Notifiable and Imported Diseases Flashcards
1
Q
What makes a disease notifiable?
A
To prevent their further spread
When it affects international trade, public health, animal welfare and wider society.
2
Q
How are notifiable diseases reported?
A
- Possible notifiable disease found
- Stay on farm and report finding immediately to APHA
- APHA duty vet will discuss the case with you. May send a veterinary inspector to the premises and give you advice on what to do next, such as restricting movement of animals or vehicles from the premises.
- If confirmed, carry out further investigations and notify additional organisations.
3
Q
What are control zones?
A
Legally defined areas where specific rules are in force which aim to prevent disease spread, which may vary on disease.
- Inner circle is a 3km radius called protection zone
- Further circle is 10km radius and is called surveillance zone
4
Q
How do we maintain disease free status?
A
Making diseases notifiable
Surveillance
Trade requirements
5
Q
What is the causative agent of foot and mouth disease?
A
A picorna virus. No cross immunity between serotypes. Highly contagious and ability to survive outside hosts
6
Q
Describe the ability to survive of foot and mouth virus?
A
- Survive for months at 4˚C
- Survive in lymph nodes and bone marrow at neutral pH. pH 6-9
- Resistant to iodophors, quaternary ammonium compounds, hypochlorite and phenols, especially in presence of organic matter
- Persists in contaminated fodder and environment for up to a month
- Persists in slurry for 6 months
7
Q
Which conditions can foot and mouth disease not survive?
A
- Progressively inactivated at temperatures above 50˚C
- pH below 6 or above 9, so destroyed in muscle when pH is below 6/after rigor mortis.
- Virus killed by UV light and desiccation
8
Q
How is foot and mouth transmitted?
A
- Direct or indirect contact via droplets
- Airborne – claimed to be up to 60 km overland and 300 km over sea
9
Q
What are the sources of foot and mouth virus?
A
- Clinically affected animals in breath, saliva, faeces, urine, milk and semen
- Incubating animals
- Meat where pH has remained above 6
- Carriers
10
Q
What is the incubation period of foot and mouth disease?
A
3-8 days
11
Q
What are early clinical signs of foot and mouth in cattle?
A
Pyrexia
Anorexia
Depression
Reduction in milk yield
Shivering
Often lameness
Usually salivation
12
Q
Where are vesicles located in foot and mouth disease in cattle?
A
Buccal mucous membranes and/or between claws and coronary band
Vesicles rupture quickly leaving erosions, secondary infection
13
Q
What are the clinical complications of foot and mouth in cattle?
A
- Super-infection of lesions
- Mastitis and permanent impairment of milk production
- Abortion
- Permanent weight loss
- Loss of efficient thermoregulation
- Myocarditis, especially in young stock
14
Q
What is the clinical presentation of foot and mouth disease in sheep?
A
- Lame, often lie down
- Foot lesions
- Lesions in dental pad
- Myocarditis fatal in many lambs
- Major problem with differential diagnosis, especially with Orf
15
Q
What is the clinical presentation of foot and mouth in pigs?
A
- Less dramatic than in cattle, but lameness may be severe and painful
- Often a high mortality in pigs
16
Q
How is foot and mouth disease diagnosed?
A
Clinical signs
Vesicular epithelial sample
Blood sample
17
Q
What is the disease control policy for foot and mouth disease?
A
- Slaughter of infected animals, animals in direct contact, animals perceived to be dangerous contacts and normal animals within exclusion zones surrounding an outbreak
- Cull of animals on infected farms within 24 hours
- Cull of animals on contiguous premises within 48 hours
- Removal of dangerous contact animals
18
Q
What is the sequence of events for a premises infected with foot and mouth disease?
A
- Notification
- Quarantine – nothing moves off the farm
- Diagnosis
- Movement control
- Appraisal
- Slaughter/disposal (burning)
- Disinfection
- Re-stocking
19
Q
Why are sheep silent shedders of foot and mouth disease?
A
- Movements of sheep often impossible to trace
- Over 90% of submitted cattle samples positive. About 60% of submitted sheep samples positive
- Major problem with Orf
- Massive sero-surveillance of sheep was needed
20
Q
How important is speed of culling and carcass disposal with foot and mouth disease?
