Lecture 5 - Part 1. FMD, ASFV & CSFV Flashcards

1
Q

Diseases are divided into categories:

A

A, B, C, D, E

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2
Q

Disease category A

A

Diseases that do not normally occur in the EU and for which immediate eradicaton measures must be taken as soon as they are detetcted.

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3
Q

Disease category B

A

Diseases which must be controlled in all member states with the goal of eradicating them throughout the EU

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4
Q

Disease category C

A

DIseases which are of relevance to some Member States and for which measures are needed to prevent them from spreading to parts of the Union that are officially disease-free or that have eradication programs for the listed disease concerned.

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5
Q

Disease category D

A

Diseases for which measures are needed to prevent them from spreading on account of their movements between member states or entry into the EU.

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6
Q

Disease category E

A

Diseases for which there is a need for surveillance within the EU.

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7
Q

Notifiable animal diseases, so Highly contagious animal diseases, first half (6)

A

Foot and mouth disease
African swine fever
Classical swine fever

Rinderpest
Lumpy skin disease
Contagious bovine pleuropneumonia

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8
Q

Notifiable animal diseases, so Highly contagious animal diseases, 2nd half (7)

A

Sheep pox and goat pox
Peste des Petits Ruminants

Contagious caprine pleuropneumonia

African horse sickness
Glanders

(Highly pathogenic) Avian influenza
Newcastle disease

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9
Q

Name 3 Vesicular animal diseases

A

Foot and mouth disease
Vesicular stomatitis
Swine vesicular disease
(Vesicular exanthema of swine virus)

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10
Q

What species are susceptible to foot and mouth disease?

A

all cloven-hoofed animals

Domestic: cattle, pigs, sheep, goats, llamas, alpacas, camels, buffalos

Wild: African buffalos, deer, moose, wild pigs, giraffes, elephants etc.

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11
Q

What species are susceptible to vesicular stomatitis disease? (4)

A

bovine
swine
goats
horses

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12
Q

FOOT AND MOUTH DISEASE (FMD) is

A

a highly infectious viral disease of cloven-hoofed species characterized by fever and vesicles in the mouth and on the muzzle, teats, and feet.

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13
Q

FOOT AND MOUTH DISEASE (FMD) is rarely fatal except for - who and why?

A

young animals due to dystrophy of the heart and skeletal muscles.

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14
Q

How many serotypes of FMDV?

A

foot and mouth disease virus

7 serotypes exist: A, O, C, SAT1, SAT2, SAT3, Asia1

Serotypes do not confer cross immunity —> vaccination!

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15
Q

FMDV belongs to what viral family?

A

foot and mouth disease virus

family Picornaviridae,
genus Aphthovirus,
is an RNA-virus

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16
Q

FMDV can be inactivated by pH of?

A

Virus can be inactivated by pH <6.5 and pH >11.

Survives in milk and milk products, bone marrow and lymph nodes.

Can persist in contaminated fodder and the environment for up to 1 month!

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17
Q

Morbidity & mortality & recovery of FMDV

A

High morbidity (100%) in all age groups
Mortality <1%

Higher in young animals (myocarditis)

Recovery in 2 weeks.

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18
Q

World distribution of FMDV?

A

Endemic: Asia, Africa, Middle-East ja South-America

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19
Q

FMDV endemic where?

A

Asia, Africa, Middle-East ja South-America

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20
Q

Transmission of FMDV.

A

Virus is excreted with all body fluids.

So if e.g. you were not to find it in the fluid of a vesicle, then you can rule out FMD.

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21
Q

Incubation period of FMDV:

A

2-14 days
Can be as little as 24h!

Depends on the viral load - the smaller the dose, the longer the incubation period.

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22
Q

FMDV viral replication occurs where (typically)?

A

inthe oropharynx (tonsils!) and/or skin

Epithelial cells lyse, formation of blisters.

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23
Q

Which species are considered maintenance hosts for FMDV?

A

Sheep and goats are considered maintenance hosts for FMD; they have mild signs which delay diagnosis and allow for aerosol, contact spread, and environmental contamination.

Sheep can carry the virus in their pharyngeal tissue for 4-6 months.

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24
Q

What is meant by indicator host?

A

indicator host because they are often the first species to demonstrate clinical signs. Lesions quickly progress and become severe.

For FMD this is cows.

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25
Q

What is meant as amplifier host?

A

Pigs are amplifying hosts of FMD; they produce large quantities of aerosolized virus, but shed for a short time and are not long-term carriers

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26
Q

Which species are considered indicator hosts for FMDV?

A

Cows because they are often the first species to demonstrate clinical signs.

