Bangladesh Agricultural University
Md. Rafiqul Islam
Level-5, Sem-2
ID- 1501171
Reg: 42814
Peste des Petits Ruminants
( PPR ) in Goat
Talk Plan
 Introduction
 Origin and spread
 Etiology
 Physical and Chemical
Action
 Economic importance
 Transmission
 Pathogenesis
 Clinical signs
 Post mortem lesion
 Diagnosis
 Differential diagnosis
 Treatment
 Prevention and
control
Introduction
• Included as List-A disease by OIE
• PPR ( Peste des Petits Ruminants) is also
known as Ovine Rinderpest or Goat Plague
• Acute , highly contagious transboundary
viral disease of goat and sheep
• Characterized by fever, sores in mouth,
oculo-nasal discharge, diarrhea,
pneumonia and ultimately death
Origin and Spread
• The first description of the disease was published in 1940
through an outbreak in Ivory Coast
• Pakistan and India: Early 1990s
• In Bangladesh, outbreaks of Peste des petits ruminants (PPR)
identified by British reference laboratory in goats since 1993.
World Wide Distribution of PPRV
Etiology
• Caused by a Morbillivirus (ssRNA) in
the family of Paramyxoviridae
• Genetically characterized into 4
groups
• 6 Structural proteins: N, P, L, M, F, H
• Incubation period: 3-6 days
Physical and Chemical
Action
Destroyed at 60˚C/60 min.
Inactivation: pH < 4.0 or >
10.0
Susceptible to alcohol,
sodium hydroxide, ether,
phenol & detergents etc
Long survival time in chilled
and frozen tissue
PPRV
Economic Importance
Highly
Fatal in
young
Morbidity:
Up to 100%
Mortality:
Varying
Goat: 55-85 %
Sheep: 45-75%
Prevalence
is higher in
mixed
population
About 22
million at risk
population in
BD
Limits
Trade &
Export
Threatens
Food
security
Production
loss & culling
Transmission
The virus is secreted in tears, nasal or ocular discharge, coughing
and in the feces of infected individual
Susceptible animals inhale droplets and likely to be infected
There is no known carrier state
 Virus may also present in semen and embryo
 Offspring can also be infected through mother by milk sucking
PPR virus penetrate the
retropharyngeal mucosa
Viremia
Specifically damage the
Alimentary system Respiratory System Lymphoid
System
Pathogenesis
Entry
Diarrhea Pneumonia
Immuno
suppression
Symptoms
 High body temperature ( Up to 41˚C)
 Diarrhea, depression , anorexia
 Ulcer in the gum (lower),dental pad,
hard palate, cheek and tongue
 Serous/ foamy/ hemorrhagic discharge
from nose
 Pneumonia
Clinical presentation of
PPR affected Goat
Post Mortem Lesion
Dehydrated carcass with fecal soiling
Congestion of the ileo-cecal valve
Blackening of the
folds of large
intestine ( Zebra
stripping)
Enlarged spleen
Edematous
lymphnode
Broncho
pneumonia
Diagnosis

Based on history
- Any recent outbreak in the case area
- Change in husbandry and trade practice
- Change in weather. i.e. Rainy season
- Movement history
 Based on clinical signs
 Post Mortem changes
 Blood examination
 Isolation and culture of virus
 Serological tests:
- PCR - AGID
- ELISA - cDNA probe
 Blue tongue
 Sheep pox
 Rinderpest
 FMD
 Contagious Caprine Pleuropneumonia (CCPP)
 Contagious ecthyma
 Nairobi Sheep Disease
 Salmonellosis
 Colibacillosis
Differential diagnosis
Line of Treatment
 Non specific symptomatic treatment
 Antibiotic therapy to prevent secondary infection
 Anti-diarrheal drug
 Anti-inflammatory drug
 Fluid therapy
A PPR Case Study at
CVASU
Species: Goat
(Jamunapari)
Age: 11 month
Weight: 13 kg
Client’s Complaint:
Diarrhea and
Increased temp.
Clinical History: Off
fed, Stomatitis and
Nasal discharge
 Treatment Given:
1) Inj. Diadin – 30 ml vial × 1
Sig: Inject 8 ml IV on 1st day followed
by 4 ml IV for next 4 days.
2) Inj. Histavet – 10 ml vial × 1
Sig: Inject 1 ml IM daily for 4 days.
3) Pow. DD-4 – 100gm pack × 1
Sig: Adm. 25gm PO, bid for 3 days.
4) Inj. Cholera Saline – 500 ml bag × 1
Sig: Inject 250 ml IV daily for 2 days.
Prevention and control
In March 2015, the FAO and OIE officially announced the global
PPR control strategy. Training and information sharing are crucial
elements for the success of this strategy.
 Strict isolation and quarantine facility
 Movement control
 Compulsory slaughter of affected animals
 Sanitation and hygiene
 Vaccination
- Ring vaccination
- Vaccination of high risk population
PPR Vaccine
 Tissue culture Rinderpest vaccine TC ID50 at 12 month of age
 Genetically engineered recombinant vaccine (under trial by
OIE)
 French attenuated PPR vaccine ( Immunity for 3 years)
 Live attenuated PPR vaccine by LRI 45 lakh doses per year
(Adopted in VERO cell culture) but poor thermal stability so cold
chain is to be maintained to preserve the potency
 Protocol:
1ml S/C at 4 months of age
Booster at 6 amonth of age
Followed by yearly vaccination
Peste des Petits Ruminants( PPR ) in Goat
Peste des Petits Ruminants( PPR ) in Goat

