease in humans (Mainil, 1999).


Poultry


Several studies have evaluated the risk for human health associated with APEC. Results of one study (Cherifi et al., 1994) concluded that animals (including chickens) are a possible source of serogroup O78 E. coli involved in septicaemic infections in humans. It has been suggested (White et al., 1990) that certain strains involved in swollen head syndrome (SHS) infections belong to a clone complex whose members have special attributes that promote involvement in invasive diseases in humans and animals.

Finally, in one study, biochemical characterization of APEC (O2) isolates from humans and animals including poultry has demonstrated that they belong to the same clonal group (Achtman et al., 1986), whereas another study (Caya et al., 1999) suggests that avian isolates recovered from cellulitis and air sacculitis possess few attributes required to cause disease in humans.


Meat inspection


The presence of E. coli strains in carcasses indicates faecal contamination. It should be noted that in most abattoirs the total coliform count is determined, whereas only VTEC and possibly ETEC, SEPEC, and APEC are threats to human health.

Moreover a visual control is not efficient since most of the involved E. coli strains do not induce macroscopic lesions. Certain strains, such as those responsible for septicaemia, mastitis or urinary tract infection may be associated with macroscopic lesions, although these strains are usually not considered to be zoonotic.


Food hygiene


Spray washes seem to be effective for removal of pathogenic E. coli due to physical removal of bacteria, rather than to the chemical nature of washes (Cutter, 1999). Irradiation with ?-rays also seems to be effective, although consumers may not be ready to eat such products.


Pathogen survival


Most E. coli strains need a water activity (aw) of more than 0.95, a pH of between 6.5 and 7.5 and a temperature of between 18 and 42°C for optimal survival. However, it is important to mention that O157: H7 strains have a different pattern. They can resist more stringent conditions, such as: an aw of less than 0.95, and a pH as low as 2.


Transmission in food


As mentioned above, transmission is mostly by the orofaecal route. For VTEC and EHEC strains, food and water should also be considered as sources of faecal contamination.

Disease Treatment

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Treatment of colibacillosis is mostly aimed at removal of the pathogenic E. coli and should be initiated as soon as possible to be effective. Diagnosis should be confirmed by culture and antibiotic sensitivity tests, as antibiotic sensitivity varies greatly among E. coli isolates. A broad-spectrum antibiotic treatment may be used initially while waiting for the results of sensitivity tests. The route of administration depends on the type of infection and choice of antibiotic. Isolates are becoming increasingly resistant to certain antibiotics such as ampicillin, neomycin, kanamycin, spectinomycin, tetracycline and sulfisoxazole.


Pigs


Diarrhoea


In newborn piglets, treatment with antibiotics may be on an individual or litter basis, by mouth or parenteral injection (Fairbrother, 1999b). Commonly used antibiotics are ampicillin, apramycin, ceftiofur, gentamycin, neomycin, spectinomycin, furazolidone and potentiated sulphur drugs. Bacteriophages have been used with success experimentally but not yet extensively applied in the field. Oral fluid therapy consisting of electrolyte replacement solutions containing glucose, is helpful for the treatment of acidosis and dehydration. The use of antisecretory drugs such as bencetimide and loperamide, alone or in combination with antibacterial drugs may be helpful.

In postweaning colibacillosis, antimicrobial and electrolyte treatment is also required and may be initially administered orally or parenterally and subsequently in the water or feed (Hampson, 1994).


Oedema disease


For pigs with oedema disease, withholding the feed is thought to impair colonization of the gut and is a valuable measure still recommended to the owners of pigs on a farm on which an outbreak has been recognized (Bertschinger, 1994). Antimicrobials are also administrated in the feed. In general, piglets showing neurological signs have a poor prognosis.


Septicaemia


Antibiotic treatment may be useful in subacute cases but is mostly ineffective after appearance of clinical signs (Fairbrother and Ngeleka, 1994). However, it may be effective to treat remaining pigs in the litter and affected piglets in adjacent litters.


