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Reovirus Flashcards

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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
Equine Encephalosis Species affected
Equids —> Horses, Donkeys, Zebras —> Clinical signs only in horses! Elephants (rare)
26
Equine Encephalosis Most susceptible
All age groups
27
Equine Encephalosis Occurence
``` Southern parts of Africa Israel outbreak (2009) ```
28
Equine Encephalosis Spread
Vector borne disease: Culicoides sp | Placental crossing!
29
Equine Encephalosis Pathogenesis
* Similar to AHS | * Blood vessel damage —> Oedema and Haemorrhages
30
Equine Encephalosis Primary replication
* Lymphatic Tissue | * Incubation period of 3-10 days
31
Equine Encephalosis Target organs
Blood vessel walls
32
Equine Encephalosis Clinical signs
* 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
Equine Encephalosis Pathology/histopathology
* Enteritis | * Liver dystrophy
34
Equine Encephalosis Treatment
* In most cases animals recover without any complication | * Anti-inflammatories, appetite stimulants and antibiotics (to prevent secondary bacterial infections) recommended
35
Equine Encephalosis Prevention and immunity
* Vector control * Control of import of horses from Africa * No effective vaccine!
36
Equine Encephalosis | Diagnosis
Virus isolation RT-PCR Serology: ELISA
37
Rotavirus infections in domestic animals Species affected
``` 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
Rotavirus infections in domestic animals Most susceptible
Few-day old animals
39
Rotavirus infections in domestic animals Occurrence
Worldwide
40
Rotavirus infections in domestic animals Spread
*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
Rotavirus infections in domestic animals Pathogenesis
* 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
Rotavirus infections in domestic animals Primary replication
Enterocytes | Incubation period of 24-48 hours
43
Rotavirus infections in domestic animals Target organs
Middle and Distal Small Intestines
44
Rotavirus infections in domestic animals Clinical signs
* 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
Rotavirus infections in domestic animals Pathology/histopathology
* 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
Rotavirus infections in domestic animals Diagnosis
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
Rotavirus infections in domestic animals Treatment
* Electrolyte therapy (possible parenteral) | * Antibiotics against bacterial co-infecitons
48
Rotavirus infections in domestic animals Prevention and immunity
* 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
Seadornavirus associated Diseases Species affected
Human pathogen but | detected in animals too
50
Seadornavirus associated Diseases Occurence
China, Java, Indonesia
51
Seadornavirus associated Diseases Clinical signs
``` Influenza-like illness: • Fever • Muscle pains • Joint pains Encephalitis ```
52
Orthoreovirus Infeciton of Domestic Animals Species affected
Cattle, Sheep, Horse, | Swine, Rabbit
53
Orthoreovirus Infeciton of Domestic Animals Most susceptible
Young animals
54
Orthoreovirus Infeciton of Domestic Animals Occurrence
Worldwide
55
Orthoreovirus Infeciton of Domestic Animals Pathogenesis
PO, Airborne Infections
56
Orthoreovirus Infeciton of Domestic Animals Clinical signs
*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
Orthoreovirus Infeciton of Domestic Animals Prevention and immunity
Cattle: Colostral immunity for up to 5 months
58
``` 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
Mainly chicken Turkey, Goose, Guinea Fowl, Muscovy Duck, Quail, Pigeon, Parrot and many other bird species too
59
``` 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
* All age groups | * No clinical signs if infection is after 10 days old!
60
``` 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
Worldwide
61
``` 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
* 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
``` 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
*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
``` 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
*Epithelial cells: • Enterocytes • Bursa Fabricii *Spreads really fast!
64
``` 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
* Tendon sheaths and joints | * Visceral Organs
65
``` 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
*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
``` 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
*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
``` 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
*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
``` 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
*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
General Characteristics of Reoviral
*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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