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Infectious diseases I & II > Lecture 7 - Part. 3 PPRV, Sheep and goat pox & CCPP > Flashcards

Lecture 7 - Part. 3 PPRV, Sheep and goat pox & CCPP Flashcards

1
Q

PPRV

A

Peste des petits ruminants virus

“Pest of Small Ruminants”

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2
Q

Peste des petits ruminants (PPR) is a

A

highly contagious viral disease of sheep and goats,

caused by Morbillivirus,

characterized by fever, necrotic stomatitis, gastroenteritis and pneumonia.

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3
Q

Peste des petits ruminants (PPR) is highly contagious viral disease of sheep and goats, caused by

A

Morbillivirus,

and characterized by fever, necrotic stomatitis, gastroenteritis and pneumonia.

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4
Q

Peste des petits ruminants (PPR) is a highly contagious viral disease of sheep and goats, caused by Morbillivirus, characterized by (4)

A

fever, necrotic stomatitis, gastroenteritis and pneumonia.

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5
Q

What bovine disease is similar to PPRV?

A

rinderpest

It is Closely related to Rinderpest virus.

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5
Q

Peste des Petits Ruminants virus (PPRV) belongs to what viral family and genus?

A

Family Paramyxoviridae, genus Morbillivirus

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6
Q

What type of virus is PPRV?

A

RNA-virus

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6
Q

How many genetic lineages does PPRV have?

A

Four genetic lineages

Closely related to Rinderpest virus

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7
Q

PPRV antibodies are cross-protective against?

A

rinderpest virus

The viruses are very similiar antigenically but are distinct viruses.

Vaccination for rinderpest can mask the presence of peste des petits ruminants.

Serological cross-reactivity also complicates some diagnostic tests.

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8
Q

Inactivation of PPRV?

A

Inactivation pH <4.0 and >11.0

Most common disinfectants can inactivate it.

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8
Q

PPRV can survive for long periods in

A

chilled and frozen tissues.

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9
Q

Host range of PPRV?

A

goats and sheep

Cattle and pigs seroconvert (so they develop antibodies) but do not develop or transmit disease. Are “dead-end hosts”.

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10
Q

Define seroconvert?

A

Seroconversion is the transition from the point of viral infection to when antibodies of the virus become present in the blood.

Given that many diagnostic tests use the presence of antibodies to infer illness, understanding seroconversion becomes a very important part of immunology and virology.

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10
Q

Morbidity of PPRV?

A

Varies by species, immunity and herd.

Morbidity in susceptible populations is 90-100%.

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11
Q

Mortality of PPRV?

A

Mortality varies.
Severe instances: 50-100%

mortality is high in Exotic ungulates.

Both morbidity and mortality rates are lower in endemic areas and in adults when compared to young.

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12
Q

Transmission of PPR mainly occurs

A

during close contact. Inhalation of aerosols is thought to be an important route of spread.

Fomites such as water, feed troughs and bedding can probably transmit PPRV for a short time, but do not remain infectious for long periods.

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13
Q

PPRV excretion

A

PPRV is shed in nasal and ocular secretions, saliva, urine and feces. It probably occurs in milk.

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14
Q

PPRV long-term carriers are

A

unlikely.

How the virus is maintained between outbreaks is not well understood.

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15
Q

Incubation period of PPRV

A

2-10 days

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16
Q

Forms of PPRV?(4)

A

peracute, acute, subacute, asymptomatic

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17
Q

Difference between rinderpest and PPRV ocular discharge?

A

in rinderpest its clear and watery

in PPRV its mucopurulent

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18
Q

PPRV is peracute in who?

A

naive populations

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19
Q

Features of Acute PPRV (7)

A

Pyrexia
Nasal and ocular discharges
(serous and then turns mucopurulent)

Hyperemic gums, necrotic oral lesions
Profuse diarrhea resutling in dehydration, emaciation

Rapid respiration, dyspnea
Abortions

Skin nodules around muzzle

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20
Q

Most cases of PPR are what form?

A

acute.

The characteristic signs are high fever and a serous nasal and ocular discharge that becomes mucopurulent.

Animals that do not die often have a prolonged convalescence.

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21
Q

Post-mortem lesions of PPRV. (5)

A

Inflammatory and necrotic lesionsin the oral cavity, GI tract.

Emaciation

Erosive lesions, “zebra stripes”

Bronchopneumonia

Enlarged lymph nodes

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22
Q

DDx for PPRV

A

Rinderpest (no pneumonia in rinderpest though)
Bluetongue

Contagious caprine pleuropneumonia
Pasteurellosis

Contagious ecthyma (skin infection)
FMD (both have oral erosions, FMD vesicles burst in 24h into erosions)

Coccidiosis
Mineral poisoning

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23
Q

When Sheep/goats with any acutely febrile, highly contagious disease signs and Oral lesions and/or GI signs, suspect what?

