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Viral Disease in Ruminant. Sukolrat Boonyayatra DVM, M.S. Clinic for Ruminant, FVM. CMU. Disease topic including:. Bovine Ephemeral Fever Bovine Respiratory Syncytial Virus Parainfluenza-3 Bovine Viral Diarrhea Infectious Bovine Rhinotracheitis Foot and Mouth Disease

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viral disease in ruminant

Viral Disease in Ruminant

Sukolrat Boonyayatra

DVM, M.S.

Clinic for Ruminant, FVM. CMU.

disease topic including
Disease topic including:
  • Bovine Ephemeral Fever
  • Bovine Respiratory Syncytial Virus
  • Parainfluenza-3
  • Bovine Viral Diarrhea
  • Infectious Bovine Rhinotracheitis
  • Foot and Mouth Disease
  • Bovine Spongioform Encephalopathy
  • Rinderpest
  • Lumpy Skin Disease
  • Papillomavirus
  • Pseudocowpox
bovine ephemeral fever

BOVINE EPHEMERAL FEVER

(Three-day sickness, Bovine Epizootic Fever, Three-day stiffsickness,

Dragon boat disease)

definition
Definition
  • a noncontagious epizootic arthropod-borne viral disease
  • cattle and water buffaloes
  • sudden onset of fever
  • depression
  • stiffness
  • lameness
  • rapid recovery
etiology
Etiology
  • Family Rhabdoviridae

1. Genus Vesiculovirus

Type Species vesicular stomatitis Indiana virus

2. Genus Lyssavirus

Type Species rabies virus

3. Genus Ephemerovirus

Type Species Bovine ephemeral fever virus

4. Genus Cytorhabdovirus

Type Species lettuce necrotic yellows virus

5. Genus Nucleorhabdovirus

Type Species potato yellow dwarf virus

epidemiology
Epidemiology
  • first described in South Africa in 1906
  • tropical, subtropical, and temperate countries in Africa, Asia, and Australia
  • Thailand since 1984
transmission
Transmission
  • Insect bite
  • not spread from cow to cow
    • Culicoides
    • Mosquitoes
clinical signs 1
Clinical Signs (1)
  • Depressed
  • High fever (105-107 F) with biphasic or triphasic fever
  • Serous ocular and nasal discharge
  • Anorexia
  • Decreased milk production
  • Weight loss
  • Stiffness and lameness
  • More severe in high BW animals
clinical signs 2
Clinical Signs (2)
  • Severe case

Muscle stiffness

Drag feet when forced to walk

Lying down, with hide limbs outstretched-

to relieve muscle cramp

Lie down for three days

clinical signs 3
Clinical Signs (3)
  • Morbidity may reach to 30%
  • Low mortality
  • Causes of the death
    • Pneumonia from secondary infection
    • Muscle damaged and inflammation from long period lying down
    • Pregnancy toxemia (fatty liver syndrome)
gross lesions
Gross lesions
  • the small amounts of fibrin-rich fluid in the pleural,peritoneal, pericardial cavities and joint capsules
  • the synovial surfaces of the spine may have fibrin plaques.
  • The lungs may have patchy edema.
  • Lymphadenitis
  • Focal necrosis can be found in major muscle groups in some cases.
hematology
Hematology
  • an absolute rise in leukocyte numbers
  • a rapid fall in circulating lymphocytes
  • a return to normal levels after 3-4 days
  • The serum fibrinogen level rises to 3-4 times the normal level and returns to normal 1-2 weeks after recovery.
  • The total serum calcium level falls to 1.8 mmol-1 during the febrile phases and returns to normal on recovery.
  • This is the biochemical event that causes the reversible early paralysis.
diagnosis
Diagnosis
  • Clinical signs
  • Sero-conversion: paired serum
    • SN test
    • ELISA
  • Gross lesion
differential diagnosis
Differential Diagnosis
  • Bluetongue
  • Babesiosis
  • Blackleg
treatment
Treatment
  • Recovery with no treatment
  • In severe cases
    • Anti-inflammatory drug: NSAIDs
    • Fluid therapy and calcium
    • Broad spectrum ABO

Recovery period3-4 wks.

prevention and control
Prevention and Control
  • Vector control
  • Vaccine: Attenuated lived virus vaccine (Australia)
bovine respiratory syncytial virus brsv
Bovine Respiratory Syncytial Virus (BRSV)
  • Bovine respiratory disease complex (BRD)
  • Synergistically infect with bacteria to cause pneumonia
    • Pasteurella haemolytica
    • P. multocida
    • Haemophillus somnus
  • 1960: The existence of BRSV
  • 1970: Isolation of BRSV from an outbreak (Switzerland)
  • 1974: Isolation of BRSV in USA
  • 1978: An attenuated lived vaccine was available in Europe.
  • 1984: An attenuated lived vaccine (USA)
  • 1988: Inactivated vaccines were commercially available in USA
etiology1
Etiology
  • Family Paramyxoviridae
    • Genus Pneumovirus
      • Human Respiratory Syncytial Virus (HRSV)
      • Bovine Respiratory Syncytial Virus (BRSV)
      • Ovine Respiratory Syncytial Virus (ORSV)
      • Turkey Rhinotracheitis virus

