pigs Flashcards
(218 cards)
1
Q
African swine fever
A
- OIE reporting disease
- very contagious infectious disease of swine, severe haemorrhagic disease
- low virulence: seroconversion
2
Q
aetiology ASF
A
- asfarviridae – genus asfivirus – ASDV
o ASFAR = African swine fever and related viruses - Double stranded, DNA virus, enveloped
- survives 11d in faeces, 300d in smoked meat, 15y in frozen meat. Stable in pH 4-13, inactivated in body fluids 30mims at 60oC
3
Q
ASF SOI
A
- SOI: infected pigs, contaminated food, places, vehicle
4
Q
ASF MOT
A
- MOT: oronasal from other pigs, PO eating waste food, tick (vector for warthog), pigs with less virulent strain infective for 1m PI
5
Q
HS ASF
A
- HS: European wild boar, African wild boar (wart hog, giant forest pig and bush pig)
- ASFV originally virus of tick, while domestic pigs and wild boars are accidental host
6
Q
pathogenesis ASF
A
- Upper resp tract replication in tonsils + LN generalised infection via bloodstream high conc of virus in all tissues, severe disruption to blood clotting mechanism
- Not fully understood
7
Q
signs ASF
A
- manifested as haemorrhagic septicaemia (like Ebola in humans)
- acute form: incubation <4 – 19days, 42oC, inappetence, incoordination, cyanosis of ears, death (6-13d), erythema, bleeding, from nose + anus, 100% mortality (high virulent strains),
o if survive = appear healthy or ‘not right’ - main target is endothelial blood vessels and destruction of it haemorrhagic
- subacute form: mortality rate 30-70%, less intense signs, abortion in pregnant sow
- chronic form: weight loss, swollen joints, skin ulcers, low mortality, if survive = carriers for life
8
Q
PM ASF
A
- haemorrhage in LN, kidneys + heart. Large and friable spleen, fluid in cavities, oedematous organs, congested lungs
- mesenteric LN – like “plum”, dark blue – because of excessive haemorrhage inside
- surface of spleen – have dark dots (haemorrhagic infarcts)
9
Q
diagnosis ASF
A
- suspicion: signs, typical lesions, enlarged spleen, enlarged LN (marble like)
VI in bone marrow/peripheral blood leukocyte cultures – hemadsorption of RBC - PCR, IF of tissue smear to detect antigen. Antigen detection ELISA
- Antibody detection 8-21d PIO (Die before antibodies)
10
Q
differential ASF
A
- CSF, acute PRRS, erysipelas, salmonellosis, circoviruses
11
Q
treatment ASF
A
- None + no vaccine
12
Q
control + Prevention ASF
A
- Slaughter of all infected + in contact, surveillance zones, disposal of carcasses
- Prevent contact of wild boar + pigs = increased biosecurity
o Movement, restrictions, cleaning + disinfection - NOT ZOONOTIC
13
Q
classical swine fever (hog cholera)
A
- OIE notifiable
- very contagious infectious disease of swine
- very similar to African swine fever
- destruction of BV’ walls with consequent haemorrhage, necrosis, infarction, inflam
14
Q
aetiology CSF
A
- genus pestivirus, family Flaviviridae, CSF virus
- RNA virus, enveloped, related to DVDV + border disease (cause antibody response in pig)
- Easily killed in environment but lives in frozen meat 4y, 15d manure, m in cured
- can occur in several forms: peracute, acute, subacute, chronic and atypical form
o atypical form = is when only the secondary bacterial infection is visible
15
Q
SOI CSF
A
- SOI: infected pig (in incubation) + wild boar + undercooked pork products
16
Q
MOT CSF
A
- MOT: direct contact (shed in urine , faeces, discharge + semen) + fomites, trans-placental persistently infected pigs (no signs)
17
Q
pathogenesis CSF
A
- Enters + replications in mucosa of gastro + resp tract + conjunctiva. After 24h – viraemia spreads multiples in tonsils, LN, spleen, liver, bone marrow, endothelial cells
- Huge damage to endothelial cells typical haemorrhagic septicaemia
- 2nd bacterial infection (salmonella, strep, clostridium Pasteurella) button ulcers in caecum + LI (pathognomic)
- pneumonia crouposa – same as colds (covid) In humans, lungs become like chewing gum
18
Q
signs CSF
A
- depends on: virulence of strain, dose, immune status of the animal
- highly virulent strains peracute and acute form – 3-7d incubation, 10d death
- low virulent strains chronic and atypical form
- incubation period vary – 2 – 14 days, more often 3-4days
- peracute form = very rare, fever, constipation diarrhoea, lethargy, death, 24-36hrs
- acute form = lower fever, haemorrhage + cyanosis of skin, generalised erythema, vasculitis in CNS = staggering + convulsions
- subacute/chronic = fever, staggering gait, cough, diarrhoea, cyanosis, death in 20-30d+, abortion
- atypical = domination of 2nd bacterial infection rather than primary viral
19
Q
PM CSF
A
- pathognomic sign - chronic form = “button” ulcers in the cecum and large intestines
- petechial haemorrhages in LN, skin, MM, viscera. Splenomegaly with multifocal infarction of margin/periphery