A
- Absolutely essential to kill clinically affected animals immediately
- Essential to kill direct in contacts within 24 hours
- Essential to kill proven dangerous contacts as soon as possible
- Disposal of disinfectant treated carcasses important but not if it interferes with logistical support for above
21
Q
How does vaccination affect foot and mouth disease?
A
Control of FMD in endemic countries relies on mass use of multivalent inactivated vaccines. Major costs of FMD in endemic countries are reduced productivity, regular vaccination and reduced access to global markets
22
Q
What was the foot and mouth epidemic affected by?
A
- Delay in notification of disease
- Difficulty in clinically detecting FMD in sheep
- Peak time of year for marketing of sheep and high frequency of sheep movements
- Marketing of infected sheep before FMD recognized in country
- Large sheep population in UK
- Cool weather
- Inadequate veterinary force
23
Q
What are the shared clinical signs of both classical and African swine fever?
A
- Sick pig – in acute form, high temperature, dull, off food
- Initially constipated
- Vomiting and diarrhoea are common sings even early in the clinical course
- Gummed up eyes
- Coughing
- Blotchy discolouration of the skin
- Abortion, still births and weak litters
- Weakness of hindquarters
- Convulsions and tremors in new born piglets
24
Q
What are the clinical signs of classical swine fever?
A
- Purple-red skin discolouration
- Anorexia
- Depression
- Ataxia
- Oedema
- Early pyrexia
- Possible conjunctivitis or diarrhoea
25
How can classical swine fever be identified post mortem?
- Enlarged, pale kidneys – sometimes petechiae
- Oedema of body cavities
- Occasional gastric ulceration
- Occasional pneumonia and pleurisy
- Acute cases have very enlarged, haemorrhagic subcutaneous lymph nodes
26
What is the main source of classical swine fever?
Pigs eating infected pork or pork products
27
How is classical swine fever spread?
Movement
Prolonged excretion of virus
Virus stable in environment
28
Why is there significant restriction on trade following classical swine fever vaccination?
Cannot differentiate between naturally infected and vaccinated animals
29
What is the virus of classical swine fever and of African swine fever?
CSF = pestivirus
ASF = asfaviridae
30
What is the vector of African swine fever?
Ornithodoros tick
31
How is African swine fever transmitted?
- Tick borne is the original form
- Direct contact is the novel form
- Recrudescence of latent infection
- Persistent in environment – environmental reservoir, enveloped virus can survive in fomites
32
What is the incubation period of African swine fever?
5-10 days
33
What are the differences between classical and African swine fever?
- ASF generally has longer incubation period
- ASF can be transmitted by ticks - direct form more common
- Spread by fomites but not wind
34
What are the control measures of swine fever?
- Commercial pig feed not swill feed
- No contact with other pigs
- Change clothes to enter housing
- Disinfect in and out
35
Why are there no available swine fever vaccines?
Difficult finding a stable antigen
36
What are the control measures for African swine fever in Europe?
- Hunting and supplemental feeding of wild boar ban
- Searching for wild boar carcasses and carcass collection centres – testing of wild boar carcasses
- Control of access to forests for commercial and tourism activities
- Passive and active surveillance
37
What is the legislation on movement of equine?
Passport and microchipped by six months
Horse imports to EU only permitted from countries free of African Horse Sickness and without vaccination
38
Depending on where a horse is travelling, what is needed from an official veterinarian?
Health certificate
Vaccinations
Blood tests
Quarantine
39
When is equine viral arteritis notifiable?
Notifiable in stallions and mares that have been mates or inseminated within 14 days
40
What are the clinical signs of equine viral arteritis?
Pyrexia
Abortion
Periorbital/scrotal/limb/mammary oedema
Conjunctivitis
Nasal/ocular discharges
Depression
Urticaria
41
How is equine viral arteritis spread?
Viraemia may be present for up to 20 days, during which the virus may spread via secretions
42
How is equine viral arteritis prevented against?
No treatment so prevent by blood testing mare and stallion before going to stud. Vaccinate stallions but not mares
43
Describe the active state of contagious equine metritis.
Main outward sign is a vulval discharge which may range from very mild to extremely profuse
44
Describe the carrier state of contagious equine metritis.
No outward signs of infection. Mare remains capable of transmitting infection as bacteria are established on the clitoris surface, clitoral fossa and sinuses, with K.pneumoniae and P.aeruginosa in the urethra and bladder.
