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Describe the important factors for biosecurity of the pig unit?

Location - preferably an area of low pig density, at least 3km from another pig unit in hilly country or on the coast. Secure perimeter fence to prevent visitors, wild pigs and other mammals entering the unit, isolation facilities off site for incoming stock, well constructed loading bay, draining towards the lorry, with gates preventing lorry drivers entering the unit from the loading bay, washing and disinfection facilities at the loading bay, lorries arriving at the farm to collect pigs should be empty, clean and disinfected. Visitors should not have been to another pig unit in the past 2,3 or 4 days. rodent and fly control should be effective and feed stores should be netted to prevent birds gaining access.


Which pathogens will a minimal disease pig herd be free from?

Enzootic pneumonia (mycoplasma hyopneumonia)
Porcine reproductive and respiratory virus infection
Pleuropneumonia (actinobacillus pleuropneumoniae)
Atrophic rhinitis (toxigenic pasteurella multocida)
Swine dysentery (bracyspira hyodysenteriae)
Streptococcal meningitis (streptococcus suis type II)
Mange (sarcoptes scabei)


What is the cause of white spot livers?

ascaris suum infection (roundworm)


What is mulberry heart disease?

A nutritional disease of the myocardium of pigs, causing sudden death in young pigs in good body condition. thought to be due to selenium/vit E deficiency. May also see hepatosis dietetica - an enlarged and mottled liver with haemorrhage.


What is the target for herd culling policy in a pig herd?

indoor herds have an average target of 38% and outdoors 45%. The target for culling sows is 6-7 parity.


What are the increasing problems with sows getting older?

Prolonged farrowings - increased stillbirth rate, more piglets overlain. Variable litter size and birth weights, problems with lactation arising from chronic mastitis and non functional teats, greater likelihood of poor fertility, lameness, endometritis, vulval discharge, cystitis/pyelonephritis.


Which management factors should be considered when investigating reproductive failures in sows?

Sow condition - level of nutrition, diet, feeding system.
Service management - boar contact, heat detection, number/timing of services, supervision, hygiene. Boar usag e- frequency, ratio of boar to sows, health of boars.
AI usage - timing, operator experience, handling of semen, quality of semen.
Seasonal effects - winter anoestrus, adverse temperature and weather conditions.
Pregnancy testing
Farrowing house management and environment - hygiene, sow comfort, farrowing supervision, speed of farrowing, neonatal care, suitable conditions for piglets, health. Sow parity, health problems, sow deaths.


Define an anoestrus gilt?

atleast 8 months of age without showing oestrus. or Cessation of oestrus cycles in the absence of pregnancy.


Define an anoestrus sow

Weaned at least 10 days without showing oestrus. Cessation of oestrus cycles int he absence of pregnancy or lactation.


what are your differentials for anoestrus?

inactive ovaries, pregnancy, undetected oestrus, irregular cycles due to persistent cl,, cystic follicles, intersexuality


What is the cause of cystic ovaries in sows?

high progesterone concentrations from adrenal cortex inhibits positive feedback mechanism of oestrogens on the pituitary gland thus inhibiting pre ovulatory surge of LH. examine for causes of environmental stress.


Which problems should you consider when sows are showing irregular returns to oestrus?

Loss during the embryonic phase up to 35 days leading to resorption or the foetal stage leading to abortion. possible - seasonal affects, overuse of boars leading to small number of embryos, vaginal discharges/endometritis, infectious reproductive diseases eg PRRS, Parvo, enteroviruses, swine influenza, erysipelas, actinobacillus pleuropneumoniae.


What are the possible causes of intrapartum deaths in sows?

Long duration of farrowing, small litters, or very large litters, where parturition is 6-7 days early or late, high parity sows, position of foetus, anorexia, carbon monoxide, high ambient temperature in late gestation (sow fatigue)


How can parturition be induced in pigs?

By injection of prostaglandin. Farrowing commences 18-36 hours later. small doses of oxytocin can be given form 20 hours post prostaglandin in order to speed up the farrowing. single large doses of oxytocin are contra indicated as this has been shown to cause dystocia.


What is a male pseudohermaphrodite?

testicles for gonads with female external genitalia.


What is a true hermaphrodite?

Both ovarian and testicular tissue in gonads with female external genitalia. Vulva often upturned and clitoris prominent.


When is reproductive failure associated with vaginal discharge in the sow seen? what is the aetiology of this?

Thick creamy or muco haemorrhagic discharge seen 10-20 days post service. May persist for weeks/months if untreated or resolve spontaneously after 1-2 weeks. Discharge may arise from vagina, uterus, bladder or kidney inflammation. Quantitiy of discharge varies from slight to copious. The aetiology is a mixed population of ubiquitous organisms eg A pyogenes, E coli, streptococci, pseudomonas. Environmental factors are important. Infection probably introduced at service when genitalia contaminated.


How can reproductive failure associated with vaginal discharge in the sow be controlled and treated?

If discharge is copious, sows are unlikely to be pregnant. Treat discharging sows promptly with long acting broad spectrum antibiotic injection or installation via AI catheter. A slight discharge in the first week after service is of no pathogenic significance - usually due to seminal debris. Do not re serve sows whilst discharging. Once recovered use AI for next service, avoid possible boar contamination. If discharge recurs or sow returns for a second/third time then cull. Adopt stringent hygiene for boar pens, service pens and sow stalls/accommodation especially that used in the first 21 days post service.


