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Epidemiology > Reovirus > Flashcards

Reovirus Flashcards

1
Q

Bluetongue

Species affected

A
  • Ruminants —> Mainly Sheep and Cattle Goats are more resistant
  • Further domestic and wild ruminants may be carriers and possible reservoirs (ex deer)
  • Serotype 8: sheep, goat and cattle
  • Serotype 25 (Toggenberg virus): Goats
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2
Q

Bluetongue

Most susceptible

A
  • Sheep are the most susceptible ruminant —> African sheep are more resistant
  • All age groups
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3
Q

Bluetongue

Occurence

A

*African origin —> worldwide
*Primarily in warmer regions, where Culicoides imicola midges occur —> endemic to Africa but due to global warming it is occurring in more and more places in the world
*Serotype 8 emerged in Europe (from Africa) in 2008 —> no significant clinical signs but trade of animals is hindered *Serotype 25 —> In Switzerland in 2008, no clinical signs
When area of serotypes is overlapping (different serotypes in 1 place) —> new serotypes will appear due to genetic reassortment

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4
Q

Bluetongue

Spread

A

*Transmission primarily via Culicoides imicola (midge) but other midges and ticks may be vectors as well.
*The propagation is in embryonated midge eggs.
*Vectors may also be infected with BTV after feeding from blood of infected vertebrates —> inoculate virus into an uninfected host animal at their next blood meal.
*Seasonal occurrence —> mainly in summer and autumn (not that much late autumn, winter and early spring) —> however not exclusively in these monthsas the midges can stay active in stables in winter
*Long distance spread:
• Vectors can travel by the wind
• Transport of infected
ruminants
*Transmission by semen is also possible
*Placental crossing

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5
Q

Bluetongue

Pathogenesis

A

*Midge bite and inoculation of virus—> lymphatic tissue > viraemia in 5-11 days —> endothelial damage —> Oedema and haemorrhages due to damages to the capillary and blood vessel walls
*Damage to mucosal surface, skin and muscle also occurs
*Transplacental infection —>
• Abortion
• Developmental anomalies (hydrocephalus, cerebella hypoplasia, jaw disorders, distortion of skull and jaw)
• Birth of viraemic lambs/calves
• May lead to immunotolerance, especially in cattle —> animal will shed the virus throughout its life, difficult to identify as they are seronegative!

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6
Q

Bluetongue

Primary replication

A

Lymphatic tissue

Incubation period of 3-7 day

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7
Q

Bluetongue

Target organs

A

Muscle and Epithelial cells

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8
Q

Bluetongue

Clinical signs

A

*Variable severity due to strain virulence, host species and breed
*Sheep:
• Fever (41.5℃ for 4-12 days) —> animals are anorexic, depressed and reluctant to
move (will be at the back of the flock when driven), dyspnoea
• Hypeaemia of the oral and nasal mucosa, serous nasal discharge (after day 1) and salivation due to lung oedema
• Conjunctivitis, eyelid oedema, lacrimation
• Oedema under the skin (subcutaneous) in head, ears, chin and neck region
• Swollen, protruding, cyanotic tongue — > Blue tongue
• Erosions on muzzle and oral mucosa (on days 2-3)
• Ulcers covered with greys necrotic membrane and purulent discharge (on days 4-7)
• Oedemas, erosions on the hoofs (coronary bands), laminitis
• Muscle damage due to virus propagation in the muscles > disturbed movements, torticollis
• Enteritis in lambs —> may be hemorrhagic
• Loss of wool, loss of weight
• Abortion, congenital defects
• Death within a week or recovery
• Mortality is 10-30% —> most animals recover
*Cattle:
• Some serotypes can be highly pathogenic
• Usually infections are subclinical making cattle asymptomatic carriers
• If clinical:
• Nasal discharge, reduced milk production
• Oedema of lips and eyelids
• Erosions and ulceration of nose, mouth, muzzle and teats with pseudomembrane formation
• Congenital defects: abortion, dummy calves, hydrocephalus, limb deformities
• Can transfer the disease back to sheep
*Goat:
• Often subclinical carriers