A

PPRV

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24
Q

Material for diagnosis of PPRV? (3)

A

Blood

Conjunctival discharges; nasal and buccal mucosae – swabs.

Lymph nodes, spleen, lung

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25
Q

Lab analyses for diagnosis of PPRV? (4)

A

Virus isolation (not always successful)
Antigen detection
PCR can detect viral nucleic acids
Serology

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26
Q

Treatment for PPRV?

A

no treatment, Euthanasia of the infected and exposed animals in stamp-out countries.

otherwise symptomatic care.

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27
Q

Prevention & control of PPRV? (4)

A

Quarantine, movement control

Euthanasia of the infected and exposed animals

Disinfection

Vaccination

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28
Q

DescribeVaccination of PPRV.

A

Is performed In Endemic areas to control it.

During outbreaks – ring vaccination of high-risk populations can be helpful.

Vaccines:
Attenuated live (Rinderpest) vaccine
Homologous, attenuated PPR vaccine
Recombinant vaccine (Capripox & PPR)

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29
Q

Sheep and goat pox is

A

1 disease but 2 viruses

Were once thought to be strains of a single virus.

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30
Q

SPV and GPV =

A

sheep pox virus & goat pox virus

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31
Q

SHEEPPOX AND GOATPOX (SPV and GPV) is

A

an acute, highly contagious disease,
caused by Capripoxvirus,
characterized by fever and papular-pustular lesions on skin and mucous membranes.

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32
Q

SHEEPPOX AND GOATPOX (SPV and GPV) is an acute, highly contagious disease, caused by

A

Capripoxvirus,

characterized by fever and papular-pustular lesions on skin and mucous membranes.

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33
Q

SHEEPPOX AND GOATPOX (SPV and GPV) is an acute, highly contagious disease, caused by Capripoxvirus, characterized by (2)

A

fever and papular-pustular lesions on skin and mucous membranes.

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34
Q

Sheeppox virus (SPV) and goatpox virus (GPV) belong to what viral family and genus?

A

Family Poxviridae, genus Capripoxvirus

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35
Q

What type of virus is SPV & GPV?

A

DNA-virus

36
Q

Why were SPV & GPV once thought to be the same?

A

Were once thought to be strains of a single virus because serology can’t distinguish them.

Recombination can occur between the viruses.

One serotype, with multiple strains.

37
Q

Define serotype.

A

Serotypes are groups within a single species of microorganisms, such as bacteria or viruses, which share distinctive surface structures.

These microorganisms, viruses, or cells are classified together based on their surface antigens, allowing the epidemiologic classification of organisms to the subspecies level.

A “strain” is a genetic variant or subtype of a microorganisms.

“serotype” or “serovar” is distinct variation within a species of bacteria or virus or among immune cells of different individuals.

38
Q

SPV & GPV can survive in what type of environmental conditions?

A

They have Prolonged survival in the environment.

Dry sheep pens < 6 months
Wool/hair < 3 months

Survives freeze-thaw cycles, though infectivity may be reduced.

39
Q

Sheep pox and goat pox are classified together with what other viral disease in the genus Capripoxvirus (family Poxviridae)?

A

lumpy skin disease virus

40
Q

Host range of SPV & GPV?

A

sheep and goats

Most isolates are host specific.

Some isolates affect both species.

Native breeds in endemic areas are less susceptible than introduced breeds (European or Australian origin).

41
Q

Morbidity of SPV & GPV?

A

Depends on breed, immunity, virus strain.

Morbidity in endemic areas 70-90% (OIE: 1 - >75%)

Newly imported up to 100%

42
Q

Mortality of SPV & GPV?

A

Mortality 5-10%

Imported, young animals <100%

43
Q

Transmission of SPV & GPV?

A

Sheep pox and goat pox viruses are usually transmitted by close contact.

Direct contact: - aerosols
Contaminative – fomites
Indirect contact - insects

44
Q

Excretion of SPV & GPV?

A

Infectious virus is found in all secretions, excretions including feces, and the scabs from skin lesions.

Contagious aerosols may also be generated from dust that contains pox scabs.

45
Q

SPV & GPV infected Animals are most contagious when?

A

before neutralizing antibodies develop (tahts seroconversion) = about 1 week after onset of clinical signs.

46
Q

No transmission of sheep and goat pox occurs in what stage of disease?