What are the typical bacteria which cause coliform mastitis in sows?

E coli, klebsiella, enterobacter spp. Bacterial species which are common in the sows environment. ORganisms come in contact with the teats through inadequate hygiene or via a piglets oral flora. Endotoxaemia is considered to be the cause of agalactia. Septicaemia does not develop.


What are the clinical signs seen in sows with coliform mastitiS?

Initial signs on day 1 or 2 post farrowing, temperature response up to 42C, listless, weak, loss of interest in piglets, prefer sternal recumbency, piglets gaunt and hungry looking, continually trying to feed, restless. skin over mammary area reddened. Sub cutaneous oedema.
Treatment - broad spectrum antibiotic, nsaids, oxytocin, care for piglets, cross fostering, fee with milk, substitute, prevent chilling.


What does Porcine reproductive and respiratory syndrome cause?

Reproductive losses in pregnant stock, increased pre weaning mortality and influenza like illness affecting all ages of pigs.


What are the clinical signs of PRRS?

Non specific illness in sows, 1-2 weeks later reproductive losses followed by unthriftiness, respiratory illness and mortality in piglets and all ages of growing stock. Effects on neonatal piglets can be severe, respiratory distress, scour, unthriftiness, high mortality. Semen quality may be impaired following infections of boars. Reproductive problems include infertility, premature farrowing, stillbirths and weakly born piglets.


How can PRRS be diagnosed?

Serology, virus isolation from aborted stilborn or non viable piglets, PCR test for virus from blood semen throat swabs.


What are the clinical signs of swine influenza?

Very similar to PRRS except respiratory signs are more widespread and severe especially if there are other endemic respiratory diseases on the farm. The virus enters the respiratory tract, multiplies rapidly in bronchial epithelim, virus dissapears by 9-10 days post infection.


How can swine influenza be diagnosed?

clinical featuers, serology (paired samples, rising titres) virus isolation from aborted piglets, infected lung in acute stage of disease.


What are the clinical signs of porcine parvo virus?

All reproductive associated, stillbirths, mummification, embryonic death, infertility, increased regular and irregular returns to oestrus, small litters, in non pregnant gilts and boars infection is of no consequence. Virus kills foetuses up to approx 70 days of gestation but pregnancy is maintained and piglets all mummified at birth or mixed mummified, stillborn and live piglets born.


How does porcine parvo virus spread?

oro nasal or veneral routes, viraemia, transplacental spread approx 10-14 days. Spreads into boar reproductive organs and semen from approx 7-21 days post infection.


How can porcine parvovirus be diagnosed?

paired maternal serology, virus detection PCR on foetal liver, serology in large fresh foetuses and stillborns.


Which is the most common leptospira serovar infecting pigs?

L bratislava is of most importance with L canicola and L icterohaemorrhagica occuring rarely.


What are the clinical signs seen with porcine leptospirosis?

abortion, stillbirths, weak piglets of reduced viability, abortion in last trimester, infertility, returns to service.


What is the pathogenesis of porcine leptospirosis?

Infection by oro nasal, venereal routes. BActeraemia, localised in renal tubules, shed in urine. Transplacental infection occurs, localises in uterus, foetal invasion, abortion 10 days - 4 weeks post infection. subclinical infection common in herds.


How can lepto be diagnosed in pig herds?

Sample sows with a history of recent abortion/infertility and assess the titres of the batch. For a foetus use antigen detection FAT or serology.


What clinical signs does streptococcus suis infection cause?

Polyserositis, joint ill, septicaemia, meningitis in young piglets.


How does streptococcus suis spread?

Infection is by aerosol or contact with carrier pigs. Bacteria colonise the tonsils, multiply and gain access to the circulation causing bacteraemia or septicaemia. The infection can localise in target tissues causing inflammation.


What are the clinical signs of streptococcus suis infection?

Joint ill occurs in suckling piglets and weaners. piglets are febrile with one or more swollen joints which are painful causing lameness. Affected piglets are reluctant to suckle or feed and rapidly fall behind the group. piglets with septicaemia show little on pathology except petechial haemorrhages of the pleura. In polyserositis there is fibrinous fluid exudation into body cavities and pericardium.


How can streptococcus suis infection be treated and prevented?

S suis is susceptible to a wide range of antibiotics. Suckling piglets are treated individually with courses of antibiotics by injection. Weaners can be treated by water or feed medication. Cases of meningitis must be removed from pens, placed in hospital accomodation and treated with antibiotics and NSAIDs by injection. Penicillin is usually highly effective. Attempts to eradicate s suis from herds by partial depopulation, medication of sows and boars with tilmicosin and thorough cleaning and disinfection of buildings has often proved unsuccessful on account of tonsilar carriage of organism by sows.


What is the cause of exudative epidermitis (greasy pig disease)

Staphylococcus hyicus - A common skin infection which can cause extensive lesions and prove fatal.


How does staphylococcus hyicus spread?

Spread is by contact with infected pigs and it can spread rapidly within groups. Trauma to the skin through teeth marks, mange infection, rough bedding or sharp projecting objects in pens predispose to infection.