“Single stranded RNA virus that replicate in the cytoplasm and mature by budding from apical cell membrane”

epidemiology1
Epidemiology
  • Worldwide distribution in the cattle population
  • High seropositive ranging from 65-75% (USA) before vaccine was introduced
  • BRSV was determined to be involved in
    • 14% of respiratory infections in UK
    • 32% of outbreaks of calf pneumonia in North Ireland
    • 53% of respiratory outbreaks in Belgium
    • 71% of the outbreaks of calf pneumonia in Minnesota
clinical signs
Clinical signs
  • Initial signs
    • A decreased appetite
    • Milk depression
    • Nasal and lacrimal discharge (serous to mucoid)
    • Increased respiratory rate
  • Progress signs
    • Elevated BT (104-108 F)
    • Dyspnea
    • Opened mouth breathing
    • Hyperpnea (abdominal breathing)
    • Cough
    • Increased bronchial and bronchovesicular sounds, and fine crackles
    • Decreased milk production
  • Duration of disease is variable, lasting from 1-2 weeks
  • Calf :more severe
postmortem findings
Postmortem findings
  • Atypical interstitial pneumonia (AIP)
  • Gross findings:
    • Initially involves the cranioventral lobes
    • Calves die from severe lung edema and interstitial pneumonia
    • Lung fail to collapse
    • Subpleural emphysema
    • Bronchial and mediastinal lymphnodes are enlarged and edema.
histopathological findings
Histopathological findings
  • Vary depending on stage of viral infection and the secondary bacterial infection
  • Bronchointerstitial pneumonia with severe bronchiolitis in cranioventral part
  • Alveolar edema and emphysema are diffusely present
  • Multinucleated syncytial cells (bronchiolar epithelium)
  • Bacterial pneumonia: suppurative or fibrous bronchopneuminia
slide27

Lung. Multinucleated syncytial cell is prominent within the bronchiole and appears to be arising from the epithelial layer. The lumen is packed with neutrophils. A few neutrophils are also transmigrating the bronchiolar wall and are in the adjacent atelectactic parenchyma. 40X

pathogenesis 1
Pathogenesis (1)
  • Virus infects epithelial cells in the pulmonary airways
  • Cytopathic changes and necrosis
  • Necrotizing bronchiolotis
  • Alveolar epithelium: interstitial pheumonia
  • Mixed inflammatory cell infiltration with a predominance of neutrophils
pathogenesis 2
Pathogenesis (2)
  • May suppress the immune system
  • Atypical interstitial pneumonia
  • Necrotizing bronchiolitis:
    • Extensive viral replication at bronchiolar epithelium
    • Dyspnea and forced expiration
    • Emphysema
immune response to infection
Immune response to infection
  • Both dies and recovery from clinically severe have antibody responses to proteins of virus (F and N): may not protective effect
  • Colostrum IgG-1 do not prevent the infection but make disease less severe
  • Cell-mediated immune responses may play a protective role
differential diagnosis1
Differential diagnosis
  • Parainfluenza-3
  • IBR
  • Mycoplasma spp.
  • Haemophilus somnus
  • etc…
diagnosis1
Diagnosis
  • Clinical signs
  • Necropsy
  • Laboratory Diagnosis

Viral isolation

Antigen Detection Enzyme Immunoassay

Immunofluorescent Antibody Staining

Detection of Nucleic acids: PCR

Serological Diagnosis

treatment 1
Treatment (1)
  • ABO: Bacterial pneumonia

- Pasteurella haemolytica

    • P. multocida
    • Haemophilus somnus
  • Anti-inflammatory agents
    • Corticosteroid
    • Antihistamine
    • NSAIDs
treatment 2
Treatment (2)
  • Antiviral therapy: Ribivarin: HRSV
  • Immunotherapy: Hyperimmune serum : HRSV
  • Supportive treatment
    • Dehydration and electrolyte imbalances
    • Anorectic animals: B-complex vitamins
prevention and control1
Prevention and Control
  • Management:
    • Stress, ventilation, maternity pen, calf-rearing area
  • Immunization
    • Passive Immunization: Modify severity of disease
    • Vaccination: Modified-lived BRSV vaccine

Inactivated BRSV vaccine

slide38

IBR, BRSV, PI-3, BVD killed vaccine + Haemophilus somnus bacterin

Killed vaccine protects against IBR, BVD, PI3 and BRSV, and Pasteurella haemolytica and Haemophilus.

infectious agents identified in the bovine respiratory disease complex
Viruses

- Bovine herpesvirus type1 (IBR)

- Bovine herpesvirus type3 (malignant catarrhal fever virus)

- Bovine herpesvirus type4 (DN-599, Movar 33/63)

- Bovine adenovirus types1 to 8

- Bovine parainfluenza virus type3

- Bovine respiratory syncytial virus

- Bovine viral diarrhea virus

- Reovirus types1 to 3

- Bovine Rhinovirus types1 and 2

- Bovine Enterovirus types1 to 7

- Calcivirus

- Influenza virus (reported from Russia)

Bacteria

Pasteurella haemolytica

Pasteurella multocida

Haemophilus somnus

Mycoplasma mycoides subspecies mycoides

Mycoplasma bovis

Mycoplasma dispar

Ureaplasma spp.

