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Veterinary systemic virology
Group Assignment + Presentation
Prepared by:
① Ayenew wudie___________________________________0514/13
② Badada Halake__________________________________0533/13
③ Bayu Mamo_____________________________________0557/13
④ Bodena Kumela_________________________________ 0724/13
⑤ Cherinet Fanta______________________________ ____0748/13
⑥ Delu
Ufaisa______________________________________0832/13
⑦ Derese Hailemeskel _____________________________0848/13
⑧ Derese Tekilu____________________________________0850/13
⑨ Dessalegn Ermiyas______________________________0860/13
⑩ Aychew Molla ___________________________________0511/13
Submitted to: Dr. Abdallahi A. Submission date: June 14/2023
College of veterinary medicine DVM
3rd
Year
REOVIRIDAE

 Respiratory enteric orphan virus( Reo)
 "Orphan virus" = without any associated disease (some)

Reoviridae
 Non-enveloped with double or triple layered capsid & icoshedral
structure 60-80 nm in diameter
 Segmented (10-12 segments) double- stranded RNA.

 Replicate in cytoplasm with intracytoplasmic inclusion bodies.

 Genetic reassortment readily takes place.
 Resistant to heat, organic solvents and non-ionic detergents.
 2 morphological forms:
General characters:
1. 'Spiked' = turret shaped projections
2. 'Smooth' = spherical
Rotavirus particles as they appear in an electron
micrograph and a diagrammatic representation
① Orthoreovirus: cause arthritis & tenocynovitis in poultry.
②
② Rotavirus : cause enteritis in neonatal farm animals.
③
③ Orbivirus: Arthropods- borne infections (Arbo), cause:
④ African horse sickness in horses, Bluetongue disease in sheep ,
and in other domestic & wild
⑤ ruminants.
⑥ Colti virus (Colorado tick fever virus): primarily infect rodents
and human but occasionally cause clinical disease in domestic
animals
Generas of Reoviridae :
 Orthoreoviruses and rotaviruses are stable over a wide
range of pH values while orbiviruses lose infectivity at
low pH value
 Blue tongue virus
 African horse sickness virus
 Epizootic haemorrhagic disease virus
 Ibaraki virus
 Equine encephalosis virus
 Palyam virus
Genus: Orbivirus
 non-contagious viral disease of sheep and other domestic and
wild ruminants.
 transmitted principally by biting midges (Culicoides spp).
 caused by serotypes of bluetongue virus (BTV) in the genus
orbivirus of the family Reoviridae.
 Twenty four serotypes of the BTV have been described.
Blue tongue
 transmitted by Culicoides imicola in Africa and Asia.
 Venereal transmission through the semen of ram and bull has
been reported.
 Can also be transmitted by embryo transfer.
 Blue tongue is of great significance in sheep and deer.
 Cattle are considered to be important reservoir of the virus.
Transmission:
 After experimental infection, the virus replicates initially in
regional lymph nodes.
 It is then carried in blood or lymph to other lymphoid tissues,
lungs and spleen where further replication takes place.
 Virus localizes and multiplies in the endothelium of small blood
vessels producing vascular damage with stasis, exudation and
tissue hypoxia.
 The initiation and development of surface lesions in areas of
tissue hypoxia relate to minor trauma and may be complicated
by secondary bacterial infection.
 Lesions are particularly evident in the oral cavity, around the
mouth and on the coronet of the hoof.
Pathogenesis and pathology
 In the bloodstream, the virus is highly cell - associated,
particularly with erythrocytes.
 Infectious virus can be detected for 35 to 60 days after
infection.
Cont....
 are diverse and varied.
 There may be:
Clinical signs:
 fever
 depression
 vascular congestion of the lips and muzzle,
 oedema of lips, face, eyelids and ear
 erosion and ulceration of oral mucosa
 excessive salivation and
 watery nasal discharges which later becomes
mucopurulent
 swollen and cyanotic tongue,
 lameness from coronotis and
 laminitis ( inflammation of laminae)
 abortion and
 mortality of up to 30%.
