Poly systemic conditions Flashcards
Nutritional polysystemic diseases
Mycotoxins
Bacterial polysystemic diseases
Clostridium novyi
Leptospirosis
Erysipelas
Strep suis
Glasser’s Disease
Pasteurellosis
Salmonellosis
E coli septicaemia
Notifiable bacterial diseases
Viral polysystemic diseases
Porcine circoviral disease (PCVD)
Porcine reproductive and respiratory syndrome virus (PRRSV)
Notifiable viral diseases
Malignant catarrhal fever
Border disease
Swine bacterial notifiable diseases
Anthrax
Bovine TB
Brucellosis (B. suis)
Swine viral notifiable diseases
Classical Swine Fever
African Swine Fever
Foot and Mouth Disease
Swine Vesicular Disease
Aujeszky’s Disease
Porcine Epidemic Diarrhoea
Teschen
Vesicular stomatitis virus
Mycotoxins
Aflatoxin
Ochratoxin
Ergot
Zearalenone
Trichothecenes
Fumonisin
Toxins produced by fungi growing on cereals or feed constituents in particularly bad (wet, rainy) growing seasons
Clinical signs: Variable and often subtle and multisystemic.
Treatment of affected animals is not usually possible but usually improvement is seen once contaminated feed is removed. Mycotoxin binders.
Aflatoxin
Apergillus spp (cotton maize, groundnut)
Hepatoxic, reduced growth, immunesuppression
Ochratoxin
Aspergillus spp., Penicillium spp
Nephrotoxic, reduced growth
Ergot toxin
Claviceps spp (pasture, cereals)
Vasocontriction, distal necrosis
Zearalenone toxin
Fusarium spp (cereals)
Estrogenic
Trichothecenes (T-2 toxin, DON)
Fusarium spp
Suppress appetite and immune system
Fumonisin toxin
Fusarium spp
Immune suppressant, hepatotoxic, damage to endothelium (oedema)
Clostridium novyi
Relatively uncommon but can be responsible for the sudden deaths of adult or heavy finishing pigs
Clostridium novyi type B.(or A).
Possible activation of spores (ubiquitous) in liver or intestinal epithelium when oxygenation is reduced
older sows or fatteners with chronic respiratory disease
sudden death; cases are only rarely found alive
Rapid decomposition of carcase. Liver pale, friable and with foam rubber appearance.
If suspected in life then parenteral antibiotic such as penicillin
vaccination using sheep 8 in 1 products,
Leptospirosis
mainly within Leptospira interrogans
In pigs L pomona is considered to be host adapted and causes significant disease around the world
L Bratislava, L Canicola, L Icterohaemorrhagica and L Australis serovars show serological evidence of activity in the UK
Initial (7-14d) leptospiraemia and septicaemia with infection of repro. tract.
Infection locates to renal interstitial cells and tubular epithelial cells (shedding in urine).
Treatment: Antibiotic therapy - especially penicillin / streptomycin, or dihydrostreptoycin in cases of acute infection.
Acute cases in younger pigs may be effectively treated with tetracycline.
Clinical signs of acute leptospirosis
Weaners and growers, associated with L canicola and L icterohaemorrhagica.
Affected pigs are pyrexic, dull and anorexic.
May show diarrhoea and jaundice.
Neurological signs and death.
Clinical signs of sub- acute leptospirosis
quite widespread in outdoor pig units.
Serological evidence of infection but no clinical signs.
Clinical signs of reproductive leptospirosis disease
3rd trimester abortion and neonatal mortality of unthrifty pigs.
Affected sows may show pyrexia, agalactia and jaundice.
Aborted fetuses may be autolysed (L. bratislava).
Porcine circovirus associated disease (PCVD)
Systemic PCVD (previously called PMWS - Post weaning multisystemic wasting syndrome)
PDNS - Porcine dermatitis & nephropathy syndrome
Porcine reproductive and respiratory syndrome virus (PRRSV).