What is the pathogenesis of staphylococcus hyicus infection?

BActeria multiply in the epidermis causing congestion, inflammation, fibrin exudation and increased sebaceous gland secretions giving the pigs a greasy feel. scabs form in the affected areas. May be fairly localised but can spread to affect large areas of skin in some piglets, causing severe pain, anorexia and death. In severe cases the skin is extremelythickened and develops deep cracks that ooze serous fluid and fibrin.


How is S hyicus treated and prevented?

S hyicus is generally susceptible to a range of antibiotics. The treatment strategy depends on umbers of pigs affected. the best response is obtained with antibiotics by injection. Antibiotic creams applied to the skin speed recovery. Severe cases should always be treated by injection and anti inflammatory agents should be used to help alleviate the severity of the lesions. Large affected groups should be treated in water or in feed.


What is the cause of glassers disease in pigs?

Haemophilus parasuis


What is the pathogenesis of glassers disease?

Haemophilus parasuis infection is characterised by fibrinous polyserositis in weaner and grower pigs. infection is by aerosol, pigs develop septicaemia, polyserositis, pneumonia and sometimes rhinitis and meningitis. Immunity develops in pigs that recover.


What are the clinical signs of glassers disease?

Occurs most commonly in weaned pigs from 1-3 months of age. onset of the disease is sudden. pigs become febrile, anorexic, show signs of pneumonia, lameness, stiffness and recumbency. there can be blotchy skin discolouration, mainly reddening of skin or peripheral cyanosis. Pigs that die acutely show fibrinous polyserositis, pericarditis and polyarthritis. Pneumonia and meningitis


What is the treatment and prevention methods for glassers disease?

H parasuis is sensitive to a wide range of antibiotics. As the disease commonly occurs in outbreak, treatment of the affected group with antibiotics in water or feed is advisable. An inactivated vaccine containing mycoplasma hyopneumoniae and haemophilus parasuis can be used in piglets for preventing /controlling both infections.


What is swine erysipelas?

Erysipelothrix rhsuopathiae is the cause of an acute disease in pigs characterised by a septicaemia and diamond shaped skin haemorrhages or a chronic syndrome characterised by polyarthritis and vegetative endocarditis.


How does infection with swine erysipelas occur?

E rhusopathiae is a soil associated organism and is carried by pigs in the tonsils. buildngs become contaminated and pigs get infected through contact. the organism is shed in faeces and urine. it is zoonotic. Pis develop immunity. however, antibodies do not appear to cross joint capusles and this allows joint infections to persist.


What are the clinical signs of swine erysipelas?

In the acute form pigs from approximately 2 months of age to adult show high temperature, lethargy, anorexia and red blotching of the skin, sudden death can occur, diamond shaped skin lesions appear 1-2 days after onset of fever. Polyarthritis affects the limb joints especially elbows and stifles. Cases with valvular endocarditis may have an obvious heart murmur and develop clinical signs of congestive heart failure.


What does m. hyosynoviae infection cause in pigs?

arthritis in growing and finishing pigs. Septicaemia folows infection by oronasal route and localisation in joints causing synovitis. pigs develop acute lameness on one or more limbs and joint capsules swell.


What must a pig owner do before buying a pig as a pet?

get a county, parish holding number that identifies where the pigs will be kept. Obtain an animal movement document from the sellar (AML2), transport in pigs in compliance with DEFRAs general license for moving pigs, and register pigs with animal health within 3 days of arrival on the premises.
Make sure the pig is properly and legally identified. Implement good bio security to protect both the health of pigs and their keepers.


what must pig owners never do?

Move pig without the proper license or walk them without obtaining a walking license. In scotland pig walking off premises is not permitted. Do not feed pigs or allow pigs acess to any waste food, kitchen scraps or food that has come from a domestic or commercial kitchen. Milk, milk products, fruit and veg may be fed aslong as they have not come from a domestic kitchen or catering outlet.


when should female pigs be spayed?

if it is not intended to breed from femaees, they should be spayed at approx 10-12 weeks of age before onset of oestrus. Vietnamese potbellied pigs and other asian types reach puberty at approx 4 moths of age (generally 2 months earlier than commercial breeds of pigs)


what wormer should be used for pigs?

avermectin on arrival and again 2 weeks later. if the premises cannot be kept worm free, pigs need to be treated with benzimidazoles every 4-6 months to avoid heavy infestations with ascaris and other parasites.


What should pigs be vaccinated against?

Erysipelas using an initial double injection course followed by 6 monthly vaccination, if it is planned to breed from gilts then they should be vaccinated against parvo virus before getting served for the first 3 parities. Vaccination of gilts against E coli and clostridium perfringens type C should be done at 6 weeks and 3 weeks before first farrowing, then 3-4 weeks before farrowing in subsequent pregnancies.


Which infections of pigs are zoonotic?

swine influenza virus, salmonellosis, streptococcus suis type II and erysipelas


What are the common problems affecting pet pigs?

Skin problems - mange, lice, ticks and fleas, insect bites. Some pet pigs develop severe thickening and crusting or flaking of the skin through insufficient zinc or essential fatty acids in feed. sunburn can affect pigs if no shelter is available in hot weather. Sunscreen should be applied. Overgrown claws tends to affect lateral claws more commonly than medial claws. Boar tusks continue to grow and will need to be trimmed. Tumours are fairly common in older pet pigs including melanoma, osteosarcoma, lymphosarcoma. Defects such as umbilical or scrotal hernias can also occur. cryptorchidism is quite common in pet pigs and the retained testicles are best removed surgically at a young age.


