GI diseases Flashcards
GI diseases of piglets 0-4 weeks
Neonatal E. coli Septicaemia Diarrhoea
Clostridium perfringens
Coccidiosis
Rotavirus
Other infectious diseases e.g. TGE, PED
Congenital problems
GI diseases in pigs older than 4 weeks
Proliferative enteropthy
Swine dysentery
Spirochaetal diarrhoea
Post weaning E. coli enteritis and oedema disease
Salmonellosis
Colitis
Torsion
Gastric ulceration
Hernia
Rectal prolapse
Helminths
Incidence of Enteric colibacillosis (E. coli diseases)
Very common - the most important cause of enteric disease in pigs.
Responsible for > 50 % of all gastro - enteropathies in neonatal piglets.
Aetiology of Enteric colibacillosis (E. coli diseases)
Various serotypes of Echerichia coli. Important pilus antigens include
K88 (F4), K99 (F5) & K987P (F6).
The majority of serotypes do not penetrate the gut wall. They adhere to the gut wall and produce enterotoxins which in turn give rise to diarrhoea, dehydration and sometimes to death.
Some produce verotoxins.
Which serotype of E. coli is invasive
Serogroup 078
organisms pass the gut wall, enter the body and produce endotoxins.
These in turn contribute to the symptoms of endotoxic shock - severe illness, septicaemia and often death with a few hours.
Epidemiology of
Enteric Colibacillosis - E coli diseases.
The problem is very widespread and few units are free from this group of diseases.
The litters of older sows with better immunity to E coli experience fewer problems than do the litters of gilts.
The organisms are found in the bowel and faeces of sows and other pigs and also in the uterus and vagina.
Large numbers of organisms can build up in heavily used farrowing crates.
Affected litters pass very large numbers of potentially pathogenic organisms increasing the risk of infection of other litters in nearby accommodation.
Infection normally gains access through the mouth - but can occur through the respiratory tract or the umbilicus.
Predisposing factors for Enteric Colibacillosis - E coli diseases
Poor hygiene, lack of colostrum, adverse temperatures - cold, damp, dirty buildings.
Sows coming into farrowing house unwashed and in very dirty condition.
Lack of food (sow’s milk).
In older pigs taking solid food - sudden changes of diet are very important.
These include the sudden introduction of creep feed or a major change of diet after weaning.
The strain of E. coli involved is also important - some are much more pathogenic than others.
Disease syndromes of Enteric colibacilloisis - E coli diseases
a. Septicaemic colibacillosis - organism undergoes systemic spread. Less common than enterotoxigenic colibacillosis.
b. Enterotoxigenic colibacillosis - organism remains in the bowel. Most common
In both conditions either a few or many members of the litter may be affected.
Clinical signs of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
Septicaemic colibacillosis -
piglets may be found dead or very weak, low T and feel cold to the touch.
May be slightly cyanotic and occasionally terminal convulsions. Often no diarrhoea at this stage. Mortality close to 100%.
Enterotoxigenic colibacillosis - diarrhoea - yellow/ green in colour.
Faecal staining on perineum, tails contaminated and hang down with reduced tone.
T subnormal or just normal. Hunched backs and drooping tails. Raised hair coat.
Loose faeces around pen.
May attempt to feed from sow but may be too weak to get to teat and hold position.
Become progressively more moribund, weak, dehydrated and comatose - if untreated many die. Surviving piglets may be stunted.
PM signs of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
Diarrhoea:
Carcase dehydrated
Dark liver
Congestion of SI with watery content
Villi often intact or mildly atrophic
Septicaemia:
Carcase in good condition
Congestion of muscles
Enlarged spleen
If they dont die immediately then:
- meningitis
- polyserositis
- polyarthritis
Diagnosis of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
Clinical signs, history of farm, PM
Differential diagnoses of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
TGE - more acute 100 % mortality, older pigs also affected.
Rota virus infection - can look very similar to E coli cases and both conditions may be present at same time, though rotavirus typically in slightly older pigs. Virus isolation.
Clostridium perfringens Type C - very sudden onset, haemorrhagic diarrhoea, characteristic PM.
Coccidiosis - usually less acute, lower morbidity and mortality. Identification of oocysts in faeces.
Porcine epidemic diarrhoea - range of ages often affected - like a mild TGE infection; confirmation by RT-PCR.
Treatment of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
Oral antibiotics e.g spectinomycin (Spectam oral doser, Ceva), neomycin.
Parenteral antibiotics (ampicillin, spectinomycin) also advisable as cannot be sure which piglets are septicaemic.
Parenteral therapy may help to reduce the risk of septicaemia.