Chlamydial agent

- Chlamydia psittaci

Infectious Agents Identified in the Bovine Respiratory Disease Complex
parainfluenza 3 virus pi 3
Parainfluenza-3 Virus (PI-3)
  • Enzootic Pneumonia
  • Etiology
    • Family Paramyxoviridae
    • Genus Paramyxovirus
pathogenesis
Pathogenesis
  • Virus infects ciliated respiratory epithelium of the upper and lower respiratory tracts and also alveolar macrophage.
  • Reduce alveolar macrophage
  • Facilitate pulmonary bacterial colonization
  • Infection of calves is rarely fatal, producing mild or subclinical cases.
epidemiology2
Epidemiology
  • World wide distribution
  • Subclinical
  • Stress produce more severe clinical case
  • Disease is commonly seen in calves 2-8 mths.
  • Thailand:
    • 1994- 1,788 of 2,070 bulk milk samples were antibody positive (86.3%)
transmission1
Transmission
  • Aerosal
  • Direct contact
clinical signs1
Clinical signs
  • Fever 104-105 F
  • Rhinitis and pneumonia
  • Cough (easily by pinching the trachea)
  • Recovery in few days
diagnosis2
Diagnosis
  • Virus isolation
  • Immunofluorescent or immunoperoxidase test
  • Serology: Hemagglutination-Inhibition (HI) Viral Neutralization
bovine viral diarrhea virus bvdv
Bovine viral diarrhea virus (BVDV)
  • BVD was first recognised in Canada and the United States in the 1940's.
  • In 1987, outbreaks of BVD occurred affecting veal calves and older cattle in New York and Pennsylvania.
  • Beginning in 1992, an outbreak of BVD affected veal calves and dairy herds in Quebec.
  • Today BVDV infections are seen in all ages of cattle throughout the world and has significant economic impact due to productive and reproductive losses.
etiology2
Etiology
  • RNA virus
    • Family Flaviviridae
      • Pestivirus

2 biotypes: cytopathogenic (cp) or noncytopathogenic (ncp)

Both biotypes of BVDV infect cattle and cause disease, but only ncp BVDV causes persistent infections.

effect of bvdv infection on cattle
Effect of BVDV infection on cattle
  • Reproductive failure: Embryonic death, Mummification, Abortions, Stillbirths
  • Repeated breeding syndrome
  • Immunosuppression
  • Congenital defects: Cerebellar hypoplasia, Cataract
  • Persistent infections: Carrier animals
  • Acute BVD
  • Bovine respiratory tract disease
  • Mucosal disease
transmission2
Transmission
  • Persistent infected animals
  • Acute infected cattle
  • Semen
  • Embryo transfer
  • Rectal sleeves
  • Contaminated water
  • Biting insect (experimentally)
effect of pregnant cow infection
Effect of Pregnant Cow Infection

Days pregnancyEffect

0-40 Embryonic death

40-120 Abortion or

Persistent Infected calf

90-160 Abortion or

Congenital defect

160-Parturition Abortion or normal calf

critical concerns
Critical concerns
  • Prenatally infected cattle and that are persistently viremic after birth
  • Postnatally infected cattle that are transiently viremic for about 2 to 10 days or possibly longer

Both groups of animal are considered as source of infection in herd.

prevalence
Prevalence
  • Prevalence survey in many areas of cattle raising countries: 60-80% of animals antibody positive
  • 1-2% PI animals
  • Variation in cattle population structure and herd management can account for the difference.
interspecies transfer
Interspecies transfer
  • Sheep
  • Wild ruminants
    • Natural infections (caribou: 40-100%)
    • Transfer (llamas: dead end)
prevalence of bvdv infections
Prevalence of BVDV infections

Seroprevalence Antigen/virus isolation

United Kingdom + +

Germany NK +

Denmark + +

Sweden + +

Norway + NK

United state + +

Thailand +(Bulk milk) NK

NK: Not Known

thailand
Thailand
  • Muaglek area: 4.4% (7/160) of dairy herds were positive for antibodies to BVDV in bulk tank milk samples (Aiumlamai et al, 1992)
  • And colleague reported 22.8% of bulk tank milk samples (473/2,070) form all over the country; Muaglek and area close by (Livestock area1) had 15.8% (Veerakul et al, 1996)
  • There are evidences of BVDV infections among pigs in Thailand (Ornveerakul et al, 1994)
  • 158 of 522 bulk milk samples are antibody positive in survey study (Ajariyakhajorn, 1999)
  • Evidences of natural exposure of BVDV in dairy cattle
clinical signs 11
Clinical signs (1)
  • Acute BVDV of young animals, 6-24 months old
    • Fever, ulcers in mouth, throat (esophagus) and intestine, diarrhea (some bloody), high mortallity