How to vaccines play an integral part in disease control in pigs?

Used in adult stock to protect them against specific diseases eg erysipelas and parvovirus. Vaccines used in adult stock to confer maternal immunity to neonatal piglets eg E coli. Vaccines used in weaners to protect them against endemic diseases in the home unit or in units to which they are destined for supply e.g mycoplasma hyopneumoniae, PRRS, porcine circovirus, haemophilus parasuis, and lawsonia intracellularis. In the event of a significant disease problems an autogenous vaccine can be made under a liscence - using the pathogen isolated from a specific farm. These vaccines are always killed.


How much medication should be added to in water medication for pigs?

healthy pigs drink 8-10% of their body weight each day. rule of thumb : 5L of water per 60kg of pis drinking from the supply point. or 100L per tonne of pig weight. water medication is the fastest method of medicating large numbers of pigs quickly. Pigs that are ill will usually continue to drink whereas they might refuse to eat. If there are high environmental temperatures the temperature within the header tank could cause products to degrade. dirty tanks and pipework and slime contamination reduce the efficacy of antibiotics. Unduly high water pressure and flow rates result in high levels of wastage with wastage of products. You should increase estimated medication by 10-12% to allow for this.


Where should pigs be injected subcut?

Behind the ear (25-75mm behind the base) for small pigs the inside thigh is an option. avoid femoral canal.


What is isowean?

This system is designed to rear growing pigs free from particular diseases. With isowean, piglets are usually weaned at 21 days. at weaning piglets are given the most appropriate antibiotic against the particular infection by injection and immediately moved to the isolated weaning accomodation. Once they attain the correct size, the batch is moved to the grower unit and subsequently to the finisher unit on an all in all out basis. they do not come into contact with other pigs and all units in the isowean programme are at least 3km for any other pig unit to prevent aerial spread of infection to pigs.


What is segregated disease control and what does it involve?

This involves eliminating diseases from the breeding stock as well as the growing pigs. This is more complex and requires careful planning in order to be successful. The system works best if all buildings on the unit can be depopulated in order to carry out effective decontamination. While the programme is taking place, piglets are sold off the farm as weaners in order to depopulate the grow-finish accomodation. this should allow the grow- finish buildings to be segregated and thoroughly cleaned. Managing the breeding stock works best if the unit is batch farowing every three weeks rather than farrowing weekly. Whilst off site the adults are medicated in feed with effective levels of the most appropriate antimicrobial agent. Once the entire unit is cleaned and the adults have been medicated for the required length of time they are re introduced to the decontaminated unit and farrowing recommences. Piglets born form the treated sows should be free from infection.


How are residues of medicines tested for in pigs?

this is assessed by testing kidney of slaughtered pigs for antibiotics and heavy metals. Strict adherence to withdrawal times is essential for preventing residue problems.


What type of virus is classical swine fever?

A highly contagious disease caused by a togavirus (in genus pestivirus)


Describe the pathogenesis of classical swine feer?

Infection is by direct contact or aerosol spread. Entry is through mucous membranes or sin abrasians. the incubation period is usually 3-4 days but can range from 5-10 days. virus i infects epithelial cells of tonsilar crypts and subsequently spreads to regional lymph nodes via lymphatic vessels. It enters the bloodstream, replicates in spleen, bone marrow and lymph nodes. Multiple haemorrhages are caused by degeneration of endothelial cells of blood vessels and thrombocytopenia resulting in poor blood coagulation. In acute CSF pigs die from acute angiopathy, shock and febrile response. Pigs infected in utero are born Persistently infected. They grow poorly and excrete virus over long periods.


How does classical swine fever survive?

It can survive for a long time in frozen or refrigerated meat, it is resistant to heat and relatively stable. It is spread by pigs, human contacts, fomites, semen and wild boar and also by aerosol form large concentrations of pigs and via infected feed and lorries contaminated by organic matter.


What are the clinical signs seen in acute CSF?

Large numbers of pigs become sick in a short period of time. they are drowsy, inactive, stand with arched backs. Others stand with drooping heads, straight tails. some may vomit and have diarrhoea. Temperature may be as high as 42C. Purple skin blotches and skin haemorrhages may be seen.


What are the clinical signs of chronic CSF?

Outbreaks are prolonged and clinical signs include diarrhoea, lameness, poor growth performance and increased mortality. There are large numbers of runty pigs which eventually die. Infertility problems occur in the herd.


What are the clinical signs of congenital CSF?

If a virulent strain is involved there is abortion If the strain is of low virulence mummificiation, stillbirth, weak or shaker pigs are born. Malformation of the visceral organs or brain occur regularly. Some pigs may be born viraemic after exposure in first trimester of pregnancy. These do not mount an antibody response. In many herds where low virulence strains are endemic the only clinical signs may be poor reproductive performance.


What are button ulcers a typical feature of?

Chronic CSF - lesions are often obscured by secondary infections in chronic cases of CSF. one of these are button ulcers of the large intestine, particularly the ileocaecocolic junction.