- chronic = as acute + button ulcers in OLI – ileocecal junction
- micro = acute = non-suppurative encephalitis with vascular cuffing, chronic = thymus atrophy + decreased lymphoid tissue
20
Q
differentials CSF-
A
- ASF, parvo, aujeszky, PRRSV, erysipelas, haemophilus suis, salt poisoning, PWD
21
Q
diagnosis CSF
A
RT-PCR – blood, nasal swabs, tonsils, LN
- IF – frozen tonsils, ELISA – herd screening culture on PK-14 cell line
- VN = gold standard
22
Q
prevention and control CSF
A
- no treatment – sanitary culling, restrict movement
- no vaccination – forbidden in free countries, ok in endemic. Live attenuated – protection within 3d (PO for wild boars in EU). subunit vaccine = less efficient but DNA capability
23
Q
porcine circovirus (PCV)
A
- PCV-1 = non-pathogenic for swine
- PCV–2 = systemic or reproductive disease, subclinical infection, PDNS
- PCV-3 = repro problems + multisystemic vasculitis, PDNS
24
Q
PCV - RD (reproductive disease)
A
- Late term abortions + stillbirths in absence or presence of other unknown repro pathogens
- PM piglets = congestion of liver, cardiac hypertrophy with multifocal myocardial discolouration
- Diagnosis
o 1. Late term abortion with hypertrophy of foetal heart
o 2. Extensive fibrosing/necrotising myocarditis
o 3. High conc of PCV-2 in foetal tissue - Differentials: PRRSV, parvo, aujeszky, lepto
25
PCV-2 SD
- Porcine circovirus 2 – systemic disease
26
aetiology of PCV-2
- PCV 2, small, non-enveloped, single strand, circular DNA. At least 4 genotypes a-d. ubiquitous. Resistant to disinfectants + irridation. Persists in swine for month
27
MOT PCV-2
- MOT = direct contact with infected pigs. Found in nasal, ocular + bronchial secretion. Saliva, urine + faeces. Maybe AI + colostrum
28
HS PCV-2
- HS = fattening 8-18w old pigs
29
risk PCV-2
- Risks = overcrowding, poor air quality, mixed ages
30
pathogenesis PCV-2
- Usually coinfection with porcine parvo, PRRSV, p.multocida, staph, strep, etc
- Not fully known but damages immune system acquired immunodeficiency
31
signs PCV-2
- Weight loss, pallor, anaemia, jaundice, dyspnoea, palpable inguinal lymphadenopathy, fever
32
PM PCV-2
- Enlarged + pale LN, atrophied thymus, thin tonsils, splenic infarcts, lung signs
- Micro = lymphocytic depletion + granulomatous inflam, intracytoplasmic inclusion bodies
33
diagnosis PCV-2
- 1. Signs of wasting
- 2. Gross + micro lesions
- 3. Present of PCV-2 antigen/DNA in microscopic lymphoid lesions (insitu hybridisation, immunohistochemistry)
- On herd level = increased mortality + pigs failing to gain weight + at least 1/5 examinated pigs meet above 3 criteria
- Can’t use qualitative PCR as virus is ubiquitous + no clinical signs is common
34
differential PCV-2
- PRRSV, chronic resp disease, Glässers, salmonellosis
35
prevent PCV-2
- Vaccine
- 4 different types – 2 = subunit vaccine, 1 is an inactivated + last is a different type of inactivated based on PCV2a + cross protects against PCV2b + PCV2d + generates cellular + humoral response
- When vaccinating piglets take into account MDA
36
PDNS
porcine dermatitis + neprhopathy syndrome
- Prevalence = <1%
37
PDNS aetiology
- Porcine circoviruses, small, non-enveloped single strand circular DNA, resistant to disinfectants + irridation
38
PDNS MOT
- MOT = direct contact with infected pigs. Found in all secretions, saliva, faeces + urine
39
PDNS HS
- HS = nursey, growing + adult pigs
40
pathogenesis PDNS
- Type 3 hypersensitivity reaction but antigen in immune complex unknown (maybe PCV-2)
41
signs PDNS
- Die within days of signs due to acute kidney failure
- Anorexia, depression, stiff gait, no fever, increased BUN + creatinine
- Irregular red/purple macules papules on skin crusts – fade after 2-3 weeks sometimes leaving scars
- Surviving pigs recover + gain weight 7-10d after start of syndrome
42
PM PDNS
- Skin lesions – necrotising vasculitis, firm, bilaterally enlarged kidneys, oedema of renal pelvis, red, pinpoint lesions on cortex
- Micro = interstitial nephritis, fibronecrotosing glomerulitis, lymphocyte depletion in lymphoid tissue
43
diagnosis PDNS
- 1. Presence of haemorrhagic/necrotising skin lesion
- 2. Presence of systemic necrotising vasculitis + necrotising + fibrinous glomerulonephritis (PM)
44
differetnaisk PDNS
- CSF, ASF, erysipelas, systemic salmonellosis
45
treatment PDNS
- None
- Antigen unknown so prevention difficult but PCV-2 vaccine has decreased number of cases
46
Porcine reproductive respiratory syndrome
- PRRS is the most costly disease of the global swine industry
47
aetiology PRRS
- ¬PRRSV – Arterivirida family, 2 species genetically diverse (1 = Europe, 2 = America + Asia)
- Small, enveloped, single stranded RNA virus, stable at freezing, inactivated by ether, chloroform + 56oC/20 min.