Mild infection: off feed, depressed, mild diarrhea and recovery

Subclinical infection with no visible signs are most common

Colostral antibodies protect most calves until 4-8 months

clinical signs 21
Clinical signs (2)
  • Acute BVDV in adult cattle (> 2 years)
    • Fever, off feed, decreased milk production, diarrhea
    • Occasionally ulcers in mouth
    • Outbreaks occur in unvaccinated cattle after introduction of new animals shedding BVD or in first calf heifers when they enter the milk string
    • During outbreaks up to 25% of adult cattle may become ill
slide67

Figure 1: Choroid plexus, filly: EHV-1 within endothelium and circulating macrophages. Peroxidase immunohistochemistry and hematoxylin.

slide68

Figure 2: Lung, calf persistently infected with bovine pestivirus (BVD virus) with bacterial bronchopneumonia. BVDV is contained within the cytoplasm of numerous cells (macrophages, endothelia, alveolar epithelium). Peroxidase immunohistochemistry and hematoxylin.

diagnosis 1
Diagnosis(1)
  • Virus Isolation
    • Persistent Infection 
      • Adults — Serum 
      • Calves — Serum if pre colostrum or older than 4 months of age. 
      • Calves — Whole blood if post colostrum and less than 4 of months age.
    • Acute Infection
      • Whole blood. 
    • Post Mortem 
      • Spleen, Peyer's patch, lymph nodes.
    • Abortion 
      • Spleen, thymus. 
diagnosis 2
Diagnosis(2)
  • Serology

Virus neutralization

FA

Immunohistochemistry test

ELISA

PCR

herd screening
Herd screening
  • Bulk milk tank (Antibodies or PCR)
  • Pre immunization antibody titers at 6-12 months of age (serology) (5-10% of unvaccinated calves)
  • Test all animals
    • Skin Biopsy : Immunoperoxidase (IPX)
    • Blood from <4 mths, serum >4 mthsfor
      • Virus isolation
      • Test again in 3 months (isolation + serology)
prevention and control2
Prevention and control
  • Elimination of Carrier Animals
    • Herd testing
    • Test calves at birth
  • Immunization
    • Modified live or killed vaccines
    • Maximize immunity pre-breeding and early gestation
  • Biosecurity
    • Closed herd
    • Test all new arrivals
    • Test newborns of new arrivals
    • Quarantine all new arrivals and reintroduced cattle for 21 days
etiology3
Etiology
  • Herpes virus (DNA virus)
    • 3 genotypes
      • BHV1: IBR
      • BHV2: Infectious pustular vulvovaginitis (IPV)

Infectious balanoposthitis (IBP)

      • BHV3: Neurologic signs
transmission3
Transmission
  • Nasal and ocular viral shedding is detected for 10-14 days after infection.
  • Aerosal
  • Venereal transmission
  • Carrier animals : virus persist in trigeminal ganglia-reactivated-viremia-shedding
pathogenesis1
Pathogenesis
  • In the respiratory disease syndrome, the virus replicates in the nasal cavity and the mucosa of the upper respiratory tract resulting in inflammation of the nasal cavity, larynx and trachea.
  • The virus may spread to the eyes causing ocular lesions.
  • The virus can become systemic and localize in various tissues including the placenta that results in fetal infection and abortion.
  • Localization in the brain leads to encephalitis.
clinical signs 12
Clinical signs(1)
  • The incubation period can be variable.
  • In feedlot cattle the disease tends to occur 10-20 days after the introduction of susceptible cattle.
  • Nasal discharge
  • Inflammation of nostrils (Red nose)
  • Erosion of nasal mucosa
clinical signs 22
Clinical signs(2)
  • Lacrimation
  • Conjunctivitis
  • High fever
  • Inappetance
  • Drop in milk production
  • late abortion (between the 5th and 8ht month of pregnancy) and placenta retention
  • 10% mortality in severe outbreak
gross lesions1
Gross lesions
  • Swelling and congestion of respiratory mucosal surfaces
  • Secondary bacterial infections produce mucopurulent nasal discharge
  • Cervical lymphnode become swallen
  • Conjunctivitis (edema and inflammation) resulting in excessive lacrimation
  • Clear ocular discharge progresses to mucopurulent
histopathological lesions
Histopathological lesions
  • Secondary bronchopneumonia or interstitial emphysema due to labored breathing
  • Rhinitis
  • Laryngotracheitis
  • Bronchitis
epidemiology3
Epidemiology
  • Infectious Bovine Rhinotracheitis (IBR) was originally recognized as a respiratory disease of feeder cattle in the western United States during the early 1950s.
epidemiology thailand
Epidemiology (Thailand)
  • 1990- Survey in central part of Thailand (12 provinces) 558/1,780 (31.3%) serum samples were positive (SN>1:2)
  • 1990- BHV1 was isolated from nasal and vaginal swab of seropositive cow after administration of dexamethazone
  • 1992- 26/40 bulk milk samples were antibody positive (37.3%)
diagnosis3
Diagnosis
  • Clinical signs
  • Necropsy
  • Laboratory diagnosis
    • Virus isolation
    • Direct fluorescent antibody test
    • ELIZA (serum and milk)
    • SN (serum)
    • PCR
vaccination 1
Vaccination(1)
  • Replicating IBR Vaccine
    • Modified Live Virus - should not be used in pregnant cows or in calves nursing pregnant cows.
      • one injection to provide protection.
      • A booster is recommended when an IBR exposure is anticipated.
  • Non-Replicating IBR Vaccine
    • Killed Virus and Chemically Altered Virus are safe to use in all cattle.
      • Requires two doses initially and an annual booster to provide adequate protection.
vaccination 2
Vaccination(2)
  • Intra-Nasal IBR Vaccine
    • Intra-nasal IBR Vaccine is safe to use in all age cattle regardless of pregnancy status.
    • short-lived Immunity
    • The vaccine of choice to stimulate rapid resistance when an outbreak of IBR is occurring or is anticipated.
    • A booster vaccination with a replicating or a non-replicating form of IBR vaccine is required to provide longer protection.
  • The basic principle of establishing an immune population before a disease appears is particularly important in the control of IBR, especially the abortion form of IBR.
prevention and control3
Prevention and Control
  • Once introduced it is difficult and expensive to eradicate IBR/IPV especially because as the disease establishes animals tend to become unapparent carriers. Systematic testing and elimination of positives has been successful in some countries. 
bovine leukosis
Bovine Leukosis
  • Etiology
    • Family Retroviridae (Oncogenic RNA virus)
      • Genus Bovine leukaemia virus (BLV)
  • 2 forms
    • Enzootic form (Enzootic Bovine Leukosis)
    • Sporadic form
epidemiology4
Epidemiology
  • Worldwide distribution
    • Prevalence increases with age
    • Dairy cattle generally have higher prevalence rates than beef cattle
      • Management factors
      • Breed susceptibility differences?
clinical signs 13
Clinical signs (1)
  • Enzootic Bovine Leukosis
    • Persistent lymphocytosis (~40% of infected cow)
    • Most infected animals (~70%) do not develop the disease.
    • Cattle 4-8 years old
    • Weight loss with/with out no appetite
clinical signs 23
Clinical signs (2)
  • Anemia
  • Decreased milk yield
  • Enlarged external and enlarged internal lymph nodes
  • Partial paralysis of the hind legs
  • Abnormal breathing
  • Bulging eyes
  • Diarrhea
  • Constipation
clinical signs 31
Clinical signs (3)
  • Sporadic form
    • Rarely cases
    • Calve <3 years old
    • 3 forms of pathological lesions
      • Calf form : animals less than 6 mths old

