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
What is meant as amplifier host?
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
26
Which species are considered indicator hosts for FMDV?
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.
27
Which species are considered amplifier hosts for FMDV?
Pigs are amplifying hosts; they produce large quantities of aerosolized virus, but shed for a short time and are not long-term carriers
28
Course of FMD disease in cows:
acute, because cows are indicator hosts for FMD.
29
Clinical signs of FMD in cattle.
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
30
Recovery time for FMD in cattle?
Recovery in 8-15 days
31
Complications of FMD in cattle?
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.
32
Clinical signs of FMD in goats and sheep.
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.
33
Clinical signs of FMD in pigs.
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
34
Cardiac change in FMD cases.
Gray or yellow streaking in the heart from myocarditis, degeneration and necrosis of the myocardium in young animals of all species (‘tiger heart’).
35
Humans can catch FMD how?
milk, or droplet transmission from ppl with it in very rare cases from animals, but disease is mild.
36
ddx for FMDV (3)
Vesicular diseases are clinically indistinguishable so they're your main ddx! vesicular stomatitis swine vesicular disease vesicular exanthema of swine
37
other ddx for FMDV other than the vesicular diseases (5)
burns - e.g. chemical, thermal rinderpest bovine viral diarrhoea and mucosal disease infectious bovine rhinotracheitis bluetongue disease
38
Material needed for Diagnosis of FMDV.(4)
an unruptured vesicle's fluid (1ml), or recently ruptured vesicle's tissue (1g) oesophageal-pharyngeal fluid blood
39
Laboratory Diagnosis of FMDV.(3)
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
40
Prevention & control of FMDV (4-5)
Biosafety measures Disinfection Emergency vaccination Strategy: stamping out + Destruction of carcasses by burning or burial
41
Classical swine fever (CSF) is also known as
hog cholera
42
CLASSICAL SWINE FEVER (CSF) is 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
CSFV stands for
Classical swine fever virus
44
Classical swine fever virus belongs to what family
family Flaviviridae, genus Pestivirus RNA-virus
45
Classical swine fever virus /CSFV serotypes
one serotype minor antigenic variability between viral strains three genotypes, ten subtypes
46
Classical swine fever virus /CSFV stability
Inactivation pH <3 and >11 Does not persist long in the environment Survives in refrigerated meat (months) and frozen meat (years)
47
Host range of CSFV
swine only! Mostly seen in autumn.
48
CSFV Morbidity & mortality
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
Transmission of CSFV via
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
Reservoir of CSFV
only infected pigs!
51
CSFV Incubation period:
2-14 days
52
CSFV Persistent viraemia in
Congenitally infected piglets Shedding of the virus for months!
53
Form of CSFV disease.
Mostly we see: subacute, chronic or atypical form of the disease. Disease is variable from acutely fatal to asymptomatic.
54
Clinical signs of CSFV acute dz
Clinical signs are similar to other swine diseases (e.g. ASF) Pyrexia (>40⁰C), huddling, weakness, anorexia, Conjunctivitis, Diarrhea, staggering, cyanosis, skin hemorrhages, death.
55
Clinical signs of subacute CSFV dz
similar to acute, but symptoms less severe. pigs may survive!
56
Clinical signs of chronic CSFV dz
anorexia, depression, fever, diarrhoea abortions, stillbirths, deformities persistently infected pigs almost always fatal
57
Clinical signs of congenital CSFV infection
persistent viraemia tremors deformities persistently infected pigs disease is almost always fatal
58
Post mortem: CSFV acute dz
Highly variable Haemorrhages Necrotic foci in tonsils Petechiae/ecchymoses on serosal and mucosal surfaces - kidneys, larynx, trachea, intestines, spleen, lungs
59
What type of post mortem ulcer is typical to chronic CSFV
necrotic foci called button ulcers, found in the: intestinal mucosa epiglottis larynx
60
Post mortem findings in congenital CSFV
cerebellar hypoplasia thymic atrophy haemorrhages deformities
61
DDx for CSFV
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
Suspect CSFV when...?
Suspect when: Characteristic post mortem signs (hemorrages in internal organs) High morbidity Clinical signs: anorexia, deaths, reproductive symptoms History of garbage/scrap feeding
62
Materials for CSFV detection.
ideally tonsil tissue but also whole blood
63
Laborarotry analyses for detection of CSFV.
Detect virus, antigens or nucleic acids Serology - ELISA or virus neutralisation, comparative neutralisation test
64
Treatment for CSFV.
There is no treatment!
65
Strategy for eradication of CSFV.
- 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
ASFV
african swine fever virus
67
AFRICAN SWINE FEVER (ASF) is 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
ASF is caused by what virus and belongs to which family
Asfivirus family Asfarviridae, genus Asfivirus “ASFAR” - African swine fever and related viruses DNA-virus!
69
How many genotypes of ASF?
23 genotypes no antigenic variability between viral strains!
70
ASF virus stimulates antibodies but
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
the only known DNA virus that is transmitted by arthropods.
ASFV The virus replicates in Ornithodoros ticks and can be transmitted to swine through the bite of the tick.
72
ASFV stability
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
ASFV can survive for how long in; 4*C blood room temp. feces putrefied blood contaminated pig pens frozen meat
4'C blood 18 months room temp. feces 11 days putrefied blood 15 weeks contaminated pig pens 1 month frozen meat 1000 days
74
Host range of ASFV:
swine African wild suids are asymptomatic carriers Ticks (Ornithodoros sp.) - natural arthropod host and reservoir of the dz
75
reservoir of ASFV
African wild suids - asymptomatic carriers (not the ticks!)
76
Morbidity & mortality of ASFV
Morbidity in naive population <100% Mortality - dependent of the virulence; high virulence <100% low virulence - lower mortality
77
Morbidity versus mortality versus case fatality rate
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
What is the treatment for ASFV?
No treatment or vaccine currently exists for this disease. So, culling.
79
Transmission of ASFV.
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
Excretion of ASFV.
Excretion: blood, tissues, secretions and excretions of sick and dead animals. Excretion starts during the incubation period.
81
Forms of ASF disease:
peracute, acute, subacute and chronic
82
Clinical form of ASFV disease depends on (4)
virus strain virulence exposure dose exposure route host
83
Incubation period of AFSV:
3-15 days Excretion starts during the incubation period. add from note bit on slide 70
84
how to identify peracute ASFV disease
sudden death with just a few lesions or no clinical signs
85
Initial signs of ASFV infection (not depending on the virulence of the virus):
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
good difference between the ambiguous or prodromal signs of ASFV versus classic swine fever is:
african swine fever: respiratory classic swine fever : diarrhea
87
Clinical signs: acute AFSV
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
Clinical signs: subacute ASFV
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
Clinical signs: chronic ASFV
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
Review this table on African swine fever disease forms.
91
Post mortem changes in acute ASFV
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
Post mortem changes in chronic ASFV
focal caseous necrosis and mineralisation of the lungs enlarged LN
93
DDx for ASFV
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
Diagnosis of ASFV
Suspect when: characteristic post mortem signs, anorexia, depression and sudden deaths in the herd
95
Material for diagnosis of ASFV
tissue samples (LN, spleen, kidney, lung), blood and serum
96
Prevention, control & Treatment for ASFV. Immobilisation and surveillance areas?
No Tx No vaccine Culling! Immobilisation areas: Protection area 3km Surveillance area 10km
97
Laboratory analyses for diagnosis of ASFV
PCR & ELISA mainly Haemadsorption test (HAD) Fluorescent antibody test (FAT) Indirect fluorescent antibody (IFA) Immunoblotting test