Aetiology: Enterotoxigenic E.coli (ETEC) K88 or F18 strains. Most problems in UK are due to K88 strains. F18 strains cause ‘oedema disease’ which is currently very rare in this country.

Pathogenesis: The same as for neonatal piglets. In ‘oedema disease’ there is toxaemia that affects the integrity of vascular endothelium allowing fluid exudation into perivascular tissues causing oedema in multiple sites.

Epidemiology: Infection is by faecal-oral route. The antibody protection acquired by piglets through colostrum wanes by the time piglets are weaned, therefore maternal vaccination has little or no protective effect at this stage. Loss of the protective effect of secretory IgA from sow’s milk and stress factors associated with weaning increase the susceptibility of piglets to post-weaning colibacillosis. Piglets that are genetically resistant to K88+ and F18 E.coli will not be affected. 

Clinical Signs: Watery diarrhoea is the main clinical sign, the severity varies. Sudden death, dehydration, metabolic acidosis, vomiting and depression may be seen. Most commonly seen in pigs 1 – 2 weeks after weaning but pigs may be affected up to 6 weeks post-weaning. Single pigs or whole pens may be affected. Where there is toxaemia associated with E.coli infection pigs may show neurological signs similar to meningitis (ataxia, recumbency, paddling limb movements) with or without diarrhoea. This occurs due to cerebrovascular angiopathy (perivascular fluid leakage and increase in intra-cranial pressure). In ‘oedema disease’ pigs show subcutaneous oedema, particularly affecting the head and eyelids.

Clinical Signs: Watery diarrhoea is the main clinical sign, the severity varies. Sudden death, dehydration, metabolic acidosis, vomiting and depression may be seen. Most commonly seen in pigs 1 – 2 weeks after weaning but pigs may be affected up to 6 weeks post-weaning. Single pigs or whole pens may be affected. Where there is toxaemia associated with E.coli infection pigs may show neurological signs similar to meningitis (ataxia, recumbency, paddling limb movements) with or without diarrhoea. This occurs due to cerebrovascular angiopathy (perivascular fluid leakage and increase in intra-cranial pressure). In ‘oedema disease’ pigs show subcutaneous oedema, particularly affecting the head and eyelids.

With K88 E. coli few specific lesions are seen on post mortem. The small intestine is congested, the contents yellow and watery throughout. Histology shows coliform attachment to small intestinal villi. In ‘oedema disease’ there is marked sub-serosal oedema affecting the stomach and colon. Oedema can also be present in other tissues. Neuropathology confirms changes of cerebrovascular angiopathy (whole brain required).

Diagnosis: Based on clinical signs, bacteriology/serotyping and histopathology.

Treatment: Should consist of oral rehydration fluids and antibiotics. If cases are sporadic pigs can be treated with antibiotics individually but in outbreak situations antibiotics are administered to entire pens or houses via feed or water. The antibiotic of choice is as per antibiotic sensitivity profile.

Prevention: Good hygiene and minimising stress factors at weaning, as described in the previous lecture, are very important. In units with regular problems of post-weaning colibacillosis, the use of a high concentration of zinc oxide in the diet (2500 – 3000ppm) for two weeks after weaning is beneficial. It controls E.coli by reducing microbiological proliferation in the gut. Zinc oxide can be incorporated in diets under veterinary prescription in the UK but this has been banned in several European countries because of concerns over high levels of zinc being spread onto fields in pig slurry. 

Aetiology: PE is caused by the obligately intracellular bacterium Lawsonia intracellularis.

Pathogenesis: L.intracellularis colonises epithelial cells of the small and large intestine. The bacteria impede maturation of the epithelial cells, they continue to undergo mitosis and form hyperplastic crypts. Intracellular bacteria and histological changes are first evident 8-10 days after exposure; lesions are most prominent 14 - 21 days post challenge. Blocking of nutrient absorption by the thickened intestinal mucosa leads to reduction in weight gain and altered feed conversion. Secondary infections cause more severe lesions – necrotic enteritis and regional ileitis. A severe form of haemorrhagic enteropathy called proliferative haemorrhagic enteropathy (PHE) can occur in cases with heavy infections.