general lymphadenopathy

widespread tumour metastasis

      • Thymic form : animals of 6-8 mths old

thymic tumour

sometimes extension into the thorax

      • Skin leucosis : a non fatal form

Young adults develop superficial cutaneous tumour that disappear spontaneously after a few weeks.

gross lesions2
Gross lesions
  • Firm white tumour masses in any organs and more commonly in lymph nodes.
  • Organs most frequently involved:
    • abomasum,
    • right auricle of the heart,
    • spleen, intestine, liver, kidney,
    • omasum, lung, and uterus
diagnosis4
Diagnosis
  • Virus isolation
  • PCR
  • Sheep inoculation
  • Serology – can be first detected 3-8 wks after infection

- calves < 6 mths old can be false positive

    • Agar Gel Immunodiffusion (AGID)
    • Milk ELISA
transmission4
Transmission
  • Mechanical transmission
    • Blood suckling insects: Tabanus spp.
  • Natural transmission
    • Transfer of infected cell Ex. Parturition.
  • Artificial transmission
    • Blood contaminated needles
    • Surgical equipment
    • Gloves used for rectal examination
important 1
Important(1)
  • Direct Losses
    • Condemnation at slaughter
    • Higher culling rates
    • Decreased reproductive performance
    • Decreased milk yields
      • Most all economic analyses have failed to distinguish various clinical entities of BLV
important 2
Important(2)
  • Indirect Losses
    • Loss of export market
    • Loss of sales to AI industry
    • Loss of sales to embryo transfer industry
    • Loss of consumer confidence
    • Expenses involved in status testing
important 3
Important(3)