How can you diagnose CSF? what should be done if this is diagnosed?

If there is any suspision - it is important to notify the local AHVLA without delay. AHVLA will visit the unit and take responsibility for confirming the diagnosis. Tonsils, spleen, LN, kidneys and distal ileum are taken for virus detection and tissues taken in formalin for histopathology.


What is the aetiology of african swine fever?

A tick borne contagious viral disease of swine caused by an iridovirus. The disease spreads through tick bites and by direct contact with infected pigs.


Do african swine fever and classical swine fever spread transplacentally?

Classical swine fever - YES
African swine fever - no


What are the hosts of african swine fever?

Warthogs - inapparent hosts. Replicates in the soft tick ornithodoros.


How is african swine fever spread from country to country?

pork products carried by people on planes, cruise liners etc as well as through wild boar. it survives readily in salted and dried pork for about a year and in frozen pork for about 2 years.


What are the clinical signs of african swine fever?

The signs are similar to CSF. there is a reluctance to stand and pigs are depressed. There is a high fever, reddened skin, moderate anorexia, but usually less than 25% mortality. in pregnant animals there is abortion and high mortality. Affected animals become progressively more reddish/blue by 5-6 days and deaths occur from 7-10 days post infection. No meningitis/encephalitis is seen in young pigs. low virulence forms may cause a mild fever and joint lesions.


What type of virus is foot and mouth disease?

It is a highly contagious vesicular disease which affects all cloven footed animals.


How is foot and mouth spread?

Infection is by aerosol and direct contact with infected animals or by direct contact with infected animals or infected material. The incubation period is from 2-7 days. Virus invades the upper and lower respiratory tract and grows initially in the pharyngeal area.


What are the clinical signs of foot and mouth disease in pigs?

Pigs usually have few lesions in the mouth. There is small hyperaemic areas on the snout, lips, coronary bands, interdigital clefts and skin. These soon develop into 1mm-3cm vesicles. The lesions coalesce to form blisters containing clear yellow fluid. Blisters rupture leaving raw epithelium and flaps of loose tissue and painful eroded areas which bleed easily. Pigs become intensely lame due to lesions on the coronary band of the feet and eventual sloughing of the hooves. Lesions can be seen on the snout in the early stages but blisters rupture fairly quickly after forming. It is not possible to differentiate the vesicular diseases on the basis of the clinical signs.


What is swine vesicular disease?

A contagious disease of pigs caused by enterovirus.


How is swine vesicular disease spread?

Infection is by direct contact with infected animals or infected material. the incubation period is from 2-7 days. The virus proliferates in the pharynx and the intestinal tract.


What are the clinical signs of swine vescular disease?

The vesicular lesions are indistingushable from those of FMD. Affected pigs have a high fever, salivate and show lameness. Recovered pigs can be infected without showing clinical signs. encephalitis may occur.


What is anthrax?

A rare bacterial infection f pigs caused by bacillus anthracis, characterised by marked swelling of the neck in pigs and deaths.


How does infection with anthrax occur?

Usually by ingestion but rarely can occur by inhalation or entry through wounds. n pigs tissues in the pharynx and neck are most commonly affected but it can become disseminated through bacteraemia and septicaemia. The bacteria produce toxins that cause necrotising changes in tissues. Organisms are shed in urine, faeces, discharges and blood. Animals that recover develop immunity. Pigs that recover remain carriers and infection can spread in faeces and slurry.


What are the clinical signs of anthrax?

Pharyngeal, septicaemic and intestinal forms of the disease occur. The pharyngeal form is characterised by extensive oedema of the throat and neck, dyspnoea and high temperature. the skin over the neck can become blackened and necrotic. there is anorexia, vomiting and death usually occurs between 12 and 48 hours after onset of signs. If anthrax is suspected do not caryr out a post mortem examination as this releases bacteria into the environment and spore formation will follow.


How can anthrax be confirmed?

Impression smear of a cervical lymph node stained polychrome methylene blue. Square ended bacilli with pink/blue capsules confirm the diagnosis. if anthrax is suspected or confirmed it must be reported to the AHVLA.


What is aujeszkys disease?

A herpesvirus infection of pigs characterised by signs of respiratory and nervous disease, high temperature and high mortality. Infection is by inhalation, virus replication occurs in the nasal epithelium then virus travels along the cranial nerves to the brain, where it causes non suppurative meningo encephalitis and myelitis.


What are the clinical signs of aujeszkys disease in newborn pigs?

The incubation period is 3-7 days, pigs have a fever 41.5C. there is diarrhoea, trembling, incoordination, dog sitting and opisthotonus. The death rate is 100%, declining to 50% by four weeks of age.


What are the clinical signs of aujeszkys disease in piglets of four weeks to five months of age?

The incubation period is 5-7 days there is anorexia from day 3. There i fever up to 41.5C form day 4 up to day 8. Nervous signs occur form day 4 and include ataxia, incoordination and convulsions. pneumonia occurs in finishers form day 4 with some strains and deaths occur after 4-5 days. Pigs that recover have finishing periods extended by 10-14 days.


What are the clinical signs of Aujeszkys disease in adult pigs?

Adult pigs show few clinical signs. there is transient anorexia and mild nervous signs. up to 50% abort on first introduction of the disease into the herd.


