cattle Flashcards
1
Q
enzootic bovine leukosis
A
Disease of cattle, infected at any age (+embryonic)
2
Q
enzootic bovine leukosis aetiology
A
- bovine leukaemia virus (BLV), delta retrovirus
- similar to human T-cell leukaemia virus, stale genome, no chronic viraemia
3
Q
EBL distribution
A
worldwide, NZ + Aus + west Europe free
4
Q
EBL epizootiology
A
- virus is present mostly in lymphocytes and can be found in blood, milk and tumours
- persistent infection – virus is maintained in cattle population
5
Q
EBL SOI
A
infected lymphocytes = blood (injection/rectal/dehorning/blood taking)
6
Q
EBL MOT
A
- horizontal – direct contact
- vectors: tabanids
- vertical: transplacentally, intrapartum + colostrum
7
Q
EBL HS
A
- increase incidence with increase age (rare <2y)
- increased in dairy cattle (closer contact)
- cattle, water buffalos and capybaras (mostly cattle)
- sheep and goats experimentally
8
Q
EBL pathogenesis
A
- infected through blood
- 4 possible outcomes after exposure to BLV
- Failure to become infected
- Remain persistent infected with no signs (most common)
- Persistent lymphocytosis
- Lymphosarcomas
9
Q
EBL signs
A
- 5-10% peracute: lymphosarcoma are growing and if they rupture they cause the bleeding (just seeing sudden death) affected spleen, adrenal glands, rupture of abomasal ulcer
- subacute to chronic – signs depend on organ affected, decreased milk, decreased weight, weakness
- 70-90% will have enlarged superficial lymph nodes
- mostly depends on where the tumour is located
- 30% >3 yo = persistent lymphocytosis – mostly subclinical
- Multicentric lymphosarcoma – LN, heart, kidneys
10
Q
EBL PM
A
- lymphosarcoma = yellow-tan, discrete nodular masses or diffuse infiltrate
- enlarged, pale organ – DD = degenerative changes
11
Q
EBL diagnosis
A
- ¬haematology = persistent lymphocytosis
- serology: AGID (serum), ELISA (serum, milk)
- exception is calf from infected mother as they have maternal antibody has until 4-6 months of age, so need to use molecular methods
- PCR of blood
- Viral isolation
- neoplastic tumours are identified by cytology or histopathology
12
Q
EBL treatment
A
- no treatment + no vaccine
- eradication programs – if farm negative for 2 consecutive years can be deemed as free and importing animals need to have 6 months free status prior to transport
- not zoonotic
13
Q
BSE
A
- listed, notifiable OIE
- progressive, fatal, infectious, neurologic disease of cattle, incubation 2-8 years
- two forms:
o classical BSE (occurs in cattle after ingesting prion contaminated feed)
o atypical BSE (occur spontaneously in all cattle populations)B
14
Q
BSE aetiology
A
- prion – proteinaceous infectious particle – (H type and L type?) accumulation of prions
- resistant to heat, freezing, UV light and chemical disinfectant
15
Q
BSE SOI
A
- classic BSE = contaminated feed
16
Q
BSE HS
A
- no sex or breed predisposition, more common in dairy (fed animal source protein)
- mostly during 1st 6 months of life + diagnosed in cattle 3-6years old
17
Q
BSE MOT
A
- not transmitted horizontally by contact or aerosols but calves from ill mum’s higher chance
18
Q
BSE PATHOGENESIS
A
- oral exposureagent replicates in peyer’s patches of ileum migration via peripheral nerves to the CNS
19
Q
BSE SIGNS
A
- initial signs are subtle and behavioural in nature and clinical onset usually after 3 months
- changes in behaviour: tremors, head shy, kicking in parlour, aggressive behaviour, nervous, reluctant to enter doorways, fine muscle fasciculations
- changes in locomotion: HL+ FL ataxia, abnormal posture, falling, recumbency, circling
- sensor disturbance: head tossing, teeth grinding, nose licking, tongue play, head rubbing/pressing, sneezing/snorting, increase salivation