Do all possible to keep piglets warm and hydrated.
Fluoroquinolones possible but should be reserved for last resort and used only based on culture and sensitivity.
Best not to take off sow - but may supplement fluid intake by allowing piglets access to electrolyte / glucose solutions in a low dish.
Must give antibiotics for full 5 days.
Steroids and NSAIDs may help reduce mortality in severely ill piglets.
Control of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
a) maximise colostral intake,
b) Strict cleanliness in farrowing accommodation - all in / all out policy best.
c) Wash sows before moving into farrowing quarters.
d) Boost piglet immunity by sow vaccination during pregnancy - a number of killed vaccines available.
E. coli vaccines - most contain pilus antigens F4, F5, F6.
Piglets receive boosted colostral immunity against E. coli and hence colostral management must be good.
Epidemiology in enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
Not always clear - may be an older litter on the unit exposed to faeces from younger scouring pigs.
The older litter’s immunity may be waning and symptoms occur.
Several litters may be affected and problem may persist on the unit for some time.
Creep feed may have been changed, increased in quantity or introduced later than normal.
In some cases no change in management has occurred.
Clinical signs of enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
Usually sudden onset of diarrhoea - pale yellow to grey in colour.
variable percentage of litter affected.
Occasional sudden death but usually loose foul smelling faeces found in the pen and sick piglets spotted.
T usually normal or slightly subnormal.
Some animals develop chronic diarrhoea and ill thrift.
Diagnosis of enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
Isolation of E. coli in heavy culture from faeces
PM shows severe inflammation of the bowel and sometimes dehydration
Treatment of enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
Oral antibiotics e.g spectinomycin (Spectam oral doser, Ceva), neomycin.
Parenteral antibiotics (ampicillin, spectinomycin) also advisable as cannot be sure which piglets are septicaemic.
Parenteral therapy may help to reduce the risk of septicaemia.
Do all possible to keep piglets warm and hydrated.
Fluoroquinolones possible but should be reserved for last resort and used only based on culture and sensitivity.
Best not to take off sow - but may supplement fluid intake by allowing piglets access to electrolyte / glucose solutions in a low dish.
Must give antibiotics for full 5 days.
Steroids and NSAIDs may help reduce mortality in severely ill piglets.
Control of enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
Reducing the environmental contamination is essential.
Prophylactic antibiotic treatment may help but is not a long-term solution.
Careful introduction of creep and using a creep with a lower protein level may help empirically.
Vaccination of piglets early in life has been used but insufficient immunity is produced to overcome the infectious challenge.
Incidence of acute post weaning enteritis
Common
Aetiology of acute post weaning enteritis
E. coli
Common serotype is F4/K88 antigen
Epidemiology of acute post weaning enteritis
Mixing of litters and the stress of fighting etc. may predispose.
Change from creep feed onto ad lib weaner ration can also be involved.
Moving pigs into a dirty, cold pen from the warmth and comfort of their farrowing quarters may also predispose to the problem.
Sudden loss of maternal milk (lactose) in diet may produce an intestinal pH which allows massive multiplication of bacteria within the bowel.
Declining non-specific and specific elements of maternal immunity are important.
Receptor for F4 is secreted into mucus in gut and absence of receptor is heritable (recessive) – selected in Danish pig population.
Clinical signs of acute post weaning enteritis
Often one or more very sudden deaths - sometimes within hours or overnight from weaning.
Other pigs have severe enteritis, T normal or low.
Flanks tucked in and pig has a dehydrated, empty appearance.
Eyes severely sunken.
Faeces watery, greenish grey and foul smelling.
Tail straight, cold and soiled.
Vocalisation - a thin reedy squeal.
Diagnosis of acute post weaning enteritis
History of weaning, possible change of food, clinical signs.
Post mortem - congested, dehydrated carcase, stomach often very full of drying meal contents.
Small intestine reddened, thin walled and fluid filled.
Confirm by culture of profuse pure growth of (often haemolytic) E. coli from faeces.
Differential diagnoses of acute post weaning enteritis
Could be part of a wider problem e.g. TGE or PED.
Salmonella infections may cause diarrhoea in this age group - pigs usually pyrexic.
Swine dysentery - usually pyrexic, dark dysenteric faeces.
Treatment of acute post weaning enteritis
Must be aggressive and supportive or more pigs will die.
Pigs must be carefully handled to avoid more stress.
Parenteral antibiotic injection - neomycin, ampicillin, spectinomycin.
Antibiotic sensitivity profile may indicate need for fluoroquinolones but these should be avoided if possible.