Cattle can carry the virus in their pharyngeal tissue for 6-24 months once infected with FMD.

Vaccination can protect from clinical signs but does not prevent development of the carrier state.

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27
Q

Which species are considered amplifier hosts for FMDV?

A

Pigs are amplifying hosts; they produce large quantities of aerosolized virus, but shed for a short time and are not long-term carriers

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28
Q

Course of FMD disease in cows:

A

acute, because cows are indicator hosts for FMD.

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29
Q

Clinical signs of FMD in cattle.

A

Pyrexia, anorexia, shivering, reduction in milk production (2-3 days), then:

smacking of the lips, grinding of the teeth, drooling, lameness, stamping or kicking of the feet.

vesicles in the mouth and on the muzzle, teats and feet

after 24h: rupture of vesicles —> erosions

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30
Q

Recovery time for FMD in cattle?

A

Recovery in 8-15 days

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31
Q

Complications of FMD in cattle?

A

tongue erosions,
superinfection of lesions,
hoof deformation,
mastitis and permanent impairment of milk production,
myocarditis,
abortions,
permanent weight loss,
loss of heat control (‘panters’)

Death of young animals from myocarditis.

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32
Q

Clinical signs of FMD in goats and sheep.

A

Are not as clear as in e.g. cattle, signs can be very mild which is why these are maintenance hosts.

Pyrexia
Lameness and oral lesions are often mild - complicates diagnosis
Agalactia

Death of young stock may occur without clinical signs.

Foot lesions along the coronary band or interdigital spaces may go unrecognised, as may lesions on the dental pad.

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33
Q

Clinical signs of FMD in pigs.

A

Pyrexia
foot lesions with lameness
(even detachment of the claw horn)

Vesicles at pressure points of the limbs, especially along the carpus (‘knuckling’)

Vesicular lesions on snout and dry lesions on the tongue

High mortality of piglets

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34
Q

Cardiac change in FMD cases.

A

Gray or yellow streaking in the heart from myocarditis, degeneration and necrosis of the myocardium in young animals of all species (‘tiger heart’).

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35
Q

Humans can catch FMD how?

A

milk, or droplet transmission from ppl with it

in very rare cases from animals, but disease is mild.

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36
Q

ddx for FMDV (3)

A

Vesicular diseases are clinically indistinguishable so they’re your main ddx!

vesicular stomatitis
swine vesicular disease
vesicular exanthema of swine

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37
Q

other ddx for FMDV other than the vesicular diseases (5)

A

burns - e.g. chemical, thermal

rinderpest
bovine viral diarrhoea and mucosal disease
infectious bovine rhinotracheitis
bluetongue disease

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38
Q

Material needed for Diagnosis of FMDV.(4)

A

an unruptured vesicle’s fluid (1ml),
or recently ruptured vesicle’s tissue (1g)

oesophageal-pharyngeal fluid
blood

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39
Q

Laboratory Diagnosis of FMDV.(3)

A

Virus isolation in cell-culture which is slow (4 days), but has high sensitivity and specificity.

Antigen ELISA - fast (hours), but may produce false positives.

RT-PCR

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40
Q

Prevention & control of FMDV (4-5)

A

Biosafety measures
Disinfection
Emergency vaccination

Strategy: stamping out

+ Destruction of carcasses by burning or burial

41
Q

Classical swine fever (CSF) is also known as

A

hog cholera

42
Q

CLASSICAL SWINE FEVER (CSF) is a

A

highly contagious disease of pigs,
caused by a Pestivirus,
characterised by high fever, lethargy, diarrhoea, vomiting and purple skin discolouration of the ears, lower abdomen and legs.

43
Q

CSFV stands for

A

Classical swine fever virus

44
Q

Classical swine fever virus belongs to what family

A

family Flaviviridae,
genus Pestivirus

RNA-virus

45
Q

Classical swine fever virus /CSFV serotypes

A

one serotype

minor antigenic variability between viral strains
three genotypes, ten subtypes

46
Q

Classical swine fever virus /CSFV stability

A

Inactivation pH <3 and >11

Does not persist long in the environment

Survives in refrigerated meat (months) and frozen meat (years)

47
Q

Host range of CSFV

A

swine only!

Mostly seen in autumn.

48
Q

CSFV Morbidity & mortality

A

Age and immune status affect mortality: piglets are more susceptible than adults.

Acute strain - high mortality (<100%)
Subacute - M&M both lower
Chronic - only few animals are affected but is always fatal!
Asymptomatic cases can occur.

49
Q

Transmission of CSFV via

A

blood, saliva, urine, faeces, tissues
Starts during incubation period, goes on for months after recovery.