How does Tuberculosis affect pigs?

Bovine Tb caused by mycobacterium bovis is an infectious disease which mainly affects cattle but can also infect other mammals including badgers, cats, dogs, deer and alpaca and has been diagnosed in domestic swine in recent years as well. Often there is a link between reported cases and cattle but rarely this is by direct contact so the suggestion is that there is a common wildlife vector. This may explain why M bovis is more commonly seen in outdoor pigs and farms with limited biosecurity where more contact with wildlife can be expected.


What is the most common type of mange in pigs?

sarcoptes scabei var suis. Mites burrow into the skin and multiply. burrowing causes intense pruritis. life cycle 14-15 days and multiplication only takes place on pigs.


What are the clinical signs seen when pigs are infected with mange?

Scratching, rubbing. Lesions presenta as small red papules and erythematous skin lesiosn especially on the head, neck axilla and hind quarters. rubbing causes crusting and thick scab formation Infestation of the ears is common and causes head shaking.


How can a diagnosis of mange be made in sheep?

Examination of ear wax from as deep within the ear as possible looking for mites, or skin scrapings from newly affected areas. apply glycerine to the skin before scraping in orer to retain the scraped material on the scalpel blade.


What is the treatment of mange in pigs?

avermectins. Treated pigs should be moved into cleaned disinfected buildins that have been sprayed with amitraz to prevent re infection.


What is pityriasis rosea?

a common skin conditions of weaners and growers of unknown aetiology. Lesions appear as irregular hyperaemic patches on the belly, flanks, groin or thighs and expand rapidly to form large lesions with intensely reddened margins. the central areas of lesions can remain reddened or may revert to normal appearance. The lesions are not pruritic and do not appear to be painful. Carcasses of infected pigs have enlarged lymph nodes usually associated with secondary bacterial infection.


What is the treatment for pityriasis rosea?

No treatment given usually a the lesions resolve spontaneously. if significant secondary bacterial infection is suspected, a course of antibiotics should be given. if the lesions are being traumatised by other pigs then move to hospital accommodation.


What is porcine dermatitis and nephropathy syndrome?

Characterised by skin and kidney lesions, due to an immune complex disorder. the cause is uncertain but the syndrome is often seen inconjunction with outbreaks of PMWS so PCV2 virus is considered to be involved. The basis of the lesions hinges on an immune complex casculitis with lesions occurring primarily in the kidney causing severe glomerulonephritis, but also in the skin causing multifocal areas of haemorrhagic dermatitis and skin necrosis. immune complexes are thought to form in excessive quantities in response to chronic antigen challenge. Spotty skin lesions are often the first indication of a problem.


How is PDNS treated and controlled?

Severely affected pigs should be euthanased as they have no hope of recovery. mildly affected pigs can be given anti inflammatory agents to try and limit the extent and severity of vasculitis. In the event of outbreaks it is worth treating younger age groups with in feed antibiotics as a means of controlling gram negative infections such as P multocida. Treating affected pigs with antibiotics has had no benefit because pigs are in the chronic stages of infection with high circulating antibody levels by the time clinical signs appear.


What is Parakeratosis?

A chronic skin disorder of pigs caused by Zinc deficiency in the diet. It is rarely seen nowadays due to the widespread use of commercial compound rations or preprepared vitamin and mineral balancers for use in home mix rations. zinc deficiency reduces the biosynthesis of essential fatty acids and that interferes with keratohyalin synthesis in the skin, resulting in parakeratosis. The lesions become very crusted, blackened, get covered in debris and fissures form in the crusts. The lesions are non pruritic. Supplementation of the diet with adequate zinc levels results in skin healing over 2-3 weeks.


What is thrombocytopenic purpura in pigs?

An immune mediated condition of young pigs characterised by multiple petechial haemorrhages in skin and other organs. it arises due to pigelts ingesting colostrum containing antibodies to their platelets.. Antibodies to foetal thrombocyte antigens develop in sows by isoimmunisation. After ingesting colosturm, piglets suffer a progressive drop in thrombocyte numbers.


How does thrombocytopenic purpura occur? what must the boar be compared to the sow?

The boar must have a different thrombocyte type to the sow and there must have been atleast one previous parity to a boar with that thrombocyte type in order for the sow to become sensitised.


What is the most common degenerative joint disease in pigs?



You see a pig dog sitting and unable to rise- what is your suspicion?

Electrocution. Affected pigs are usually frothing at the mouth and burn marks may be seen at the point of contact, usually on the snout or lips.


What are the differential diagnosis for causes of sudden death in pigs?

septicaemia, mulberry heart disease, porcine stress syndrome, meningitis, abdominal accidents, gastric haemorrhage, notifiable diseases, acute toxicity.


What is the cause of PMWS?

Porcine Circovirus 2. Infected piglets become viraemic with localisation of PCV2 in several organs, most notably the lymphoid tissues, lung and kidney. in the spleen and Lymph nodes it has a direct effect on lymphoid follicles, lung and kidney.


What are the clinical signs of PMWS?

PMWS affects piglets mainly between 6-12 weeks of age. clinical signs are variable but include anorexia, weight loss, lethargy, coughing and hairy gaunt appearance. Enlarged peripheral lymph nodes are an important feature in wasting piglets.