Urinary tract infections (UTI)


An antibiotic therapy with broad-spectrum or combined antimicrobials, such as sulfamides with trimethoprim, is recommended to eliminate bacteria responsible for UTI (Fairbrother and Ngeleka, 1994). Prolonged parenteral treatment with broad spectrum or combined antimicrobials may be recommended, although subclinical UTI often persists after treatment. Treatment of affected sows with specific antimicrobial drugs before parturition may be helpful.


Ruminants


Diarrhoea


If antibiotherapy, with a limited number of antibiotics such as cephalosporin or enrofloxacin (Kyriakis et al., 1997) due to the increasing number of resistant strains, is important in the treatment of colibacillosis due to E. coli, it is very important to rehydrate animals and to establish the homeostasis with fluid and electrolyte therapy.

In calves, correction of body water, electrolytes and acid-base abnormalities is achieved by using 2-5 litres of an oral or intravenous rehydration solution (Groutides and Michell, 1990b,a; Michell et al., 1992).


Septicaemia


Empiric antimicrobial therapy should include a Gram-negative and Gram-positive spectrum. Antimicrobial drugs with a Gram-negative spectrum of activity include third-generation cephalosporins (ceftiofur), trimethoprim-sulfonamides (TMS), fluoroquinolones (enrofloxacin), aminoglycosides, sulfonamides, and tetracyclines. The bacteriostatic action and frequency of antimicrobial resistance to tetracyclines and nonpotentiated sulfonamides limits their effectiveness in septic calves. Fluoroquinolones such as enrofloxacin are bactericidal and have an appropriate Gram-negative spectrum of activity suitable for treatment of Gram-negative septicaemia. In countries where it is legal to use enrofloxacin for treatment of neonatal calf septicaemia, a dosage rate of 2.5 to 5 mg/kg every 24 h has been suggested as appropriate for calves (Smith, 2001). It is often difficult to treat animals with septicaemia (for example with anti-endotoxin drugs) because veterinarians do not have the time to intervene before death. Drugs that may help in treating symptoms of endotoxic shock include the cyclo-oygenase inhibitor flunixin meglumine combined with dexamethasone and the lazaroid drug tirilazad mesylate (Fairbrother, 1999a). Treatment with antiserum against the endotoxin of E. coli strain J5 may delay onset of clinical signs but appears to have little effect on mortality rate.


Mastitis


Spontaneous recovery without treatment is a common course for most cases of E. coli mastitis. However, some cases become very severe, with acute toxicity and sometimes death of the cow (Smith, 2001). If antimicrobial treatment is required, antibiotics can be administered parenterally or by intramammary infusion. Acute and peracute mastitis may be treated with antimicrobials and always require supportive therapy (fluid and electrolytes) and non-steroidal anti-inflammatory agents (Radostits et al., 2000).


Poultry


Colisepticaemia


Antibiotics (ampicillin, chloramphenicol, chlortetracycline, oxytetracyclin and neomycin) are commonly used to treat birds for E. coli infection. Isolates should be tested for antibiotic sensitivity because isolates of E. coli from poultry are frequently resistant to these drugs (Gross, 1994). Some treatments are used to increase efficacy of the immune system, such as ascorbic acid (100 mg/kg), corticosterone and deoxycorticosterone.


Cellulitis


Cellulitis is usually not detected in live birds, and hence treatment is not generally undertaken.

Prevention and Control

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Immunization and vaccines


Pigs


Diarrhoea


If the dam has not been exposed to ETEC present in the environment of the piglets, her colostrum will not contain specific antibodies necessary for protection against adherence and proliferation of ETEC. Any disease process causing agalactia in the sow will diminish transfer of colostrum. Mastitis may also affect colostrum production. For neonatal colibacillosis, passive treatment with hyperimmune gamma-globulin from pigs immunized with E. coli F4(K88) can reduce the severity of diarrhoea in piglets (Jiang et al., 1995).