NSAIDs or steroid injections for shocked dehydrated animals.
Offer electrolyte solution and antibiotic in warmed water.
Reduce food drastically and re - introduce carefully and slowly.
Control of acute post weaning enteritis
Reduce predisposing causes especially sudden dietary changes.
Hygiene improvements and avoidance of stress of all kinds.
Strategic in-feed antibiotic therapy around weaning may help if high incidence in weaned litters (based on antibiotic sensitivity; colistin is effective and resistance is unusual).
Some success with using zinc oxide in diet at 2000 ppm for 2 weeks, but there is focus on reducing high levels of Zn in diets for environmental reasons; also because ZN may bind other essential nutrients.
Incidence of CLostridium perfringens Type C infection (haemorrhagic enterotoxaemia)
Cases encountered from time to time.
Much less common than E. coli but usually much more virulent.
Mostly seen in first 7 days of life.
Aetiology of Clostridium perfringens Type C infection (haemorrhagic enterotoxaemia)
Clostridium perfringens Type C.
Type B seen occasionally as cause of piglet enteritis.
Type A much less pathogenic.
Epidemiology of Clostridium perfringens Type C infection (Haemorrhagic enterotoxaemia)
Infection carried on skin of some sows and also in faeces of affected piglets.
Usually seen on farm as an outbreak with a number of litters being affected.
Occasionally becomes endemic on unit but may have many months between batches of cases.
Clinical signs of Clostridium perfringens Type C infection (Haemorrhagic enterotoxaemia)
First sign is often one or more piglets being found dead.
Often in good condition and may have evidence of bloody faecal staining on perineum.
Other piglets dull, depressed, diarrhoeic - faeces may initially be pale but are often dark red and contain blood and necrotic debris.
The anus can be slightly swollen and reddened.
Temperature may be briefly elevated but soon becomes subnormal.
Piglets can appear normal and then be found dead an hour or so later.
Several pigs in litter usually affected and several litters involved.
Note - older piglets may be less severely affected.
Diagnosis of Clostridium perfringens Type C infection (Haemorrhagic enterotoxaemia)
Sudden onset of clinical signs and bloody diarrhoea.
Post mortem -
piglets in good condition.
Stomach often full of milk.
Small intestine dark red and necrotic.
May see localised peritonitis but piglet usually dead before this can develop.
May see fibrin tags in the lumen of the abnormal bowel.
To confirm - direct or cultural evidence of causal organism.
PCR available for detection of the various toxins.
Differential diagnoses of Clostridium perfringens Type C infection (Haemorrhagic enterotoxaemia)
other causes of neonatal diarrhoea.
Coccidiosis may show haemorrhagic diarrhoea and oocysts found in faeces.
Treatment of Clostridium perfringens Type C infection (Haemorrhagic enterotoxaemia)
Little hope for severely ill piglets.
Always treat whole litter and preferably others in farrowing house.
Oral ampicillin and parenteral ampicillin for each piglet for 3 - 5 days.
In severe cases can help immunity by an injection of Lamb Dysentery antiserum.
Control of Clostridium perfringens Type C infection (Haemorrhagic enterotoxaemia)
Vaccinate sows to ensure good colostral immunity.
Gletvax 6 (MSD) can be used to vaccinate sow against E. coli (various strains) and also Clostridium perfringens Types B, C & D.
Sow is vaccinated 6 weeks before farrowing with second dose 2 weeks before farrowing.
Sheep clostridia vaccines e.g. Heptavac P have been used in emergency.
May also help to dose neonatal piglets with oral and parenteral antibiotics if insufficient time for effective use of vaccine.
Incidence of Clostridium perfringens Type A and B
Less common than Type C
Epidemiology of Clostridium perfringens Type A & B
A much less severe disease than haemorrhagic enterotoxaemia.
Has a high morbidity but low mortality. Mostly affects pigs <3 weeks of age.
Clinical signs of Clostridium perfringens Type A & B
Signs of yellow, watery diarrhoea.
Can have creamy pink diarrhoea in type A, as well as dramatic loss of condition.
Dull, sunken eyes, and flanks
Affects weaners as well
Diagnosis of Clostridium perfringens Type A & B
Clinical signs, culture, identification of organism PCR.
Pathology (especially microscopic lens).
Culture from intestinal scrapings. Gram smear.
Toxin detection to distinguish between strains - PCR. DD: E. coli, Rota, Coccidia (may appear together).
Marked response to penicillin therapy.
Pathology of Clostridium perfringens Type A and B
Pale carcase
Severely inflamed intestines
Fillled with haemorrhagic contents
Villous atrophy
Treatment of Clostridium perfringens Type A and B
Parenteral and oral antibiotic for 3 - 5 days - e.g. Ampicillin.
