GI diseases Flashcards
1
Q
GI diseases of piglets 0-4 weeks
A
Neonatal E. coli Septicaemia Diarrhoea
Clostridium perfringens
Coccidiosis
Rotavirus
Other infectious diseases e.g. TGE, PED
Congenital problems
2
Q
GI diseases in pigs older than 4 weeks
A
Proliferative enteropthy
Swine dysentery
Spirochaetal diarrhoea
Post weaning E. coli enteritis and oedema disease
Salmonellosis
Colitis
Torsion
Gastric ulceration
Hernia
Rectal prolapse
Helminths
3
Q
Incidence of Enteric colibacillosis (E. coli diseases)
A
Very common - the most important cause of enteric disease in pigs.
Responsible for > 50 % of all gastro - enteropathies in neonatal piglets.
4
Q
Aetiology of Enteric colibacillosis (E. coli diseases)
A
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.
5
Q
Which serotype of E. coli is invasive
A
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.
6
Q
Epidemiology of
Enteric Colibacillosis - E coli diseases.
A
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.
7
Q
Predisposing factors for Enteric Colibacillosis - E coli diseases
A
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.
8
Q
Disease syndromes of Enteric colibacilloisis - E coli diseases
A
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.
9
Q
Clinical signs of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
A
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.
10
Q
PM signs of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
A
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
11
Q
Diagnosis of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
A
Clinical signs, history of farm, PM
12
Q
Differential diagnoses of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
A
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.
13
Q
Treatment of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
A
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.
14
Q
Control of enteric colibacillosis (E. coli diseases) in neonatal piglets (first 3 days)
A
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.
15
Q
Epidemiology in enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
A
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.
16
Q
Clinical signs of enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
A
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.
17
Q
Diagnosis of enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
A
Isolation of E. coli in heavy culture from faeces
PM shows severe inflammation of the bowel and sometimes dehydration
18
Q
Treatment of enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
A
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.
19
Q
Control of enteric colibacillosis (E. coli diseases) in Unweaned older piglets < 3 weeks
A
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.
20
Q
Incidence of acute post weaning enteritis
A
Common
21
Q
Aetiology of acute post weaning enteritis
A
E. coli
Common serotype is F4/K88 antigen
22
Q
Epidemiology of acute post weaning enteritis
A
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.
23
Q
Clinical signs of acute post weaning enteritis
A
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.
24
Q
Diagnosis of acute post weaning enteritis
A
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.
25
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.
26
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.
27
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.
28
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.
29
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.
30
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.
31
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.
32
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.
33
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.
34
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.
35
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.
36
Incidence of Clostridium perfringens Type A and B
Less common than Type C
37
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.
38
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
39
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.
40
Pathology of Clostridium perfringens Type A and B
Pale carcase
Severely inflamed intestines
Fillled with haemorrhagic contents
Villous atrophy
41
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.
42
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.
43
Eimeria suis
Carried and shed by sows
May affect weaners
Warm and moist climate in the farrowing house may inhibit sporulation
44
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
45
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.
46
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.
47
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.
48
Pathology of coccidiosis
SI thickened with creamy-watery contents, necrosis, villous atrophy.
49
Histology of coccidiosis
fibronecrotic enteritis and intracellular coccidial forms.
50
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.
51
Aetiology of cryptosporidiosios
Cryptosporidium parvum
52
Epidemiology of Cryptosporidiosis
Organism is present in normal pigs and is mostly asymptomatic.
Cryptosporidiosis may be concurrent to other enteric diseases.
Potential zoonosis.
53
Clinical signs of Cryptosporidiosis
If present, diarrhoea and ill – thrift, <12 wks.
54
Diagnosis of Cryptosporidiosis
Oocysts detectable in faeces using MZN staining; eliminate other causes of diarrhoea
55
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.
56
Aetiology of rotavirus infection
Group A rotaviruses most important in pigs
57
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.
58
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.
59
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.
60
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.
61
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.
62
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).
63
Incidence of Transimssible Gastroenteritis (TGE)
Currently very low. Have been epidemics in the past.
