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Flashcards in Infectious disease 2 Deck (69)
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1
Q

Describe the neurological signs of canine distemper

A
  • Circling, head tilt, nystagmus
  • Paralysis
  • Convulsions, fitting, involuntary “chewing”
  • Viral inclusion bodies in CNS (skin, GIT, bronchi etc)
  • Death in 2-4 weeks
2
Q

Outline the effect of canine distemper on teeth

A
  • Enamel hypoplasia
  • Most of enamel on teeth gone, poor teeth
  • Epithelium laying down enamel on teeth affected
  • Infection attacks developing adult teeth
3
Q

Describe old dog encephalitis and how this relates to canine distemper

A
  • Dementia, blindness, circling
  • Often in distemper vaccinated dogs
  • CSF normal - virus come in and gone again by the time signs are seen
4
Q

What is the cause of feline infectious peritonitis?

A

Feline coronavirus

5
Q

Which cats are more susceptible to feline infectious peritonitis?

A
  • Younger cats (<1yo)
  • More common in pure breed cats (e.g. Bengal, Birman)
  • History of stress e.g. neuter, trauma
6
Q

What are the 2 types of feline infectious peritonitis?

A

Wet and dry

7
Q

Outline the pathogenesis of feline infectious peritonitis

A
  • Infection with FCoV
  • Either mild or subclinical enteritis OR FIPV
  • FIPV able to replicate in macrophages
  • Immune complex formation which leads to vasculitis
  • Either get effusions (wet) or pyogranulomatous lesions (dry) developing
8
Q

Describe the clinical signs of wet FIP

A
  • Ascites
  • Pleural effusion
  • Fever
  • Anorexia
  • Depression
9
Q

Describe the clinical signs of dry FIP

A
  • Signs may be vague
  • Fever
  • Anorexia
  • Depression
  • Ocular lesions (uveitis)
  • Neurological signs
  • No effusion
10
Q

Describe the neurological signs that may be seen with FIP

A
  • Variable, depends on site of inflammatory lesions (cranial, cerebellar, spinal cord)
  • Paresis, ataxia, hyperaesthesia, convulsions, beahvioural changes
  • Look for involvement of other body systems (ocular, renal, intestinal)
  • Uveitis
11
Q

Discuss potential reasons for the conversion from FCoV to FIP

A
  • Reason unknown
  • Probably mutation of virus (recombination or spontaneous)
  • Stress
  • Viral load
  • Inappropriate immune response (poor cellular immune response)
12
Q

Outline the treatment of FIP

A
  • Generally palliative
  • Treat secondary bacterial infections
  • Corticosteroids may reduce clinical signs by reducing immune complex formation
  • Interferon suggested but lack of evidence in favour
  • Polyprenyl immunostimulant
13
Q

Outline the diagnosis of pestiviruses

A
  • History of abortion etc. in flock/herd
  • Clinical signs
  • Detection of serum/milk antibody suggests exposure
  • Detection of virus
  • Post mortem
14
Q

Describe methods for the detection of pestiviruses

A
  • ELISA for virus antigen, RT-PCR, virus isolation
  • Pooled blood samples, ear tag samples (when apply tag produce small circle of skin)
  • Pooled samples indicated if there is need for individual sampling
15
Q

Outline the control of pestiviruses

A
  • Control programs in place
  • Cull PIs as soon as identified
  • Aim for BVD free status in herd
  • National Voluntary Industry led scheme in England
16
Q

Describe the diagnosis of feline parvovirus

A
  • Clinical signs
  • History
  • MRI (not usually needed, will not change management)
  • PM
17
Q

Outline the control of parvovirus

A
  • Vaccination (attenuated live and inactivated virus available) once MDA weans after ~8 weeks
  • Boost every 1-3 years
  • Cannot use live in pregnant queens
  • Vaccinate dams to cover early period of neonatal development
  • Prevent exposure of kittens to FPV in environment
  • Use effective disinfectant (bleach 1:32 dilution) and maintain quarantine in vet practie
18
Q

Describe the diagnosis of Schmallenberg virus

A
  • Serology (ELISA) so antiviral antibody
  • RT-PCR for virus in tissue at PM
  • RT-PCR on blood (EDTA) to detect virus RNA in acute phase of infection
19
Q

What samples can be used for serology to test for Schmallenberg?

A
  • Paired samples collected 2-3 week interval to demonstrate rising antibody titre in order to diagnose individual cases
  • Single sample to show exposure
  • Bulk milk sample good for herd screening
20
Q

What is the main disadvantage of using RT-PCR on blood for Schmallenberg virus?

A

Difficult, will only get positive result prior to clinical signs as virus will be gone once these emerge

21
Q

Outline the prevention of Schmallenberg virus

A
  • Inactivated live virus vaccine available but poor uptake by farmers
  • Used in non-pregnant animals
  • Duration of immunity not yet determined
22
Q

What methods are used in the diagnosis of Borna virus?

