Virology

1. Herpesviridae
More than 90% adults have been infected
(Chayavichitsilp P et. al.2009)

4. 1. Attachment
2. Penetration
3. Capsid Transport to N
4. Capsid Transport via MT
5. Release of Viral genome
6. Genome Replication
7. Preformed Capsid
8. Viral Genome encapsidation
9. Primary Envelopment
10. Perinuclear space
11. De envelopment
12. Secondary envelopment
13. Transport to cell surface
14. Release

5. Latency

6. Infectious Bovine Rhinotracheitis
• BHV-1
• Rhinotracheitis
• Vulvovaginitis
• Conjunctivitis
• respiratory disease
• Economic Losses

7. Transmission
• Respiratory & Genital Secreations
• Aerosol transmission
• Reactivation of latency following
transportation and parturition
• Semen of infected bull also contain virus

8. Pathogenesis
• Replication occurs in the mucous membranes
of the upper respiratory tract
• Secondary Bacterial infection
• Viraemia leads to fetal death rarely

9. Signs and Symptoms
• Temperature, nasal discharge
• Respiratory signs
• Morbidity 100%
• Mortality 10%

10. Diagnosis
• Swabs collected from the eyes, nares and
genitalia
• Viral antigen can also be detected using ELISA

11. Control
• Vaccine

12. Infectious laryngotracheitis
• Highly contagious
respiratory disease of
chickens
• Caused by Gallid herpes-
virus 1 (GaHV-1)
• Infection is transmitted
through aerosols

13. Signs and Symptoms
• Coughing
• Oculonasal discharge
• Bloodstained Mucous

14. Control
• Vaccination

15. Marek’s disease
• Caused by Gallid herpesvirus 2 (Marek’s disease
virus)
• oncogenic virus
• Major economic significance in the poultry
industry
• Infected birds remain carriers for life
• Transportation, vaccination, handling and beak
trimming are stress factors that increase
susceptibility to disease

16. Pathogenesis
• Following inhalation, virus replicates locally
• Persistent cell-associated viraemia results in
dissemination of the virus throughout the
body
• Infection of epithelial cells in feather follicles
• Cytolysis of these results in shedding of virus
particles into the environment
• Lymphoid Tumor

17. Clinical signs
• Birds between 12 and 24 weeks of age are
most commonly affected
• Clinically, Marek’s disease presents as partial
or complete paralysis of the legs and wings
• outbreaks with mortality as high as 70%

18. Control
• Vaccination

19. Retroviruses
• Enveloped
• RNA viruses
• Single strands of RNA
• Two linear, positive-
sense
• Core proteins
including
The enzymes reverse
transcriptase
 Integrase

20. • Reverse transcriptase
acts as an RNA-
dependent DNA
polymerase
• Three Major genes:
gag (Structural
Proteins)
pol (Enzymes)
env (Envelop
Glycoproteins)

21. Replication cycle
1:Binding,2:Fusion,3:Uncoating, 4:Reverse Transcription, 5: Nuclear Import, 6:
Integration, 7: Transcription, 8: Assembly, 9: Budding, 10: Release, 11: Maturation.

22. Replication cycle

24. Avian Leukosis
• B cell lymphoma
• Following infection, virus spreads throughout
the body

25. Signs
• The incubation period for lymphoid leukosis is
usually more than 4 months
• Affected birds become inappetent, weak and
emaciated.
• depressed egg production and fertility

26. Diagnosis
• ELISA
• PCR

27. Prion-BSE
• Unconventional infectious agents
• Can infect animals and humans without
inducing an immune response
• A unique group of neurodegenerative diseases
characterized by neuronal degeneration
• Protein Mutatiion

28. • Slow progressive neurodegenerative disease
• long incubation periods
• changes in the brain
• Neurological signs
• restlessness or nervousness, particularly after
sudden noise or movement
• Fine tremors of the head and neck and
incoordination