Oral electrolytes.
Litters at immediate risk: long acting amoxicillin.
Hygiene in farrowing environment - spores only killed by flames or lime wash, washing of sows before entering farrowing house.
Vaccination of type B, C, and D.
Aetiology of coccidiosis
A number of species found in pigs.
Isospora suis - especially important
in suckling piglets (10-20 days old).
Eimeria suis and E. porci are among those species found in older pigs.
Eimeria suis
Carried and shed by sows
May affect weaners
Warm and moist climate in the farrowing house may inhibit sporulation
Cryptosporidium parvum (not a coccidian strictly)
Zoonosis
Differ slightly from other coccidia
- develop in microvillus border of enterocytes rather than deep in the cytoplasm
- oocysts already sporulated when excreted and contain sporozoites (no sporocysts)
- 90% asymptomatic, if associated with rotavirus infections severe clinical signs may appear
Epidemiology of coccidiosis
Isospora suis is mainly acquired from the faeces of other pigs but rarely from the sow.
Eimeria species are however contracted from carrier sows.
Infestation can build up both on outdoor units and also in damp indoor accommodation - especially with solid floors.
Clinical signs of Coccidiosis
Ill-thrift and diarrhoea are seen.
Piglets from 5 - 21 days are most commonly affected.
Diarrhoea may be pale and pasty or yellow and fluid in consistency – continuing for around 7 days.
Some vomiting of curd-like material.
Growth rate is depressed and piglets look thin and stunted.
Young adults may show signs of ill-thrift caused by coccidiosis.
Mortality can reach 20% in untreated cases.
Damage to small intestinal wall leads to susceptibility to other pathogens.
Diagnosis of coccidiosis
Clinical signs, poor response to antibiotic therapy, presence of oocysts in faeces which should be identified to determine their species.
Samples should be collected from recovering piglets since shedding does not peak until 3-4 days into scouring.
Pathology of coccidiosis
SI thickened with creamy-watery contents, necrosis, villous atrophy.
Histology of coccidiosis
fibronecrotic enteritis and intracellular coccidial forms.
Treatment and prevention of coccidiosis
Toltrazuril (Baycox) is now licensed for use in pigs.
Pigs are dosed once on d3, d4 or d5 according to optimum effect (just before onset of clinical signs), and then may be repeated at d10 if necessary.
The drug will reduce ongoing diarrhoea but is best used as a prophylactic.
Focus on hygiene and reduce exposure to oocysts.
The use of effective disinfectants such as Oocide (Antec), or other ammonium based products, flame disinfection, lime washing.
Scrupulous attention to hygiene (washing of sows on entry to farrowing etc) and a batch based farrowing system are key.
Aetiology of cryptosporidiosios
Cryptosporidium parvum
Epidemiology of Cryptosporidiosis
Organism is present in normal pigs and is mostly asymptomatic.
Cryptosporidiosis may be concurrent to other enteric diseases.
Potential zoonosis.
Clinical signs of Cryptosporidiosis
If present, diarrhoea and ill – thrift, <12 wks.
Diagnosis of Cryptosporidiosis
Oocysts detectable in faeces using MZN staining; eliminate other causes of diarrhoea
Treatment of Cryptosporidiosis
Anti-protozoal drugs may help but no convincing benefit.
Supportive treatment including electrolytes when necessary.
Importance of stringent hygiene in farrowing house to avoid build up of sporocysts.
Aetiology of rotavirus infection
Group A rotaviruses most important in pigs
Epidemiology of rotavirus infection
Ubiquitous (100% slaughter pigs have antibodies).
Very resistant in the environment (7-9 months in buildings).
Can be involved in piglet enteritis at a number of stages.
Subclinical infection is also common and rotavirus can be involved in enteric diseases at the same time as other organisms such as E. coli.
The sow is the main source of infection, but also environmental carryover.
Sows have quantities of IgA in their milk, which is highly beneficial in ensuring some immediate piglet immunity.
Rotavirus can be a particular problem in intensive systems where there is a constant throughput of farrowing sows with no rest of accommodation between batches.
Infected enterocytes of the small intestine are shed. A and C result in villous atrophy.
Clinical signs of rotavirus infection
Diarrhoea - very fluid to semi - formed faeces sometimes pale yellow in colour with floccules.
Piglets often quite bright and may recover spontaneously within a few days.
Rapid loss of condition, depression, anorexia, maybe vomiting, mortality is about 33%.