48
SOI PRRS
- SOI: infected pigs + contaminated semen – carrier pig for 86-157d. in semen for 93d post infection
49
MOT PRRS
- MOT: direct contact, semen, aerosol (9km), fomites, transplacental, experimental via flies
50
pathogenesis PRRS
- Replicates in monocyte derived cells displaying CD163 – splenic red pulp + lamina propria + peritoneal macrophages + Kupffer cells
- 2 clinical phases: reproductive failure and post weaning respiratory disease
51
repro PRRS
- Increased stillborn, mummified, premature birth + weak born. Anorexia + agalactia in sows = increased preweaning mortality. Can last 1-4 months
52
respiratory PRRS
- Thumping resp pattern in suckling pigs
- Can become chronic – decreased daily gain + increased mortality 25%
- Histo = severe necrotising interstitial pneumonia
- Acute infection – disease when highest viral titre, then decrease + most pigs not viraemic by 21-28d post infection
- Persistence – viraemia stops + no clinical disease
- Extinction – shedding ends, can be up to 250d post exposure
- Once introduced to herd, becomes endemic in almost all cases regular/occasional outbreaks in nursery/grower/finisher pigs
- Often isolated with strep suis, E.coli, mycoplasma, corona, flu
53
diagnosis PRRS
- ELISA to detect IgG (after 7-10d + lasts 144d), can’t differentiate non-viraemic carriers from animals that have cleared virus. Nuclei sequencing, VI, IHC, serum, blood, tonsil, lung, BAL, semen, oral fluid specimen
54
treatment PRRX
- No effective treatment OIE
55
control PRRS
- PRRSV free gilts + boars, isolation + acclimatisation, all in all out, cleaning. Test on arrival + after 14d
- Herd closure technique – strict quarantine + testing, PRRSV free stock/semen, cleaning, disinfection
- MLV to decrease shedding + prevent econ losses
- Infection eventually induces immunity and control initial infection but variable protection for future infection
56
public health PRRS
- no public health significance
57
GD PRRS
After infection of a naive herd, exposure of all members of the breeding population is inconsistent, leading to development of naive, exposed, and persistently infected subpopulations of sows.
58
atrophic rhinitis
- 2 forms =
o non-progressive - Cause = b.bronchiseptica – mild transient, minor effect on growth + performance. Reversible
o progressive – cause = toxigenic p. multocida (alone or w b.bronchi) severe, poor growth + irreversible
59
MOT AR
nose-nose contact, aerosol, via milk
60
HS AR
- HS = affected at any age (esp p. multocida) (3-8w)
61
risks AR
- Risks = intensive production – high dust + ammonia, high crowding. Outbreaks after mix new pigs
62
pathogenesis AR
- B. bronchiseptica colonises resp tract + destroys mucosal epithelium + ciliostasis
- P. multocida part of normal flora but colonises when mucosa damage (in tonsils + tonsillar crypts) produces PAT (p.multocida toxins)
- PAT causes snout shortening + turbinate atrophy + interferes with remodelling + formation of bone
63
signs AR
- Appear at 3-8w old – sneezing, coughing + inflammation of lacrimal duct, epistaxis. Lateral deviation or shortening o upper jaw. Turbinate atrophy. Decreased growth rate + feed conversion
64
PM AR
- Lesions – transversal section of nasal cavity at 2nd premolar pale mucosa, purulent material, softening + atrophy of turbinates. Turbinate structure may be able to return to normal by 18w post infection
65
diagnosis AR
- Signs + culture of toxigenic P.multocida (tonsils + nasal cavity)
66
differentials AR
- PAR, b.bronchispetica, PCMV, necrotic rhinitis (f.necrophorum)
67
control AR
- Rarely observed in modern swine production, bacteria-toxoid mixture -vaccinate sows 6+2w before farrowing = high colostral immunity. Intranasal MLV of b.bronchi for young pigs
- Vaccinated = subclinical carreires still (decreased pathogen load but doesn’t completely prevent)
68
treatment AR
- Decreased prevalence + load of p.multocida by vaccinating sows or atb for piglets (susceptibility testing) treat growing pigs to decrease severity of changes – change environemt -increase ventilation: all in all out, cleaning. B.bronchi = tulathromycin, oxytetracycline
69
inclusion rhinitis
- PCMV (porcine cytomegalovirus) family Herpesviridae, ubiquitous – nearly all pigs. Sensitive to chloroform + ether
70
GD inclusion rhinitis
worldwide
71
MOT IR
oro-nasal route, congenital
72
SOI IR
ocular + nasal discharge, urine + cervical fluid
73
HS IR
rare disease but fatal systemic disease in 1-5w piglets. Latent infections possible. Can occur in immunologically susceptible herds (previously infected), including foetuses
74
pathogenesis IR