64
Aetiology of Transmissible Gastroenteritis (TGE)
TGE virus - member of the Coronaviridae family
65
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.
66
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).
67
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.
68
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.
69
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.
70
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.
70
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.
71
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.
72
Aetiology of Porcine Epidemic DIarrhoea
A Coronavirus (Alphacoronavirus).
73
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.
74
Diagnosis of Porcine Epidemic Diarrhoea
Detection of virus by RT-PCR; Serology by ELISA.
75
Differential diagnoses of Porcine Epidemic Diarrhoea
TGE is the major differential for the hot Asian strains, other wise for less virulent strains consider enteric colibacillosis, coccidiosis, Clostridium perfringens Type C, Rotavirus.
76
Treatment and control of Porcine Epidemic Diarrhoea
No effective treatment.
Electrolytes in water and general nursing care may help.
In recent USA outbreak, advice was given to euthanize all piglets <10 days of age where those piglets were born to sows without existing colostral antibody.
Vaccines (inactivated and subunit) are in development but none gives solid protection to date, although may be helpful in reducing mortality.
77
Classical swine fever
Diarrhoea and occasionally vomiting are seen in some cases of Classical Swine Fever.
Other symptoms especially CNS signs are usually present.
Affected pigs normally have very high fever and are non - responsive to antibiotic therapy.
The disease is Notifiable and must be reported to APHA.
78
Nectrotic stomatitis
Occasionally seen in piglets whilst on sow.
Infection with Fusobacter necrophorum- may gain access to the soft tissues of mouth through injury - including bites and careless use of tooth clippers.
Foul smelling lesions seen on cheeks, lips and tongue. Mild pyrexia.
Piglets may have difficulty in feeding.
Treatment by antibiotic injection; oxytetracycline usually effective. Gentle debridement of accessible necrotic tissue speeds recovery.
79
Congential and hereditary conditions affecting the GI tract
Atresia Ani
Cleft palate
Macroglossus
Short mandible
80
Incidence of Atresia Ani
Common - may occur in 0.3%
81
Aetiology of atresia ani
Thought to be a recessive gene with incomplete penetrance
82
Epidemiology of atresia ani
May involve just one or (more commonly) several piglets in the litter.
Both male and female are affected. In the male total rectal obstruction is present.
In the female piglet faeces are sometimes passed through a recto-vaginal fistula.
83
Clinical signs of atresia ani
Absence of the anus may be spotted within a short time of birth.
The perineum may be distended by the obstructed rectum just beneath the skin.
On other occasions the rectum terminates at the pelvic inlet or within the pelvis. In such cases dullness, progressive inappetance and a distended abdomen may be seen.
In female piglets with a fistula small faecal pellets may be seen emerging through the vulva.
Affected piglet may survive 3 - 10 days after birth.
84
Treatment of Atresia Ani
If the rectum is immediately beneath the perineal skin a cruciate incision can be made through the perineal skin and into the rectum, with local anaesthesia.
Faecal material escapes and usually the anal opening remains patent.
85
Incidence of cleft palate
Uncommon
86
Aetiology of cleft palate
Thought to be inherited in some cases - possibly through an autosomal recessive gene.
Also may follow Hemlock poisoning in the sow.
87
Clinical signs of cleft palate
Piglet soon seen to be ill-thriven.
Unable to swallow milk – with leakage from nostrils; secondary pneumonia may occur.
88
Treatment of cleft palate
Not attempted – euthanasia. Review data on incidence to identify heritable or toxic factors.
89
Macroglossus
Uncommon,
Cause unknown but probably genetic.
One or more piglets in litter born with very large tongues.
Affected animals unable to close their mouths or swallow.
The defect is incompatible with life.
Euthanasia and investigate genetic background.
90
Short mandible
Uncommon but is seen in the humpy backed pig syndrome which has been described in large whites
91
Enteric disease in pigs from weaning onwards
Porcine proliferative enteropathy complex
Swine dysentery
Spirochaetal colitis/diarrhoea
Post weaning E. coli enteritis
E. coli bowel oedema
Salmonellosis
Non-specific colitis
Yersinia spp. infection
92
Incidence of porcine proliferative enteropathy complex
Widespread.