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9
Q

Bluetongue

Pathology/Histopathology

A
  • Haemorrhages in the airways, oral cavity, rumen
  • Cyanosis, oedema and erosions on the mucous membranes
  • Lambs —> haemorrhage gastroenteritis
  • Myocardial and muscle dystrophy
  • Cerebellar hypoplasia in aborted foetuses and in newborns
  • Endothelial necrosis, inflammation, thrombosis
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10
Q

Bluetongue

Diagnosis

A

Seasonality, clinical signs and PM lesions —> suspicion of disease —> further testing requirements since disease is notifiable!
Detection of virus: RT- PCR
Virus isolation rarely used
Serology: ELISA, CF, AGID, VN

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11
Q

Bluetongue

Treatment

A

No effective treatment

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12
Q

Bluetongue

Prevention and immunity

A

*In non endemic countries > Measures for control:
• Restrictions (restriction zone 20km, protection zone 100km, surveillance zone 150km)
• Slaughter of affected animals, vector control and monitoring
• Separation of seropositive pregnant animals, virological testing of newborns —> detect immunotolerant lambs and calves!
• Emergency vaccination (inactivated vaccine) —> because of genetic reassortment if we immunise an animal with a live vaccine,
the virus in the vaccine will produce another serotype!
(like Influenza)
*In endemic countries —>
Attenuated vaccines:
• Africa: polyvalent since
multiple serotypes in the area
• Other countries: serotype specific, monovalent
• Can be foetopathogenic
• Problems —> shedding of the vaccine strain, infection of vectors, risk of reversion

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13
Q

African Horse Sickness

Species affected

A
  • Equids —> Horses, Donkeys, Zebras, Mules etc
  • Zebras are the natural reservoirs
  • Rarely: Elephant, Camel. Dog, Ferret —> no clinical signs
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14
Q

African Horse Sickness

Most susceptible

A

All age groups

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15
Q

African Horse Sickness

Occurence

A
  • African origin —> spread to other parts of the world
  • Primarily in warmer regions —> endemic to Africa, Europe is currently free —> but due to global warming it is expected to be introduced soon
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16
Q

African Horse Sickness

Spread

A

*Transmitted by arthropod vectors:
• Midges/gnats (Culicoides sp) —> Biological vectors
• Mosquitoes (Cilicidae) —> mechanical vectors
• Rarely ticks (Hyaloma, Ripicephalus) —>mechanical vector Culicoides sp prefers warm, humid weather —> seasonality
*Not directly contagious between horses
*Indirect transmission by semen, urine and discharges too
*Infection of carnivores by consumption of infected horse meat, blood or organs

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17
Q

African Horse Sickness

Pathogenesis

A
  • Midge bite and inoculation of virus —> lymphatic tissue—> viraemia in 4-8 days (horse); in 28 days (zebra and donkey) > damage to lymph and blood vessels —> oedema, haemorrhages —> pulmonary oedema, cardiopathy —> death
  • Vascular problems which produce visible signs in lungs and subcutaneous tissue
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18
Q

African Horse Sickness

Primary replication

A

Lymphatic tissue

Incubation period of 5-7 (2-14) days

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19
Q

African Horse Sickness

Target organs

A

Blood vessel walls

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20
Q

African Horse Sickness

Clinical signs

A

*Variable severity
*Peracute, Pulmonary form:
• If many infected arthropods bite the same horse
• Fever (40-41℃), general weakness, sweating, red conjunctiva
• Dyspnoea, foamy nasal discharge, coughing
• Circulatory problems —> lung oedema —> protein rich exudate —> appears in alveoli and bronchi —> forced breathing —> egg-white like, protein rich foam produced —> gas exchange not possible if lung is filled with this foam
• Sudden death (within 24 hours)
*Acute, Respiratory form:
• Fever (40-41℃), respiratory symptoms, foamy nasal discharge
• Death within one week due to congestive heart failure, anoxia or both
*Subacute, Cardiac, Oedematous form:
• The most frequent form
• Oedema of the subcutaneous tissue
• Oedema around the eyes, lips, head, tongue, throat —> Hippo Head
• Later, oedema in the neck and chest
• Lung oedema —> excess load on the right side of heart, right ventricle will need stronger force to pump blood —> cardiac failure
• In final stages, haemorrhages appear in conjunctiva and under the tongue
• Death due to cardiac dysfunction 4-8 days after the onset of clinical signs
• If animals survives, oedema disappears within 3-8 days
*Mixed form (Respiratory and Cardiac):
• Fever (40-41℃), milder respiratory signs
• Oedema and death
*Chronic, Febrile form:
• Recurrent fever, higher in afternoons (max 40℃), lower in mornings
• Rarely other clinical signs, maybe reddened conjunctiva
• Mainly in donkeys, zebras and immune/ vaccinated horses
*Mortality varies:
• Horse: 70-96%
• Mule: 50%
• Donkey: 10%
• Zebra: 0% —> survives the infection but carriers and sheds the virus for a long term