 Clinical signs and postmortem findings are suggestive
 Laboratory confirmation requires isolation and identification
of the virus or demonstration of BTV-specific antibodies
 Samples: unclotted blood from febrile animals or fresh spleen
and lymph node collected at post mortem
 Virus isolation in embryonated egg inoculated intravenously
 Antigen detection by ELISA
 Serology: CFT, AGID, Indirect IF, and Indirect ELISA
 Neutralization test and HI test
 PCR
Diagnosis
 Vector control
 Live attenuated vaccine for protection against virulent virus
of homologous serotype
 Polyvalent vaccine in regions where more than one
serotype is prevalent
 Live attenuated vaccine may be teratogenic when used in
pregnant animals during the first half of gestation
 Live attenuated vaccine virus may revert to virulence
 Killed adjuvanted vaccine can induce protection but
requires booster dose. It is more expensive to produce.
Control
 non-contagious disease of horse, mules and donkeys.
 Aetiology: African horse sickness virus (AHSV), an orbivirus.
 The AHS subgroup is made up of nine serotypes of AHSV and
they are distinguishable by neutralization tests.
 AHS is endemic in subtropical and tropical Africa.
 Outbreak have also been reported in some parts of Asia
(Middle East, India, Pakistan)=serotype 9 and Europe (Spain
and Portugal)=serotype 4
African horse sickness
 transmitted by haematophagous insects.
 major vector is Culicoides imicola (a species of Afro-Asian midge).
 C.imicola once infected remains infected for life.
 warm climate of Africa supports the multiplication of the midge
and endemic disease occurs only in regions where C. imicola is
constantly present.
 Outbreaks occurs majorly during the warm humid season
(summer).
 may be isolated from clinically normal maintenance hosts such as
the zebra and African donkey.
Transmission
 The primary sites of viral replication are believed to be
regional LNs, spleen and lungs.
 Viraemia persists throughout the febrile period, typically 4
to 8 days.
 In zebras and donkeys, viraemia may last up to 4 weeks.
 Endothelial cells are important sites of secondary viral
replication, resulting in increased vascular permeability,
oedema, haemorrhage and intravascular coagulation.
 Post - mortem findings include diffuse pulmonary oedema,
hydrothorax, ascites and hydropericardium.
Pathogenesis and pathology
① A peracute pulmonary form characterized by depression, nasal
discharge with rapid progression to severe respiratory distress.
Mortality is close to 100%
② a subacute cardiac form manifesting as conjunctivitis, abdominal
pain and progressive dyspnoea
③ subacute oedematous swelling of the head and mouth are most
obvious in the supraorbital fossae, palpebral conjuctiva and
intermandibular space.
④ Mortality rate is up to 70%.
⑤ A combination of pulmonary and cardiac features (mixed form).
⑥ a mild or subclassical form termed horse sickness fever observed
in zebra and donkeys.
Four clinical forms of AHS are recognized:
Clinical signs
Peracute pulmonary form Subacute cardiac form
 characteristic clinical signs and postmortem findings
 samples: blood, lymph nodes, spleen
 virus isolation in embryonated eggs or cell culture as well as
intracerebral inoculation of newborn mice
 identification of isolated virus by immunoflourescence and
typing by virus neutralization with monovalent antiserum or
competitive ELISA
 reverse-transcriptase (RT)- PCR can be used for detection of
viral RNA.
 serological test by CFT, AGID, ELISA and serum neutralization
tests.
Diagnosis
 vector control, quarantine and vaccination
 attenuated vaccines both monovalent and polyvalent
containing up to four serotypes are available, vaccines do
not prevent viraemia.
 Vaccine virus can revert to virulence and be transmitted by
vectors.
 Vaccinated animals can not be differentiated serologically
from those with foal infection.
 inactivated vaccines based on serotype 4 are effective in
preventing both clinical disease and viraemia.
 a polyvalent vaccine must be used if there is a risk of
exposure to different serotypes
Control
 Veterinary microbiology and microbial disease, 2nd
edition.P J Quin ,B K Markey, F C Leonard, E S Fitz
patrick, S Fanning , P J Hartigan. Ch. 69 P. (635-643)
,Reoviridae.