Seen in post weaning pigs aged 10 weeks onwards but occasionally in younger (mostly as proliferative enteropathy) and also in young adults (mostly as proliferative haemorrhagic enteropathy).
93
Aetiology of Porcine proliferative enteropathy complex
Lawsonia intracellularis
94
Epidemiology of Porcine proliferative enteropathy complex
Spread via the faeco-oral route and infection can be brought in by carrier pigs.
Organism found in wild boar.
The organism is obligate intracellular and causes proliferative replacement of gut epithelial cells by adenomatous tissue.
Survival in buildings for up to 2 weeks and rodents may carry for longer.
Sows a possible source of seeding to piglets.
95
Clinical signs of Porcine proliferative enteropathy complex
Proliferative enteropathy / PIA - usually in pigs 4 - 6 weeks post weaning.
Affected pigs dull, poor appetite and poor food conversion. Temperature usually normal.
May see grey / pale diarrhoea (like wet cement) but not in all animals. Chronically affected animals fail to thrive.
Proliferative haemorrhagic enteropathy (PHE) -
usually young adults.
May have sudden death and sometimes passage of haemorrhagic faeces.
Animal may be pale due to heavy blood loss into the bowel.
T normal.
96
Diagnosis of Porcine proliferative enteropathy complex
Clinical signs, age group involved, identification of organism in faeces
or gut wall.
PCR test on faeces sample.
97
Post mortem of Porcine proliferative enteropathy complex
proliferative enteropathy - inflammation of small intestine with thickening and some necrosis of the wall of the terminal ileum.
Haemorrhagic form - large amounts of blood in bowel lumen. Some fibrin tags on gut epithelium.
98
DIfferential diagnoses of Porcine proliferative enteropathy complex
Swine dysentery - usually develops more slowly - PIA sudden onset of haemorrhage,
Bleeding from Gastric / oesophageal ulcers - post mortem examination confirms,
Intestinal haemorrhagic syndrome - usually associated with whey diet
Clostridium perfringens Type C - usually younger pigs.
99
Treatment of Porcine proliferative enteropathy complex
Treat clinically affected animals with parenteral oxytetracycline or tiamulin.
Vitamins to help blood replacement in cases of PHE.
In contacts - oxytetracycline or tiamulin in water. Also tylosin or lincomycin - spectinomycin (Lincospectin, Zoetis), valnemulin (Econor, Novartis) in food or water
100
Control of Porcine proliferative enteropathy complex
Vaccination (Enterisol Ileitis – Boehringer) – gives 17 weeks protection after in-water addition of live attenuated organism.
Strategic antibiotic therapy. Improve hygiene.
Whole building destocking & disinfection helps.
Caution with incoming potential carrier pigs – but even high health herds likely to carry.
101
Incidence of swine dysentery
Had declined in prevalence but now re-emerging, interest in regional eradication plans.
Mostly affects pigs aged 8 - 16 weeks but occasionally adults in naive herd.
Severe economic losses arise through poor food conversion.
102
Aetiology of swine dysentery
Brachyspira hyodysenteriae (formerly Treponema & Serpulina); B. hampsonii is an emergent strain of equivalent virulence.
103
Epidemiology of swine dysentery
Direct pig to pig or indirect spread.
Passes through stomach unaffected by gastric pH.
Can be carried by rodents.
Stresses including overcrowding, mixing, and moving all predispose. Morbidity <75%.
Mortality can reach 25%.
104
Clinical signs of swine dysentery
Muco-haemorrhagic diarrhoea - i.e. dysentery, but not always at first.
Temperatures may be normal or slightly raised.
Poor appetite and rapid weight loss.
Abdominal discomfort and loose faeces in pen.
Perineal staining.
Diarrhoea greyish black with blood and mucus.
Occasional deaths.
If untreated some recover spontaneously others develop chronic, irreversible bowel damage.
105
Diagnosis of swine dysentery
Herd history, clinical signs.
Usual methods include FAT, PCR and culture.
Important to make diagnosis based on clinical signs and pathology / histopathology as well as culture or PCR since non-virulent strains of B. hyodysenteriae exist.