Transmission occurs via the faecal-oral route. Pigs develop mucosal immunity and infection generally resolves in 21 – 28 days. Within infected groups pigs can shed L.intracellularis for up to 10 weeks. 60% or more farms in the UK are infected. PE is most common in the post-

weaning pig between 6 and 14 weeks of age. PHE is more common in susceptible adult gilts introduced into an infected environment. PHE cases have a high mortality rate.

The subclinical/chronic form is the most common one in the UK Clinical cases have diarrhoea and failure to sustain growth despite normal feed intake. With necrotic enteritis or regional ileitis pigs show severe loss of condition and often scour persistently. Most cases of PE recover spontaneously but within groups there is considerable size variation among the pigs. Cases of PHE are pale and have diarrhoea which ranges in colour from black and tarry to port- wine. Pigs are anorexic and dull. Such cases require urgent antibiotic treatment. 

Lesions most common in the terminal 50cm of small intestine and the proximal third of the colon. The intestinal wall is visibly thickened and the overall diameter increased. Cases of necrotic enteritis show a coagulative necrosis with marked inflammatory exudation superimposed on an established lesion of PE. In regional ileitis the gut is rigid (hosepipe-like). In PHE the mucosa is turgid and oedematous. Large blood clots and heavily blood-stained liquid are present in the ileum and colon. 

Clinical signs, demonstrating L.intracellularis in faeces using PCR, post mortem examination and histopathology. Herds can be screened by pooling diarrhoeic samples for PCR testing. Serology (L.intracellularis IFAT) can be used to determine the seroconversion profile in the herd. This can be used in control strategies. 

Treatment and Prevention: Oral antibiotic treatment of clinically affected groups (e.g. chlortetracycline, tylosin, tiamulin). Where PE is endemic in growing pigs, vaccination (MLV) is necessary to minimise production losses. It takes 3 weeks for the immunity to be effective, thus vaccination needs to take place 6 weeks before clinical signs (or sero-conversion) are seen. Another option is strategy medication but problems are that time of infection is variable and thus the antibiotics are too early (no build-up of immunity) or too late (intestines already damaged). Some strains may remain viable for 1-2 weeks at 5C in the environment. Only quaternary ammonium compounds and iodine-based compounds show bactericidal activity against L.intracellularis. Cases of PHE need a parenteral antibiotic treatment, tetracycline is the drug of choice. 

Aetiology: The spirochaete Brachyspira hyodysenteriae has major economic consequences for pig production world-wide

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Pathogenesis: The organism colonises the large intestine in 2 – 4 days, multiplies in the crypts, invades the goblet cells and causes damage and disruption to epithelial cells. Typhlocolitis develops within 5 – 7 days of infection. Goblet cell hyperplasia and excess mucus production occurs resulting in diarrhoeic faeces containing mucus and sometimes blood. Some strains of B.hyodysenteriae appear to have a low virulence potential and in such cases, clinical disease and pathology are very mild or sub-clinical.

Infection is by faecal-oral route. The main risk of introducing infection is sub- clinically-infected pigs, infected pig lorries and contaminated boots worn by visitors. Vermin (rats and mice) and dogs can also carry infection. When newly introduced into a susceptible herd all ages of pigs from 6 weeks of age and upwards (including adults) can become affected. In herds with endemic infection the disease is mainly seen in growing and finishing pigs between 2 – 5 months of age. Herds classed as ‘minimal disease’ are free from swine dysentery.

Diarrhoea starts from 5 – 7 days post infection, fresh blood may be seen in faeces and excess mucus is a feature from 10 days post infection. Clinical disease lasts 10-14 days. Affected pigs show signs ranging from moderate diarrhoea to severe illness and death. Pigs with haemorrhagic diarrhoea appear gaunt, weak, become anorexic and severely lethargic. High mortality rates can occur in severe outbreaks.

Lesions are confined to the large intestine, in particular the proximal colon. Lesions include mucosal congestion and thickening with excess mucus overlying the mucosa, mucosal haemorrhage, diptheresis, erosion and ulceration. Fibrinous serositis may be present over the colon and the colonic lymph nodes are congested and enlarged.