45
How is contagious equine metritis prevented against?
Establishing freedom from infection before breeding – pre-breeding swabs
46
If a pre-breeding swab for contagious equine metritis is positive, what must be done?
Notify APHA, stop breeding and investigate source and extent. Isolate and treat infected horses, swab horses at risk, disinfect all equipment for breeding, inform all owners, inform breeders association and anyone with stallion’s semen.
47
How is contagious equine metritis treated?
1. Clean penis/clitoris with chlorhexidine solution for 5 days
2. Apply nitrofurazone ointment
3. Uterus normally self-clears
4. Re-test
48
What are the clinical signs of acute equine infectious anaemia/swamp fever?
- Fever
- Depression
- Increased heart and respiratory rate
- Haemorrhaging
- Haemorrhagic diarrhoea
- Ataxia
- Rapid weight loss
- Jaundice
49
What are the clinical signs of chronic equine infectious anaemia/swamp fever?
- Recurring bouts of fever, depression, anaemia, weakness or weight loss
- Interspersed with periods of normality
50
What is the other possible form of equine infectious anaemia/swamp fever?
Subclinical - may show not clinical signs
51
How is equine infectious anaemia/swamp fever transmitted?
- Insect vectors such as biting flies
- Administration of infected blood products (including plasma) and unauthorised blood-based veterinary medicinal products
- Contaminated veterinary or dental equipment
- Placenta or contaminated colostrum
- Semen (uncommon)
52
What are the clinical signs of the primary cutaneous form of epizootic lymphangitis in horses?
- Cord-like appearance of sub-cutaneous lymph vessels
- Especially limbs, neck and chest
- Development of a series of pyogranulomas
- Discharge from these contains yeast-like cells of the pathogen
53
How is epizootic lymphangitis spread?
Flies
Contaminated equipment
Live in soil for up to 15 days
54
What is the incubation period of epizootic lymphangitis?
Weeks to months
55
How is epizootic lymphangitis diagnosed?
See organisms in pus
Gram stain
Confirm with culture
Serology
56
How is epizootic lymphangitis treated?
Amphotericin B IV
Removing scabs
Cleaning
Topical iodine
57
What is glanders and farcy?
Serial development of ulcerating nodules in the upper respiratory tract, lungs, and skin
58
How can glanders and farcy be distinguished?
If the nodules are mainly in the nostrils, lungs and other internal organs = glanders
If the nodules are mainly on the surface of the horse’s limbs or body = farcy
59
How can glanders and farcy be contracted?
- Ingesting food or water contaminated with nasal discharges of carrier animals
- Contact with harness components
- Ingestion of meat from affected horses
60
What is African horse sickness?
Insect-borne viral disease of horses
61
What happens following transmission of African horse sickness?
- Viral replication within regional lymph nodes occurs
- Viraemia
- Spread to spleen, lymphoid tissue and lungs
62
Describe the pulmonary syndrome of African horse sickness.
Sudden death, pyrexia, respiratory distress, frothy nasal discharge
63
Describe the cardiac syndrome of African horse sickness.
Pyrexia, subcutaneous oedema, periocular petechial haemorrhages, colic, lasts several weeks
64
Describe the cardiopulmonary syndrome of African horse sickness.
Most common combination of others, die 3-6 days after developing fever
65
Describe AHS fever syndrome of African horse sickness.
Usually donkeys/zebra with acquired immunity. Fever and supraorbital fossa oedema, self-limiting. No treatment for AHS
66
How is African horse sickness diagnosed?
Blood and organ PCR and ELISA
67
What is dourine?
Venereal disease of equine
68
What are the clinical signs of vesicular stomatitis in horses?
Mucosal vesicles and ulcers in the mouth
Systemic signs such as anorexia, lethargy and pyrexia
69
How is West Nile virus transmitted?
Migrating carrier birds to mammals through the bite of various mosquito species
70
How does West Nile virus cause neurological symptoms?
Travels through the bloodstream to the brain and the spinal cord, resulting in an inflammation which can cause severe and potentially fatal neurological symptoms. Clinical signs in 3-15 days
71
How is West Nile virus diagnosed, treated and prevented?
Serology
Supportive treatment
Vaccination, reduce exposure to mosquitoes
72
What is type A avian influenza?
An infection of the respiratory, alimentary and nervous systems. Wildfowl are the natural hosts.