106
Post mortem of swine dysentery
lesions mainly in large bowel, SI mostly unaffected.
Carcase emaciated and later chronic gut wall damage.
Colon affected: serosal oedema, mucosa thickened, diphtheritic material, bloody mucus.
Contents brownish red, fould smelling fluid, varying portions of blood streaked mucus.
107
Differential diagnoses of swine dysentery
Classical Swine Fever – will have fever, plus CNS and respiratory signs, while dysentery is rare in CSF.
Porcine colonic spirochaetosis - milder and B. hyodysenteriae not present.
E. coli infections - non - pyrexic. Small Intestine involved. Culture.
Salmonellosis - usually higher temperature, and yellow diarrhoea.
Yersinia infection - lower grade diarrhoea and ill - thrift.
Intestinal haemorrhagic syndrome or Gastric / oesophageal ulceration
108
Treatment of swine dysentery
Start as soon as possible and advisable to treat whole group.
Parenteral injection of e.g. tiamulin, tylosin (some resistance), lincomycin etc.
Water or feed medication for in-contacts - e.g. tiamulin for 4 weeks). Also valnemulin in food (Econor, Novartis).
109
Control of swine dysentery
Feed highly digestible food.
No vaccine available.
Eradication – total depopulation, disinfection, rest, and repopulation with clean stock.
Partial depopulation of grower/finisher pigs with medication of sows (e.g. with tiamulin) and suckling piglets, with disinfection of entire unit and drains.
Increasing interest in regional eradications in the UK.
110
Spirochaetal colitis/diarrhoea
An enteric disease of pigs caused by spirochetes other than Brachyspira hyodysenteriae.
111
Incidence of spirochaetal colitis/diarrhoea
Mostly seen in young weaned pigs but occasionally seen in adults.
112
Aetiology of spirochaetal colitis/diarrhoea
Spirochaetes including Brachyspira pilosicoli, B. intermedia, and B. innocens.
113
Epidemiology of spirochaetal colitis/diarrhoea
As for Swine Dysentery, including rodent, but also dog carriage.
Low digestibility diets predispose, with raised delivery of fermentable residues to colon.
114
Clinical signs of spirochaetal colitis/diarrhoea
Diarrhoea, very occasionally dysentery.
T 39 - 40 C.
Poor weight gain and some chronic cases of diarrhoea.
Many recover without treatment.
Large intestine lesions only.
Mucus and reddening but blood rare.
Colonisation of colonic mucosa interferes with water absorption.
115
Diagnosis of spirochaetal colitis/diarrhoea
Clinical signs, PCR on faeces, and culture (with negative results for B. hyodysenteriae).
A much milder disease than Swine Dysentery.
116
Treatment and control of spirochaetal colitis/diarrhoea
As for Swine Dysentery.
Also tylosin.
Change from pellets to meal.
117
Clinical signs of post weaning E. coli enteritis
>95% of diarrhoea in recently weaned pigs.
Grey brown watery diarrhoea. Rough hair coat.
Pyrexia may occur (40.6 degrees). Morbidity 20-50%.
Outcome: dehydration, recovery with reduction in growth rate, remain stunted, mortality in uncomplicated cases <10%.
118
Similarities between post weaning enteritis and oedema disease
Same age group (recently weaned)
May occur together in one pig
Share certain virulence factors
Some strains cause both disease
119
Incidence of E coli bowel oedema
Less common than it was when pigs were weaned at 8 weeks.
May see in very traditional small scale systems.
120
Aetiology of E coli bowel oedema
Verotoxin-producing strains of E. coli, including F18 group.
121
EPidemiology of E coli bowel oedema
Usually occurs within 10 days of weaning.
One or more animals in the litter affected.
Predisposing factors thought to include excessive feed (unbalance in gut flora), sudden change of diet, too fine particle size in the food, sudden loss of maternal milk.
122
Clinical signs of E coli bowel oedema
Affected pigs are dull and less interested in food than others.
Temperature - mostly normal or subnormal.
Mild ataxia may be seen and animals appear to lose control of their forelegs and try to move with their shoulders flexed and forelimbs being pushed along the floor.