- PCMV replicates in nasal mucosa +/or lacrimal glands
- Cell associated viraemia 14-21d PI in 3wo+
- Shed in nasal secretions for 10-30d
- Congenitally infected pigs excrete virus until death
- In growing pigs – spreads to nasal mucosal glands, harderian glands, kidney tubules + rarely epididymis + oesophagus glands
- In foetus/neonates = infects capillary endothelium + sinusoids of lymphoid tissue systemic spread
75
signs IR
- Incubation be 10–20days
- Depress, anorexic, sneezing, nasal exudate, dyspnoea, rhinitis, neuro signs
- Neonates sudden death/ shivering, sneezing, resp distress, decreased weight, rhinitis
- 3w+ = subclinical – mild-death
- Generally self-limiting
76
diagnosis IR
- PCR, VI from swabs of nasal secretions, scraping or whole blood. Whole herd ELISA – no antibody in neonatal serum
- PM = turbinate mucosa, lungs, pulmonary macrophage from BAL, kidney
- Micro = basophilic intranuclear inclusion bodies in cytomegalic cells of nasal mucosa
77
differential IR
- CSF, enterovirus, parvo, PRRSV, PCV2, PRV
78
prevention and control IR
- No vaccine + no treatment
- Care when bringing in new stock – reactivation of latent infections or primary infection of susceptible herds
79
eryispela
- an infectious disease mostly of growing or adult swine
- it may be clinically inapparent, may cause acute illness involving many animals, or be a chronic disease characterized by enlarged joints, lameness, and endocarditis
80
aetiology erysipeal
- ersipelotrix rhusiopathiae, G+, nonmotile, facultative anaerobe, ubiquitous – 50% adult pigs
- 32 serotypes – cases caused by 1a, 1b + 2
- Very resistant in environment – 1-5, in faeces, 3 y at 5oC in water + soil, 9m in carcass
81
SOI erysipela
- SOI = healthy carriers, faeces, oronasal secretions
82
MOT erysipela
- MOT = contaminated feed, water or faeces through skin abrasion
83
HS erysipela
- HS = 3-12m old + 1y+
- Stress + change in weather (hot) increase in incidence
84
pathogenesis erysipela
- PO entry – infects tonsils/GI mucosa, can survive + replicate in macrophages. Or enter through skin abrasion bacteraemia in 24h if no immune response septicaemia
- Damage to capillaries + synovial membrane shock like generalised coagulopathy
- Severe = haemolysis + ischemic necrosis
- Sequestration of bacteria into cytoplasm of chondrocytes protection from immunity chronic arthritis
- Acute, subacute, chronic or inapparent
85
signs erysipela
- Acute = growing + finishing pigs
o Acute death, depression, fever, anorexia, painful joints, excessive squealing. Diamoni skin (disappears 4-7d), abortion
- chronic form
o after acute or on its own. Enlarged joints, lameness, infertility. Vegetative valvular endocarditis resp distress on exertion, lethargy, cyanosis + death
o sloughing of necrotic skin lesions/ears, decreased growth
86
PM erysipela
- acute = skin lesions, enlarged + congestive. LN, oedematous + congested lungs, spleno + hepatomegaly. Petechial haemorrhage on kidneys + heart
- chronic = proliferative, granular growths on heart + valves, embolism + infarctions. Enlarged joints, increased viscosity of synovial fluid. Joint fibrosis
87
diagnosis eryisepal
- signs, response to atb, demonstration of bacteria/DNA culture/PCR/ IHC blood
- IHC good if atb used already
- diamond skin lesions – pathognomonic
88
differential erysipela
- salmonellosis, CSF, strep suis, PDNS, glassers, mycoplasma hyosynoviae
89
treatment erysipela
- penicillin q12h for min 3d, NSAIDs, good response in 24-36h
90
prevention erysipela
- prevention = erysin -inactivated. Give when 8w+ + breeding ones after 6m again + 2x.y
91
public health erysipela
- zoonosis = butchers, farmer, vet – swollen finger
92
strep suis
- one of the most important pathogen of swine
93
aetiology strep suis
- G+, non-motile, facultatively anaerobic alpha haemolytic + catalase negative
- 35 serotypes based on capsular antigens
- Categories as: highly pathogenic, weakly pathogenic + avirulent
- Capsular polysaccharide = most important virulence factor
- Normal inhabitant of upper resp tract (tonsils)
94
SOI Strep
- SOI = carrier pigs. House flies carry for 5d
95
MOT strep
- MOT = piglets colonised from vaginal secretions during birth + while nursing. Mixing pigs
96
HS strep
- HS = post weaned piglets <2w-20w. intro of highly virulent strains into naïve herd or carriers develop disease with stress (overcrowding, poor ventilation, mixing pigs)
- Incidence = <5%,mortality up to 20%
97
pathogenesis strep
- Can spread systemically from nasopharynx septicaemia = death
- Hematogenous + lymphatic spread
- Potentially can reach blood via intestine