20
Q
BSE DIAGNOSI
A
prions cannot be isolated and only be conclusively confirmed in post-mortem
21
Q
PM BSE
A
- ¬no abnormalities in gross pathology
- diagnosis is dependent on histological findings
- brainstem, (pathognomonic) bilaterally symmetric intracytoplasmic vacuolation of neurones and grey matter neutrophil – no longer the method of choice for BSE confirmation
- immunologic detection of PrPres in medulla oblongata samples
o ELISA – ‘rapid test’ – principal screening tools
o ICH or western immunoblot – confirmatory methods
22
Q
transmissible spongiform encephalopathies
A
- BSE, scrapie, chronic wasting disease of Cervidae, transmissible mink encephalopathy, feline spongiform encephalopathy, creutzfeld-jakob disease, kuru, fatal familial insomnia
23
Q
differentials of BSE
A
- Nervous ketosis, hypomagnesemia, lead poisoning, rabies, toxicosis, trauma, neoplasia
24
Q
Treatment BSE
A
- no effective treatment and affected animals will inevitably die
25
Q
control of BSE
A
- ¬prohibition of feeding of sick to cattle, national and/or local guidelines – reporting, passive and active surveillance
- High risk tissues aren’t allowed to enter food chain (brain, spinal cord, eyes, intestine’s)
26
Q
public health BSE
A
- eating infected tissue/iatrogenic – average incubation period is estimated to be 11-12 years
- psychiatric symptoms followed by neurological signs. Cognitive function gradually deteriorates
27
Q
aetiology of foot and mouth disease
A
- picornaviridae – genus aphthovirus, non-enveloped, single, RNA, 7 serotypes (A,O,C, SAT-1,2,3, Asia 1) no cross protection between types
28
Q
Tenacity of FMD
A
- very resistant survive in poo 1 m, carcasses 48hr + frozen meat years
- inactivated by >56oC, drying, 2% NaOH, vinegar. Travel 150 miles over sea + 6 miles land
29
Q
EPIZOOTIOLOGY OF FMD
A
- only 12 variants is enough to infect cow via resp route, 20 pig and 10 in sheep (pigs high resis)
30
Q
FMD SOI
A
- animals: incubation, sick, re-convalescence
- aerosol, saliva, faeces, urine, milk and semen, contaminated fomites, water, food, soil
31
Q
FMD MOT
A
- direct and indirect contact, contaminated food, water, straw and barn manure
32
Q
FMD POE
A
- MM of the upper GI and respiratory system (inhalation, ingestion, skin wounds, MM)
33
Q
FMD HS
A
- domestic animals – ruminants and cloven-hoofed animals
- horses are resistant to FMD, wild animals – main natural reservoir African buffalo
34
Q
pathogenesis of FMD
A
- oronasal (inhalation in rum, oral pigs) replication in mucosa of pharynx 1o vesicles (aphte) rupture infective liquid exhaled into environment
- viraemia 18-36 in blood to mucosal, skin or organ cells (heart)
- 2ndary vesicles rupture 1-3 days (2nd phase of infection) virus exhaled + shed
- after vesicles ruptured erosions remains – secondary bacterial infections are possible
- virus is epitheliotropic and myotrophic (myodegeneration – tiger heart) – in young animals
35
Q
FMD signs
A
- clinical onset around 4 days
- incubation variable 2-14d cattle, 3-8d rums, >2d pig
- fever, vesicular lesions on tongue, hard palate, lips, muzzle, coronary band, interdigital cleft, teats
- drooling, stamping feet, lying down, lameness, 2nd bacterial infection = exungulation
- decreased BW, decreased milk production. Sudden death in calves, recovery in 2-3w, mortality only 1-5% in adults. Carriers for 30m (cattle), 9m (sheep)
36
Q
diagnosis FMD
A
- RT-PCR (epithelium, milk, serum, oesophageal-pharyngeal fluid)
- Ag-ELISA, CFT, VI primary bovine or calf thyroid cells
- Ig vesicular epithelium – only OIE labs for containment. Group 4 pathogens for confirmation
- Serology for trade to test efficacy of vaccination have to know if vaccinated (ELISA, VN, CFT)
37
Q
PM FMD
A