What is the cause of transmissible gastroenteritis in pigs?

TGE is a highly infectious coronavirus of pigs that causes diarrhoea and dehydration in pigs of all ages and high mortality in young pigs. In the intestine, infection spreads rapidly along the entire length of the small intestine causing diffuse changes. there is acute degeneration of the epithelium at the tips of the villi, the epithelium detaches resulting in severe villus atrophy. Absorption of fluid and nutrients form the small intestine is severely reduced, piglets develop watery diarrhoea, dehydration and hypoglycaemia.


Why are outbreaks of TGE now rare in the UK?

Due to the presence of another coronavirus infection in pigs - porcine respiratory coronavirus.


What are the clinical signs of transmissible gastroenteritis?

In susceptible herds, the disease presents as explosive outbreaks of diarrhoea affecting all ages of pigs. Diarrhoea is watery and yellowish in young pigs and watery grey in pigs from weaning onwards, vomiting may occur.Nursing sows develop diarrhoea and agalctia.


What is the cause of porcine epidemic diarrhoea ?(PED)

It is a highly contagious coronavirus infection of pigs that causes diarrhoea in all ages of pigs and a high mortality in suckling pigs, caused by a coronavirus. the PED virus. Similar to TGE except virus replication is confined to the intestine. Villus atrophy, severe diarrhoea and dehydration occurs.


What are the clinical signs of PED?

explosive outbreaks of diarrhoea similar to TGE. A sharp drop in feed consumption can be recorded in the 1-2 days preceeding the outbreak of diarrhoea. Vomiting is seen. Sows develop agalactia. Pigs are affected with diarrhoea for 7-10 days and recover thereafter.


What is porcine inclusion body rhinitis? What is it caused by?

PIBR is caused by a cytomegalovirus (herpesvirus) and results in outbreaks of rhinitis in young suckling piglets. Infection is by the oronasal route. Foetuses infected in late gestation are born sero negative.


What are the clinical signs of porcine inclusion body rhinitis?

Rhinitis is ususally confined to suckling piglets between 10 days and 3 weeks of age. They show sneezing, respiratory difficulty, dyspnoea, difficulty with suckling, weight loss and lethargy. morbidity is high and mortality can reach 50%. SMEDI syndrome can occur in sows.


What are the five types of congenital tremor?

A1 - classical swine fever.
A2 - viral agent not yet characterised
A3 - hereditary in male landrace pigs
A4 - hereditary in british saddleback pigs
A5 - toxic - organophosphate treatment of sows during pregnancy


Describe the pathogenesis of congenital tremor type A2?

An unknown viral agent that affects non immune pregnant sows or gilts at approximately day 30 -40 of gestation. the agent affects foetal neurological development causing varying degrees of cerebellar hypoplasia and hypomyelinogenesis. Newborn piglets show neurological deficits ranging from mild trembling to severe body shaking making piglets unable to stand or suckle. In piglets that survive the first seven days, the tremor gradually disappears. Piglets are usually normal by 4-5 weeks of age. No clinical signs are apparent in any older pis. Cerebellar hypoplasia might be apparent.


How does bordetella bronchispetica cause disease in pigs?

It colonises the nasal passages of suckling piglets causing rhinitis, sneezing and mild tubrinate atrophy. it can also affect the lungs, particularly the cranial lung lobes causing purulent pnuemonia. Toxins are produced byt he bacteria. these are then absorbed and cause turbinate atrophy in 14-21 days due to a reduction in osteoid fibres in the turbinates. turbinate atrophy resolves following antibiotic treatment.


What is the cause of enzootic pneumonia in pigs?

Mycoplasma hyopneumonia organisms remain on the surface of the bronchial epithelium betwen cilia and a chronic infection is established. infection impedes normal ciliary clearance of mucus and inflammatory reaction occurs. High levels of infection occur when large numbers of pigs are in the same airspace and the throughput is continuous. Lesions are red to fawn in colour and clearly demarcated from normal lung.


What is the cause of pneuropneumonia in pigs?

Actinobacillus pleuropneumonia. Bacteria are inhaled and colonise the respiratory passages, especially the alveoli in the caudal lung lobes. Bacteria multiply and rapidly prouce Apx toxins causing congestion and oedema of alveolar tissues, necrosis and vascular thrombosis.


What are the pathological lesions of APP?

Pigs that die as a result show severe pleuropneumonia, the caudal lung lobes in particular show multiofcal raised haemorrhagic lesions approx 3cm in diameter. there is pleurisy overlying these lsions and pelurisy can extend to the cover the entire lung. Haemorrhagic frothy fluid is present in the airways.


How can diagnosis of APP be made?

presence of APP can be confirmed by PCR testing. Toxin gene PCR testing can also be used to determine the virulence potential of isolates.


Which respiratory viral infections cause pneumonia in pigs?

PRRS virus, swine influenza, porcine circovirus type 2 and porcine respiratory coronavirus.


What is progressive atrophic rhinitis?

A severe bacterial rhinitis causing permanent turbinate atrophy caused by toxigenic pasteurella multocida. P multocida colonises the nasal passages and strains that cause PAR have the Tox A gene and produce a dermonecrotic toxin. The toxin causes degeneration and necrosis of osteoblasts and accelerated osteoclastic activity. Deviation of the septum may occur in association with the turbinate atrophy. Sneezing in weaners is the earliest clinical signs. Pigs that have been affected for 2-3 weeks or mroe show shortening of the snout with or without deviation. growth rates are depressed as pigs eat less.