Immunization of the mother with a vaccine containing the appropriate adhesins will effectively protect young animals from ETEC infection following sufficient transfer of maternal antibodies (Osek et al., 1993; Wassel et al., 1999). One of the earliest vaccination techniques consisted of taking the small intestinal contents from a piglet with diarrhoea, culturing it and feeding the culture to pregnant sows, usually about one month before parturition. This method is effective and confers a lasting immunity, although it is contraindicated in herds where endemic swine dysentery, clinical cases of erysipelas, or dysentery due to Clostridium perfringens are present. Commonly used commercially available vaccines are given parenterally and may be killed whole-cell bacterins or purified fimbrial vaccines. Both types of vaccine appear to work equally well and are usually given 6 weeks and 2 weeks before parturition. Bacterins usually contain strains representing the most important serogroups and producing the fimbrial antigens F4(K88), F5(K99), F6(987P), and F41. The latter type of vaccines usually contain the same four purified fimbrial antigens. In cases where use of commercially available vaccines appears to be ineffective, it would be important to identify the E. coli serotypes involved for possible inclusion in an autogenous bacterin.

In postweaning colibacillosis, protection against colonization with F4(K88)- and F18-positive E. coli may be accomplished by feeding eggs produced by vaccinated hens. Few commercial vaccines are available for the prevention of postweaning colibacillosis. Oral vaccination of piglets before or at the time of weaning using live attenuated or autogenous strains of F4(K88)- or F18-positive E. coli may protect pigs against infection (Hampson, 1994; Bertschinger, 1999).


Oedema Disease


Administration of toxoids consisting of genetically modified or detoxified verotoxin (VT, Stx) significantly reduces oedema disease in experimentally challenged pigs. These vaccines are not yet commercially available.


Septicaemia


In outbreaks, identification of the causative serogroup(s) and immunization of the pregnant sows with an autogenous vaccine may be useful (Fairbrother and Ngeleka, 1994).


Ruminants


Diarrhoea


Immunoglobulin levels may be estimated by the zinc sulfate or sodium sulfite turbidity tests during the first 48 h after birth (Fairbrother, 1999a). Immunodefecient calves may be treated with plasma from an adult animal originating from the same area or with colostrum taken from an older cow in the herd and stored frozen until time of use. Oral administration of specific anti-F5(K99) monoclonal antibodies or powdered egg yolk from hens immunized with F5(K99) to calves within the first 12 h after birth appears to prevent colonization by F5(K99)-positive ETEC isolates and to reduce the severity of clinical signs and mortality rate.

The vaccination of pregnant cattle 6 weeks and 2 weeks before parturition with killed whole-cell ETEC bacterins or purified K99 fimbrial vaccines appears to effectively protect calves against ETEC infections (Butler and Clarke, 1994). Mixed infections with ETEC and other enteropathogens may not be effectively prevented by immunization with ETEC vaccine alone. Commercial E. coli bacterins will be effective if they contain the same fimbrial antigen as that responsible for the calf diarrhoea problem. Vaccination may be repeated annually. The calf must ingest an adequate quantity of immune colostrum as soon as possible after birth.


Septicaemia


Septicaemia due to E. coli can be totally prevented by an adequate transfer of colostral immunoglobulins. Administration of hyperimmune serum raised against the predominant serogroups of E. coli associated with colisepticaemia in a particular geographical area may be useful in calves known to be at risk due to failure of colostral transfer. Administration of hyperimmune anti-J5 serum appears to delay the onset of bacteraemia but not to affect the final mortality rate. Immunization of pregnant cattle late in gestation with vaccines including the E. coli serogroups associated with colisepticaemia in a particular area results in reduced mortality and may be useful for calves that would otherwise receive marginal levels of circulating immunoglobulins.