- Can reach CNS by invasion of brain microvasculature or choroid plexus epithelium
98
signs strep
- Fever, anorexia, depression, shifting lameness, sudden death with no signs, meningitis = ears back, squinting eyes, incoordination, dog sitting, paddling, convulsions. Polyarthritis
- Endocarditis in growing pigs – dyspnoea, cyanosis
99
PM strep
- Lymphadenopathy, meningitis, arthritis, endocarditis, polyserositis, fibropurulent exudates, splenomegaly + petechial haemorrhage – septicaemia signs
- Swollen joints + cardiac valvular vegetation
- Micro = neutrophilic meningitis + choroiditis, hyperaemia meningeal BV + fibrinopurulent or suppurative epicarditits
100
diagnosis strep
- Signs, lesions, age of animals + history, isolation + identification by MALDI-TOF
- Tonsil swab PCR – based on recN gene for ‘true’ S. suis
101
differential strep
- Polyserositis (h. parasuis or m.hyorhinis), endocaridit by e.rhusiopathiae, sepsis (e.coli, salmonella, actinobacillus)
102
treatment strep
Prompt parenteral penicillin for 5d, NSAIDs
103
control strep
Good hygiene. Inactivated whole cell vaccine – ineffective
104
public health strep
- Serotype 2 enters skin/mm or undercooked pork (zoonosis serotype 2)
- Zoonosis = septicaemia + meningitis with permanent deafness, endocarditis + arthritis, mortality 7%
105
staph auerues
- G+, non-motile, aerobe/facultative anaerobe. Catalase +
- Present on pig skin + environment sporadic cases
o Usually skin infection /sepsis, mastitis, vaginitis, metritis, endocarditis, osteomyelitis
- MRSA = subclinical herd infections worldwide
106
exudative epidermis
greasy pig
107
greasy pig aetiology
- ¬staphylococcus hyicus, g+, nonmotile, aerobe, catalase, virulent + avirulent strains
- Virulence linked to production of exfoliative toxins - ExLA, ExLB, ExLC, ExLD, SHETa + SHETb – epidermolysins
108
SOI greasy
carrier pigs
109
MOT greasy
abrasion on skin, feet, face, legs
110
HS greasy
5-60d old piglets, morbidity 10-90%, case fatality 50-75%
111
risks greasy
stress, agalatcia, 2o infection, bite wounds
112
pathogenesis greasy pig
- Toxins decrease cell-cell adhesion of keratinocytes in superficial epidermis blisters
- Exfoliation sebaceous exudation + crust formation accumulation of greasiness
- Exudate dries deep cracks + fissures
- Degen + sloughing of renal epithelium (due to dehydration)
- Death due to dehydration, loss of serum proteins + electrolytes
113
signs greasy
- Listlessness, reddening of skin, depression + anorexia with sudden onset. Thickening of skin, red/brown macules around eyes/nose/lips/ears – sebum exudates
- Erosions on coronary band + heel. No pruritus/irritation
- Acute = death in 3-5d, if recover, decrease growth
- Chronic = older, thick, crusty lesions
114
PM greasy
- White precipitate in renal papillae, pelvis + ureters, mild ulcerative glossitis + stomatitis
- Dehydration, lung congestion + inflammation of peripheral LN
115
diagnosis greasy
- Signs + maybe bacterial culture
116
differentials greasy
- swinepox, skin necrosis, pityriasis rosea, parakeratosis, sarcoptic mange, erysipelas
117
treatment greasy
- enrofloxacin, amoxicillin, TMPs but do atb sensitivity (resistance)
- antiseptic spray – 0.05% chlorhexidine every day, fluids + electrolytes
- sensitive to penicillin G, erythromycin and rifampicin
118
prophylaxis greasy
- good hygiene, decrease humidity, soft bedding, isolate affected + avoid mixing. Clip needle teeth of newborn piglets (decrease skin lesions for fighting) autogenous bacteria vaccine to decrease incidence in chronic affected herd
- vaccinate sows 2+4w before farrowing
119
porcine respiratory disease complex PRDC
- Actinobacillus pleuropneumonia
- Enzootic pneumonia (mycoplasma)
- Exudative epidermitis (greasy pig)
- Glässers disease (polyserositis)
120
polyserositis
glassers disease
121
aetiology glassers
- haemophilus parasuis, small, pleomorphic, gram-negative, 21 (15) serovars, fasticidous. Commensal of upper resp
122
GD glassers
worldwide
123
SOI glassers
carrier pigs
124
MOT glassers
direct pig-pig contact, aerosol
125
HS glassers
young 4-8wo pigs (occasionally adults) piglets exposed early in life + colostral antibodies protect -active immunity by 7-8w old. If no immunity – fulminating diease
- Predisposing = stress
126
pathogenesis glassers
- ¬poorly understood. Primary pathogen or + PRRSV bacteramia localises at many sites
- Predilection for leptomeninges + brain stimulates inflammation
- On serosal surfaces – inflammation + fibrinous exudate
- Damage to vasculature
- Can avoid phagocytosis, decrease antigen presentation to pulmonary alveolar macrophages = delay antibody production