A
  • Histopathology
  • RT-PCR
  • Confirmation on PM examination
23
Q

Describe the PM findings that would indicate the animal was positive for Borna virus

A
  • Non-suppurative polioencephalomyelitis
  • Medullary, cerebellar, pons, thalamic lesions
  • Demonstrate virus antigen in lesions by using antibody staining
24
Q

Outline the control of Louping ill

A
  • Vaccination of lambs before onto pasture after MDA has waned, and any new lambs brought in
  • Following vaccination probably protected for life due to natural re-infection
  • Vector control
  • Max period of tick activity in Spring, once temps are over 70degreesF, lasts 1-2 months
25
Q

Describe the diagnosis of canine distemper virus

A
  • Virus isolation from smears and swabs from conjunctiva
  • Immunofluorescence using Ab to detect viral antigen in ocular/nasal smears
  • RT-CR
  • Serology (IgM, rising IgG titre)
  • Histopathology showing inclusion bodies on histopath PM
  • Inclusion bodies on blood/conjunctival smears
26
Q

Describe the prevention of canine distemper

A

Vaccination very effective, usually modified live vaccine

27
Q

Describe the diagnosis of FIP

A
  • History and clinical signs may be suggestive
  • Histopath shows cahracteristic lesions
  • Peritoneal/pleural fluid
  • FCoV antibody titre
  • Albumin:globulin ratio
  • Alpha1 acid glycoprotein (ACP)
  • Haematology
28
Q

Describe the peritoneal/pleural fluid findings in FIP

A
  • High protein content (elevated gamma globulins)

- Viscous yellow fluid, may clot

29
Q

Discuss the use of FCoV antibody titre in the diagnosis of FIP

A
  • Titre of 0 makes FIP unlikely
  • NB in very end stage of effusive, all antibodies tied up in immune response and may get very low titres, but this is rare
  • Only indicates FCoV infection
  • Healthy cat with titre of FCoV does not have FIP
30
Q

Describe the albumin:globulin ratio in FIP

A
  • Serum A:G<0.4 suggestive, ruled out by ratio >0.8

- Rise in globulin, fall in albumin

31
Q

Describe the alpha1 acid glycoprotein (ACP) in FIP

A
  • > 1500ug/ml is suggestive

- Non-specifically raised in inflammation, goes very high with FIP

32
Q

Describe the haematology findings in FIP

A

Anaemia, netrophilia (left shift), lymphopaenia

33
Q

Describe the control of FIP

A
  • Maintain FCoV free catteries (isolation, use of seronegative stud males)
  • Manage catteries effectively: early weaning of kittens from infected dams at 5 weeks before MDA wanes, prevents exposure to virus from dam if removed early
  • Vaccination not available in UK and poor efficacy
34
Q

List the notifiable diseases with neurological signs

A
  • Rabies
  • SEs
  • Aujesky disease
  • Teschen disease
  • West Nile Virus
  • Equine encephalomyelitis
  • Classical Swine Fever
35
Q

List the main reservoirs for genotype 1 (classical rabies) viruses

A
  • Fox (western Europe)
  • Dog (middle east, Africa, eastern Europe)
  • Bat (north and south America)
  • Raccoon (North America)
  • Skunk (North America)
36
Q

Describe the pathogenesis of rabies

A

From bites, travels up sensory nerve into brain

37
Q

List the clinical signs of furious rabies

A
  • Restlessness, anxiety
  • Loss of fear of humans
  • Aggression, biting
  • Hyperaesthesia
38
Q

List the clinical signs of dumb rabies

A
  • Salivation
  • Dysphagia
  • Depression
  • Paralysis of limbs, neck and head
39
Q

Describe the diagnosis of rabies

A
  • History and clinical signs
  • Isolation of suspected case and send for PM
  • Histopathology of CNS tissue, PCR, staining for viral antigen
  • Virus isolation in cell culture or by intracerebral injection into mice
40
Q

Describe the histopathology findings that indicate rabies

A
  • Inclusion bodies, encephalitis

- Viral antigen staining

41
Q

Outline the control of rabies

A
  • Quarantine
  • Vaccination of dogs and cats
  • Neutering of stray dogs
  • PetTravel schemes
  • Vaccine baits for control in wild populations
42
Q

Describe the control of BSE

A
  • Feed bans
  • Removal of SRM
  • Over 30 months rule for slaughtered animals
43
Q

Describe the clinical signs of BSEs

A
  • Highly variable
  • nervous, hyperexcitable, aggressive
  • Weight loss
  • Drop in milk yield
  • Ataxia, hypermetria
  • Bruxism
44
Q

Describe the clinical signs of scrapie

A
  • Nervous, excitable, head tremors
  • Pruritus, alopecia
  • Scratch reflex (nibbling)
  • Weight loss
  • Goats can also be affected
45
Q

Describe the control of TSEs

A
  • Legal requirement to report animal suspected of being affected
  • Compulsory Scrapie Flock Scheme
  • Flock genotyping
  • Culling
  • 2 year period of TSE testing with negative results before a flock or herd is free of movement restrictions
46
Q

What is Aujesky’s disease?