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21
Q

African Horse Sickness

Pathology/histopathology

A

*Pulmonary oedema, hydrothorax, hyperaemia
• Septae of the lung become visible, looks much more like a cattle’s lung
*Oedema under the skin in the connective tissues
*Mucosal haemorrhages
*Hyperaemic visceral organs
*Fibrinous exudate in thoracic cavity
*Haemorrhages on serosal surfaces, renal cortex and spleen
*Epicardial and endocardial damage
*Ascites in abdominal cavity

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22
Q

African Horse Sickness

Treatment

A

Seasonality, clinical signs, PM lesions —> suspicion of disease —> further testing required since disease is notifiable!
Detection of virus: RT-PCR
Virus isolation in suckling mouse brain, BHK, vero cells
Detection of antigens: ELISA
Serology: ELISA, CF, AGID, V

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23
Q

African Horse Sickness

Prevention and immunity

A

No effective treatment

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24
Q

African Horse Sickness

Diagnosis

A

*In AHS free countries:
• Avoid introduction of infected animals
• Restriction of equine importation (especially zebras for zoos) from endemic countries
• If permission of importation granted —> animal should spend 30 days in quarantine and should be tested for the
virus
• Insecticide treatment against ectoparasites
• Dogs are potential carriers so monitor dogs as well
• Outbreak control:
• Sanitary prophylaxis
• Restriction, Slaughtering of affected/viraemic animals
• Insect control
• Vaccination of all animals within the safety zone with live (attenuated) or inactivated type specific vaccines twice
• Long term surveillance and monitoring
*In endemic countries:
• Immunisation with attenuated, polyvalent vaccines offer protection for
a few years

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25
Q

Equine Encephalosis

Species affected

A

Equids —> Horses, Donkeys, Zebras —> Clinical signs only in horses!
Elephants (rare)

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26
Q

Equine Encephalosis

Most susceptible

A

All age groups

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27
Q

Equine Encephalosis

Occurence

A 
Southern parts of Africa
Israel outbreak (2009)
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28
Q

Equine Encephalosis

Spread

A

Vector borne disease: Culicoides sp

Placental crossing!

29
Q

Equine Encephalosis

Pathogenesis

A
  • Similar to AHS

* Blood vessel damage —> Oedema and Haemorrhages

30
Q

Equine Encephalosis

Primary replication

A
  • Lymphatic Tissue

* Incubation period of 3-10 days

31
Q

Equine Encephalosis

Target organs

A

Blood vessel walls

32
Q

Equine Encephalosis

Clinical signs

A
  • Not primarily a neurological disease!
  • Fever (1-5 days), restlessness, inappetence, elevated heart and respiratory rates
  • Oedema of lips and eyelids
  • Inflammation of mucosa and blood vessels
  • Discolouration of mucousmembranes due to congestion and icterus
  • Neurological signs due to oedema of brain
  • Abortion during the first 5-6 months of pregnancy
  • Most infections are subclinical and affected horses usually show mild clinical signs and recover uneventfully
  • Mortality is under 5%
33
Q

Equine Encephalosis

Pathology/histopathology

A
  • Enteritis

* Liver dystrophy

34
Q

Equine Encephalosis

Treatment

A
  • In most cases animals recover without any complication

* Anti-inflammatories, appetite stimulants and antibiotics (to prevent secondary bacterial infections) recommended

35
Q

Equine Encephalosis

Prevention and immunity

A
  • Vector control
  • Control of import of horses from Africa
  • No effective vaccine!
36
Q