PCV2 enteric disease (PCVD-ED)
Porcine respiratory disease complex (PCV2 in lung disease PCV-LD)
Systemic PCVD (previously called PMWS - Post weaning multisystemic wasting syndrome)
PCV2 is ubiquitous
Most sows are immune after field exposure as piglets but occasionally persistent viraemic sows/gilts occur and these can transfer infection to fetuses and neonates
Most infection occurs during the post-weaning period (between 10-16 weeks), after the decline in colostral immunity
chronic wasting, anaemia with pallor of the skin and enlarged lymph nodes
Some animals show signs of diarrhoea and respiratory signs. Some develop gastric ulcers. A high proportion of affected pigs die - at least 30%.
carcase is emaciated and jaundiced. The spleen and LNs are enlarged. The kidneys may be swollen and have visible white spots
prevention by vaccination of sows or piglets around weaning - no specific treatment
PDNS - Porcine dermatitis & nephropathy syndrome
Ventrocaudal skin lesions
Low morbidity (importance of differential diagnosis).
Type III hypersensitivity dermonecrosis
Immune complex mediated glomerulopathy
Generalised lymphadenopathy and oedema in severe cases
Porcine reproductive and respiratory syndrome virus (PRRSV)
Abortion, still birth, low viability, low litter size.
Naïve dam exposed to PCV2 at insemination or during pregnancy
Uncommon
PCV2 enteric disease (PCVD-ED)
Enteritis in 6 – 18wk old pigs
Granulomatous thickening of ileum and enlarged mesenteric lymph nodes
Porcine respiratory disease complex (PCV2 in lung disease PCV-LD)
Key clinical observations:
* Coughing, dyspnoea
* Lethargy and inappetence
* Reduced growth
Many other organisms also found usually
Malignant catarrhal fever
Caused by Ovine Herpes Virus 2 (PCR confirmation).
Signs rather like those in cattle including ocular discharge, respiratory signs, corneal opacity plus developing respiratory signs.
No response to antibiotics.
Border disease virus
Clinical signs of polysystemic disease included failure to thrive, respiratory disease, enteritis, neurological signs, and anaemia.
These signs could not be distinguished form low-virulence classical swine fever.
Diagnosis was made by detection of BDV DNA by PCR on brain and other tissues.
Classical swine fever
highly infective pestivirus
infection of pigs which causes both acute disease and chronic inapparent disease.
Notifiable
UK eradication in 1967 - 80,000 pigs slaughtered in the 2000 outbreak
Spread is mainly directly from pig to pig
Heat and acid stable- survives in environment (pig pens for <4weeks, and frozen pork for 1500d, hams for 330d).
Virus localises in the tonsil with systemic viraemia within 24 hrs.
Clinical signs arise from targeted attack of systemic endothelial cells
No treatment effective - slaughter policy
Acute classical swine fever
First signs within 10 day of infection.
Some sudden deaths especially in young pigs.
Many severely depressed with high temperatures - 41.5 - 42.5 C - anorexic and bury themselves in straw.
Reluctant to move and may walk with swaying gait.
Initially constipated then diarrhoea and vomiting.
Ocular discharge with eyelids stuck together.
Purple blotchy discolouration of skin especially ventral abdomen and necrosis of ear tips.
Nervous signs include circling incoordination, muscle tremors and convulsions.
Chronic classical swine fever
Seen with low virulence strains of virus.
Affected pigs are dull, anorexic and fail to thrive.
Areas of skin discolouration and dermatitis may be seen.
Pigs susceptible to secondary bacterial infection & glomerulonephritis.
Congenital neonatal tremors and reduced reproductive efficiency may be observed.
Congenital classical swine fever
Usually low virulence strain of virus.
Affected sows show mild pyrexia, may abort or produce small litters with mummified piglets.
Some piglets born with viraemia.
Piglets may show cerebellar hypoplasia and type A1 congenital tremor.
Other pigs grow initially but fail to thrive and die before maturity.
Post mortem signs of classical swine fever
Systemic haemorrhagic lymphadenopathy:
* Strawberry lymphnodes
* Tonsil necrosis
Viral vasculitis:
* Petechiation and ecchymosis
* Skin, kidney, bladder and lung.
* Infarcts in spleen
* Button ulcers on caecal epithelium
Cerebellar hypoplasia:
* Congenital tremors
African swine fever
high morbidity and mortality.
large icosahedral DNA virus (Iridovirus) which replicates in the cytoplasm of infected cells.