- changes on myocardium – focal necrosis – “tiger heart”
38
Q
DD FMD
A
- to exclude all stomatitis of other aetiologies, especially – vesicular stomatitis
39
Q
prophylaxis FMD
A
- no treatment - eradication by law – immediate stamping out, burning carcasses properly etc
- countries: FMD-free wo vaccine, free w vaccine, suspended FMD-free w/wo vaccine + unrecognisedv
40
Q
vaccination FMD
A
- decision is only by WHO
- inactivated vaccine give immunity for 4-6m against specific serotypes in enzootic countries
41
Q
control FMD
A
very very strict measures it’s OIE
42
Q
Vesicular stomatitis
A
- viral infectious disease of livestock + very benign disease
- USA, endemic in south America + Mexico
43
Q
aetiology of vesicular stomatitis
A
- vesiculovirus, family rhabdoviridae
- RNA virus, bullet shaped, 2 serotypes VS-NJ (new jersey) most virulent and VS-IN (Indiana)
44
Q
epizootiology vesicular stomatitis
A
- disease more frequent during summer, seasonality, disappear with 1st cold days
- in tropical areas whole year
- morbidity is 5-10%
45
Q
MOT OF Vesicular stomatitis
A
MOT= direct contact + w animals w lesions + biting insects (horse flies and gadflies)
46
Q
HS of vesicular stomatitis
A
- HS: horses, cows, rarely swine
47
Q
signs of vesicular stomatitis
A
- incubation 3-15 days
- fever, ptyalism, ulcers (start as vesicles) coronitis, lameness, decreased appetite
- self-limiting – resolves in 10-14d
48
Q
diagnosis of vesicular stomatitis
A
- clinically unreliable, CFT, VN-test and ELISA, VI from vesicular fluid, epithelium from lesion or swab from lesion
49
Q
differential of vesicular stomatitis
A
- clinically undistinguishable from FMD (horses don’t get FMD), swine vesicular disease + vesicular exanthema
50
Q
treatment of vesicular stomatitis
A
- recover spontaneously, supportive care – soft feed, fluid, antiseptics prevent 2o bac infection
51
Q
prophylaxis of vesicular stomatitis
A
- strong isolation of infected herd, disinsection
- vaccination with modified inactivated vaccine
52
Q
public health - vesicular stomatitis
A
- ZOONOTIC – self-limiting, influenza like disease, lasting 3-5d
- Rare = vesicles on buccal mucosa, lips, nose + encephalitis
- wear PPE when handling affected animals
- reportable to state + federal officials in USA = affected premises put in qurantine
53
Q
shipping fever pneumonia
A
- acute, multifactorial + complex disease with respiratory syndrome
54
Q
shipping fever aetiology
A
- primary infection: mycoplasma bovis, m. dispar, m. bovirhinis
- secondary bacterial infection: mannheimia haemolytica, Pasteurella multocida, strep, staph
- viral: parainfluenza 3, bovine respiratory syncytial, BDV
- environmental + management factors (transport, weaning, temperature, dust)
55
Q
SOI of shipping
A
sick animals, older animals with subclinical infection
56
Q
MOT of shipping
A
contact, aerogenous, contaminated equipment and objects
57
Q
POE of shipping
A
respiratory tract
58
Q
HS of shipping
A
young growing cattle (6m-2y) but all ages susceptible (calves and beef)
- morbidity 80-100%, mortality 5%
59
Q
pathogenesis of shipping
A
- stress factor + viral = decreased immunity proliferation of commensal bacteria
- bacteria colonise lower resp tract bronchopneumonia w cranioventral distribution in lungs
- endothelial + alveolar epithelial damage
- macrophages attract neutrophils to lungs
- pathogens in fluid breathed in + gravity causes cranioventral lesions
- usually 2w after transport (2-5d)
60
Q
signs of shipping
A
- Depend on pathogen/host immunity etc
- Fever, nasal discharge, anorexia, cough, harsh + increased RR
- Bacterial = mucopurulent discharge, open mouth breathing, pleuritis friction rubs, dull sound on percussion (f. necrophorum abscess)