Mastitis


Parenteral immunization of cattle during the dry period with a vaccine containing the E. coli strain J5 reduces the rate of clinical coliform mastitis (Hill, 1994). Use of such vaccines does not prevent E. coli mastitis or alleviate the severe effects of endotoxin but would be a valuable complement to good management. Intramammary immunization with J5 vaccine increases IgG and IgM titres in the serum and whey during dry period and early in lactation, as compared to subcutaneous vaccination (Smith et al., 1999; Rainard, 1983; DeGraves and Fetrow, 1991). However, the route of administration does not appear to influence the effect of the vaccine on systemic and local signs of clinical mastitis in an experimental challenge model.


Poultry


Colisepticaemia


Immunization of chickens with killed or attenuated live bacteria usually confers a good protection against infection with the homologous strain contained in the vaccine. However, protection against infection with E. coli strains of different serogroups is less effective (Dho-Moulin and Fairbrother, 1999). Immunization of breeders results in passive immunity against infection by E. coli of the same serogroup for up to 2 weeks after hatching. Use of sonicated bacteria (Heller et al., 1991) or highly purified fimbriae (Gyimah et al., 1986; Suwanichkul et al., 1987) as antigens for vaccination have proved to be effective against infection with E. coli possessing the appropriate fimbriae. Vaccines against E. coli are not widely used, probably because of the wide variety of serogroups involved in field outbreaks.


Cellulitis


Vaccination is not usually employed as a control measure for cellulitis.


Husbandry Methods and Good Practice


Pigs


Diarrhoea


Neonatal colibacillosis

Piglets should be maintained at an adequate temperature, 30 to 34°C for unweaned pigs, free of drafts and on a low-heat-conducting floor (Fairbrother, 1999b). Good hygiene in the farrowing area helps to reduce the numbers of E. coli being presented to the piglet. Farrowing crate design is important in minimizing the faecal contamination of the farrowing area. Drinking water and creep feed should be clean and fresh and not contaminated with faecal material.

Quarantine should be practised to control the introduction of E. coli of different pathotypes into the herd, as animals in the herd will have little immunity to E. coli fimbrial antigens with which they have not had contact. Farrowing crates should be thoroughly cleaned and disinfected between litters. An all-in/all-out farrowing system with thorough disinfection between batches will greatly reduce the E. coli population in the environment.

Postweaning colibacillosis

Management factors predisposing piglets to postweaning diarrhoea should be addressed (Hampson, 1994). Increasing the age or weight at weaning is helpful. The temperature in the weaning house should start between 28 and 32°C, with a minimum of drafts and temperature changes. A good quality creep feed should be made available, especially in piglets weaned before 4 weeks of age. Weaner diets should be highly digestible, not contain high quantities of soybean meal, and ideally should be based on milk proteins, although the latter may not be economically possible. Good hygiene should be maintained, with daily removal of faeces and thorough cleaning and disinfection of pens between batches of pigs.

Several strategies may contribute to reducing the build-up of pathogenic E. coli in the intestine after weaning. Prophylactic antimicrobials are often used but should be avoided due to the alarming increase in drug resistance caused by their use. Addition of organic acids to the water supply or weaner diets may reduce gastric acidity and minimize survival of ingested E. coli. ZnO dietary supplementation effectively controls postweaning diarrhoea in pigs, but does not seem to affect bacterial colonization of the gut as faecal excretion is constant (Mores et al., 1998). Modification of the feed by adding soluble fibres seems to be effective (McDonald et al., 1999). Lactobacillus spp. inoculation appears to inhibit ETEC strain adhesion (Bomba et al., 1997; Jin et al., 2000). Other probiotics have also experimentally demonstrated efficiency (Fujiwara et al., 1999; Kyriakis et al., 1999). Many of these measures tend to delay the onset of postweaning diarrhoea rather than preventing it completely.


Oedema disease


There are several different approaches to prevention and control of oedema disease in pigs. Diets with reduced nutrient contents or limited amounts (twice daily feeding of only a quantity which is immediately consumed) of conventional diets (Smith and Halls, 1968) can be provided for the first 2-3 weeks after weaning. Prophylactic antimicrobials are often used but should be avoided due to the alarming increase in drug resistance following their use. Probiotics may be used, although the results are variable.