Bilateral eyelid oedema is seen and pigs may appear blind and deaf.
If handled, pigs have a muffled bubbly squeal.
Deterioration is rapid and within 12 hours affected pigs may be in lateral recumbency, breathing with a forced expiration and unconscious.
Death follows in almost every case.
Very occasionally pigs recover but may be left with a mild CNS defect such as a head tilt or mild ataxia.
123
Diagnosis of E coli bowel oedema
History of late weaning, or over-feeding, and clinical signs.
Laboratory tests: culture/swab, detection of F and O serotypes and toxin types.
Sensitivity test.
124
Post mortem of E coli bowel oedema
ideally shortly after death - marked oedema of gastric wall, laryngeal and mesenteric oedema.
125
DIfferential diagnoses of E coli bowel oedema
Other CNS diseases like Strep suis Type 2 - meningitic
signs including nystagmus are not seen and no joint involvement with bowel oedema.
126
Treatment of E coli bowel oedema
Nothing very effective once clinical signs – prognosis very guarded.
Can try parenteral antibiotic e.g. apramycin, and NSAIDs may help.
Rest of litter - try to prevent cases developing.
Reduce food intake.
127
Control of E coli bowel oedema
General care at weaning time, avoidance of over feeding, and try to avoid other predisposing factors
128
Incidence of salmonellosis
Zoonotic and a constant threat to the pig industry.
Condition is notifiable by APHA to DEFRA.
S Typhimurium predominated.
Surface contamination very low in well run abattoirs and human risk should be quite low.
129
Aetiology of salmonellosis
Salmonella enterica serotype Typhimurium is the serotype most frequently found in pigs in the UK.
A wide range of other serotypes include monophasic Salmonella 4,[5]:i:- (a recently emerged subgroup of S. Typhimurium), S. Derby, and S. London have been reported.
Salmonella cholerae suis is a pig-adapted species but is now very rare.
130
Epidemiology of salmonellosis
Can have direct and indirect spread.
Carrier animals are common and the organisms may be found in their tonsils or bowel.
Piglets acquire infection from the sow or from other pigs after weaning.
Stress - plays a major part in predisposition as it does in other animals - overcrowding, transport, poor hygiene.
Group-level antibiotic treatment for other diseases such as Streptococcal meningitis can trigger an switch from subclinical to clinical Salmonellosis.
Risk of human infection - from pigs or contaminated carcasses is important
131
Clinical signs of salmonellosis
Vary from acute sudden deaths with septicaemia to enteritis and
subclinical carriers.
Seen in pigs 6 - 26 weeks.
Septicaemic form - Pigs may be found dead, others in group are dull, pyrexic, anorexic, reluctant to move, may show purple cyanosis, CNS signs occasionally
Acute enteritis - pigs dull, anorexic, pyrexic, profuse watery, yellow diarrhoea, some deaths.
Chronic diarrhoea - severe weight loss and chronic scour. Intermittent pyrexia. Some develop rectal stricture. Pigs may become emaciated and totally anorexic and death may ensue.
132
Diagnosis of salmonellosis
Any high temperature in scouring pigs should lead one to suspect salmonella.
Purple skin discolouration suspicious but occurs with other septicaemias.
Confirmation is by faecal culture and isolation.
Antibody ELISA for use on serum and meat juice indicates historic or ongoing exposure.
133
Post mortem of salmonellosis
Septicaemic form - multiple haemorrhages including petechiae in kidneys - can resemble Classical Swine Fever.
Enteritis - severe bowel inflammation with infarcts and ulcers; mesenteric LNs enlarged.
Chronic enteritis - may see necrotic enteritis, especially colitis and or typhlitis, with destruction of much of the mucosal surface.
134
Differential diagnoses of salmonellosis
Classical Swine Fever - important differential - also very pyrexic and septicaemic, but would also expect skin petechiation and reporiductive signs.
Acute swine erysipelas - no diarrhoea.
Swine dysentery - less pyrexic.
E. coli infections - usually non - pyrexic and no haemorrhage into bowel or ulceration.
Acute E coli post weaning enteritis.