- Typical body position with open mouth breathing
61
Q
PM of shipping
A
- atelectasis, emphysema in lung lobes, firm Serofibrinous exudate in thorax + fibrinous pleuritis
- hyperaemia, hypertrophic, necrotic bronchial LN
- stage of pneumonia varies within the affected tissue
- micro = alveoli flooded with haemorrhage, fibrin + oedema. Various stages of consolidation
62
Q
diagnosis of shipping
A
- bacteria are commensal so increase culture specificity by BAL/deep nasopharyngeal swabs
- PCR – m. haemolytica/viruses
- Serology for BHV-1 (2nd can be lower than 1st) VN, ELISA, HI
- Histopathology + culture from lungs PM
63
Q
differentials of shipping
A
- Pneumonia: viral/mycoplasma/bacterial/aspiration, calf diphtheria, lungworm, AHF,
64
Q
treatment of shipping
A
- antimicrobials: oxytetracycline, tilmicosin, trimethoprimsulfadoxine, sulfonamides, penicillin
- 1 treatment, but severely ill may relapse + need every day or 2-3x a day up to 3-5d
- symptomatic therapy – NSAIDs, bronchodilators
65
Q
prophylaxis of shipping
A
- feedlot management + improvement of animal housing, all in all out system
- biosecurity measures, quarantine all animals new to the farm
- MLV and killed virus (KV) vaccine (on arrival to feedlot or 2-3w before transport)
66
Q
public health of shippign
A
no human transmission
67
Q
infectious bovine rhinotracheitis
A
- highly contagious, respiratory (feedlot) or genital infection
68
Q
aetiology of IBR
A
- bovine herpesvirus-1 (BHV-1)
- family: Herpesviridae
o BHV-1.1 = respiratory and abortions
o BHV-1.2 - BHV-1.2a = abortions, BHV-1.2b = venereal infections
o BHV-1.3 (now 1.5) = neurovirulent (encephalitis subtype)
69
Q
SOI IBR
A
sick animals, latently infected animals, fomites
70
Q
MOT IBR
A
direct routes (nasal and genital secretions), indirect (people and equipment)
71
Q
POE IBR
A
: MM of upper respiratory tract, vagina or prepuce
72
Q
HS IBR
A
affect young and older cattle (younger more often) = beef feedlot (severe), more often in cold (overcrowding)
73
Q
pathogenesis IBR
A
- BHV-1 = not life threatening but predisposes to 2nd bact infection maybe death
- Colonises MM of upper resp tract + replications in tonsils conjunctiva
- Bronchopneumonia from aspiration of exudate/ decrease pulmonary defence
- Establishes latency in trigeminal + sacral ganglia (reactivated w stress)
74
Q
signs IBR
A
- incubation 3-7days
- respiratory infection (IBR)
o fever, anorexia, coughing, hypersalivation, conjunctivitis, RED NOSE, grey necrotic foci on septal mucosa + pseudodiptheric yellow plaques, abortion (<100d after infection) - genital
o frequent urination, elevated tail, mild vaginal discharge papules on vulva ulcers (recover in 10-14d if no bacterial infection)
o if bacteria = uterus inflamed + transient infertility
o ulcers on penis, decrease libido, painful erection - calves = pyrexia, nasal discharge, diarrhoea, resp distress, death
75
Q
PM IBR
A
- petechial haemorrhage + focal necrosis in upper resp tract
- increase LN, Serofibrinous exudate in airways, 2nd bacterial pneumonia
- aborted foetus = focal necrotising hepatitis
76
Q
DIAGNOSIS OF IBR
A
- Epizootioloigcal data + clinical signs
- PCR, serology (not for abortion), ELISA
- Abortion = PCR, VI, fluorescent antibody staining foetal tissue
77
Q
differential IBR
A
- shipping fever, pasteurellosis, mucosal disease, malignant catarrhal fever, calf diphtheria
78
Q
TREATMENT IBR
A
- atb for secondary bacterial infection
79
Q
prophylaxis IBR
A
- DIVA vaccine -differentiating infected from vaccinated animals
- MLV or killed. IM/int4ransal MLV (IM in pregnant = abortion)
- MLV at 6-8m, before breeding then q1y. calves 2-3w before entry to feedlot
- recommended for intensive breeding units
80
Q
public health IBR