A provisional diagnosis can be made on the basis of the clinical signs (blood, mucus and mucofibrinous exudate), history, gross pathology and microscopic examination of colonic mucosal smears for large spirochaetes. Confirmation of the diagnosis requires histopathological

examination and specific detection of the agent by culture or PCR. There are no reliable serological tests for B.hyodysenteriae infection as yet.

Tiamulin and valnemulin are the drugs of choice but lincomycin is also effective in some cases. Macrolides (Tylan and Aivlosin) have a variable level of success). Individual sick pigs should be treated with parenteral antibioticsl. Good hygiene, management (all- in, all-out), cleaning and disinfecting buildings between batches and strategic medication of pigs before being moved into clean buildings are required. Some strains of B.hyodysenteriae have developed resistance against one or more antimicrobials, so sensitivity testing is advisable if herds fail to respond to treatment. More often, failure to achieve a satisfactory response to treatment is on account of the presence of other infectious agents that are not responsive to the above antibiotics eg, salmonella. There are no vaccines available.

Eradication of the disease can be done in several ways; 1) complete depopulation of the herd with thorough cleaning and disinfecting plus a minimum of three weeks vacant, re-stock with SPF pigs 2) depopulation of the growing herd (all pigs from weaning to finishing), sows moved off-site for a minimum of two weeks and medicated in feed (tiamulin 10mg/kg bodyweight), thorough cleaning and disinfecting of empty buildings, sows moved back to farm, suckling piglets get injected with tiamulin, pigs weaned thereafter remain on the farm 3) depopulation of the growing herd (all pigs from weaning to finishing), sows stay on farm and receive in feed medication as in (2), thorough cleaning and disinfecting of empty buildings and sow accommodation as best possible. 

Aetiology: The spirochaete Brachyspira pilosicoli.

Pathogenesis: The pathogenesis is similar to B.hyodysenteriae except that the degree of inflammation is milder and haemorrhage is not a feature unless the infection is complicated by another infectious agent. The infection does not usually result in fatalities.

Clinical signs: Affected pigs show signs ranging from cow-pat type diarrhoea to watery grey diarrhoea. Pigs retain normal appetite and vigour. Morbidity within infected groups can range from 10 – 50%. Affected pigs show reduced growth rates resulting in significant size variation within groups and adverse economic effects for herd production.

Porcine colonic spirochaetosis epidemiology

Epidemiology: Infection is by faecal-oral route. Pigs become infected from a contaminated environment and from in-contact pigs that are shedding infection (poor biosecurity). The organism can survive for several weeks in wet anaerobic conditions. Pigs may shed infection for six weeks. The infection is prevalent in UK pig herds and it is involved in approximately 50% of colitis outbreaks, either as the sole pathogen or as a co-infection.. This is a zoonotic infection which can cause chronic colitis in immuno-compromised individuals.
In herds with endemic infection the disease is mainly seen in growing and finishing pigs between 6 – 16 weeks of age. There is considerable risk of infection whenever there is frequent mixing, continuous pig flow, poor ventilation/sanitation and high stocking densities.

Pathology: Lesions are similar in type and distribution to swine dysentery except they are less severe and the mucosa is seldom haemorrhagic.

Porcine colonic spirochaetosis treatment and prevention

Treatment and prevention: Control of infection follows the same principles and procedures as for swine dysentery. B.pilosicoli is susceptible to the same antimicrobial agents. As yet no resistance has been recorded among UK isolates. 

Aetiology: Salmonellosis is caused by serovars of Salmonella enterica (e.g. typhimurium, derby, choleraesuis). In Britain, S.typhimurium is the most prevalent serovar of pigs with S.derby second. S.choleraesuis is rare.
Pathogenesis: Most pathogenic salmonellae have fimbriae and flagella which are involved in attachment and invasion. The organism multiplies in the small intestine. Diarrhoea is a result of malabsorption and fluid leakage from the necrotic inflamed bowel.