29. Flaviviridae
• ssRNA
• Positive sense
• Icosahedral

30. Replication Cycle

31. Birnaviridae
• Non-enveloped, double-stranded RNA viruses
• with icosahedral symmetry
• Replicate in cytoplasm

32. Infectious bursal disease
• highly contagious disease of young chickens
• infectious bursal disease virus (IBDV)
• Infection, which is usually acquired by the oral
route
• Virus is shed in the faeces for up to 2 weeks
after infection and can remain infectious in
the environment of a poultry house for several
months

33. • Within hours of ingestion, virus can be detected
in macrophages and lymphoid cells in the caeca,
duodenum and jejunum
• Infection spreads to the bursa of Fabricius where
rapid replication results in dissemination to other
tissues

34. Clinical Signs
• Affected birds are depressed and inappetent
and show evidence of diarrhoea and vent
pecking
• Morbidity ranges from 10% to 100% with a
mortality rate up to 20%

35. Diagnosis
• Swollen oedematous bursa at post-mortem
are often sufficient for diagnosis
• Specimens of bursa, spleen or faeces are
suitable for virus isolation
• Reverse transcriptase-PCR can be used for the
diagnosis of IBD

36. Control
• Cleaning and effective disinfection
• Vaccination

37. Poxviridae
• largest viruses
• Enveloped DNA viruses
• linear double-stranded DNA
• 100 proteins including several virus-encoded
enzymes

39. Contagious ecthyma
• poxvirus
• Goats, camels and
humans
• transmitted
through direct
contact

40. Pathogenesis
• Epitheliotropic
• Wart-like lesions following entry through skin
abrasions
• virus replicates in epidermal keratinocytes
• Infected cells release a vascular endothelial
growth factor, which stimulates angiogenesis in
the skin
• Virus encodes a number of factors that interfere
with immune response

41. Signs
• The disease primarily affects young sheep
• lesions most often occur on the commissures
of the lips and on the muzzle

42. Control
• Vaccination

43. Sheeppox and goatpox
• capripoxvirus strains
• Recent genetic studies suggest that sheeppox
virus and goatpox virus are phylogenetically
distinct viruses

44. Pathogenesis
• The virus replicates locally either in the skin or
in the lungs
• Spread to the regional lymph nodes is
followed by viraemia and replication in various
internal organs
• Lung lesions present as multiple nodular areas

45. Control
• Vaccine

46. Crimean–Congo hemorrhagic fever
(CCHF)
• viral disease
• CCHF outbreaks have a case fatality rate of up to
40%
• fever,
• muscle pains,
• headache,
• vomiting,
• diarrhea, and
• bleeding into the skin.

47. • Onset of symptoms is less than two weeks
following exposure
• spread by tick bites or contact with livestock
carrying the disease

48. • Virus enter to the monocytes, macrophages,
and dendritic cells
• Subsequent maturation occurs by budding in
the cisternae of the Golgi apparatus
• Disseminate to regional lymph nodes and to
whole body through lymph and blood

49. Paramyxoviridae
• Large enveloped viruses
• Negative-sense
• Single-stranded RNA
• Replicate in the cytoplasm
• Cause rinderpest, peste des petits ruminants,
canine distemper, Newcastle disease

51. Peste des petits ruminants
• goat plague
• Acute contagious disease of small ruminants
• peste des petits ruminants virus (PPRV)

52. Transmission
• Close contact
• Aerosols
• Movement of animals
• gathered together in preparation for sales

53. Pathogenesis
• After inhalation of the virus, multiplication
occurs in the pharyngeal and mandibular
lymph nodes
• Viraemia develops within 3 days
• spread to other lymphoid tissues and to the
mucosae of the respiratory and digestive
tracts
• Immunosuppression follow necrosis in
lymphoid tissues
• virus is
• shed in all secretions and excretions

54. Clinical signs
• The incubation period is about 4 days
• Affected goats exhibit fever, dry muzzle and
nasal discharge
• Erosions on the mucous membrane
• Ulcers develop in the mucosae
• Conjunctivitis with ocular discharge
• Diarrhoea, which results in dehydration
• Tracheitis and pneumonia

55. • Mortality rates more than 70%

56. Diagnosis
• Suitable specimens include nasal and ocular
swabs, and scrapings of buccal and mucosae
• Laboratory confirmation is based primarily on
virus isolation in tissue culture and on antigen
detection