A
- no human transmission but OIE listed
- eradicate = serology surveillance, cull reactors, biosecurity + vaccination
81
Q
Malignant catarrhal fever
A
- severe often fatal lymphoproliferative disease coryza gangrenosa bovum
- quickly inactivated in environment (3h)
- incubation = 14-200d, if survive- lifelong infection
82
Q
aetiology of MCF
A
- herpesviridae, genus: macavirus, subfamily: gammaherpesvirinae, family: Herpesviridae
- AHV-1 natural host (wildebeest), OHV-2 (domestic sheep + goats)
- AHV-2: nonpathogenic + CpHV-2 natural host: domestic goats
83
Q
MCF HS
A
Bison >1000x more susceptible than cattle
84
Q
MOT MCF
A
nasal secretion direct contact + aerosol
85
Q
AHV-1 MCF
A
- wildebeest infected at perinatal period by horizontal + maybe intrauterine transmission
- shed virus until 4-6 months of age
- transmitted by direct contact/ airborne routes
86
Q
OHV-2 MCF
A
- lambs are infected usually at 3-6 months by aerosol + shed virus at ~6-9months of age
- virus is quickly inactivated by sunlight
87
Q
AHV-1 AND OHV-2
A
- similar clinically + pathologically, course = peracute-chronic and severe vasculitis
88
Q
pathogenesis of mcf
A
- unresolved
- non-specific cytotoxicity caused by small fragments of infected lymphocytes causing proliferation + dysregulation of cells
89
Q
signs of MCF
A
- fever, depression, decreased milk production, serous discharge from eyes + nose with matting of hair
- cattle = increased LN, peripheral corneal opacity, hypopyon erosion + mucopurulent discharge of upper resp, ocular + oral mucosa, lameness, stupor, aggression (CNS)
- deer + bison = sudden death
- cattle that survive = erythema + exudation between digits + heels, skin cracking, hair loss, haemorrhagic cystitis
90
Q
diagnosis MCF
A
- signs with low morbidity, history of contact with sheep/goat/wildebeest
- PCR – blood, kidney, LN, brain and ELISA
91
Q
PM MCF
A
- Inflammation + necrosis of resp, alimentary + urinary epithelium, generalised lymphoid proliferation + necrosis + widespread vasculitis
92
Q
differentials MCF
A
- BVDV, blue tongue, rinderpest, FMD, IBR, if CNS signs – can resemble rabies + tick encephalitis
93
Q
treatment MCF
A
- none consistently effective, supportive + decrease stress
94
Q
prevention MCF
A
- preventing contact between carriers and clinically susceptible species remains the primary control method
- no vaccine is available
- sheep can be free if early weaning + isolation
95
Q
infectious bovine keratoconjuncitivits
A
- highly contagious and infectious ocular
96
Q
aetiology of IBK
A
- maybe Moraxella bovoculi, or M.bovis
- mycoplasma, chlamydia spp, BHV-1, bovine adenovirus
97
Q
SOI OF IBK
A
- secretions from eye, nose or vagina, carriers
- flies = mechanical vector + irritant
98
Q
MOT OF IBK
A
- direct contact, aerosol and fomites, mechanical vectors (flies)
99
Q
HS IBK
A
- cattle- young cattle commonly in their first summer, immunologically naïve cattle
- increases In spring, peaks in summer and decreases in fall
100
Q
pathogenesis of IBK
A
- bacterium adheres to corneal epithelium via fimbriae + pilli proteins
- produces B-haemolysin toxin, cytotoxic toxin, pathogenic fibrinolysis, phosphatase, hyaluronidase etc
- invades lacrimal + tarsal glands
101
Q
signs of IBK
A
- photophobia, blepharospasm, epiphora, oedema, ulcer
- stage 1: excessive tearing and increased sensitivity to light
- stage 2: 1+ ulcer spreads + cornea becomes increasingly cloudy
- stage 3: ulcer covers most of cornea, inflammation goes deeper
- stage 4: spontaneous recovery in 3-5 weeks, ulcer heals and reduces, leaving a scar
- severe = blindness in 48-72hr
102
Q
diagnosis of IBK
A
- signs + microbial culture (aerobic for Moraxella)
- fluorescent antibody testing