Peste des Petits Ruminants ( PPR ) in Goat

  • 1.
    Bangladesh Agricultural University Md.Rafiqul Islam Level-5, Sem-2 ID- 1501171 Reg: 42814
  • 2.
    Peste des PetitsRuminants ( PPR ) in Goat
  • 3.
    Talk Plan  Introduction Origin and spread  Etiology  Physical and Chemical Action  Economic importance  Transmission  Pathogenesis  Clinical signs  Post mortem lesion  Diagnosis  Differential diagnosis  Treatment  Prevention and control
  • 4.
    Introduction • Included asList-A disease by OIE • PPR ( Peste des Petits Ruminants) is also known as Ovine Rinderpest or Goat Plague • Acute , highly contagious transboundary viral disease of goat and sheep • Characterized by fever, sores in mouth, oculo-nasal discharge, diarrhea, pneumonia and ultimately death
  • 5.
    Origin and Spread •The first description of the disease was published in 1940 through an outbreak in Ivory Coast • Pakistan and India: Early 1990s • In Bangladesh, outbreaks of Peste des petits ruminants (PPR) identified by British reference laboratory in goats since 1993.
  • 6.
  • 7.
    Etiology • Caused bya Morbillivirus (ssRNA) in the family of Paramyxoviridae • Genetically characterized into 4 groups • 6 Structural proteins: N, P, L, M, F, H • Incubation period: 3-6 days
  • 8.
    Physical and Chemical Action Destroyedat 60˚C/60 min. Inactivation: pH < 4.0 or > 10.0 Susceptible to alcohol, sodium hydroxide, ether, phenol & detergents etc Long survival time in chilled and frozen tissue PPRV
  • 9.
    Economic Importance Highly Fatal in young Morbidity: Upto 100% Mortality: Varying Goat: 55-85 % Sheep: 45-75% Prevalence is higher in mixed population About 22 million at risk population in BD Limits Trade & Export Threatens Food security Production loss & culling
  • 10.
    Transmission The virus issecreted in tears, nasal or ocular discharge, coughing and in the feces of infected individual Susceptible animals inhale droplets and likely to be infected There is no known carrier state  Virus may also present in semen and embryo  Offspring can also be infected through mother by milk sucking
  • 11.
    PPR virus penetratethe retropharyngeal mucosa Viremia Specifically damage the Alimentary system Respiratory System Lymphoid System Pathogenesis Entry Diarrhea Pneumonia Immuno suppression
  • 12.
    Symptoms  High bodytemperature ( Up to 41˚C)  Diarrhea, depression , anorexia  Ulcer in the gum (lower),dental pad, hard palate, cheek and tongue  Serous/ foamy/ hemorrhagic discharge from nose  Pneumonia
  • 13.
  • 14.
    Post Mortem Lesion Dehydratedcarcass with fecal soiling Congestion of the ileo-cecal valve Blackening of the folds of large intestine ( Zebra stripping) Enlarged spleen Edematous lymphnode Broncho pneumonia
  • 15.
    Diagnosis  Based on history -Any recent outbreak in the case area - Change in husbandry and trade practice - Change in weather. i.e. Rainy season - Movement history  Based on clinical signs  Post Mortem changes  Blood examination  Isolation and culture of virus  Serological tests: - PCR - AGID - ELISA - cDNA probe
  • 16.
     Blue tongue Sheep pox  Rinderpest  FMD  Contagious Caprine Pleuropneumonia (CCPP)  Contagious ecthyma  Nairobi Sheep Disease  Salmonellosis  Colibacillosis Differential diagnosis
  • 17.
    Line of Treatment Non specific symptomatic treatment  Antibiotic therapy to prevent secondary infection  Anti-diarrheal drug  Anti-inflammatory drug  Fluid therapy
  • 18.
    A PPR CaseStudy at CVASU Species: Goat (Jamunapari) Age: 11 month Weight: 13 kg Client’s Complaint: Diarrhea and Increased temp. Clinical History: Off fed, Stomatitis and Nasal discharge  Treatment Given: 1) Inj. Diadin – 30 ml vial × 1 Sig: Inject 8 ml IV on 1st day followed by 4 ml IV for next 4 days. 2) Inj. Histavet – 10 ml vial × 1 Sig: Inject 1 ml IM daily for 4 days. 3) Pow. DD-4 – 100gm pack × 1 Sig: Adm. 25gm PO, bid for 3 days. 4) Inj. Cholera Saline – 500 ml bag × 1 Sig: Inject 250 ml IV daily for 2 days.
  • 19.
    Prevention and control InMarch 2015, the FAO and OIE officially announced the global PPR control strategy. Training and information sharing are crucial elements for the success of this strategy.  Strict isolation and quarantine facility  Movement control  Compulsory slaughter of affected animals  Sanitation and hygiene  Vaccination - Ring vaccination - Vaccination of high risk population
  • 20.
    PPR Vaccine  Tissueculture Rinderpest vaccine TC ID50 at 12 month of age  Genetically engineered recombinant vaccine (under trial by OIE)  French attenuated PPR vaccine ( Immunity for 3 years)  Live attenuated PPR vaccine by LRI 45 lakh doses per year (Adopted in VERO cell culture) but poor thermal stability so cold chain is to be maintained to preserve the potency  Protocol: 1ml S/C at 4 months of age Booster at 6 amonth of age Followed by yearly vaccination

Editor's Notes

  • #3 Pest of small ruminants/pseudo-rinderpest of small ruminants
  • #20 Proper disposal of carcass and disinfection