73
How can avian influenza be categorised?
Ability to cause severe disease (pathogenicity) in avian species as either highly pathogenic (HPAI) or low pathogenic (LPAI).
Properties of their haemagglutinin (H1-H18) and neuraminidase (N1-N11) surface glycoprotein ‘spikes’ (peplomers).
74
Name 2 surface glycoproteins of avian influenza and their purposes.
Haemagglutinin – important for entering host cell
Neuraminidase – important for virus release from host cells
75
What does the avian influenza genome being in 8 segments allow?
Allows genetic recombination in host cells simultaneously infected with more than one virus = ‘antigenic shift’
76
What is the significance of pigs to avian influenza?
Pigs seem to be ‘mixing vessels’ – they are susceptible to both human and avian viruses. Over 50% of UK the UK pig herd is now kept outdoors.
77
What are the functions of haemoagglutinin on avian influenza viruses?
- Recognition of target vertebrate cells
- Binds target cell sialic acid-containing glycoprotein receptors
- Entry of the viral genome into the target cells by fusion of host endosomal membrane with the viral membrane
78
What are the functions of neurominidase on avian influenza viruses?
- Promotes release of progeny viruses and their spread to uninfected surrounding cells
- Cleaves sialic acid residues from viral proteins, preventing aggregation of viruses
79
How does haemagglutinin partly determine pathogenicity of avian influenza?
The change in haemagglutinin structure requires its amino acid chain to be nicked by a host cell-associated protease. Susceptibility of the virus haemagglutinin to host cell proteases is an important determinant of virus pathogenicity
80
What are the clinical signs of avian influenza?
Sudden onset
Depression, inappetance
Oedema of head
Cyanosis of comb and wattles
Respiratory distress
Diarrhoea
Egg drop
Weakness of death
81
How can avian influenza be identified post-mortem?
- Congestion and haemorrhages of organs
- Necrotic foci in liver, lungs, spleen, kidneys
- Fibrinous pericarditis
- Peritoneal and air sac exudate
- Egg peritonitis
82
List the differential diagnoses for avian influenza.
Newcastle disease
Fowl cholera
Infectious laryngotracheitis
Infectious bronchitis
Duck viral enteritis
83
Which forms of avian influenza are notifiable?
H5 or H7 and highly pathogenic
H5 or H7 and not highly pathogenic
Other Haemagglutinin and highly pathogenic
84
When would avian influenza be considered a pandemic?
R0 > 1 could lead to a pandemic
85
How has HPAI H5N1 spread so rapidly?
- Exotic bird trade and illegal movement of captive birds
- Wildfowl migration
- Domestic poultry trade
86
Which avian influenza serotypes are of concern?
H5N1
H5N6
H5N8
87
When should suspicion of avian influenza be reported?
Failure to do so is an offence
Reporting dead wild birds:
1+ dead birds of prey or owl
3+ dead gulls or wild waterfowl
5+ dead birds of any species
88
What is the government response to HPAI avian influenza outbreaks?
- Infected premises – all birds culled following confirmation of infection
- Protection zone – 3km radius
- Surveillance zone – 10km radius
- Prevention zones
- Additional housing measures
89
Why is it rare to diagnose bovine TB via clinical signs?
Due to compulsory routine testing
90
What are the clinical signs of bovine TB seen in advanced stages of infection?
- Weight loss
- Mild pyrexia, reoccurring
- Weak reduced appetite
- With/without moist cough
- With/without swollen lymph nodes
- With/without chronic mastitis
91
What are the clinical signs of bovine TB in camelids?
Rapid weight loss – BCS 5-6/10 to 1-2/10 in 2 weeks
Chronic respiratory signs – tachypnoea and possible dyspnoea/cough
92
Why do camelids already have extensive lesions before clinical signs appear in bovine TB?
Camelids have increased lung efficiency
93
How does bovine TB further differ in camelids?
Increased zoonotic risks due to spitting
No routine TB testing in camelids
94
How is bovine TB transmitted?
- Inhalation (primary) or ingestion
- Calves infected by ingesting infected milk
- Spread – respiratory, faeces, urine, milk, semen
- Badgers are known to be a reservoir/maintenance host of M.bovis
95
What appears in the organs system of primary infection of bovine TB?