A

Aka pseudorabies, Alpha-herpesvirus

47
Q

Describe the clinical signs of Aujesky’s disease in pigs and how this varies by age

A
  • Reproductive (abortion, still birth, resorption) and enurological signs
  • Neonatal pigs more severely affected: listless, tremors, incoordination, hypersalivation, convulsions, death in 1-2 days
  • Suckling pigs: less severe but high mortality, circling, paddling of legs, V/D
  • Weaners: lower death rate, respiratory signs, fever, death rate <10%
    e
48
Q

Describe the epidemiology of Aujesky’s disease

A
  • Endemic in Asia, South and central America
  • Canada, USA, UK, Denmark etc. disease free but risk of reintroduction
  • Spread via oronasal secretions, milk, semen, transplacental
  • Pig movement
  • Windborne spread over short distances
  • Secondary infection of sheep/cattle by aerosols, dogs/cats by ingestion of meat
49
Q

Describe the clinical signs of Aujesky’s disease in cats

A

Sudden death

50
Q

Describe the clinical signs of Aujesky’s disease in dogs

A
  • Jaw and pharyngeal paralysis
  • Salivation
  • Scratching
  • Death
51
Q

Describe the clinical signs of Aujesky’s disease in cattle

A
  • Mad itch: biting, licking, rubbing
  • Often unilateral
  • Staggering
  • Aggression
  • Circling
  • Death
52
Q

Describe the control of Aujesky’s disease

A
  • UK free of disease, if found, slaughter quickly

- In endemic areas have vaccines with attenuated marker vaccine

53
Q

What is Teschen disease?

A

Porcine enteroviral encephalomyelitis

54
Q

Describe the clinical signs of Teschen disease

A
  • Fever and depression

- Followed by: incoordination, paraplegia, paralysis

55
Q

Evaluate the risk of Teschen disease in the UK

A
  • Never reported in UK

- No recent outbreaks worldwide

56
Q

What is West Nile Virus?

A

ssRNA Flavivirus

57
Q

Describe the epidemiology of West Nile Virus

A
  • Maintained in mosquitos and birds
  • Problem when passed to dead end hosts e.g. humans, horses
  • Spread to USA from Africa, now endemic
  • In UK and Europe mainly sporadic cases
58
Q

Describe the clinical signs of West Nile virus

A
  • Most horses no dsiease following bite by infected mosquito, silent, seroconvert
  • Encephalitis and/or meningitis in 33% of sick animals
  • Ataxia, lethargy, facial paralysis, blindness, seizures, recumbency
59
Q

Describe the diagnosis of West Nile Virus

A
  • Clinical signs
  • Detection of anti-iviral antibodies with ELISA
  • PM examination of brain
60
Q

Outline the treatment of West Nile Virus

A

Supportive Therapy only

61
Q

Describe the control of West Nile Virus

A
  • Vaccination of horses with killed virus vaccine or canarypox recombinant vaccine
  • Reduce opportinities for insect vectors to flourish
  • Insect repellents
  • Stabling to avoid exposure
  • Use of animals as sentinels of disease
62
Q

What is equine encephalomyelitis caused by?

A

Alphavirus - WEE, VEE, EEE

63
Q

Describe the clinical signs of equine encephalomyelitis

A
  • Fever/depression
  • Fatal febrile encephalomyelitis
  • Photophobia, head pressing, blindness, dysphagia, ataxia
64
Q

Outline the control of equine encephalomyelitis

A

Vaccination and vector control

65
Q

What is classical swine fever caused by?

A

Pestivirus

66
Q

Describe the epidemiology of classical swine fever

A
  • Spread by movement of pigs, mechanically or in infected pig products
  • Feeding of swill implicated as part of spread
  • Present in wild boar in some parts of EU
  • Most recent UK outbreak 2000
67
Q

Describe the clinical signs of classical swine fever

A
  • Erythema, petechiae
  • Fever >40degreesC
  • Depression, anorexia
  • Piglets show convulsions, tremors
  • Constipation, diarrhoea
  • Abortions, stillbirths
  • Haemorrhagic lesions on multiple organs
68
Q

List the differentials for classical swine fever

A
  • Porcine dermatopathy and nephropathy

- African swine fever

69
Q

List the notifiable causes of neurological disease that are also zoonotic

A
  • Equine encephalomyelitis
  • West Nile Virus
  • TSEs
  • Rabies