Equine Encephalosis

Diagnosis

A

Virus isolation
RT-PCR
Serology: ELISA

37
Q

Rotavirus infections in domestic animals

Species affected

A 
A: Majority of mammals and birds
B: Human, swine, cattle, sheep, rat —> Zoonosis!
C: Swine, rarely human —> Zoonosis!
D: Bird
E: Swine
F: Bird
G: Bird
38
Q

Rotavirus infections in domestic animals

Most susceptible

A

Few-day old animals

39
Q

Rotavirus infections in domestic animals

Occurrence

A

Worldwide

40
Q

Rotavirus infections in domestic animals

Spread

A

*From infected faeces, water
and environment, fomites
*Not germinative, but present in the surface of the egg —> infection of day old chicks
*Widespread —> almost all adult animals are seropositive and have been infected at some point during their lifetime

41
Q

Rotavirus infections in domestic animals

Pathogenesis

A
  • PO infection —> Enterocytes of gut —> Epithelial damage —> Villus atrophy —> Osmotic diarrhoea, exsiccosis
  • Virus is shed in faeces in high titres
  • Frequent simultaneous infection with parvo-, corona-, astroviruses and E.coli, cryptosporidia
42
Q

Rotavirus infections in domestic animals

Primary replication

A

Enterocytes

Incubation period of 24-48 hours

43
Q

Rotavirus infections in domestic animals

Target organs

A

Middle and Distal Small Intestines

44
Q

Rotavirus infections in domestic animals

Clinical signs

A
  • Mainly in 1-2 weeks of age
  • Sudden massive watery diarrhoea
  • Vomitting and dehydration
  • Loss of appetite, weakening, retarded body weight gain
  • Mortality is low —> deaths are mainly due to concomitant pathogens
  • Recovery by the end of second week
  • Immunity develops with each infection so subsequent infections are less severe and adults are rarely clinically affected
  • If signs develop at an older age, it is usually more serious as there is immunosuppression in the background
45
Q

Rotavirus infections in domestic animals

Pathology/histopathology

A
  • Undigested, liquid content in the intestines
  • Enlarged and dilated intestinal loops
  • Inflammation of the enteric mucosa
  • Villus atrophy and blunting
  • Animals survive as the deeper layers (Lieberkuhn crypts) of the intestine remain intact —> able to regenerate
46
Q

Rotavirus infections in domestic animals

Diagnosis

A

Age, Clinical Signs and PM lesions —> Suspicion of disease
Virus detection: RT-PCR, IF
Antigen detection: ELISA
Serology
Since virus is shed in high titres, it is easy to detect

47
Q

Rotavirus infections in domestic animals

Treatment

A
  • Electrolyte therapy (possible parenteral)

* Antibiotics against bacterial co-infecitons

48
Q

Rotavirus infections in domestic animals

Prevention and immunity

A
  • Strict hygiene (parturition, hatching, litter, individual keeping)
  • Ensure sufficient colostrum uptake
  • Inactivated, usually polyvalent vaccines (+ Corona and parvovirus, E.coli) —>
  • Vaccination of pregnant cows twice in the third trimester > immunity passed on to offspring via colostrum
49
Q

Seadornavirus associated Diseases

Species affected

A

Human pathogen but

detected in animals too

50
Q

Seadornavirus associated Diseases

Occurence

A

China, Java, Indonesia

51
Q

Seadornavirus associated Diseases

Clinical signs

A 
Influenza-like illness:
• Fever
• Muscle pains
• Joint pains
Encephalitis
52
Q

Orthoreovirus Infeciton of Domestic Animals

Species affected

A

Cattle, Sheep, Horse,

Swine, Rabbit

53
Q

Orthoreovirus Infeciton of Domestic Animals

Most susceptible

A

Young animals

54
Q

Orthoreovirus Infeciton of Domestic Animals

Occurrence

A

Worldwide

55
Q

Orthoreovirus Infeciton of Domestic Animals

Pathogenesis

A

PO, Airborne Infections

56
Q

Orthoreovirus Infeciton of Domestic Animals

Clinical signs

A

*Usually no clinical signs!
-Respiratory and Enteric (diarrhoea) signs
-Frequent with bacterial co infections
• Cattle: mild enteritis and pneumoenterits
• Sheep: enteritis and pneumoenteritis
• Horse: respiratory disease, usually with bacterial co-infections
• Swine: detection from diarrhoea and encephalitis cases, zoonotic potential
• Rabbit: diarrhoea