Nodular granulomatous lesions – tubercles. Necrosis, caseation, calcification
96
What’s the main route of transmission of M. bovis from cattle to people?
Unpasteurised milk
97
What are the advantages and disadvantages of diagnosing bovine TB via culturing bacteria (gold standard)?
- Time consuming as a slow growing microorganism, 2+ months
- Culturing of respiratory tract secretions gives positive results in <20% of naturally infected animals
+ Allows genome sequencing to support epidemiological investigations
98
What are the advantages and disadvantages diagnosing bovine TB via PCR?
+ Newly developed PCR can detect M. bovis from tissue samples collected at postmortem
+ Much quicker than culture, 3 weeks to report a result
- Cannot be used in live animals
99
What are the advantages and disadvantages of diagnosing bovine TB via serology?
- Antibody responses vary in magnitude and often not detected until a few months after infection
+ Approved for use in testing Camelids
100
What is SICCT?
Single intradermal comparative cervical tuberculin test.
101
How does a SICCT test work?
- Measures the animals immune response to the bacterium
- Triggers an inflammatory response and a reaction (swelling/lump) develops at the injection site.
- Delayed type hypersensitivity reactions to bTB infection detectable from 6 weeks after infection
- Skin thickness measured before and again after 72 hours
102
What are the possible SICCT test results?
Clear (negative)
Fail (reactor or positive result)
Inconclusive (IR) – the animal shows a reaction to bovine tuberculin greater than the avian, but not strong enough to be classified as a reactor
103
What can be found at post mortem inspection if positive for bovine TB?
Visible lesions (VL) – lesions typical of TB in carcass. Commonly in LNs of thorax, lungs, and head. Seen in approx. 36% reactors in HRA and edge regions
104
What is the specificity of SICCT testing?
High specificity of 99.98% – equates to one false positive per 5,000 disease-free animals tested. Contrary to farmers beliefs. Testing for immunity not active infection
105
What is the sensitivity of SICCT testing?
Low Sensitivity 50 to 80% – however well the test is carried out we are leaving some infected animals (false negatives) on farm
106
Why does SICCT testing have low sensitivity?
- Stage of infection
- Immunosuppression
- Recurrent testing (frequency)
- Anergy/overwhelming infection
- Operator factors: human error, injection site, tuberculin storage
107
What are the advantages of interferon gamma testing for bovine TB?
- Earlier detection – estimating from 3 weeks post infection
- Greater sensitivity of all available test – less false negatives
- Can identify animals anergic to SICCT
- Laboratory-based test – objective, no degree of subjectivity
- Does not interfere with subsequent tests – increased test frequency is possible
- Use in conjunction with the skin test
108
What are the disadvantages of interferon gamma testing for bovine TB?
- Blood must be delivered to the lab in good condition within 24 hours of collection
- Blood samples must be kept warm between 17 ⁰C and 27 ⁰C
- Lower specificity – 3/4 false positives per 100 so only used in infected herds
- Expensive at £24 per cow
109
What is the result of a positive result of bovine TB in pre-movement testing?
Movement restrictions. It is an offence to move cattle that have not been TB tested 60 days before their movement
110
What is post-movement bovine TB testing?
- Carried out 60 to 120 days after movement to premises
- It is an offence if not carried out
111
How can a herd be protected from bovine TB?
- Restrict contact between cattle and badgers
- Manage cattle feed and water
- Stop infected cattle entering the herd
- Reduce risk from neighbouring herds
- Minimise infection form cattle manure
112
Is there a vaccine for bovine TB?
Currently no legal vaccine available – use of vaccines would stop us being able to trade abroad.
Need to differentiate vaccinated animals from non-vaccinated animals
113
Name 6 imported diseases.
Rabies (notifiable)
Leishmania
Dirofilaria immitis
Babesia
Anaplasma
Ehrichia
114
What is the infection timeline for rabies?
- Incubation 3 weeks to 6 months, usually 1 month
- Clinical signs 1-2 months post exposure, up to 6 months
- Virus shedding 1 day in cats, 5 days in dogs before development of clinical signs
115
Name the 3 phases of rabies and a common factor between them.
Prodromal
Furious
Paralytic
All end in death
116
Describe the prodromal phase of rabies.
Lasts 1-3 days – with/without wound and local irritation. Pyrexia, behavioural changes, mydriasis with/without decreased PLR
117
Describe the furious phase of rabies.