References
THANK YOU!!

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Vet. viro . Reoviridae.pptx

  • 1. Veterinary systemic virology Group Assignment + Presentation Prepared by: ① Ayenew wudie___________________________________0514/13 ② Badada Halake__________________________________0533/13 ③ Bayu Mamo_____________________________________0557/13 ④ Bodena Kumela_________________________________ 0724/13 ⑤ Cherinet Fanta______________________________ ____0748/13 ⑥ Delu Ufaisa______________________________________0832/13 ⑦ Derese Hailemeskel _____________________________0848/13 ⑧ Derese Tekilu____________________________________0850/13 ⑨ Dessalegn Ermiyas______________________________0860/13 ⑩ Aychew Molla ___________________________________0511/13 Submitted to: Dr. Abdallahi A. Submission date: June 14/2023 College of veterinary medicine DVM 3rd Year
  • 3.   Respiratory enteric orphan virus( Reo)  "Orphan virus" = without any associated disease (some)  Reoviridae  Non-enveloped with double or triple layered capsid & icoshedral structure 60-80 nm in diameter  Segmented (10-12 segments) double- stranded RNA.   Replicate in cytoplasm with intracytoplasmic inclusion bodies.   Genetic reassortment readily takes place.  Resistant to heat, organic solvents and non-ionic detergents.  2 morphological forms: General characters: 1. 'Spiked' = turret shaped projections 2. 'Smooth' = spherical
  • 4.
  • 5. Rotavirus particles as they appear in an electron micrograph and a diagrammatic representation
  • 6. ① Orthoreovirus: cause arthritis & tenocynovitis in poultry. ② ② Rotavirus : cause enteritis in neonatal farm animals. ③ ③ Orbivirus: Arthropods- borne infections (Arbo), cause: ④ African horse sickness in horses, Bluetongue disease in sheep , and in other domestic & wild ⑤ ruminants. ⑥ Colti virus (Colorado tick fever virus): primarily infect rodents and human but occasionally cause clinical disease in domestic animals Generas of Reoviridae :
  • 7.
  • 8.  Orthoreoviruses and rotaviruses are stable over a wide range of pH values while orbiviruses lose infectivity at low pH value  Blue tongue virus  African horse sickness virus  Epizootic haemorrhagic disease virus  Ibaraki virus  Equine encephalosis virus  Palyam virus Genus: Orbivirus
  • 9.  non-contagious viral disease of sheep and other domestic and wild ruminants.  transmitted principally by biting midges (Culicoides spp).  caused by serotypes of bluetongue virus (BTV) in the genus orbivirus of the family Reoviridae.  Twenty four serotypes of the BTV have been described. Blue tongue
  • 10.  transmitted by Culicoides imicola in Africa and Asia.  Venereal transmission through the semen of ram and bull has been reported.  Can also be transmitted by embryo transfer.  Blue tongue is of great significance in sheep and deer.  Cattle are considered to be important reservoir of the virus. Transmission:
  • 11.  After experimental infection, the virus replicates initially in regional lymph nodes.  It is then carried in blood or lymph to other lymphoid tissues, lungs and spleen where further replication takes place.  Virus localizes and multiplies in the endothelium of small blood vessels producing vascular damage with stasis, exudation and tissue hypoxia.  The initiation and development of surface lesions in areas of tissue hypoxia relate to minor trauma and may be complicated by secondary bacterial infection.  Lesions are particularly evident in the oral cavity, around the mouth and on the coronet of the hoof. Pathogenesis and pathology
  • 12.  In the bloodstream, the virus is highly cell - associated, particularly with erythrocytes.  Infectious virus can be detected for 35 to 60 days after infection. Cont....
  • 13.  are diverse and varied.  There may be: Clinical signs:  fever  depression  vascular congestion of the lips and muzzle,  oedema of lips, face, eyelids and ear  erosion and ulceration of oral mucosa  excessive salivation and  watery nasal discharges which later becomes mucopurulent  swollen and cyanotic tongue,  lameness from coronotis and  laminitis ( inflammation of laminae)  abortion and  mortality of up to 30%.
  • 14.