A

in the prepapular stage (e.g. animals early in dz or those dying peracutely).

Also no chronically infected carriers!

47
Q

transmission of sheep and goat pox is reduced when?

A

once papules have become necrotic and neutralizing antibody is being produced (about 1 week after onset).

48
Q

incubation period of sheep and goat pox?

A

4-21 days (usually 1-2 weeks)

49
Q

Forms of SPV & GPV? (3)

A

Forms: papulovesicular, nodular and hemorrhagic form

50
Q

First signs of SPV & GPV? (3)

A

Fever

Skin lesions: erythematous macules that become hard papules later on.

Superficial lymph nodes enlarge.

51
Q

Describe The PAPULOVESICULAR FORM of SPV & GPV? (3)

A

is common.

Papules become necrotic in the center, surrounded with hyperemia.

Sharply demarcated scabs over the necrotic area.

52
Q

Describe the nodular form of SPV &GPV. (4)

A

Is uncommon, called ‘stonepox’.

Papules become nodules.

Epidermis, dermis and subcutaneous tissues are involved.

Nodules become necrotic, hairless scars eventually.

53
Q

Describe the flat hemorraghic form of SPV & GPV. (3)

A

is uncommon

affects European goat breeds

Papules coalesce over the body, animal invariably dies.

54
Q

Clinical signs of SPV & GPV. (min. 4)

A

Lesions on mucous membranes and intestines along with systemic signs.

Salivation, loss of appetite
Rhinitis, conjunctivitis or blepharitis with mucopurulent discharges.

Respiratory signs:
coughing,
nasal discharge,
dyspnea

Diarrhea
Depression, emaciation
Abortions sometimes

55
Q

Recovery time of SPV & GPV.

A

Recovery takes weeks or longer, may leave permanent scars.

Secondary bacterial infections (incl. pneumonia) are common; death can occur at any stage.

56
Q

Post mortem lesions of SPV & GPV? (min. 4)

A

Skin lesions: macules, papules and/or necrotic lesions and scabs; oedema, hemorrhage, congestion.

LN: enlarged, edematous, hemorrhage, congested.

Mucous membranes of the eyes, nose, mouth, vulva and prepuce can be necrotic or ulcerated.

Lung lesions: congestion, oedema, nodules (up to 5 cm diameter).

57
Q

DDx for SPV&GPV? (9)

A

Contagious ecthyma (= skin infection, “deep impetigo”)
Bluetongue

Dermatophilosis/ Streptothricosis (rain rot-skin infection)
Mange (e.g. psoroptic mange/sheep scab)

Photosensitization or utricaria
PPRV

Parasitic pneumonia
Multiple insect bites
Caseous lymphadenitis

58
Q

Suspect what when: febrile animals with full-thickness skin lesions and enlarged LNs.

A

SPV/GPV

59
Q

Material for diagnosis of SPV/GPV? (3-4)

A

Blood

Skin biopsies;
scabs, skin lesions.

lymph nodes and their aspirates

lung lesions

60
Q

Lab diagnosis of SPV/GPV?

A

Virus isolation in cell cultures

Antigens: AGID or ELISA

PCR – can detect capripoxvirus genomes but can’t distinguish them from goat vs sheep unless you add another test called RFLP.

Serology can identify GPV and SPV as capripoxviruses, but cannot distinguish these two viruses from each other.

61
Q

Treatment for SPV/GPV?

A

no treatment

62
Q

Prevention & control of SPV/GPV. (4)

A

In the event of an outbreak: isolation up until 45 days from resolution of clinicial signs or slaughter of herd.

Quarantines and movement control
Disinfection
Vaccination

63
Q

Vaccination against SPV/GPV. (3)

A

Vaccination in endemic areas.

Live attenuated lends immunity for up to 2 years.

Inactivated/killed gives only short-term immunity.

64
Q

CONTAGIOUS CAPRINE PLEUROPNEUMONIA in finnish.

A

vuohen tarttuva keuhkorutto

65
Q

CCPP =

A

CONTAGIOUS CAPRINE PLEUROPNEUMONIA

66
Q

CCPP is caused by what pathogen?

A

the bacteria Mycoplasma capricolum subsp. capripneumoniae

67
Q

CONTAGIOUS CAPRINE PLEUROPNEUMONIA (CCPP) is a

A

highly contagious disease of goats,

caused by Mycoplasma capricolum subsp. capripneumoaniae,

and is characterized by respiratory disease and high mortality.