Zoonotic Potential

  • BLV will infect human cells
  • No study has linked BLV to human disease
    • Most not willing to deny potential exists
    • Molecular technology should be able to provide definitive answer
prevention and control4
Prevention and Control
  • Use individual sterile needles for transdermal injection or blood collection.
  • Disinfect tattoo equipment between animals.
  • Use electric dehorners, or disinfect dehorning equipment between animals.
  • Replace examination gloves and sleeves between animals.
  • Use milk replacer to feed preweaned calves.
  • Heat-treat or pasteurize colostrum.
  • Use BLV-seronegative recipients for embryo transfer.
  • Wash and rinse instruments in warm water, then submerge in an appropriate disinfectant.
eradication
Eradication
  • Tested all calves >six months of age
  • removal or segregation of infected cattle from non-infected cattle
  • Three consecutive negative herd tests at 60- to 90-day intervals are then required for the herd to be certified as BLV-free.
  • recertified annually by a repeated negative test of the entire herd
etiology4
Etiology
  • Family Picornaviridae
  • Genus Aphthovirus
  • Serotypes
    • O, A, C, Asia1, SAT1, SAT2 and SAT3
    • Asia1 in Asia and Middle East
    • SAT1-3 in Africa
    • O, A, C in European country and world wide
    • Free from FMD: Scandinavia, Great Britain, North and Central America, Australia and New Zealand
resistant and sensitivity
Resistant and Sensitivity
  • Sensitive
    • Sunlight
    • UV
    • Temp >50 C
    • pH changes
slide118
Host
  • All domestic and wild cloven-footed animals
  • Susceptibility: cattle>pig>sheep>goat
  • Pigs are amplifying host which can cause airborne transmission.
transmission5
Transmission
  • 2 main routes of infection:
    • Aerosal
    • Ingestion
  • Modes of Transmission:
    • Direct contact
    • Indirect contact (mechanical transfer)
      • Air borne spread up to 10 kms
factors favoring the spread of fmd
Factors favoring the spread of FMD
  • 1. Massive production and excretion of FMDV by infected animals (incubatory carrier)
  • 2. Prolonged survival of FMDV outside animal body
  • 3. Airborne spread of virus over long distances
  • 4. Persistent carrier stage in domestic and wild animals recovered from apparent and inapparent infection.
  • 5. The ready spread of infection either by direct contact or through animal products, formites or aerosals.
  • 6. The multiplicity of virus antigenic forms which do not confer cross-protection against each other.
clinical signs 14
Clinical signs(1)
  • Incubation period 2-14 days
  • Fever (usually fall in about 48 hrs)
  • Anorexia
  • Depression
  • Drop in milk production
  • Development of vesicles on mouth and feet
  • Ruptured vesicles leading to salivation and lameness
clinical signs 24
Clinical signs (2)
  • Vesicular lesions occuring on udder and teats may become permanently infected.
  • Loss of condition and cessation of growth which may prolonged.
  • Lameness is prominent sign in pig.
  • Mortality is limited to young animals.
  • Inapparent infection: goat>sheep>pig>cattle
biological basis for vaccination 1
Biological Basis for Vaccination (1)
  • Lack of cross-protection
  • RNA virus, like FMDV, mutate at a rate higher than DNA virus.
  • The wide range of antigenic variants within the serotypes.
  • Vaccinated ruminants may become subclinical carrier of FMDV following contact with virus.
  • Parenteral immunization with inactivated FMDV vaccine is poor stimulator of mucosal humoral immunization.
biological basis for vaccination 2
Biological Basis for Vaccination (2)
  • The rapidity of FMDV replication allows little opportunity for immunological memory to play a role in immunity to infection.
  • Repeated prophylactic vaccination is necessary for the maintenance of protective serum antibody titers in susceptible livestock.
  • Recovery from and protection against reinfection with FMD are related to the development of serum-neutralizing antibody in the cattle.
the role of vaccination in fmd control strategy 1
The Role of Vaccination in FMD Control Strategy (1)
  • Antigenically appropriate vaccine
  • Regularly ascertained the relationship between field isolates and the vaccine strains
  • In calf, the primary vaccination should be 4 months.
  • Revaccination may be given 4-12 mths intervals depending upon local epidemiological advice and the quality of vaccine.
the role of vaccination in fmd control strategy 2
The Role of Vaccination in FMD Control Strategy (2)
  • Prophylactic
    • Annually, bi-annually, tri-annually
    • Common practice: >1 strain of a particular serotype in FMD vaccine
    • Mass prophylactic vaccination
  • Emergency in FMD free country
    • Slaughter of all infected and susceptible in-contacted animals
    • Define zone around the outbreak
    • Control virus spread by movement control and disinfection
    • Emergency vaccination: ring vaccination
the role of vaccination in fmd control strategy 3
The Role of Vaccination in FMD Control Strategy (3)
  • Emergency in FMD infected country
    • Treat animal, mild disinfection, protective dressing to inflammed area, administration of flunixin meglumine.
    • Declare infected zone, ring zone within a radius of 16-24 km.
    • Control human and animal movement
    • Disinfection: 1-2% of NaOH or Formaline,

4% of Sodium carbonate

    • Mass Vaccination
cautions and remarks
Cautions and Remarks
  • The maintenance of a serum antibody-negative national herd is essential for international trade.
  • Find the source of outbreak
  • Confirm subtype of virus
    • Complement fixation test
    • ELISA
    • RT-PCR and sequencing for molecular epidemiology
  • Careful imitative virus
  • The carrier stage in vaccinated and unvaccinated cattle may persist for as long as 6 mths and be capable of causing new out break in all species.
etiology5
Etiology
  • Prion protein

(PrP)

history
History
  • Great Britain in 1985:
    • Dead cattle with clinical signs of nervous system abnormality: atxia, salivation, etc.
    • “Mad cow disease”
    • 167,000 cases and death animals
    • Infectious agent: prion protein (PrP)
    • Contaminated in meat and bone meal
jekyll and hydes prions
Jekyll and Hydes Prions

The wild type prion (PrPc) is found in the secretory pathway of

cells expressing the protein(1)and moves to the plasma

membrane where it is anchored by its GPI tail (2).There it may

bind to an extracellular ligand (possibly copper) (3) before being

cycled from the membrane into endocytic vesicles (4). At some

point its cargo is released and the protein either passes to the

lysozome for degradation or back to surface for another round of

ligand binding. In this respect it resembles many other

membrane-resident proteins. The pathogenic form(PrPSc) also

finds its way to endocytic vesicles where it co-opts some of the

wild type form to become pathogenic (5). PrPSc is resistant to

degradation, a hallmark of the infectious form, so accumulates.