127
signs glassers
- Peracute-acute onset
- Best pigs affected first-sudden death or after2d
- High fever, severe coughing, abdo breathing, swollen joints
- CNS signs – tremor, paddling, lateral recumbency
- Chronic = decreased growth rate due to severe fibrosis in thoracic + peritoneal cavities
128
PM glassers
- Peracute = petechiae in some tissues. Increased fluid in cavities
- Acute = fibrinous polyserositis, polyarthritis + meningitis, cranioventral consolidation. Swollen joints
- Chronic = fibrosis of pericardium + pleura
- Micro = vasculitis, microhaemorrhages, DIC, fibropurulent exudate
129
diagnosis glassers
- ¬PCR from pleura, pericardium, peritoneum, joints, brain
- Multiplex PCR to differentiate virulent from non-virulent
- Commensal so not significant in upper resp tract
130
differential glasser
- Strep suis, actinobacillosis suis, septic E.coli, e.rhusiopathiae
131
treatment glasser
- Penicillin – all pigs not just ones showing signs
132
control glasser
- All in all out, control PRRSV, decrease stress
- Formalin killed bacterins – protection between isolates from same serovar good, but protection unreliable
- Vaccinate sow before farrowing or piglets at 1-3w
133
porceine enzootic pneumonia
- Mycoplasmal pneumonia, chronic, mild,
134
aetiology porcine enzootic pneumonia
- Mycoplasma hyopneumoniae, host-specific, pleomorphic, no cell wall, small rapidly inactivated in environment, survives longer in cold
- Part of porcine resp disease complex
135
GD PEP
worldwide
136
SOI PEP
carrier pigs - persists in lungs for months (7)
137
MOT PEP
- MOT = direct contact, aerosol (several km), via milk (mot common from gilts)
138
HS PEP
- HS = all ages suscepgtible (colonised in 1st few weeks of life) incidence of lung lesions highest in 3-5m old pigs
139
pathogenesis PEP
- ¬Inhalation attaches to the cilia + surface epithelium by adhesin proteins clumping, loss of cilia, cell death, and decreased mucus ciliary clearance
- Suppression of macrophages + immunity. Exudate settles cranioventrally
- Hyperplasia of mucus secreting cells
- Inflammation spreads alveolitis, atelectasis, obstruction
- 2nd bacterial infection increased severity death
140
signs PEP
- Onset most evident at 18-20w old
- Persistent, non-productive cough, most obvious when pigs are rounded. Morbidity high, mortality low
- Affects of disease uneven – impaired growth rate + feed conversion
- Most severe in naïve herds, predisposing = season, stress, parasites, mixing pigs
141
PM PEP
- Lungs are grey/purple + consolidated in apical + cardiac lobes. Old lesions well-demarcated + scarred. Mucopurulent exudate on cut surface
- Micro = perivascular + peribronchiolar cuffing, lymphoid hyperplasia
142
diagnosis PEP
- PCR from lower airway better. Very difficult to culture
- ELISA on herd basis but antibodies develop slowly + can’t differentiate vaccinated
- If of impression smear of cut lung. PM best
143
treatment PEP
- Lincomycin, enrofloxacin in feed/water/infection.
144
control PEP
- Bacteria vaccine = decreased lung lesions + signs but doesn’t prevent infection. Vaccinate sows 1-2 w before farrowing or piglets at 1-3 w old
- All in all out, cleaning, repopulation with SPF herd, gilt acclimatisation
145
swine pleuropneumonia
- highly contagious sudden onset, short clinical course, high morbidity, and high mortality.
- restricted to swine.
146
aetiology pleuropneumonia
- Actinobacillus pleuropneumoniae, Gram-, haemolytic
- Two biotypes, 15 serotypes - secretes 4 exotoxins (ApxI-IV (together = RTX toxins produced endotoxin)
147
SOI pleuropneumonia
carrier pigs (survives)
148
MOT pleuropneumonia
nose-nose contact, aerosol limited
149
HS pleuropneumonia
young (weaner/finisher pigs) <6 months
150
risks pleuropneumonia
poor ventilation, chilling, stress
151
pathogenesis pleuropneumonia
- Colonises + adheres to tonsils in non-immunised/stressed pigs inhalaed + adheres to aveoli epithelium
- Swallowed by macrophage macrophage killed by toxins (Apx1)
- Multiples + produces toxins inflam pleuritis + destruction of lung tissue
- Vasculitis thrombosis infarction
- Sudden death due to endotoxic shock
152
signs pleuropenumonia
- Sudden onset + rapid spread. Peracute – chronic death w/o clinical signs. 80% mortality in 10-16w old. Severe resp distress, ‘thumps’, open mouth breathing, bloody, frothy nasal + oral discharge. Fever, anorexia, not moving. Abortion in sows, cyanosis
- Survivors = decreased growth, pleurisy, abscess
153
PM pleuropnemonia
- Bilateral severe fibronecrotic + haemorrhagic pneumonia with fibrinous pleuritis. Pericarditis, dark, swollen lungs, necrotic bullae, froth in trachea