- multiplex PCR for different Moraxella spp
103
Q
differential of IBK
A
- trauma, parasites (thelazia), foreign body
- IBR = upper resp signs + conjunctivitis, keratitis + ulceration rare
- MCF = resp sign s+ 1o uveitis + associated keratitis
104
Q
treatment of IBK
A
- Oxytetracycline/tulathromycin systemically (based on susceptibility results)
- Eye patch, partial tarsorrhaphy, topical atropine, NSAIDs, shade
105
Q
prophylaxis of IBK
A
- fly and dust control and pasture management
- several vaccines but because of multiple strains of bacteria, the vaccine isn’t consistently effective
106
Q
TB
A
- infectious granulomatous zoonotic disease
- OIE listed
107
Q
aetiology of TB
A
- Mycobacterium tuberculosis complex: M.bovis, m. caprae, m.tuberculosis
- G+, acid fast
- Persists in environment: Cold, dark, moist conditions
- Don’t grow outside of a host + Multiply in culture cells approximately every 20 hours
108
Q
SOI TB
A
cattle (reservoir for m.bovis)
109
Q
MOT OF TB
A
aerosol or ingestion, bites (badgers) intrauterine + coital = rare
110
Q
HS TB
A
o maintenance = cow, badger, ferret, deer
o Spillover = sheep, goat, horse, dog
111
Q
pathogenesis of TB
A
- Inhaled bacteria phagocytosed by alveolar macrophages
- Bacteria proliferates granuloma made of dead + degenerate macrophages surrounded by epithelioid cells, granulocytes, lymphocytes + MNGC
- Caseous necrotic centre surrounded by granulation tissue = tubercle
- Initial granulomatous lesions = 1o complex
- 1o complex = remain stable or progress slowly/rapidly
- Acute miliary TB = generalised + rapidly fatal dissemination of complexes through vascular + lymphatics
112
Q
signs of TB
A
- Latent, subclinical, severe
- Progressive emaciation, lethargy, anorexia, diarrhoea, low grade fluctuating fever
- Bronchopneumonia, moist productive cough, dyspnoea, enlarged draining LN
113
Q
PM TB
A
- Lesions = granulomas – yellow, caseous, calcified In LN + organs
114
Q
diagnosis TB
A
- Intradermal tuberculin test infect purified protein derivatives of m.bovis + m. avium. Measure skin thickness 72hours later, Swelling = delayed hypersensitivity reaction
- Single comparative intradermal TB test used if lots of avian TB or para TB
- Culture = 8w, PCR, interferon gamma assay
115
Q
prevention + control TB
A
o Test + cull, abattoir surveillance
o Test + separate, biosecurity, PM meat inspection etc
116
Q
treatment TB
A
- ¬not practical due to public health concerns
117
Q
public health TB
A
- All m. tuberculosis complex sp are zoonotic. Zoonotic TB = m.bovis is resistant to pyrazinamide
- Prevent zoonosis = pasteurise milk
- BGG vaccine for badgers + maybe people
118
Q
BVD
A
- high morbidity with a mortality of >25%
- OIE mucosal disease
119
Q
aetiology BVD
A
- BVDV – bovine viral diarrhoea virus, family: flavivirdae, genus: pestivirus
- RNA virus
- 2 genotypes: BVDV1 and BVDV 2 (antigenetically different)
- 2 biotypes: cytopathic and non-cytopathic (most predominant)
o noncytopathic = most common + most important. Crosses placenta, invades foetus and leads to persistent infection
o cytopathic = only associated with mucosal disease in animals that are already persistently infected with the non-cytopathic type
120
Q
SOI BVD
A
= cattle persistently infected with non-cytopathic are reservoirs. Acutely infected. Fomites
121
Q
MOT BVD
A
horizontal: direct/ indirect, AI/coitus, vertical: transplacental transmission (any stage during pregnancy – just with different results)
122
Q
POE BVD
A
oronasal mucosa (inhalation or ingestion of virus)
123
Q
HS BVD
A
cattle, wild ruminants, swine, sheep, goats and camelids
- Persistently Infected = when non-cytopathic BVDV transmitted transplacentally during 1st 4m of foetal development. Calf if immunotolerant.