135
Treatment of salmonellosis
A range of antibiotics can be used but their use should only be considered where there is evidence of disease (i.e. not as a tool to reduce shedding in sub-clinical situations).
Sensitivity testing should be done to allow adaptation of plans since resistance is common.
Drugs include trimethoprim / sulpha, apramycin, neomycin.
Fluoroquinolones should be reserved unless no other option.
Parenteral treatment for ill and pyrexic animals and NSAIDs (ketoprofen) useful.
Fluid therapy not really practical if large numbers involved but oral electrolyte should be made available if possible.
Also antibiotics in water for sick and in contact animals.
136
Control of salmonellosis
Acidification of food and water (formic acid) can be beneficial in controlling infection through stabilising beneficial gut flora.
Inclusion of sodium chlorate in water reduces shedding.
Wet feeding or meal versus pelleted feed is beneficial through effects on gut flora.
Use of barley instead of wheat in home milled feeds is helpful
Improvements in hygiene.
Vaccination is an option, although none yet specifically licensed in pigs in the UK.
137
Incidence of non-specific colitis
Up to 5 percent of UK herds may have the problem.
Mostly affects pigs of 8 - 10 weeks of age.
More common on farms where hygiene is poor.
138
Aetiology of non-specific colitis
Unknown but may involve the following:
a. Unsuitable nutrition - may include excesses of ingredients such as soya, rape and peas. Also too finely ground food. The pelleting process may destroy trace elements and caramelize carbohydrates. Pantothenic acid deficiency may predispose.
b. Chronic parasitism - including Oesophagostomum
c. Chronic infection - including Rotavirus, chronic TGE etc.
139
Clinical signs of non-specific colitis
Mild looseness.
Symptoms mostly mild but overall food conversion and growth rates may be reduced.
Growing pigs 6-14 weeks.
Diarrhoea with loss of condition. Sometimes inflammation of the colon - few if any obvious colonic lesions.
140
Diagnosis of non-specific colitis
Careful investigation of feeding and management.
Search for known pathogens in faeces and possibly at post mortem.
141
Treatment of non-specific colitis
Tackle specific pathogens where found.
Strict hygiene.
Dietary adjustments.
142
Other GI diseases
Torsion
Gastric ulceration
Abdominal hernias
Rectal prolapse
143
Incidence of torsion
Sporadic cases are rare but can occur in clusters where a dietary basis.
Can be limited to stomach, SI, LI, or a combination and may involve spleen and part of liver.
144
Aetiology of torsion
Excited activity predisposes (once a day feeding, lairage).
Liquid based feeding (whey) and fermentation of these feeds predispose.
Intake of large quantity at one time (once per day feeding).
145
Clinical signs of torsion
sudden death, abdominal distension, pain, salivation, circulatory shock.
146
Diagnosis of torsion
Usually at post mortem, plus history.
147
Pathology of torsion
Carcase pale
Abdominal distension
Dilated intestines 'pop out'
Rotation anticlockwise 180 degrees at root of mesentery
Intestinal loops reddish black
Mesenteric vessels extremely engorged
Stomach distended
Spleen can rupture causing hemiperitoneum
148
Treatment and control of torsion
Mild cases (abdominal distension) can attempt exercise to dissipate gas.
Most cases require euthanasia.
Review dietary management and procedures and if appropriate reduce the whey element in wet feeds.
149
Incidence of gastric ulceration
Constant threat but clinical cases uncommon.
The non - glandular oesophageal part of the stomach is mostly involved.
150
Aetiology of gastric ulceration
Predisposing causes include:
Stress - of any kind including disease and overcrowding.
Parasitism - especially Hyostrongylus rubidus
Diet - especially too fine particle size. Also high unsaturated fat levels. Lack of roughage e.g. no straw in diet. Starvation.
Ongoing other diseases: Post-weaning multisystemic wasting syndrome PMWS.
151
Epidemiology of gastric ulceration
Initial lesion may be hyperkeratosis in pars oesophagea.
Leads to ulceration, exposure of blood vessels and haemorrhage.
Mostly seen in pigs approaching finishing weight.