Neurotoxicity is probably linked to the conversion event itself,

perhaps through its interference with normal PrPc turnover,

because there is considerable evidence to show that the accrued

PrPSc is not inherently toxic.

resistance to physical and chemical action
RESISTANCE TO PHYSICAL AND CHEMICAL ACTION
  • Temperature:Preserved by refrigeration and freezing. Recommended physical inactivation is porous load autoclaving at 134–138°C for 18 minutes (this temperature range may not completely inactivate).
  • pH:Stable over a wide range of pH.
  • Disinfectants:Sodium hypochlorite containing 2% available chlorine, or 2 N sodium hydroxide, applied for >1 hour at 20°C, for surfaces, or overnight for equipment.
  • Survival:Recommended decontamination measures will reduce titres but may be incompletely effective if dealing with high titre material, when agent is protected within dried organic matter, or in tissue preserved in aldehyde fixatives. Survives in tissues post-mortem after a wide range of rendering processes. Related hamster scrapie infectivity can survive interment in soil for 3 years and dry heat of 1 hour at temperatures as high as 360°C.
transmission6
Transmission
  • BSE occurs as a result of dietary exposure to feedstuffs containing infected meat and bone meal (MBM).
  • No cases of BSE have been recorded as a result of iatrogenic transmission, but this is a potential means.
  • There is some evidence of a maternally associated risk for calves born to affected cows. The biological mechanisms involved are unknown, but this effect is insignificant in the epidemiology.
  • There is no evidence of horizontal transmission of BSE between cattle.
  • Occurrence of new variant Creutzfeldt-Jakob disease (CJD) suggests zoonotic potential via oral exposure.
sources of agent
SOURCES OF AGENT
  • Central nervous system (including eye) of naturally occurring clinically affected cases. Infectivity detected in the distal ileum of experimentally infected cattle is presumed associated with lymphoreticular tissues.
clinical signs 15
Clinical signs (1)
  • Mean incubation period is 4-5 years.
  • Subacute or chronic, progressive disorderThe main clinical signs are neurological:
    • Apprehension, fear, increased startle, or depression
    • Hyper-aesthesia or hyper-reflexia
    • Adventitial movements: muscle fasciculations, tremor and myoclonus
    • Ataxia of gait, including hypermetria
    • Autonomic dysfunction: reduced rumination, bradycardia and altered heart rhythm.
clinical signs 25
Clinical signs (2)
  • Pruritis, seen in scrapie, occurs also but is not usually a prominent sign.
  • Loss of body weight and condition.
lesions
Lesions
  • There are no gross post-mortem changes.
  • A characteristic spongiform encephalopathy is present in most cases.
diagnosis 11
Diagnosis(1)
  • Identification and Isolation of the agent
    • There is no available diagnostic test for the BSE agent.
    • Bioassay of brain tissue of terminally affected cattle or other species by parenteral inoculation of mice is the only method currently available for detection of infectivity. This is impractical because of minimum incubation periods approaching 300 days.
diagnosis 21
Diagnosis(2)
  • Serological test
    • The absence of detectable immune responses in BSE or other transmissible spongiform encephalopathies precludes serological tests.
  • Other test
    • Histopathological examination of the brain from clinically affected cases for characteristic bilaterally symmetrical spongiform changes of grey matter and subsequent immunohistochemical demonstration of accumulations of disease specific PrP.
    • Examination for fibrils, homologous with scrapie-associated fibrils (SAF) by electron microscopy or electrophoretic separation and immunoblotting for detection of the disease specific isoform of PrP in extracts of unfixed, fresh or frozen brain.
prevention and control5
Prevention and control
  • Free countries
    • Targeted pathological surveillance to occurrences of clinical neurological disease.
    • Safeguards on importation of live ruminant species and their products.
    • Policy and procedures for importation of embryos.
  • Countries with cases in cattle
    • Slaughter and compensation for ascertainment of cases.
    • Controls on recycling of mammalian protein.
    • Effective identification and tracing of cattle.

http://www.oie.int/eng/maladies/fiches/a_B115.htm

thailand actions to prevent bse
Thailand Actions to Prevent BSE
  • กระทรวงเกษตรและสหกรณ์
    • ไม่อนุญาตให้นำเข้าอาหารสัตว์ที่มีส่วนผสมของเนื้อ กระดูก และเลือด จากประเทศอังกฤษ (13 มิ.ย. 2540)
  • กรมปศุสัตว์
    • ให้ชลอการนำเข้าโค และอาหารสัตว์ที่มีส่วนผสมของเนื้อของสัตว์เคี้ยวเอื้องจากกลุ่มประเทศยุโรป (England, Denmark, etc.)
  • สถาบันวิจัย และมหาวิทยาลัย จัดเผยแพร่ความรู้สู่สาธารณชน
    • Review article: Prof. Peerasak Chantaraprateep et al., 1998. Thai J Vet Med. Vol. 28, No. 1:17-55
rinderpest