- Transplacental trans later = abortion, malformations/healthy calves w antibodies against BVDV
124
Q
pathogenesis BVD
A
Pathogenesis – acute infection
- Infection of immunocompetent susceptible animal with non-cytopathic or cyto BVDV
Pathogenesis – mucosal disease
- Infect MM of resp + GI system, replication in epithelial cells, diarrhoea in 6m-1yo, immunosuppression
- Virulent BVD2 = thrombocytopenia + haemorrhagic syndrome
125
Q
signs BVD
A
- Depend on organ involved, duration, strain, immune status
- Most common = subclinical infection with no signs then seroconversion
- Acute = mild severe enteric disease with high mortality, biphasic fever, depression, decreased milk, inappetence, increased RR, excessive lacrimation + nasal secretion + diarrhoea
o Signs 6-12d after infection, last 1-3d. recovery quick
o Replicates in lymphoid tissue = immunosuppression = increased severity of intercurrent infections (IBR + RSV, corona etc)
o BVDV2 = fever, oral ulcerations, lesions on coronary band + ID clef, diarrhoea, petechia on MM, prolonged bleeding from injection sites, increased LN
o Severity of acute depends on virulence of strain + animals, not viral biotype - Infection of preg = decreased conception rate (at time of fertilisation)
o 1st 4m = embryonic resorption, abortion, PI
o 4-6m = malformation of eye + CNS
o Fetal mummification, premature birth, weak calves born
126
Q
mucosal disease BVD
A
- Unknown, but highly fatal when PI cattle become superinfected with cytopathic BVDV
- Usually spontaneous mutation of PI
- Non-cytopathic cytopathic BVDV
- Cytopathic is then antigenically similar to non-cytopathic so doesn’t induce immune response
- Acute = fever, leukopenia, dysenteric diarrhoea, inappetence, erosion on nares + muoth + death within few days
- Chronic = weeks-months. Intermittent diarrhoea + gradual wasting. Coronitis + lesions of skin + interdigital clef - lameness
127
Q
patio BVD
A
Patho acute
- Erosion + ulcers through GI tract, haemorrhagic + necrotic peyer’s patches
Patho chronic
- ¬less pronounced but similar to acute focal ulcerations of cecum, proximal colon or rectum. Sunken peyer’s patches
128
Q
diagnosis BVD
A
- History, signs + gross/micro lesions, Lab when signs minimal PCR
- paired sera + 4x increase = recent infection due to vaccine use + high prevalence
- isolation from blood, nasal swab = active
- formalin fixed ear notch for IHC = no need for repeat sampling (VI from blood) + able to distinguish transiently infected + PI from amount of virus
129
Q
treatment BVD
A
supportive
130
Q
control BVD
A
- good biosecurity, eliminate PI, vaccination
- quarantine, test embryos + semen
- screen herds with PCR etc
131
Q
immunoprophylaxis BVD
A
- MLV needs to contain both strains
- Don’t use in pregnant as BVDV is fetotropic + immunosuppressive
- Inactivated vaccine for pregnant – protection is short – calves protected for 3-6m
- Booster before first breeding
132
Q
winter dysentry
A
- Acute, highly contagious GI disorder
133
Q
aetiology WD
A
- bovine coronavirus (BCoV),
- survive in low temps + low UV light
- fam: Coronaviridae, genus: betacoronavirus, subgenus: embecovirus
134
Q
WD GD
A
- worldwide, northern climate when housed indoors over winter
135
Q
SOI WD
A
carrier animals, fomites, visitors
136
Q
MOT WD
A
feco-oral or aerosol
137
Q
HS WD
A
adults recently calved most susceptible
138
Q
RISKS WD
A
cold temp, diet changes, poor ventilation, closed confinement
- High morbidity, low mortality
139
Q
pathogenesis WD
A
- Replication in resp tract (nasal turbinates, trachea) or GI tract in enterocytes
- Inflam mediators cause hypersecretion in SI + colon diarrhoea in claves
- Destruction of epithelial cells in colonic crypts transudation of extracellular fluid + blood
140
Q
SIGNS WD
A
- incubation 3-8 days
- acute onset of fluid diarrhoea + huge decrease in milk production
- faeces = dark green/black, maybe blood/mucus, little odour
- nasolacrimal discharge, cough, dehydration, depression, faeces return to normal in 2-3d, on herd level subsides in 1-2w but milk production can take months to return
141
Q
PATHOLOGY WD
A
- SI dilated + flaccid, mucosal hyperaemia, linear streaks, pinpoint haemorrhages along colon + caecum