Spreads directly between pigs mainly through the respiratory tract.
Pigs that survive may be persistently viraemic
Infection of URT and gut:
○ Primary viraemia with infection of endothelium and lymphoid cells.
○ Vasculitis and immune complex mediated disease.
○ Surviving pigs are persistent shedders for <46d (inneffective Ab)
thrombocytopaenia with widespread ecchymotic haemorrhages. Occasional button ulcers in caecum.
No effective treatment or vaccines
Notifiable
Acute african swine fever
Pyrexia initially for approx. 4 days then T falls as other signs develop; severe depression, weak hind legs, ocular discharge, diarrhoea and cough.
Skin discolouration and ecchymoses.
Convulsions and death may follow within a few days.
Mortality <100%.
Abortion.
Chronic africa swine fever
Pyrexia, depression - later become emaciated with oedematous swellings over joints.
May become enzootic with recovery of some animals.
Foot and mouth disease
endemic in parts of the Far East, S. America, Africa, Asia. Major UK outbreak 2001
Aphthovirus which is a member of the Picornaviridae family
highly contagious.
Morbidity is often 100%. Mortality is lower with 2% adults and 20% young animals dying
Spread easily with infection gaining access via the mouth and respiratory systems. Virus establishes in oro-pharynx.
Airborne infection
Pyrexia with depression and anorexia.
Lameness is observed and vesicles develop on snout and coronary band.
Hooves may be shed.
Vesicles coalesce leaving areas of skin denuded of epithelium. Younger stock more susceptible than adults and some sudden deaths occur.
Myocarditis seen at PM in young pigs.
No effective treatment - slaughter policy. Notifiable
Swine vesicular disease
clinical signs indistinguishable from Foot & Mouth Disease. Pigs usually recover within 2 - 3 weeks.
enterovirus of the Picornaviridae family.
Spread by direct pig to pig contact and through feeding uncooked pig products. airborne infection does not occur.
Short episode of pyrexia (T 41C) and anorexia.
Evidence of lameness is then seen with backs arched, reluctance to move – especially on solid surfaces. Vesicles are seen on coronary band and less commonly seen on snout, tongue and lips.
Horn of hoof may occasionally shed.
Signs normally disappear within 2 - 3 weeks.
No treatment effective or necessary
Notifiable
Seneca valley virus
Global emergence in Americas (and Asia) since 2002.
Anticipate arrival in Europe
* Lesions indistinguishable from FMDV and swine vesicular disease.
* Not notifiable.
* Potential to disrupt supply chains and lead to complacency
Anthrax
Potentially zoonotic.
Bacillus anthracis. Large G+, toxigenic, spore-forming
Entry via oropharynx and gut (abrasions).
Local proliferation and toxin production, occasional septicaemia. Sudden or delayed deaths, or recovery with immunity.
Pharyngeal form: pyrexia, upper neck swollen and oedematous, dyspnoeic/dysphagic, non-painful, depression, vomiting, death
Enteric form: diarrhoea, dysentery and death.
Septicaemic form - sudden death in younger pigs with pulmonary lesions.
Notifiable
High doses of penicillin for in contacts
TB in pigs
Relatively uncommon infectious disease of pigs whose incidence may rise with rising levels of infection in the cattle population.
A number of mycobacteria can infect pigs but M avium - intracellulare is the most common in the UK (not notifiable).
M bovis affects pigs in some countries and is reported in outdoor production systems in the South West of UK (notifiable).
Mycobacterium bovis
uncommon in UK
Infection by inhalation and ingestion.
Organism often settles in the lymph nodes of the head, neck and or mesentery often with no clinical signs. May occasionally ulcerate to skin surface.
No treatment
Mycobacterium avium
Infection is by ingestion of organism brought by wild or domestic birds or contaminated bedding. Pig to pig transmission can also occur.
Often symptomless but infected submandibular / submaxillary or other gut associated lymph nodes found at slaughter
Lesions are usually small granulomatous or caseous. Usually no clinical signs but occasional generalised infection with weight loss and diarrhoea.
No treatment