Direct contact
Indirect contact (fomites)

Entry portal: ingestion, membranes, skin abrasions.
Less common: aerosol, semen, vectors

50
Q

Reservoir of CSFV

A

only infected pigs!

51
Q

CSFV Incubation period:

A

2-14 days

52
Q

CSFV Persistent viraemia in

A

Congenitally infected piglets
Shedding of the virus for months!

53
Q

Form of CSFV disease.

A

Mostly we see: subacute, chronic or atypical form of the disease.

Disease is variable from acutely fatal to asymptomatic.

54
Q

Clinical signs of CSFV acute dz

A

Clinical signs are similar to other swine diseases (e.g. ASF)

Pyrexia (>40⁰C), huddling, weakness, anorexia, Conjunctivitis, Diarrhea, staggering, cyanosis, skin hemorrhages, death.

55
Q

Clinical signs of subacute CSFV dz

A

similar to acute, but symptoms less severe.
pigs may survive!

56
Q

Clinical signs of chronic CSFV dz

A

anorexia, depression, fever, diarrhoea

abortions, stillbirths, deformities

persistently infected pigs

almost always fatal

57
Q

Clinical signs of congenital CSFV infection

A

persistent viraemia
tremors
deformities

persistently infected pigs disease is almost always fatal

58
Q

Post mortem: CSFV acute dz

A

Highly variable
Haemorrhages
Necrotic foci in tonsils

Petechiae/ecchymoses on serosal and mucosal surfaces - kidneys, larynx, trachea, intestines, spleen, lungs

59
Q

What type of post mortem ulcer is typical to chronic CSFV

A

necrotic foci called button ulcers, found in the: intestinal mucosa
epiglottis
larynx

60
Q

Post mortem findings in congenital CSFV

A

cerebellar hypoplasia
thymic atrophy
haemorrhages
deformities

61
Q

DDx for CSFV

A

ASF
Acute PRRS
Porcine dermatitis and nephropathy syndrome
Erysipelas
Salmonellosis
Eperythozoonosis
Actinobacillosis
Glasser’s disease
Aujeszky disease
Thrombocytopenic purpura
Warfarin poisoning
Heavy metal toxicity
… and other generalized septicemic or hemorrhagic conditions.

61
Q

Suspect CSFV when…?

A

Suspect when:
Characteristic post mortem signs (hemorrages in internal organs)
High morbidity
Clinical signs: anorexia, deaths, reproductive symptoms
History of garbage/scrap feeding

62
Q

Materials for CSFV detection.

A

ideally tonsil tissue

but also whole blood

63
Q

Laborarotry analyses for detection of CSFV.

A

Detect virus, antigens or nucleic acids

Serology - ELISA or virus neutralisation, comparative neutralisation test

64
Q

Treatment for CSFV.

A

There is no treatment!

65
Q

Strategy for eradication of CSFV.

A
  • rapid control via culling of infected animals and preemptive slaughter
  • Restriction of movements
  • Emergency vaccination
  • Prophylactic vaccination in endemic areas – not in EU!
  • ring vaccination in occurrence of an outbreak
66
Q

ASFV

A

african swine fever virus

67
Q

AFRICAN SWINE FEVER (ASF) is a

A

moderately contagious* disease of pigs, caused by Asfivirus, characterised by pyrexia, haemorrhages and high mortality.

  • In books it is still ‘highly contagious’ but now we have new information
68
Q

ASF is caused by what virus and belongs to which family

A

Asfivirus

family Asfarviridae, genus Asfivirus
“ASFAR” - African swine fever and related viruses

DNA-virus!

69
Q

How many genotypes of ASF?

A

23 genotypes

no antigenic variability between viral strains!

70
Q

ASF virus stimulates antibodies but

A

the antibodies do not neutralise the virus!

The lack of neutralizing antibodies is one of the reasons that explains the absence of an effective vaccine against ASFV nowadays

71
Q

the only known DNA virus that is transmitted by arthropods.

A

ASFV

The virus replicates in Ornithodoros ticks and can be transmitted to swine through the bite of the tick.

72
Q

ASFV stability

A

Inactivation pH <3.9 and >11.5

Serum increases the resistance of the virus
(pH 13.4 - 21h vs 7 days with serum)

Remains viable for long periods in blood, faeces and tissues (pork products!)

73
Q

ASFV can survive for how long in;

4*C blood
room temp. feces
putrefied blood
contaminated pig pens
frozen meat

A

4’C blood 18 months
room temp. feces 11 days
putrefied blood 15 weeks
contaminated pig pens 1 month
frozen meat 1000 days

74
Q

Host range of ASFV:

A

swine

African wild suids are asymptomatic carriers

Ticks (Ornithodoros sp.) - natural arthropod host and reservoir of the dz

75
Q

reservoir of ASFV

A

African wild suids - asymptomatic carriers
(not the ticks!)