152
Clinical signs of gastric ulceration
Mostly sub-clinical
Sows at parturition
Reduced growth rate
Anaemia
Intermittent melaena
Laboured breathing
Rarely haemorrhagic vomit (pathognomic)
Pain (teeth grinding and rigid back)
Anorexia
Sudden death
Mortality 1-2% (sudden death of pig in good condition)
153
Diagnosis of gastric ulceration
Clinical signs.
Post mortem - extensive ulcerated area, stomach full of blood. Kits available to test for occult blood in faeces.
154
Differential diagnoses of gastric ulceration
other causes of blood in GI tract - including Swine Dysentery - usually many pigs involved and initial high temperature. Damage to gut wall also in Salmonellosis.
155
Treatment of gastric ulceration
In valuable anaemic living pig might try intraperitoneal blood transfusion in valuable and anaemic pig.
Encourage haemopoesis e.g. with multi - vitamin injection.
Use of omeprazole or ranitidine (proton pump inhibitors; not licensed in pigs) fed to each animal may encourage healing of ulcer.
Euthanise pigs in severe pain or with haemorrhagic vomit.
156
Fundic gastric ulcers
These may be an incidental finding in diseases including Classical Swine Fever, Salmonella cholerae suis.
High infestations with Hyostrongylus rubidus may also cause ulcerative damage in this part of the stomach.
Role of Helicobacter - found in pigs and also in people with gastric ulcers is not known.
157
Abdominal hernias
Inguinal and umbilical hernias are common.
If very large their covering skin may be excoriated by rubbing along the ground leading to ulceration. Umbilical hernias occasionally suffer from strangulation of the bowel.
Commonly 9-14 week old growers. Ventral/inguinal swellings.
Intestinal contents can be replaced.
Can lead to growth retardation and intestinal strangulation.
Large hernias touching the ground: risk of infection, ulceration, rupture.
Management:
Small hernias should be checked to ensure reducible. Hernia rings <8cm are prone to strangulation and must be monitored carefully. Euthanasia where this occurs. Most pigs will progress to slaughter OK.
Larger hernias: potential for injury/rupture is greater but risk of strangulation may be less. If ulcerated or touching ground then euthanise. Liaise with abattoir OV before sending for slaughter and ensure careful transport and lairage. Surgery is usually uncomplicated but occasionally bowel resection is required and the costs are prohibitive and likely not justifiable on commercial grounds.
158
Incidence of rectal prolapse
Quite common.
Mostly sporadic but can be a herd problem.
Males more commonly affected.
Pigs aged 12 - 20 weeks most commonly affected
159
Aetiology of rectal prolapse
Usually linked to straining and increased intra-abdominal pressure.
Chronic diarrhoea and / or cough predisposes.
Also prolonged oral medication with tylosin.
Occasionally linked to mycotoxins such as zearelenone poisoning from oestrogenic Fusarium.
160
Clinical signs of rectal prolapse
Intermittent or constant exposure of rectal mucosa.
In sows vaginal prolapse may also be present.
Prolapse damaged by contact with environment and damage from other pigs.
May have severe haemorrhage.
161
Complications of ractal prolapse
trauma of rectum - peritonitis, scar formation.
162
Treatment of rectal prolapse
Separate affected pigs to prevent cannibalism.
If very close to finishing may be able to send for slaughter.
Can resect surgically under general anaesthetic; but euthanasia might be appropriate in many circumstances.
NSAIDs and long acting antibiotics to prevent infections.
Avoid/treat causal factors
163
Helminth parasites of pigs
Hyostrongylosis
Oesophagostomiasis
Ascariasis
Trichuris infestation
Lungworm
Hepatosis cysticercosa
Liver fluke disease
164
Incidence of Hyostrongylosis
Quite common.
Surveys have shown that up to 30% sows may be infested.
Younger pigs - less commonly involved but can be at risk.
165
Aetiology of hyostrongylus
Hyostrongylus rubidus - the red stomach worm of pigs.
166
Epidemiology of hyostrongylosis
Adult worms are red, 1 cm in length, live on the gastric mucosa where they inflict damage resulting in protein loss.