Septicaemia


Prevention of infection should focus on reduction of numbers of pathogenic E. coli in the environment of the piglets and in providing sufficient colostrum at birth (Fairbrother and Ngeleka, 1994). Good hygiene, especially washing and disinfection of the farrowing pens will result in a reduced infection rate. Young piglets should be maintained at an even temperature of 35°C for the first week of life.


Mastitis and urinary tract infections (UTI)


For mastitis, hygiene measures such as protecting the teats by a discontinuous disinfection (Lam et al., 1997) are important. Also, drastic reduction of the sow's ration, thus decreasing the incidence of agalactia, may be effective. Bacteriological checking of every sow after farrowing may decrease the incidence of UTI (Fairbrother and Ngeleka, 1994). Keeping the udder dry and warm is important. Recumbent sows should be encouraged to stand and drink.


Ruminants


Diarrhoea


Calves should be maintained at an adequate temperature in an area free of draughts to reduce the effects of chilling on intestinal motility and resistance to enteric infection (Fairbrother, 1999a). New animals should be quarantined to avoid introduction of different pathotypes to which the existing calves have very little immunity. Calving pens should be thoroughly washed and disinfected between batches of calves, to reduce the population of pathogenic E. coli in the immediate environment. It has been found that the longer calving houses are used, the greater the incidence of E. coli infection.

Lactobacillus spp. inoculation seems to inhibit ETEC strain adhesion (Bomba et al., 1997; Jin et al., 2000). Other probiotics have also experimentally demonstrated efficacy (Fujiwara et al., 1999; Kyriakis et al., 1999).


Septicaemia


The principles of prevention of septicaemia in calves are to ensure adequate colostral intake, boost specific and non-specific immunity, and reduce the possibility of introduction/spread of infectious agents. Calves should be maintained at an adequate temperature in an area free of draughts to reduce the effects of chilling on intestinal motility and resistance to systemic infection (Fairbrother, 1999a). New animals should be quarantined to avoid introduction of different pathotypes to which the existing calves have very little immunity. Calving pens should be thoroughly washed and disinfected between batches of calves, to reduce the population of pathogenic E. coli in the immediate environment. It has been found that the longer calving houses are used, the greater the incidence of E. coli infection (Smith, 2001).

When colostral intake is not adequate, plasma is routinely used to increase immunoglobulin levels. Between 1 and 4 L of plasma have been infused intravenously to raise immunoglobulin G (IgG) levels, although the optimum amount is not known.


Mastitis


The single most important procedure in the prevention of contagious mastitis is the consistent use of postmilking disinfectant teat dips. Environmental mastitis is more difficult to control and does not respond to contagious mastitis control programmes. Consequently, prevention of environmental mastitis is based on prevention of the transmission of potential pathogens from the environment to the mammary gland, rather than the identification and treatment or isolation of infected cows. This is more often accomplished by optimal sanitation, including clean housing, clean bedding, and use of free stall housing designs (Smith, 2001).

Feeding strategies are an important component of environmental mastitis control programmes. The streak canal remains open for a variable but relatively short time after each milking, closing within 2 h after milking. Providing fresh, palatable feedstuffs after each milking will increase the interval that cows remain standing and enhance teat-end hygiene (Smith, 2001).

Proper nutrition is critical for the cow to maintain optimal immune function and disease resistance. In particular, vitamin E and selenium deficiencies have been associated with an increased incidence of clinical mastitis due to Gram-negative bacteria. When environmental mastitis is present in a herd, all of the cows, including those that are dry or non-lactating, should receive a balanced diet, including micronutrient supplementation. Blood selenium and vitamin E concentration can be monitored during late gestation and early lactation (Smith, 2001).