57
Q

Orthoreovirus Infeciton of Domestic Animals

Prevention and immunity

A

Cattle: Colostral immunity for up to 5 months

58
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Species affected

A

Mainly chicken Turkey, Goose, Guinea Fowl, Muscovy Duck, Quail, Pigeon, Parrot and many other bird species too

59
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Most susceptible

A
  • All age groups

* No clinical signs if infection is after 10 days old!

60
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Occurrence

A

Worldwide

61
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Spread

A
  • Spread by contact with infected faeces and discharges, contaminated litter
  • Also fomites and environment
  • Germinative infections!
  • Infected chickens, after hatching will spread the disease horizontally
62
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Pathogenesis

A

*Germinative infections —> foetopathy
*Trypsin sensitivity:
• Trypsin resistant strains (frequent) —> Mainly PO infections —> infection in intestines—> diarrhoea
• Trypsin sensitive strains (severe) —> Airborne/ *Percutaneous infection —> infection in lungs PO, Airborne, Transcutaneous (injuries) Infections —> Enterocytes and Bursa Fabricii —>Epithelial damage —> Viraemia:
• Tendon sheaths and joints —> inflammation
• Visceral organs —> necrotic and inflammatory foci
*Several strains can be isolated from clinically healthy birds —> subclinical infections
*Factors affecting severity of
disease:
• Age, species and breed of host
• Immunological status, resistance, immunosuppression (because of other diseases ex CAV, IBDV)
• Virulence and biotype of virus strain
• Infection route and titre
• Concomitant infections

63
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Primary replication

A

*Epithelial cells:
• Enterocytes
• Bursa Fabricii
*Spreads really fast!

64
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Target organs

A
  • Tendon sheaths and joints

* Visceral Organs

65
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Clinical signs

A

*Tenosynovitis-arthritis:
• Clinical signs mainly in 4-8 week old broilers due to the animals getting heavier
• In poor housing conditions, disease may occur even up to 15-16 weeks
• Lameness and arthritis
• Swollen knee, tarsal, metatarsal joints (uni or bi-lateral)
• Subcutaneous haemorrhages on the metatarsal area
• Deformed toes, swaying gait, paralysis-like signs
• Rupture of gastrocnemius muscle tendon (Achilles tendon) —> Lameness
increases
• Swollen thoracic bursa: Animals will lay on the floor on the sternal crest which pushes on the thoracic bursa
• Animals will not eat or drink as cannot move —> poor body weight gain, loose weight
• Frequent co-infections with Mycoplasma synoviae and Staphylococcus sp
• Morbidity 5-50%, mortality 2-10%
• In milder cases recover within 4-6 weeks
• Frequent subclinical infections
*Generalised form:
• Necrosis, inflammation and degenerative processes of visceral organs
• Immunosuppression
*Runting-Stunting Syndrome in Chickens or Poult Enteretis and Mortality Syndrome in Turkeys:
• Together with parvo-, adeno-, astro-, hepe-, corona-, enteroviruses, avian nephritis virus —> complex disease with about a dozen different viruses joined by bacteria
• PEMS: sudden increases in mortality in 1-4 week old turkeys
• Enteritis, diarrhoea, retarded development
• Developmental problems of bones and feathers
• Cartilage necrosis
• Foetopathies —> Helicopter/Chopper Disease, ruffled feathers