76
Q

Morbidity & mortality of ASFV

A

Morbidity in naive population <100%

Mortality - dependent of the virulence;
high virulence <100%
low virulence - lower mortality

77
Q

Morbidity versus mortality versus case fatality rate

A

morbidity = cases of illness

mortality = the cases of death that occur in a population

case fatality rate = the proportion of cases that die from a specified disease among all individuals diagnosed with the disease

78
Q

What is the treatment for ASFV?

A

No treatment or vaccine currently exists for this disease.

So, culling.

79
Q

Transmission of ASFV.

A

Direct contact
Indirect contact

feeding on garbage containing infected meat
fomites

biological vectors - ticks (Ornithodoros sp)
Within tick vector: transstadial, transovarial, sexual transmission.

Route: oronasal, via tick bites

80
Q

Excretion of ASFV.

A

Excretion: blood, tissues, secretions and excretions of sick and dead animals.

Excretion starts during the incubation period.

81
Q

Forms of ASF disease:

A

peracute, acute, subacute and chronic

82
Q

Clinical form of ASFV disease depends on (4)

A

virus strain virulence
exposure dose
exposure route
host

83
Q

Incubation period of AFSV:

A

3-15 days

Excretion starts during the incubation period.

add from note bit on slide 70

84
Q

how to identify peracute ASFV disease

A

sudden death with just a few lesions or no clinical signs

85
Q

Initial signs of ASFV infection (not depending on the virulence of the virus):

A

intermittent low fever, appetite loss, weight loss, respiratory signs

Also with strains of higher virulence the initial signs are the same; we might not see the signs of acute disease because pigs die before they can develop.

Only in post mortem we can see some hemorrages in internal organs.

86
Q

good difference between the ambiguous or prodromal signs of ASFV versus classic swine fever is:

A

african swine fever: respiratory

classic swine fever : diarrhea

87
Q

Clinical signs: acute AFSV

A

short IP: 3-7 days
high fever (<42⁰C), anorexia, lethargy, weakness, recumbency

cyanotic skin blotching on the ears, tail, lower legs and hams

abdominal pain, constipation or diarrhoea (mucoid —> bloody)

dyspnea, vomiting, nasal and conjunctival discharges, neurologic signs

abortions
leucopenia
death in 5-10 days

88
Q

Clinical signs: subacute ASFV

A

caused by moderately virulent strains
similar clinical signs than in acute dz, just less severe

mortality is low in adults
very high in young animals

fever, thrombocytopenia and leukopenia may be transient - affected pigs die or recover within 3-4 weeks

89
Q

Clinical signs: chronic ASFV

A

caused by strain with low virulence.

intermittent low fever, appetite loss, weight loss, depression, respiratory signs, necrosis in areas of skin, chronic skin ulcers, arthritis
pericarditis, adhesions of lungs, swelling over joints.

can go on for months (2-15 months)

can be fatal, though low mortality

90
Q

Review this table on African swine fever disease forms.

A
91
Q

Post mortem changes in acute ASFV

A

haemorrhages in LNs
petechial haemorrhages of the kidneys
congestive splenomegaly

oedematous areas of cyanosis in hairless parts
cutaneous ecchymoses on the legs and abdomen

excess of pleural, pericardial and/or peritoneal fluid

92
Q

Post mortem changes in chronic ASFV

A

focal caseous necrosis and mineralisation of the lungs
enlarged LN

93
Q

DDx for ASFV

A

classical swine fever - needs lab to distinguish!
Porcine reproductive and respiratory syndrome (PRRS)
Erysipelas
Salmonellosis

Aujeszky’s disease - younger animals
Pasteurellosis
Porcine dermatitis and nephropathy syndrome
Actinobacillosis

other septicaemic conditions
heavy metal toxicity

94
Q

Diagnosis of ASFV

A

Suspect when: characteristic post mortem signs, anorexia, depression and sudden deaths in the herd

95
Q

Material for diagnosis of ASFV

A

tissue samples (LN, spleen, kidney, lung), blood and serum

96
Q

Prevention, control & Treatment for ASFV.

Immobilisation and surveillance areas?

A

No Tx
No vaccine

Culling!

Immobilisation areas:
Protection area 3km
Surveillance area 10km

97
Q

Laboratory analyses for diagnosis of ASFV

A

PCR & ELISA mainly

Haemadsorption test (HAD)
Fluorescent antibody test (FAT)
Indirect fluorescent antibody (IFA)
Immunoblotting test