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BOVINE EPHEMERAL FEVER.ppt

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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
   Bovine Spongioform Encephalopathy
   Rinderpest
   Lumpy Skin Disease
   Papillomavirus
   Pseudocowpox
BOVINE EPHEMERAL
FEVER

(Three-day sickness, Bovine Epizootic Fever,
Three-day stiffsickness,
Dragon boat disease)
Definition

   a noncontagious epizootic arthropod-borne
    viral disease
   cattle and water buffaloes
   sudden onset of fever
   depression
   stiffness
   lameness
   rapid recovery
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

   first described in South Africa in 1906
   tropical, subtropical, and temperate countries
    in Africa, Asia, and Australia
   Thailand since 1984
Transmission

   Insect bite
   not spread from cow to cow
       Culicoides
       Mosquitoes
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)
   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)
   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

   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

   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

   Clinical signs
   Sero-conversion: paired serum
       SN test
       ELISA
   Gross lesion
Differential Diagnosis

   Bluetongue
   Babesiosis
   Blackleg
Treatment

   Recovery with no treatment
   In severe cases
     Anti-inflammatory drug: NSAIDs
     Fluid therapy and calcium

     Broad spectrum ABO

    Recovery period 3-4 wks.
Prevention and Control

   Vector control
   Vaccine: Attenuated lived virus vaccine
    (Australia)
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
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”
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
   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

   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

   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
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
Immunohistochemistry staining
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)
   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

   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 diagnosis

   Parainfluenza-3
   IBR
   Mycoplasma spp.
   Haemophilus somnus
   etc…
Diagnosis

   Clinical signs
   Necropsy
   Laboratory Diagnosis
    Viral isolation
    Antigen Detection Enzyme Immunoassay
    Immunofluorescent Antibody Staining
    Detection of Nucleic acids: PCR
    Serological Diagnosis
Treatment (1)

   ABO: Bacterial pneumonia
    - Pasteurella haemolytica
       P. multocida
       Haemophilus somnus
   Anti-inflammatory agents
       Corticosteroid
       Antihistamine
       NSAIDs
Treatment (2)
   Antiviral therapy: Ribivarin: HRSV
   Immunotherapy: Hyperimmune serum :
    HRSV
   Supportive treatment
       Dehydration and electrolyte imbalances
       Anorectic animals: B-complex vitamins
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
                  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                                    Bacteria

- Bovine herpesvirus type1 (IBR)           -   Pasteurella haemolytica
- Bovine herpesvirus type3 (malignant      -   Pasteurella multocida
     catarrhal fever virus)                -   Haemophilus somnus
- Bovine herpesvirus type4 (DN-599,        -   Mycoplasma mycoides subspecies
     Movar 33/63)                              mycoides
- Bovine adenovirus types1 to 8            -   Mycoplasma bovis
- Bovine parainfluenza virus type3         -   Mycoplasma dispar
- Bovine respiratory syncytial virus       -   Ureaplasma spp.
- Bovine viral diarrhea virus
- Reovirus types1 to 3                     Chlamydial agent
- Bovine Rhinovirus types1 and 2
- Bovine Enterovirus types1 to 7           - Chlamydia psittaci
- Calcivirus
- Influenza virus (reported from Russia)
Parainfluenza-3 Virus (PI-3)

   Enzootic Pneumonia
   Etiology
       Family Paramyxoviridae
       Genus Paramyxovirus
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.
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%)
Transmission

   Aerosal
   Direct contact
Clinical signs

   Fever 104-105 F
   Rhinitis and pneumonia
   Cough (easily by pinching the trachea)
   Recovery in few days
Diagnosis

   Virus isolation
   Immunofluorescent or immunoperoxidase
    test
   Serology: Hemagglutination-Inhibition (HI)
               Viral Neutralization
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.
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

   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
Transmission

   Persistent infected animals
   Acute infected cattle
   Semen
   Embryo transfer
   Rectal sleeves
   Contaminated water
   Biting insect (experimentally)
Effect of Pregnant Cow Infection

Days pregnancy               Effect

    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

1.   Prenatally infected cattle and that are
     persistently viremic after birth
2.   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 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

   Sheep
   Wild ruminants
       Natural infections (caribou: 40-100%)
       Transfer (llamas: dead end)
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
   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 (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 (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
Lesion on Nose
Lesion on nose,
foamy saliva
Mucosal lesions on tongue and GI tract
Lesion on hard
palate
Ataxia resulting from congenital infection
Cerebellar hypoplasia resulting from congenital infection
Fluorescent Antibody test for noncytopathic virus
Figure 1: Choroid plexus, filly: EHV-1 within endothelium and
circulating macrophages. Peroxidase immunohistochemistry and
hematoxylin.
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)

   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)
   Serology
    Virus neutralization
    FA
    Immunohistochemistry test
    ELISA
    PCR
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 mths for
           Virus isolation
           Test again in 3 months (isolation + serology)
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
Infectious Bovine
Rhinotracheitis (IBR)

    Red nose
Etiology

   Herpes virus (DNA virus)
       3 genotypes
           BHV1: IBR
           BHV2: Infectious pustular vulvovaginitis (IPV)
                    Infectious balanoposthitis (IBP)
           BHV3: Neurologic signs
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
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 (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 (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 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