68
Q

CONTAGIOUS CAPRINE PLEUROPNEUMONIA (CCPP) is a highly contagious disease of goats, caused by

A

Mycoplasma capricolum subsp. capripneumoaniae,

and is characterized by respiratory disease and high mortality.

69
Q

CONTAGIOUS CAPRINE PLEUROPNEUMONIA (CCPP) is a highly contagious disease of goats, caused by Mycoplasma capricolum subsp. capripneumoaniae, and is characterized by (2)

A

respiratory disease and high mortality.

70
Q

The causal agent of CCPP belongs to what family?

A

bacterial Family Mycoplasmataceae

And is a Member of the Mycoplasma mycoides cluster.

71
Q

Describe the stability of Mycoplasma capricolum subsp. capripneumoniae. (3)

A

Short-lived, fragile in the environment.

Many disinfectants can inactivate (e.g. 70% ethanol).

72
Q

Host range of CCPP.

A

goats

Cases also in some wild ungulates (Tibetan antelope (Pantholops hodgsonii) and Arabian oryx (Oryx leucoryx)).

CCPP has been Reported in many countries in Africa, Asia and the Middle East.

73
Q

CCPP Seropositivity status of most herds.

A

In some herds and in endemic areas, most animals may be seropositive but in Asia: <5 – 44% are seropositive.

74
Q

Morbidity of CCPP.

A

Morbidity <100%

75
Q

Mortality of CCPP.

A

Mortality 70-100%

76
Q

Transmission of CCPP.

A

Direct (close) contact via droplets.

Route: respiratory (inhalation)

77
Q

Excretion of CCPP.

A

respiratory secretions

78
Q

IP of CCPP.

A

6-10 days (2 days to 4 weeks)

79
Q

Forms of CCPP. (3)

A

Peracute, acute and chronic forms.

80
Q

Describe Peracute CCPP.

A

death within 1-3 days withminimal clinical signs

81
Q

Describe acute CCPP. (5-8)

A

Very high fever, lethargy, anorexia

Coughing and labored respiration.
Cough is frequent, violent, productive.

In final stages may not be able to move, stands with front legs wide apart, neck stiff and extended.

Saliva dripping continuously
May grunt or bleat in pain

Pregnant goats can abort
Death in 7-10 days

82
Q

Describe subacute CCPP.

A

milder than acute of course, coughing mainly following physical activity

83
Q

Describe chronic CCPP.

A

chronic cough, nasal discharge and bedilitation (= serious weakening)

84
Q

POST MORTEM lesions of CCPP.

A

Can be Unilateral or bilateral pneumonia and serofibrinous pleuritis with straw-colored fluid in the thorax.

Regional (bronchial) LNs are enlarged.

85
Q

Describe pulmonary necropsy findings in CCPP cases. (4)

A

Unilateral or bilateral pneumonia and serofibrinous pleuritis with straw-colored fluid in the thorax.

On cut surface: lung is granular with copious straw-colored exudate.

Pea-sized, yellow nodules; surrounded by areas of congestion.

Varying degrees of lung consolidation or necrosis.

Image: Acute contagious caprine pleuropneumonia showing large quantities of pleural fluid and “port wine”–colored hepatized lung lobes in a goat.

86
Q

DDx for CCPP.

A

Other pulmonary mycoplasmoses such as:

Mycoplasma mycoides subsp. capri
M. mycoides subsp. mycoides (large colony type)
M. capricolum

87
Q

Material for diagnosis of CCPP. (5)

A

Lung tissue
Exudate from lunglesions
Pleural fluid
Regional LNs
Blood

88
Q

Lab analyses for diagnosis of CCPP.

A

Identification of the agent – PCR
Detecting antigens – cross-reactions!
Serology (antibodies)

Note: Difficult to isolate from clinical material!

89
Q

Describe Serology (antibodies) in CCPP.

A

Antibodies become detectable 7-9 days after the first clinical signs; animals with acute CCPP rarely develop measurable titers before death.

Cross-reactions with otehr mycoplasma spp.!

Good to use on a herd basis.

90
Q

Treatment of CCPP.

A

ABs (tetracyclines, fluoroquinolones, macrolides)
Can be effective if given early enough.

Treated animals may still be potential carriers since complete elimination of mycoplasma is rare so treatment not recommended, instead stamping out is.

91
Q

Eradication of a CCPP outbreak: (5)

A

Quarantines (45-180 d)
Movement controls
Slaughter of infected and exposed animals
Cleaning an disinfection of the premises
Vaccination

92
Q

How is CCPP controlled in endemic areas? (4)

A

In endemic areas:
flock testing, slaughter, on-site quarantine.

Vaccination

Infectious diseases I & II (33 decks)

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