57. Control
• A modified live PPRV vaccine

58. Newcastle disease
• The most important avian paramyxovirus
• Newcastle disease was first described in 1926
when severe outbreaks were reported in
Newcastle, England
• chickens, turkeys,pigeons, pheasants, ducks
and geese is susceptible
• Strains of NDV differ in their virulence

59. Five groups or pathotypes
1. Viscerotropic velogenic isolates causing
severe fatal disease characterized by
haemorrhagic intestinal lesions
2. Neurotropic velogenic isolates causing acute
disease characterized by nervous and
respiratory signs with high mortality
3. Mesogenic isolates causing mild disease
4. Lentogenic isolates causing mild or
inapparent respiratory infection
5. Asymptomatic enteric isolates associated

60. • Factors such as the host species, dose, age of
bird and environmental conditions influence
the severity of clinical signs
• Virulent strains may arise from progenitor
viruses of low virulence following passage in
chickens

61. Transmission
• Virus is shed in all excretions and secretions
• Transmission usually occurs by aerosols or by
ingestion of contaminated feed or water
• Virus, which can survive in carcasses for some
weeks, is present in all organs of acutely
affected birds and in eggs.
• wild birds can contribute to the spread of
infection
• Pigeons are susceptible to all strains of NDV
and may play a role in the transmission of
Newcastle disease

62. Pathogenesis
• Viral replication, which occurs initially in the
epithelia of the respiratory and intestinal
tracts
• Spread to the spleen and bone marrow
• Viraemia results in infection of other organs
including lungs, intestine and CNS
• The extent of spread within the body relates
to strain virulence
• the replication of lentogenic strains is
confined to the respiratory and intestinal
epithelia

63. Clinical Signs
• The incubation period is usually about 5 days
• Respiratory, gastrointestinal and nervous signs
occur in chickens
• Highly virulent strains may produce sudden high
mortality
• The mortality rate in fully susceptible flocks may
be close to 100%.
• signs in these flocks include weakness and a
decrease in egg production
• Gasping, oedema of the head and neck and
greenish diarrhoea
• wing paralysis, leg paralysis, torticollis and muscle
• spasms

64. • Mesogenic strains usually cause respiratory
disease
• Lentogenic strains do not produce disease in
adult birds but may produce respiratory signs in
young birds.
• Humans may develop a transitory conjunctivitis if
exposed to high concentrations of NDV

65. Diagnosis
• Tracheal and cloacal swabs from live birds are
suitable for virus isolation
• Haemagglutination-inhibition test using specific
antiserum confirms the presence of NDV
• The mean death time (MDT) using embryonated
eggs has been employed to classify isolates as
velogenic (embryonic death (ED) in less than 60
hours),
mesogenic (ED between 60 and 90 hours)
lentogenic (ED after more than 90 hours)

66. Control
• General control measures
• A combination of vaccination and slaughter
policies is frequently employed

67. Infection caused by bovine respiratory
syncytial virus
• Pulmonary disease, caused by bovine
respiratory syncytial virus
• Infection has been recorded in sheep and
goats with isolates designated as ovine
respiratory syncytial virus and caprine
respiratory syncytial virus

68. Epidemiology
• Infection in cattle is common. Moderate to
severe respiratory signs often develop in
infected calves
• Infection in adult animals is usually mild or
subclinical
• Transmission occurs through aerosols or
through direct contact with infected animals

69. • Transportation, overcrowding or adverse
weather conditions lead to outbreaks of the
disease

70. Pathogenesis
• The virus replicates primarily in the ciliated
epithelium of the respiratory system
• Destruction of bronchiolar epithelium results
in necrotizing bronchiolitis
• Bovine respiratory syncytial virus is considered
to be immunosuppressive
• This effect, along with the accumulation of
cellular debris and exudate in pulmonary
airways, facilitates bacterial proliferation

71. Clinical signs
• Affected animals are typically between 3 and 9
months old
• The incubation period is 2 to 5 days
• Clinical signs, which range from mild to severe,
include fever, nasal and lacrimal discharge,
coughing
• Mild respiratory disease is followed by apparent
recovery
• Mortality in these outbreaks may reach 20%