Heavy infestation may cause necrosis and ulceration of the gastric mucosa.
The life cycle is direct.
Some larvae enter a resting stage in the gastric mucosa of sows and are activated by the hormone changes of pregnancy and lactation.
Worm egg counts rise in infested sows increasing the risk to piglets.
167
Clinical signs of hyostrongylosis
Loss of condition, anorexia, poor breeding performance.
May see melaena and occasionally vomiting.
Hyostrongylus is often involved in the Thin Sow Syndrome (a feature of early parity sows that do not take in sufficient feed in their first lactation).
168
Diagnosis of hyostrongylosis
Clinical signs, worm egg count, elevated plasma pepsinogen.
Post mortem may reveal severe damage to the gastric mucosa.
169
Differential diagnosis of hyostrongylosis
Other causes of weight loss including poor feeding.
170
Treatment and control of hyostrongylosis
Anthelminitic programme
170
Incidence of oesophagostomiasis
Quite common and easily overlooked.
Surveys have shown that 80%
of UK sows may be infested with 30% younger pigs.
Incidence likely higher in outdoor pig units.
171
Aetiology of oesophagostomiasis
Oesophagostomum dentatum and Oesophagostomum quadrispinulatum.
The pig nodular worms.
171
Epidemiology of oesophagostomiasis
Adult worms 1.5 cm long and live in the colon and caecum.
Direct life cycle.
Larvae thought not to survive long in indoor units.
Despite this infestations in indoor units can reach pathological proportions.
172
Clinical signs of oesophagostomiasis
Diarrhoea in heavy infestations.
Weight loss, poor food conversion and low milk yield in sows.
173
Treatment and control of oesophagostomiasis
Anthelmintic strategy
174
Incidence of ascariasis
Widespread in the pig population.
Direct clinical signs less common but consequences of infestation - especially milk spot liver and reduced feed conversion - can be very important.
175
Aetiology of ascariasis
Ascaris suum.
The common pig round worm.
Recent genome sequencing shows A. suum to be the same organism as A. lumbricoides (human roundworm) – so, zoonotic.
176
Epidemiology of ascariasis
Adult worms white and very large - up to 40 cm.
Life cycle direct.
Eggs extremely resistant - can survive away from pigs for up to 7 years and hence dangers of infestation from field where no pigs have lived for some years.
Cleaning of accommodation difficult to ensure all eggs removed.
177
Clinical signs of ascariasis
Reduced growth rate and poor food conversion.
Occasional sudden deaths caused by obstruction of small intestine, intussusception, blockage of bile duct - latter causing jaundice.
Larval migration thought to cause milk spots in liver which may lead to liver rejection at slaughter.
May see coughing and diaphragmatic lobe pneumonia caused by migrating larvae.
178
Diagnosis of ascariasis
Clinical signs, worm egg count, liver abattoir reports.
An ELISA test for serum antibody now available.
179
Trichuris infestation
Found frequently (25% UK pigs) as the small whip worm Trichuris suis in the caecum.
Rarely causes clinical disease in the UK but cases of ulcerative typhlitis reported overseas.
Controlled by most anthelmintic programmes.
180
Lungworm disease
Infestation with Metastrongylus apri the pig lung worm occurs in the UK.
The incidence is likely to increase with the development of more outdoor units with access to the intermediate host - the earth worm.
181
Hepatosis cysticercosa
Mostly sheep & cattle, less commonly pig.
Intermediate stage of Taenia hydatigena.
Only be recognised at PM.
182
Liver fluke disease
Infestation with Fasciola hepatica is seldom diagnosed in the UK.
Increasing numbers of outdoor units may increase the risk of exposure to the intermediate host - the snail Limnea truncatula which lives in muddy damp environments.
No flukicide drugs are currently licensed for use in pigs in the UK so follow cascade.
183
Worm control programmes
In feed wormers are easily given possibly every 6 months but this drives resistance.
Injectable wormers and in-water wormers can be sure that each pig is treated.
Macrocyclic lactones (e.g. ivermectin) have a wide range of activity including mange (Sarcoptes scabei).
Flubenol (flubendazole, Elanco) is widely used in-water and effective.