66
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Pathology/histopathology

A

*Tenosynovitis-arthrits:
• Arthritis in knee and metatarsal joint
• Deformed toes
• Haemorrhages on synovial membranes of joints
• Erosions on synovial cartilage
• Accumulation of fibrinous exudate in the hock joint and tendon sheaths
• Rupture of gastrocnemius tendon
• Enlarged diaphysis of the o.metatarsalis
• Ankylosis: consequence of chronic alteration of the joint —> due to long lasting inflammation, the joint will become stiff
• Oedema, haemorrhages, heterophil granulocyte infiltration of tissues
• Synovial cell hypertrophy and hyperplasia
• Villous proliferation on synovial membranes
• Scar tissue, fusion between tendons and tendon sheaths
*Generalised form:
• Greysih foci on liver, enlarged liver, liver dystrophy, inflammatory cell infiltration (reactive infiltration to remove necrotic cells of liver)
• Greyish foci and degenerating epithelial cells of pancreas and kidney —> atrophy of these organs
• Nephrosis
• Haemorrhages and perivasculitis in the brain stem
• Thymus atrophy, lesions in Bursa Fabricii and bone marrow
• Myocarditis, ascites in goslings
• Hydropericardium in chicken (together with Adenovirus) —> pericardium filled with fibrin rich yellowish fluid *RSS, PEMS:
• Enlarged, dilated intestinal loops with watery content
• Ascites

67
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Diagnosis

A

*Tenosynovitis-arthritis:
• Virus isolation on embryonate eggs or chicken liver cell culture —> cell rounding, synctia, cytoplasmic inclusion bodies
• Experimental infections of
day-old chickens: inoculation of joints and muscles (not routine)
• RT-PCR
• Serology: VN, AGID, ELISA

68
Q 
Depending on strain:
• Malabsroption Syndrome
• Enterits, Runting Stunting Syndrome, Poult Enteritis Mortality (PEMS)
• Tenosynovitisarthritis
• caused by S1133, WU2937
• Helicopter Disease, Blue-Wing Disease
• Hydropericardium
• Respiratory Disease
• Immunosuppression

Prevention and immunity

A

*Tenosynovitis-arthritis:
• Avoid early (<2 weeks old) infection by appropriate hygiene —> maternal antibodies prevent early infection (chicken with no yolk immunity —> infection will start very early)
• Immunisation with appropriate vaccines!
• Vaccines need to contain the specific strain for the animal to be immunised (ex must contain S1133 strain against tenosynovitis-arthritis)
• Chicken with yolk immunity:
• Vaccination at 5-7 weeks with attenuated strain, repeat at 11 weeks old
• Before laying season (age
18-22 weeks):
• With inactivated vaccine
• Chicken without yolk immunity:
• Vaccination on day 1
• Vaccination of Reovirus is antagonising the Marek’s disease vaccination so one
needs to choose one or the other RSS, PEMS:
• Hygiene
• Technology
• Vaccination —> no vaccine against all of the other viruses participating in the RSS but there is against reoviruses —> an animal can still have RSS/PEMS with the vaccination, just not caused by reoviruses

69
Q

General Characteristics of Reoviral

A

*Linear dsRNA, segmented with 10-12 segments, with an icosahedral double layered capsid and without an envelope
*Family reoviridae has 2 subfamilies:
• Sedoreovirinae —> without projections on the surface, still surface
• Spinareovirinae —> with surface projections
*Resistance is diverse within genuses:
• Orbivirus: Least resistant, pH5, inactivation in the environment within 1-2 days, however it is an arbovirus so no need to have a lot of resistance in the environment
• Orthoreovirus: pH3, 56℃ for over 30 minutes, resistant in the environment, cation stabilisation —> since they’re causing enteric problems they need to pass the stroma
and be acid resistant. Also resistant to drying out.
• Avian Orthoreovirus —> Very resistant in environment —> can survive up to 3 years!
• Rotavirus: Most resistant pH3 11, 60℃ for over 30 minutes, resistant in the environment *Biological properties:
• Segment reassortment —> Genetic diversity
• Isolation is the easiest in Orthoreoviruses (others more difficult)
• Relatively euryxen viruses
• Orbiviruses are arboviruses —> midges and mosquitos act as biological vectors —> the virus propagates in the insects (different from mechanical vectors —> insect transmits the virus without virus propagation) • Orthoreoviruses —> haemogluttinates
• Antigenicity:
• Common surface antigen —> Serological cross reactions
• Protective antigen (VN) might be serotype specific —> within the same virus species there are different serotypes, so serotype specific protection occurs —> different vaccines needed for different serotypes

Epidemiology (16 decks)

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