  • 15.  Clinical signs and postmortem findings are suggestive  Laboratory confirmation requires isolation and identification of the virus or demonstration of BTV-specific antibodies  Samples: unclotted blood from febrile animals or fresh spleen and lymph node collected at post mortem  Virus isolation in embryonated egg inoculated intravenously  Antigen detection by ELISA  Serology: CFT, AGID, Indirect IF, and Indirect ELISA  Neutralization test and HI test  PCR Diagnosis
  • 16.  Vector control  Live attenuated vaccine for protection against virulent virus of homologous serotype  Polyvalent vaccine in regions where more than one serotype is prevalent  Live attenuated vaccine may be teratogenic when used in pregnant animals during the first half of gestation  Live attenuated vaccine virus may revert to virulence  Killed adjuvanted vaccine can induce protection but requires booster dose. It is more expensive to produce. Control
  • 17.  non-contagious disease of horse, mules and donkeys.  Aetiology: African horse sickness virus (AHSV), an orbivirus.  The AHS subgroup is made up of nine serotypes of AHSV and they are distinguishable by neutralization tests.  AHS is endemic in subtropical and tropical Africa.  Outbreak have also been reported in some parts of Asia (Middle East, India, Pakistan)=serotype 9 and Europe (Spain and Portugal)=serotype 4 African horse sickness
  • 18.  transmitted by haematophagous insects.  major vector is Culicoides imicola (a species of Afro-Asian midge).  C.imicola once infected remains infected for life.  warm climate of Africa supports the multiplication of the midge and endemic disease occurs only in regions where C. imicola is constantly present.  Outbreaks occurs majorly during the warm humid season (summer).  may be isolated from clinically normal maintenance hosts such as the zebra and African donkey. Transmission
  • 19.  The primary sites of viral replication are believed to be regional LNs, spleen and lungs.  Viraemia persists throughout the febrile period, typically 4 to 8 days.  In zebras and donkeys, viraemia may last up to 4 weeks.  Endothelial cells are important sites of secondary viral replication, resulting in increased vascular permeability, oedema, haemorrhage and intravascular coagulation.  Post - mortem findings include diffuse pulmonary oedema, hydrothorax, ascites and hydropericardium. Pathogenesis and pathology
  • 20. ① A peracute pulmonary form characterized by depression, nasal discharge with rapid progression to severe respiratory distress. Mortality is close to 100% ② a subacute cardiac form manifesting as conjunctivitis, abdominal pain and progressive dyspnoea ③ subacute oedematous swelling of the head and mouth are most obvious in the supraorbital fossae, palpebral conjuctiva and intermandibular space. ④ Mortality rate is up to 70%. ⑤ A combination of pulmonary and cardiac features (mixed form). ⑥ a mild or subclassical form termed horse sickness fever observed in zebra and donkeys. Four clinical forms of AHS are recognized: Clinical signs
  • 21. Peracute pulmonary form Subacute cardiac form
  • 22.  characteristic clinical signs and postmortem findings  samples: blood, lymph nodes, spleen  virus isolation in embryonated eggs or cell culture as well as intracerebral inoculation of newborn mice  identification of isolated virus by immunoflourescence and typing by virus neutralization with monovalent antiserum or competitive ELISA  reverse-transcriptase (RT)- PCR can be used for detection of viral RNA.  serological test by CFT, AGID, ELISA and serum neutralization tests. Diagnosis
  • 23.  vector control, quarantine and vaccination  attenuated vaccines both monovalent and polyvalent containing up to four serotypes are available, vaccines do not prevent viraemia.  Vaccine virus can revert to virulence and be transmitted by vectors.  Vaccinated animals can not be differentiated serologically from those with foal infection.  inactivated vaccines based on serotype 4 are effective in preventing both clinical disease and viraemia.  a polyvalent vaccine must be used if there is a risk of exposure to different serotypes Control
  • 24.  Veterinary microbiology and microbial disease, 2nd edition.P J Quin ,B K Markey, F C Leonard, E S Fitz patrick, S Fanning , P J Hartigan. Ch. 69 P. (635-643) ,Reoviridae. References