Lasts up to 7 days - irritability/excitability with/without vocalisation, aggression, hyperaesthesia, hypersalivation, with/without ataxia, tremors and seizures
118
Describe the paralytic phase of rabies.
Flaccid paralysis, laryngeal, pharyngeal, masticatory paralysis causing dysphonia, salivation, dropped jaw. Coma/death (within 10 days onset)
119
What is leishmania?
- Intracellular protozoan parasite
- Vector-borne – sandflies
- Multisystemic disease
- Zoonotic potential
120
Why is leishmaniosis a persistent disease?
Prolonged pre-clinical phase
121
What are the less typical routes of infection of leishmania?
Vertical
Venereal
Iatrogenic (transfusions)
122
Describe subclinical leishmaniosis.
Robust T-cell mediated response typically eliminates so no signs
Subclinical infection = chronic disease reservoir
123
What are the clinical signs of leishmaniosis?
Cutaneous lesions
Lymphadeno/splenomegaly
Glomerulonephritis
Polyarthritis
Uveitis
Myositis, vasculitis
Lethargy
Inappetence
Pyrexia
124
How does leishmaniosis present on haematology?
Non-regenerative anaemia common
- High mean cell volume
- Low haemoglobin, haematocrit and RBCs
125
How does leishmaniosis present in biochemistry?
Can get azotaemias.
- High urea, creatinine, total protein, globulin, sodium, chlorine, phosphorus, glucose
- Low albumin and A:G ratio
126
How does leishmaniosis present on urinalysis?
Urine protein creatinine ratio being large is most typical of leishmania
127
How is leishmaniosis treated?
1. Meglumine antimonate or miltefosine for 28 days
2. Allopurinol for 6-12 months
3. Manage complications – renal supportive therapies
4. Monitor - CBC, chem, urine
128
What is dirofilaria immitis commonly known as?
Heartworm but different to vasostrongylus vasorum
129
Describe the affect of L5 of dirofilariasis in the pulmonary arterial system.
- Heavy infections to the right heart and great veins
- Worm induced pulmonary vasculopathy with/without pulmonary hypertension due to scarring, especially caudal lobar vessels
- Right sided heart failure
130
What are the clinical signs of dirofilariasis?
Chronic exercise intolerance
With/without signs of pulmonary disease
Pressure loaded right heart
With/without glomerulonephritis
With/without aberrant migration
131
What results from a pressure loaded right heart due to dirofilariasis?
Eccentric hypertrophy
With/without decompensation
Leading to right heart failure
With/without caval syndrome
Cranial vena cava is compressed/obstructed
132
How is dirofilariasis prevented?
Macrocytic Lactones (ivermectin, moxidectin, selamectin, eprinomectin) monthly
Or milbemycin oxime monthly
Both arrests L3/L4 development
133
How is dirofilariasis treated?
- Both adulticidal and microfilarial therapy required
- Medical possibly with surgical retrieval if very heavy burdens
- With/without concurrent prednisolone, anti-thrombotics, doxycycline
134
What are the clinical signs of babesiosis?
Haemolytic anaemia
With/without pigmenturia and jaundice
Thrombocytopenia
Splenomegaly
Multiorgan failure and death
135
What are the 2 species of babesia regarded as large and small babesia?
Babesia canis = large
Babesia gibsoni = small
136
How is large and small babesia treated?
Large – imidocarb dipropionate
Small – atovaquone + azithromycin most effective
137
How is anaplasma transmitted?
Ixodes ricinus
138
What are the clinical signs of anaplasma?
May carry asymptomatically
Lethargy
Pyrexia
Inappetence
Thrombocytopenia
With/without other cytopenias
139
What are the clinical signs of acute ehrichlia canis?
Lethargic
Pyrexic
Inappetant
Weight loss
Thrombocytopenia
140
What are the clinical signs of severe systemic ehrlichia canis?
Lymphadeno/splenomegaly
Uveitis
Oculo-nasal discharge
Platelet dysfunction/haemorrhage
Neurological/myopathy
141
How is ehrlichia canis diagnosed?
- Thrombocytopenia and/or pancytopenia
- Lymphocytosis
- Hyperglobulinaemia
- Cytology with/without buffy coat
- Serology – in-clinic ELISA. Massive titres in chronicity
- PCR – blood/marrow, reduced sensitivity in chronicity
142
How is ehrlichia canis treated?