Affected piglets grow slowly after weaning leading to uneven weaning weights.
Diagnosis of rotavirus infection
Virus isolation from piglet faeces – PAGE, FAT, ELISA, PCR tests available for both antigen and antibodies.
Post mortem - fluid filled small intestines, some milk in stomach and carcase dehydration. Small intestine distended and filled with creamy fluid - thin walled. Villous atrophy, villous fusion and crypt hyperplasia.
DIfferential diagnoses of rotavirus infection
must identify cause to eliminate a number of other infections including: TGE, Porcine epidemic diarrhoea (PED) - coronavirus,
Enteric colibacillosis - may occur with rotavirus, Coccidiosis, Clostridium perfringens Type C.
Treatment of rotavirus infection
No specific treatment.
Can offer oral electrolytes of piglets will drink.
Removal of milk for 24 hrs which can be useful in calves is seldom practical with piglets.
Probably best to prescribe oral antibiotics e.g. Neomycin, Apramycin etc. in case E. coli is present too.
Can seldom be sure of diagnosis until results of culture and virus tests are available.
Control of rotavirus infection
Concerted improvement in hygiene and farrowing room biosecurity.
All in / all out system with thorough cleaning and resting between batches.
Ensure good colostrum uptake.
No commercial vaccine available.
Expose gilts to faeces of older sows.
Feed back of piglet faeces to sows at least 4 weeks before farrowing helps in severe confirmed outbreaks but may exacerbate in milder cases (since chances of sows shedding at farrowing may be enhanced).
Incidence of Transimssible Gastroenteritis (TGE)
Currently very low. Have been epidemics in the past.
Aetiology of Transmissible Gastroenteritis (TGE)
TGE virus - member of the Coronaviridae family
Epidemiology of Transmissible gastroenteritis (TGE)
TGE is a highly contagious disease affecting pigs of all ages in a naïve herd.
It has a high morbidity and a high mortality.
The virus can enter the body orally and by aerosol; also carried by birds, vehicles and carrier pigs between adjacent farms.
Epidemics are seen mostly in the winter months.
The disease can become endemic on farms with continuous production of pigs after an earlier epidemic.
Piglets receive IgA immunity in their mother’s milk but after weaning have little immediate immunity and are at risk of infection; allows disease to become endemic.
Clinical signs of epidemic TGE
A sudden explosive outbreak of disease affecting almost all the pigs on the farm.
Youngest pigs worst affected and almost 100 % mortality for piglets < 10 days of age.
Acute diarrhoea and vomiting.
T - mostly normal or slightly subnormal.
Diarrhoea is watery, foul smelling greenish yellow.
Vomitus - yellow.
Severe diarrhoea, depression, dehydration, prostration and death in neonatal piglets.
Diarrhoea in adult pigs lasting a few days (note: it is very unusual to see diarrhoea in adult sows and boars - TGE is one of the few conditions in which this occurs).
Clinical signs of endemic TGE
Recurrent outbreaks of diarrhoea in piglets > 6 days of age.
Seen in partially immune large herds in which animals with poor immunity were exposed to the virus and developed diarrhoea.
In some such herds further acute epidemics occurred after 9 months or so depending on immune status of dams.
Diagnosis of TGE
Based on virus detection in the faeces (or oral fluid) of affected animals using RT-PCR.
An ELISA test is also available for detection of specific serum antibodies.
Pathology of TGE
Piglets in poor and dehydrated condition.
The stomach is empty and the gut wall is thin and transparent with green coloured fluid clearly visible within the lumen.
Villous atrophy is visible histologically.
Differential diagnoses of TGE
Few conditions produce such severe devastation as TGE and affected farrowing houses have the appearance of battlefields with large number of dead piglets.
All pigs on the farm including adults affected.
Treatment of TGE
none effective.
Little chance of success with neonatal piglets.
Older pigs - electrolyte solutions for oral consumption may aid recovery.
Some success with oral administration of serum from recovered sows in SAME herd – i.e. giving immune globulins direct to gut.
Prior discussion with DVM and VMD is necessary for this approach.
Control of TGE
Good biosecurity essential to prevent TGE access to farm.
Exposure of gilts and sows to infection at least 4 weeks before farrowing will ensure good colostral protection.
Vaccination available overseas – but not effective or available in UK.
Aetiology of Porcine Epidemic DIarrhoea
A Coronavirus (Alphacoronavirus).
Epidemiology of Porcine Epidemic Diarrhoea
May start in finishing pigs on farm and then spread to breeding stock and neonatal piglets through fomite spread.
Can be transmitted by carrier pigs, vehicles and other contacts.