Rinderpest

Cattle Plague

etiology6
Etiology
  • Family Paramyxoviridae
  • Genus Morbilivirus
  • Only one serotype
  • Susceptible species
    • Cattle and buffaloes
    • Sheep and goats
    • Asiatic pigs
    • Wildlife
history1
History
  • Host: cattle, sheep, goats, camels, wild ruminants and pigs
  • First established in 1754
  • A major disease of livestock through most of the 19th century in Great Britain
  • An OIE Class A disease reflecting its serious economic impact
transmission7
Transmission
  • By direct or close indirect contacts
  • Shedding of virus begins 1-2 days before pyrexia in tears, nasal secretions, saliva, urine and faeces
  • Blood and all tissues are infectious before the appearance of clinical signs
  • Infection is via the epithelium of the upper or lower respiratory tract
  • No carrier state
clinical signs 16
Clinical signs (1)
  • Incubation period: 3 to 15 days (usually 4 to 5 days)
  • Peracute form
    • This form is seen in highly susceptible and young animals.
    • The only signs of illness are a fever of 104-107o F (40-41.7o C), congested mucous membranes, and death within 2 to 3 days after the onset of fever.
clinical signs 26
Clinical signs (2)
  • Classical form: four stages
    • Incubation period
    • Febrile period (40-42°C) with depression, anorexia, reduction of rumination, increase of respiratory and cardiac rate
    • Mucous membrane congestion (oral, nasal, ocular and genital tract mucosae)
      • intense mucopurulent lachrymation and abundant salivation
      • anorexia - necrosis and erosion of the oral mucosae
      • this phase lasts 2-3 days
    • Gastrointestinal signs appear when the fever drops: profuse haemorrhagic diarrhoea containing mucus and necrotic debris. Severe tenesmus. Dehydration, abdominal pain, abdominal respiration, weakness, recumbency and death within 8-12 days. In rare cases, clinical signs regress by day 10 and recovery occurs by day 20-25
slide173

Conjunctivitis and mucopurulent exudate

in the early stage of RP infection.

slide175

Excessive salivation

in the early stage

of RP infection.

clinical signs 32
Clinical signs (3)
  • Subacute form
    • Clinical signs limited to one or more of the classic signs.
    • Low mortality rate
  • Atypical form
    • Irregular pyrexia and mild or no diarrheoa.
    • The lymphotropic nature of rinderpest virus favours recrudescence of latent infections and/or increased susceptibility to other infectious agents.
gross lesions3
Gross lesions
  • Either areas of necrosis and erosions, or congestion and haemorrhage in the mouth, intestines and upper respiratory tracts
  • Enlarged and oedematous lymph nodes
  • White necrotic foci in Peyer's patches
  • 'Zebra striping' in the large intestine
  • Carcass emaciation and dehydration
slide182

Hyperemia of the cecum and colon with accentuation

of lesions (hemorrhage) at the ceco-colic junction

epidemiology5
Epidemiology

The Global Rinderpest Eradication Program (FAO)

eradication1
Eradication
  • Only one serotype
  • Recovered or properly vaccinated animals are immune for life
  • No vertical transmission, arthropod vector, or carrier state
  • RPV is an ideal virus to be targeted for eradication.
  • Thailand is a rinderpest free country.
lumpy skin disease

Lumpy Skin Disease

Pseudo-urticaria, Neethling virus disease, exanthema nodularis bovis, knopvelsiekte

etiology and host
Etiology and Host
  • Family Poxviridae
  • Genus Capripoxvirus
  • Host: Cattle, Buffaloes, Giraff
  • First described in Northern Rhodesia in 1929
  • An OIE list A disease
transmission8
Transmission
  • Insect vector
    • Mosquitoes (e.g. Culex mirificens and Aedes natrionus)
    • Flies (e.g. Stomoxys calcitrans and Biomyia fasciata)
clinical signs2
Clinical signs
  • Inapparent to severe disease
  • Fever (40-41.5°C) either transitory or lasting up to 2 weeks
  • Swellings or nodules in the skin and generalization.
  • Depression, anorexia, excessive salivation, oculonasal discharge, agalactia and emaciation
  • The nodules may become necrotic and sometimes deep scabs form (which are called 'sittast')
  • Lameness resulting from inflammation and necrosis of tendons, and from severe oedema of brisket and legs
  • Superficial lymph nodes enlarged to four-to-ten times their normal size
  • Complications: severe mastitis and loss of the quarter

permanent lameness

abortion, intrauterine infection, and temporary sterility in bulls and cows may occur.

eradication2
Eradication
  • Slaughter of all infected and in-contact cattle
  • Vaccination
questions

Questions?

“About the test”