- Micro = widespread degeneration + necrosis of colonic glandular epithelium
142
Q
DIAGNOSIS WD
A
- PCR, ELISA of faeces (specimen collected 1-3d after onset of diarrhoea)
- Seroconversion 8w apart
143
Q
differentials WD
A
- BVD, enteric salmonellosis, coccidiosis,
- differentiate with signs, no mucosal lesions (BVD) + negative faecal culture (salmonella) + flotation (coccidia)
144
Q
treatment WD
A
- Recover spontaneously, supportive (fluids, palatable feed, free choice salt)
- NO vaccine
145
Q
control WD
A
- 2w isolation of new cattle, in outbreak – biosecurity, restrict access
146
Q
viral enteritis in valces
A
corona
rota
toro
noro
astro
kobuvirus
147
Q
bovine coronavirus
A
- replicates in epithelium of upper resp tract + enterocytes
- similar lesions to rota but also effects LI atrophy of colonic ridges
- profuse watery diarrhoea, maybe blood clots
- found in healthy + diseases
- recovered can shed low levels for weeks
148
Q
rotavirus
A
- most common
- group A (most important) + group B
- replicates in mature absorptive + enzyme producing enterocytes on villi of SI rupture + sloughing of enterocytes
- doesn’t infect immature enterocytes
- virulent strains = loss exceeds replacement decreased absorptive area
- pale yellow diarrhoea – lots of mucus, lasting 4-8d
- in calves under 3w
- after 3m not susceptible
149
Q
torovirus
A
- coronavirus family
- infected in 2-5d of life
- found in horses, swine + humans
150
Q
astrovirus
A
- Common in calves but uncommon in adult cattle
151
Q
kobuvirus
A
Signs
- Voluminous soft-liquid faeces with lots of mucus lasts around 3d, corona can become chronic
Differential
- Bacterial enteritis – fever, more severely ill
Diagnosis
- ¬isolation of pathogen in fresh faeces or PM. Calf side test kits using immune chromatography
Treatment
- Fluids + electrolytes, glucose, NSAIDs only when hydrates
- Contraindicated = GI motility modifiers
Prevention and control
- ¬good hygiene, separate age groups, good colostrum
- Vaccinate dam 6 + 2w before birth (rota + corona)
o Variable results
152
Q
lumpy skin disease
A
- LSD is a vector, poxviral disease with significant morbidity in cattle
- mortality rate is generally low
- OIE
- GD = Africa, middle east, turkey, balkans
153
Q
aetiology of lumpy
A
- LSD virus, family poxviridae, genus: capripox
- Stable in environment, lives 33d in necrotic skin nodules + 18d in dried hides
154
Q
SOI lumpy
A
old skin lesions
155
Q
MOT lumpy
A
-
- MOT = not fully understood, w saliva experimentally through water, mosquito = vector, atrogenic. Tick = reservoirs. Intrauterine yes – lesions on aborted calf
156
Q
HS lumpy
A
- Incidence increases in wet summer weather
- HS: cattle + buffalo
157
Q
pathogenesis lumpy
A
- Localised swelling at the site of inoculation after 4-7days + increased regional LN
- Generalized eruption of skin nodules usually 7-19days after inoculation
- replicates inside macrophages, fibroblasts, BV endothelial cell Vasculitis, thrombosis + infarction in severe cases
- Viraemia after the initial fever for 2 weeks
158
Q
signs lumpy
A
- Incubation 4-14 days up to 5weeks
- Fever, lacrimation, nasal discharge, hypersalivation, characteristic eruption on head, neck, perineum, genitalia, udder + limbs, increased LN, 2nd bact after 2-3w
- Lesions become harder + necrotic
- ‘sitfast’ = plug of necrotic tissue surrounded by ring of living tissue slough scar
- Necrotic plaques in GI + resp tract dyspnoea + GIS
159
Q
PM
A
- Well circumscribed, firm, round, painful nodules involving cutis + mucosa. Creamy grey/yellow on cut surface
- Very characteristic
- Vasculitis, thrombosis, perivascular fibroplasia, intracytoplasmic eosinophilic inclusions in keratinocytes, macrophages + endothelial cells
160
Q
diagnosis of lumpy
A
- Signs, PCR, histopathology, virus isolation
161
Q
differentials of lumpy
A
- Pseudo-lumpy skin (BHV-2) usually milder + confined to mammary gland. PCR to distinguish
- Pseudo cow pox, parapoxvirus, insect bites, urticaria etc
162
Q
control of lumpy
A
- Attenuated vaccine, cull positive, quarantine limited, proper carcass disposal, cleaning etc
- Economic losses due to decreased milk + hide damage
- NOT ZOONOTIC