Poultry


Colisepticaemia


The disease can be prevented by controlling environmental contamination in order to avoid predisposing respiratory infections (Dho-Moulin and Fairbrother, 1999). Also, it would be important to reduce and control intestinal contamination by E. coli of pathogenic serogroups. Effective control measures include disinfection of egg surfaces with formaldehyde within 1 h of laying, maintenance of hygiene in the litter, and chlorination of the drinking water. Pathogenic serotypes can be competitively excluded from the intestinal tract by seeding newly hatched chicks with the intestinal flora of resistant chickens (Weinack et al., 1982). Infection of the respiratory tract can be reduced by maintaining mycoplasma-free birds, and by controlling environmental parameters such as humidity, ventilation, and dust and ammonia in the air.


Cellulitis


An approach to the prevention of this disease would similarly include reducing intestinal contamination by E. coli of pathogenic serogroups, as for colisepticaemia. In experimental conditions, addition of vitamin E to the feed appears to inhibit the formation of cellulitis lesions (Macklin et al., 2000).

References

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Links to Websites

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WebsiteURLComment
Beef Industry Food Safety Councilhttp://www.bifsco.orgThe Beef Industry Food Safety Council (BIFSCo) brings together representatives from all segments of the beef industry to develop industry-wide, science-based strategies to solve the problem of E. coli O157:H7 and other food borne pathogens in beef.
Canadian Research Network on Bacterial Pathogens of Swinehttp://www.medvet.umontreal.ca/reseau/ang/index.htmThis contains details about the research network, which includes working groups on Escherichia coli, Actinobacillus pleuropneumoniae and Actinobacillus suis, Streptococcus suis, and public health. The main aims of the network are to produce molecular and immunological tools and to develop vaccines.
Center for Veterinary Medicine (FDA)http://www.fda.gov/cvm/default.htmlThe Center for Veterinary Medicine (CVM) regulates the manufacture and distribution of food additives and drugs that will be given to animals. These include animals from which human foods are derived, as well as food additives and drugs for pet (or companion) animals.
E. coli as Pathogenshttp://web.bham.ac.uk/bcm4ght6/path/path.htmlThe page is designed to bring together views and comments about E. coli as both human and animal pathogens. It discusses them from the points of view of diseases and infections they cause as well as the various phenotypic characteristics. The page was written by Karl Bettelheim and Gavin Thomas.
E. coli Genome Project, University of Wisconsinhttp://www.genome.wisc.edu/
Montreal University: Escherichia coli laboratoryhttp://www.medvet.umontreal.ca/ecoli/The primary aim of the site is to help professionals such as veterinary clinicians, diagnosticians, pathologists, microbiologists and teachers and students to keep up to date on, and more easily understand the rapidly evolving areas of classification and identification of pathogenic E. coli and the pathogenesis of infections due to these bacteria. Secondly, the services and reagents offered by the laboratory are outlined on this site.
Pathogenic E. coli lecturehttp://www.bact.wisc.edu/bact330/lectureecoliLecture on pathogenic Escherichia coli by Kenneth Todar, University of Wisconsin-Madison, Department of Bacteriology.
PennState College of Agricultural Sciences: Management of human exposure to farm animalshttp://ecoli.cas.psu.edu/farm/default.htmThis site was developed to provide guidelines for control and transmission of bacteria such as E. coli O157:H7 from farm animals to humans. These guidelines are applicable for humans visiting petting zoos on farms, fair displays, farm shows, and game preserve environments.
PennState College of Agricultural Sciences: The E. coli Reference Laboratoryhttp://www.vetsci.psu.edu/ecoli.cfmThe Gastroenteric Disease Laboratory is located in the Department of Veterinary Science at The Pennsylvania State University, under the direction of Dr. Chobi DebRoy. This laboratory functions as a reference center by accepting diagnostic cultures for characterization from outside sources. Standard strains, micro-screening sera, and testing kits are available to diagnostic laboratories and research institutions in the USA and Canada for a nominal fee.
PigHealth.com: E. coli Infections in Visitors to Farmshttp://www.pighealth.com/ecoli.htmA summary of reports of zoonoses and precautions to prevent zoonoses caused by on-farm contact between humans and animals.

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