   Secondary bronchopneumonia or interstitial
    emphysema due to labored breathing
   Rhinitis
   Laryngotracheitis
   Bronchitis
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)
   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%)
Diagnosis

   Clinical signs
   Necropsy
   Laboratory diagnosis
       Virus isolation
       Direct fluorescent antibody test
       ELIZA (serum and milk)
       SN (serum)
       PCR
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)
   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 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

   Etiology
       Family Retroviridae (Oncogenic RNA virus)
           Genus Bovine leukaemia virus (BLV)


   2 forms
       Enzootic form (Enzootic Bovine Leukosis)
       Sporadic form
Epidemiology

   Worldwide distribution
       Prevalence increases with age
       Dairy cattle generally have higher prevalence
        rates than beef cattle
           Management factors
           Breed susceptibility differences?
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 (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 (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 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
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
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)

   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)
   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)
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 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

   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
Foot and Mouth Disease
(FMD)
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

   Sensitive
       Sunlight
       UV
       Temp >50 C
       pH changes
FMD survival times in animal samples

       Organ and condition        Time
        Lymphnode at 4 C         120 days
       Bone marrow at 4 C        210 days
      Skeletal muscle at 4 C      2 days
     Frozen carcass (no rigor)   6 months
Host

   All domestic and wild cloven-footed animals
   Susceptibility: cattle>pig>sheep>goat
   Pigs are amplifying host which can cause airborne
    transmission.
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

   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 (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 (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
Period of excretion of FMDV related to
onset of clinical signs
           Source      Time (days)
            Saliva      -10 to +9
           Airborne     -1 to +4
             Milk       -4 to +4
           Semen        -4 to +7
         Feces/urine    -1 to +6
           Lesions      0 to +11
Pillars of rumens
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)

   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)
   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)
   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)
   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

   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.
Bovine Spongiform
Encephalopathy

   BSE, Mad cow disease
Etiology

   Prion protein
    (PrP)
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
    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
   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.
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

   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 (1)

   Mean incubation period is 4-5 years.
   Subacute or chronic, progressive disorder

    The 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 (2)
   Pruritis, seen in scrapie, occurs also but is
    not usually a prominent sign.

   Loss of body weight and condition.
Lesions

   There are no gross post-mortem changes.

   A characteristic spongiform encephalopathy
    is present in most cases.
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 (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 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

   กระทรวงเกษตรและสหกรณ์
                                         ี              ้
     ไม่ อนุญาตให้ นาเข้ าอาหารสัตว์ ท่ มีส่วนผสมของเนือ กระดูก และเลือด จาก

       ประเทศอังกฤษ (13 มิ.ย. 2540)
   กรมปศุสัตว์
                                               ี             ้           ้ ้
     ให้ ชลอการนาเข้ าโค และอาหารสัตว์ ท่ มีส่วนผสมของเนือของสัตว์ เคียวเอือง

       จากกลุ่มประเทศยุโรป (England, Denmark, etc.)
            ั
    สถาบันวิจย และมหาวิทยาลัย จัดเผยแพร่ ความรู้ ส่ ูสาธารณชน
     Review article: Prof. Peerasak Chantaraprateep et al., 1998. Thai J Vet

       Med. Vol. 28, No. 1:17-55
Rinderpest


   Cattle Plague
Etiology

   Family Paramyxoviridae
   Genus Morbilivirus
   Only one serotype
   Susceptible species
       Cattle and buffaloes
       Sheep and goats
       Asiatic pigs
       Wildlife
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
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 (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 (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
Conjunctivitis and mucopurulent exudate
   in the early stage of RP infection.
Purulent discharge and conjuctivitis
Excessive salivation
 in the early stage
  of RP infection.
Oral erosions
Erosions of buccal mucosa and gingiva
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 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
Sloughing of the epithelium over a necrotic Peyer's patch
Ulcerations in the mucosa of the upper colon
Hyperemia of the cecum and colon with accentuation
 of lesions (hemorrhage) at the ceco-colic junction
Hyperemia and hemorrhages in the longitudinal folds
           of the colon - Zebra striping
Hemorrhage in the mucosa of the gall bladder
Epidemiology   The Global Rinderpest Eradication
                       Program (FAO)
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


   Pseudo-urticaria, Neethling virus
   disease, exanthema nodularis bovis,
   knopvelsiekte
Etiology and Host

   Family Poxviridae
   Genus Capripoxvirus
   Host: Cattle, Buffaloes, Giraff
   First described in Northern Rhodesia in 1929
   An OIE list A disease
Transmission

   Insect vector
       Mosquitoes (e.g. Culex mirificens and Aedes
        natrionus)
       Flies (e.g. Stomoxys calcitrans and Biomyia
        fasciata)
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.
A calf affected with LSD; note the large skin nodules
Nodules (N) and sittasts (S) in a Balidy cow
       in Egypt affected with LSD
An LSD (pox) lesion in the trachael mucosa
LSD lesions in the lung are areas of atelectasis
           and interlobular edema
Eradication

   Slaughter of all infected and in-contact cattle
   Vaccination
Papillomavirus or Warts
Pseudocowpox
Pseudocowpox
Questions?


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