- In chronic cases -lesions more localised + organised
154
diagnosis pleuropneumonia
- Explosive onset, signs + pathology
- PCR, isolation + ID of A. pleuropneumonia that needs V factor (NAD) supplement for growth
- ELISA can help ID infected herds + serotypes
155
treatment pleuropnemonia
- Parenteral ceftiofur, tilcomycin, tetracyclines etc
- Then in feed/water to decrease mortality. Susceptibility testing good
- Chronic = unresponsive
156
post weaning disease
- E.coli enterotoxemia
- Low mortality
157
post weaning aetiology
E.coli that was genes for enterotoxins + F18 fimbrial adhesions can be same bacteria that causes oedema disease
158
SOI PWD
contaminated environment + sow
159
MOT PWD
PO ingestion of bacteria
160
HS PWD
just weaned piglets due to receptors arising
161
pathogenesis PWD
- E.coli ingested + colonises SI epithelial cells that have F18 receptors
- Produces enterotoxins which changes water + electrolyte influx of SI malabsorptive diarrhoea dehydration metabolic acidosis + maybe death
162
signs PWD
- Diarrhoea similar to neonatal diarrhoea but less severe (peaks 3w post weaning)
163
diagnosis, treatment + prevention PWD
- Similar to/same as: oedema disease, colibacillosis/neonatal diarrhoea
- PWD + oedema disease can occur on their own, both in same outbreak or in the same pig
o All caused by E.coli – just depends if they strain produces just Stx2e just enterotoxins or both
- Can breed pigs without F18 receptors so resistant to E.coli – but in landrace pigs, they are extra susceptible to stress
164
PRCV
- Naturally occurring deletion mutant of TGEV
165
MOT PRCV
- MOT = direct contact/airborne (travels several km)
166
HS PRCV
- HS = all ages, infects all pigs before 10-15w old after passively acquired MDA decrease, can persist in herd throughout year or disappear in summer + reappear in winter
167
path PRCV
- Tropism for resp tract
168
signs PRCV
- Usually subclinical/self-limiting, cough, dyspnea, abdo breathing, depression, anorexia, decreased growth rate. Severity increases if coinfection with PRRSV
169
PM PRCV
- Consolidation of lung, bronchointerstitial pneumonia, peribronchiolar + perivascular lymphohistiocytic cuffing
170
diagnosis PRCV
- PCR, detect viral antigen/nucleic acids in lungs
171
types of immunity PRCV
- 1. PRCV – induced active immunity to TGEV
- 2. Passive lactogenic immunity (TGEV infected sow) for piglets
- 3. PRCV-induced passive immunity to TGEV
172
swine dysentry
- Mucohaemorrhagic diarrheal disease limited to LI of pigs (bloody scours)
173
aetiology SD
- brachyspira spp – hyodysenteriae, hampsonii + suanatina (strongly beta haemolytic) anaerobic spirochetes, G- 8 species that colonise pigs
- occupy special niches in LI of birds + mammal
- B. hyodysenteriae = motile with chemotaxis + Visco taxis towards mucin (associates with gut mucosa) survives in wet poo 4m
174
SOI SD
- SOI = faeces of infected pigs, contaminated lagoon water, contaminated vehicles
175
MOT SD
- MOT = feco-oral
176
HS SD
- HS = grower – finisher pigs. Strongly influenced by diet
177
path SD
- Not fully understood
- PO proliferates in LI + cause degeneration + inflammation of mucosa, hypersecretion of mucus + multifocal haemorrhage on mucosa surface
- Diarrhoea due to decreased ability of mucosa to reabsorb, Na + Cl (+ water)
178
signs SD
- The incubation period is usually 10–14days, Morbidity 90%, mortality 30%
- Anorexia + soft faeces watery faeces containing blood, mucus + shreds of white fibrinous exudate + staining of perineum
- Dehydration + weight loss, often starts after diet changes, spreads gradually
- Pigs recover over several w but growth stays decreased
179
PM SD
- ¬mesocolonic oedema, swollen mucosa of caecum + colon
- Pseudomembrane of fibrin, mucosa + blood
- Micro = typhlocolitis, neutrophilic inflam lymphoplasmacytic + goblet cell hyperplasia
180
diagnosis SD
- Signs + PM usually sufficient
- Histo lesions in LI. Isolation of strongly B-haemolytic brachyspira by anaerobic culture
- PCR of faeces/smear of mucosa but culture better for haemolytic phenotype confirmation
181
differentials SD
- Intestinal spirochaetosis, salmonellosis, whipworm
182
treatment SD
- Atb pleuromutilin’s, lincomycin, tylosin in water for 5-7d
183
prevention SD
- Treat carriers + clean + disinfect facilities
- Reservoir (rodent + waterfowl) control, more soluble fibre (sugar beet pulp) in feed. All in-all out
- Quarantine + treat new pigs from reliable source
184
transmissible gastroenteritis (TGE)
- Coronaviral enteritis - OIE
- TGE is reported worldwide.