How does ETEC cause disease in pigs?

ETEC adhere to the mucosa of the small intestine. they colonise the small intestine and produce one or more enterotoxins. The toxins act in the gut and stimulate hypersecretions of mucin and electrolytes resulting in acute diarrhoea and dehydration.


How is E coli spread?

Faecal oral route. lack of colostrum and low ambient temperatures lead to increased susceptibility.


What are the clinical signs of E coli?

Watery diarrhoea, dehydration, metabolic acidosis, vomiting and depression or sudden death. Most common in pigs 0-4 days of age and can appear as early as 2-3 hours after birth. Single piglets or whole litters may be affected.


How can E coli in piglets be prevented?

Maternal vaccination is effective but good management, hygiene, ensuring adequate ambient temperature and colostrum intakes are also very important.


How does rotavirus cause disease in pigs?

rotavirus replicates predominantly int he cytoplasm of differentiated small intestinal epithelial cells. it results in small intestinal villous atrophy and severe enteritis.


What are the clinical signs of rotavirus?

Signs range from mild diarrhoea and dehydration to severe fatal diarrhoea. Diarrhoea affects piglets mainly between 5-14 days of age and lasts from 2-5 days.


How can rotavirus be diagnosed?

Detection of rotavirus in faecal samples using PAE. Faecal samples should be collected in the acute phase of the disease:highest concentrations of porcine rotavirus are shed during the first 24 hours after the start of diarrhoea.


What species usually causes coccidiosis in pigs?

Isospora suis.


How should piglets with coccidoisis be treated?

Toltrazuril orally at 3-5 days of age. Repeat treatment might be required 4-5 days later.


What are the clinical signs of clostridium perfringens type C enteritis in pigs?

Fatal necrotic enteritis occurs mostly in piglets from 12 hours to 7 days. beta toxin is very sensitive to trypsin. trypsin secretion is absent in pigs of less than 4 days of age. Piglets may be found dead. If noticed ill, watery haemorrhagic diarrhoea is profuse, the rectal temperature falls to 35C and the animal dies. less acute cases may survive 2 days. the reddish brown liquid faeces contains shreds of necrotic debris.


What antibiotic can be used during the outbreak of clostridium?



What are the clinical signs of cryptosporidiosis in pigs?

Watery yellow brown diarrhoea usually from 7 days of age or more and persists or several days with piglets showing dehydration and weight loss.


What is the cause of porcine epidemic diarrhoea?

an alpha coronavirus, related to the virus causing TGE.


what are the clinical signs of PED?

Introduction into a naive herd typically results in severe diarrhoea, vomiting with very high morbidity and mortality levels. within 2-4 days.


What is oedema disease of pigs?

E coli infection with F18 strain - in oedema disease there is toxaemia that affects the integrity of the vascular endothelium allowing fluid exudation into perivascular tissues causing oedema in multiple sites. Infection is by faecal oral route. Pig sshow subcutaneous oedema, particularly affecting the head and eyelids.


What is the cause of proliferative enteropathy in pigs?

PE is caused by the obligately intracellular bacterium lawsonia intracellularis. 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. 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.


What do cases of proliferative haemorrhagic enteropathy shows?

this occurs in heavy infections with L intracellularis. Cases of PHE are pale and have diarrhoea which ranges in colour from black and tarry to port wine. pigs are anorexic and dull.


What is the cause of swine dysentery?

brachyspira hyodysenteriae. The organism colonises the large intestines in 2-4 days, multiplies in the crypts, invades the goblet cells and causes damage and disruption to epithelial cells.


What are the clinical signs of swine dysentery?

Diarrhoea starts from 5-7 days post infection, fresh blood may be seen in the faeces and excess mucus is a feature from 10 days post infection. clinical diseases 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.


What is the treatment of choice for swine dysentery?

Tiamulin and valnemulin.


What is the cause of porcine spirochaetal diarrhoea?

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


What are the clinical signs of porcine colonic spirochaetal diarrhoea?

Affected pigs show signs ranging from cow pat type diarrhoea to watery grey diarrhoea. pigs retain normal appetite and vigour. In herds with endemic infection the disease is mainly seen in growing and finishing pigs between 6-16 weeks of age.


Which type of salmonella serovars most commonly affect pigs?

S typhimurium, S derby second, S cholerasuis is rare.


What are the clinical signs of salmonella infection in pigs?

On the majority of farms infection is sub clinical. when diarrhoea occurs it is initially watery and yellow without blood or mucous. later blood may appear sporadically in the faeces. acutely affected pigs are febrile, dull, dehydrated and have a decreased feed intake. sometimes pigs remain unthrifty and may develop rectal strictures.


What is the species of stomach worm that can affect pigs? What other parasites can give rise to enteritis and colitis?

Hyostrongylus rubidus 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 through regular use of broad spectrum anti parasitic agents such as the avermectins.


What are gastric ulcers linked to in pigs?

Feed processing and dietary factors, too fine particles, pelleted feed, low fibr econtent of the diet. Helicobacter pylori may also play a role in ulcer development.