Infection is via the faecal-oral route and is most common in pigs from weaning to about 4 months of age. Salmonellae are hardy, ubiquitous and can survive for years in suitable

organic substrates. High animal density, stress of transport and intercurrent disease are assumed to increase the shedding by carriers as well as the susceptibility of exposed pigs. There can be a long carrier-state following infection. Sources of infection include other pigs, vermin, birds and humans. 

Clinical Signs: On the majority of pig farms infection is sub-clinical. When diarrhoea occurs it is initially watery and yellow, without blood or mucus. Later, blood may appear sporadically in the faeces. Acutely affected pigs are febrile (40.6-41.7C), dull, dehydrated and have a decreased feed intake. Sometimes, pigs remain unthrifty and, occasionally, may develop rectal strictures. 

Pathology: S.enterica serovar typhimurium infection causes a range in severity of lesions from focal mild enteritis or colitis to diffuse necrotic enteritis, colitis or typhlitis. Mesenteric lymph nodes are enlarged. The gut contents may be watery with some necrotic material. 

Diagnosis: Clinical signs, bacteriology and pathology.

Treatment: Antibiotic treatment (oral) is only indicated in the event of outbreaks causing clinical illness in pigs. Isolation of sick pigs, scrupulous cleaning and disinfecting of pens and restricting movement of pigs and staff from contaminated to clean areas is necessary.

Prevention: Control depends on good biosecurity incl cleaning and disinfecting buildings between batches. High temperature processing of feed and preventing feed contamination is essential. Control of rodents is very important as they can carry large numbers of salmonellae in the intestine. The use of killed salmonella vaccines in breeding-age animals reduces the prevalence of infection. Serology can be used to monitor the disease situation. To improve food safety a national salmonella surveillance scheme based on ‘meat juice’ serology from slaughtered pigs was started in 2002. This scheme detects herds that have high salmonella prevalence so that appropriate control measures can be applied. 

Hyostrongylus rubidus (stomach worm) can colonise the stomach causing weight loss especially in adult breeding stock. Parasites that can give rise to enteritis and colitis are Ascaris suum, Trichuris suis and Oesophagostomum spp. On most units parasitic infections are well controlled though regular used of broad spectrum anti-parasitic agents such as the avermectins. If parasitic infections are suspected faeces samples can be examined for worm eggs. 

Aetiology: Factors linked to feed processing and dietary factors (high wheat diets) are important. Particle size (too fine), pelleted feed and low fibre content of the diet are known risk factors. Interruption of feed intake is another cause of ulcer development in the pars oesophagea. Helicobacter pylori-like bacteria might play a role in ulcer development.

Pathogenesis: The pars oesophagea does not secret mucus. Small feed particles results in greater fluidity of stomach contents and increased mixing resulting in loss of the pH-gradient between the pars oesophagea and the pyloric region. Gastric acid and pepsin coming in contact the unprotected epithelial lining of the pars oesophagea are thought to be the cause of ulceration.
Epidemiology: Common in the UK. Animals of any age can be affected but highest incidence in pigs 3-6 months of age.
Clinical Signs: Most gastic ulcers are undetected. If ulcers are severe, pigs can be found dead due to sudden severe haemorrhage into the stomach. If blood-loss occurs more slowly, pigs become pale and anaemic and pass black, tarry faeces.
Pathology: Ulcers of the pars oesophagea vary in size and are readily evident. Scarring may be present in cases of severe ulcer that have survived. Rarely, this can lead to occlusion of the oesophageal opening into the stomach.
Diagnosis: Based on clinical signs/post mortem.
Prevention: Eliminating risk factors. 

Intestinal, gastric, splenic and hepatic lobe torsions are all seen in pigs. Rough movements and manipulations and a rapid intake of food and water and possibly the fineness of ground feed stuffs have all been identified as risk factors. Intestinal volvulus around the root of the mesentery is a common cause of death in pigs. 

‘Whey bloat’ can occur in pigs with unlimited access to fresh whey. Sudden excessive intestinal fermentation causes gaseous over-distension and increased intra-abdominal pressure. If severe, this occludes venous return via the major mesenteric veins and this proves fatal. The intestines have the haemorrhagic appearance of intestinal volvulus around the root of the mesentery but no twist can be found at PM examination.