- Possible zoonosis
185
aetiology TGE
- ¬porcine coronaviruses (TGE virus)
- Porcine resp coronavirus = naturally occurring deletion mutant of TGEV
- Survives in water/sewage d at 25oC and w at 4oC
186
SOI TGE
- SOI = carrier pigs, contaminated environment
187
MOT TGE
- MOT = aerosol, direct contact
188
HS TGE
- HS = all ages susceptible
- Epidemic = when animals are TGEV/PRCV sero neg + susceptible (in winter more severe)
- Endemic = persistence of virus + disease in herd due to influx of susceptible pigs (sows transfer various degree of immunity)
189
pathogenesis TGE
- Destruction of jejunal enterocyte decrease enzymatic activity in SI + severe segmental villous atrophy
- Disruption of digestion + decrease absorptive surface malabsorptive diarrhoea, dehydration + metabolic acidosis
- Can replicate in mammary tissue + shed in milk
190
signs TGE
- Infection with PRCV = decreased severity of TGEV disease, watery diarrhoea, yellowish, weight loss, dehydration
- Under 7 d old = die in 3-4d – high mortality
- 3+w old = profuse diarrhoea, resolving in a few d maybe vomiting
- Older = anorexia, depression, agalactia, diarrhoea
- Endemic = hard to differentiate from rota, E.coli, PEDV
191
PM TGE
- Thin walled SI filled with watery content, undigested milk in colon
- Micro = severe villi shortening/loss of neutrophilic inflam of lamina propria
192
diagnosis TGE
- PCR of faeces/oral samples to differentiate PEDV, TGEV + PDCV
- IHC fixed tissues
- Serology for surveillance but difficult as TGEV + PRCV have similar antibodies
193
treatment TGE
- Supportive – lots of water, warm environment. Antibiotics if needed
194
control and prevention TGE
- Inactivated/attenuated vaccines available – sows
- Piglets protected by nursing immune sows
- Strict sanitation + biosecurity
195
eliminate TGE
- New breeding stock, feed infected pig intestine to pigs, all in all out
196
colibacilosis
(Neonatal E.Coli diarrhoea + Post weaning diarrhoea (PWD))
Neonatal E.coli diarrhoea
197
aetiology of colibacilosis
- Enterotoxigenic strain of E.coli (ETEC), pathogenic antigenic types = F4, F5, F6, F18 + F41 (produce enterotoxins)
198
MOT colibaciolosis
per oral
199
HS colibacillosis
- HS = enteric colibacillosis = nursing + weaning pigs, neonatal (F4), postweaning (F4/F18) genetic predisposition – not all pigs express receptors for all fimbrial adhesions
200
pathogenesis colibacilosis
- appropriate predisposing factors fimbriae adhere to/colonise absorptive epithelial cells of jejunum + ileum
- ETEC proliferate enterotoxins produced disease (fluid + electrolyte secretion into lumen diarrhoea + dehydration)
201
signs colibacilosis
- Profuse watery diarrhoea, rapid dehydration, acidosis + death
- Rarely collapse and die before diarrhoea
- Neonatal = diarrhoea 2-3h after birth, gilt litters more affected than sow
- Less severe = inflamed anus/perineum
202
diagnosis colibacilosis
- ¬histologic observation of coliform colonisation of SI brush borders + isolation from SI
- Isolation of E.coli alone = non-diagnostic
- Genotyping PCR assay to detect fimbrial type + enterotoxin genes
203
differentials colibacilosis
- Cl. Difficile, Cl. perfringens A + C, TGEV, PEDV, rotavirus, PRRSV
- In suckling pigs 5 days and older, Isospora suis must also be considered.
204
treatment colibacilosis
- Prompt atb + restore fluids + electrolytes have to confirm E.coli + do sensitivity testing
205
prevention and control colibacilosis
- ¬good hygiene, no damp/cold, vaccination
- Vaccinate pregnant with pilus specific/killed whole cell
- Weaned pigs = live attenuated F4/F18 strain without enterotoxins
- Pigs w/o receptors for F4 +F18 = naturally resistant
- Take SI content from piglets with diarrhoea, culture in milk + feed culture to pregnant sow
- 2x parenterally at 3 or 4weeks apart, the 2nd 2–3weeks prior to parturition.
- IgG protects gut against E.coli
206
oedema disease
- Can be sporadic or affect whole herd
- Can be with PWD or alone (depends if E.coli strain present has genes for enterotoxins)
207
aetiology of oedema disease
- Haemolytic E.coli that produces F18 fimbrial adhesions + shiga toxin 2e (Stx2e)
- Serogroups = O138, O139, O141
208
SOI oedema disease
- SOI = contaminated environment or sow
209
MOT oedema disease
- MOT = ingestion of bacteria
210
HS oedema disease
- HS = healthy, rapidly growing nursery pigs. Young (<10d old) less susceptible as don’t have F18 fimbriae receptors yet
211
risks oedema disease
- Risks = stress + high protein diet
212
pathogenesis oedema disease
- Ingestion of E.coli + colonise intestinal epithelial cells that have F18 receptors
- Stx2e = inhibits protein synthesise cell death enters blood stream + targets vascular endothelium --> fluid leakage oedema
- Stx2e readily binds to RBC spreads submucosa of stomach, mesocolon, eyelids, larynx + rain highly susceptible to Stx2e
- oedema, haemorrhage, intravascular coagulation + micro thrombosis
213
signs oedema disease
- Occurs 1-2w post weaning + affects healthiest pigs
- Sudden death without signs. CNS signs – ataxia, recumbency, periocular oedema, swelling of forehead + submandibular region, dyspnoea + anorexia, strange noises
- Morbidity 30-40%, mortality up to 90%
- Subclinical = vascular lesions + decreased growth rate
- Chronic = d- w after intestinal infection, failure to grow, circling, limb muscle atrophy
214
PM oedema disease
- Subcut oedema + oedema of submucosa of stomach (esp glandular region) fluid is gelatinous
- Fibrin strands in peritoneal cavity + maybe haemorrhage
215
diagnosis oedema disease
- Signs, culture of SI to find E.coli but sometimes not present after death
- PCR for F18 + Stxe2e to confirm EDEC
- Serotyping good to track persistence
216
treatment oedema disease
- Often ineffective as Stx2e bound to receptors when signs occur
- Atb in water to exposed + atb susceptibility testing
217
control oedema disease
- High fibre, low protein diet, decreased feed given to weaned pigs
- Breed resistant pigs but also more suspectable to stress
218
vaccine oedema disease
- 1. E.coli bacteria for sows to protect piglets
- 2. PO live non-pathogenic F18 vaccine for pig
- 3. Genetically modified recombinant Stx2e vaccine for young pigs