Doxycycline, minimum 4 weeks. Clinical improvement typically within a few days. Regardless, frequently organism persists
143
Is treatment of leishmania highly effective and results complete cure?
Treatment results in high rate of clinical remission 65-100% dogs respond but parasitological cure is rare.
144
You want to run a test for heartworm – what does the in-clinic point of care ELISA SNAP 4Dx test for (regarding heartworm)?
Adult female heartworm antigen
145
What infectious agents does the SNAP 4Dx test for?
Dirofilariasis/heartworm antigen
Anaplasma
Ehrlichia
Borrelia
146
What are spongiform encephalopathies?
A group of disease characterised by progressive vacuolisation of brain cells. Resulting symptoms – chronic progressive nervous symptoms, progressive debilitation, death
147
Define a prion.
The infectious protein hypothesis proposed that the protein was specified by a host gene, but that its structure became altered to form a proteinaceous infectious particle.
148
What are prions resistant to?
Irradiation
149
What is the resistance of scrapie?
Very resistant to any kind of inactivation
150
What causes disease in transmissible spongiform encephalopathies?
The failure of prions to be degraded by the host cell (protease K) leads to their build up in the cell
151
How are transmissible spongiform encephalopathies transmitted?
- Transfer of mis-folded PrPsc will also transmit the disease between animals
- Oral route – the normal prion gene is expressed at high levels in neural and lymphoid tissue
- Mis-folded prions can be identified by monoclonal antibodies in the lymph nodes of the oropharynx and GI tract before brain lesions develop
152
What are the clinical signs of TSEs?
Trembling
Ataxia
Rubbing
Incoordination
Recumbency
Death
153
What is scrapie?
Fatal brain disease (a transmissible spongiform encephalopathy) of sheep and goats
154
What are the additional clinical signs of scrapie?
Changes in temperament/behaviour
Repeated scratching
Nibbling/grinding teeth
Excessive wool loss
Skin damage
155
What are the changes in behaviour seen with scrapie?
Excitable
Drooping ears
Increased nervousness or fear response
Lagging behind
Aggression
Depression or vacant stare
156
What are the changes in posture and movement seen with scrapie?
Trembling
Unusual high stepping trot
Severe incoordination
Stumbling
Standing awkwardly
Weak hind legs
Unable to stand
Weight loss and death
157
How is scrapie prevented?
Transmitted via infected birth fluids, membranes and placenta.
So sheep should not eat placenta.
158
What is the problem with scrapie control?
No vaccine
No treatment
159
What is BSE?
Bovine SE. Clinical disease lasts several weeks. Invariably progressive and fatal
160
How do cattle become infected with BSE?
Only common feature is the use of commercially produced compound feed containing meat and bone meal (ruminant derived)
161
How to meat and bone meal become infected?
- Scrapie infected sheep used for animal derived protein
- Exposure to rare sporadic BSE
162
What are the clinical signs of BSE?
- Exaggerated fear response
- Reluctance on corners, doors, milking
- Occasional aggression
- Kicking when milked
- Head held low
- High stepping gait (particularly hind legs)
- Skin tremors
- Loss of condition
- Recumbency
163
What variant of BSE is caused in people?
- Creutzfeld Jacob Syndrome
- Mainly younger people
- From onset of signs to death: average of 6 months
164
How is BSE diagnosed?
Ante mortem – clinical signs
Post mortem – histopathology and antibody based tests for PrPSc protein. Western blot with brain, immunocytochemistry (ICC) with brain, tonsil, third eyelid, ELISA with spinal cord/brainstem
165
How is BSE controlled?
- Cattle tracing system
- Feed control
- Over 30 month scheme
- Offspring cull scheme
- Testing - sheep/goat surveillance
166
How does feed control control BSE?
Prohibition of all mammalian protein to ruminants, prohibition of mammalian meat and bone meal to any farmstock, ban of MMBM at feed handling premises.
167
What is the over 30 month scheme?
Slaughtered at dedicated abattoirs, meat banned for human consumption, carcasses incinerated or rendered and destroyed
168
What are offspring cull schemes?
Maternal transmission only remaining route, animals born after ban at risk from infection by dam slaughtered, all offspring of female BSE cases born within 2 years of diagnosis culled.
