Peste des petits ruminants (PPR) is a contagious and acute viral disease of small ruminants characterized by fever, sores, diarrhea, and pneumonia. It is caused by a virus in the genus Morbillivirus and family Paramyxoviridae. The virus primarily affects goats and sheep through respiratory or oral transmission. Clinical signs include fever, nasal and ocular discharge, sores in the mouth, and later respiratory and digestive signs. At the microscopic level, it causes necrosis of epithelial cells and formation of syncytial cells in mucosa. There is no treatment, and vaccination is the main control method.

1. PESTE DES PETITS
RUMINANTS (PPR)
ABHIJITH SP
CVAS POOKODE

2. INTRODUCTION
 Contagious and acute febrile viral disease of
sheep and goats mainly, characterized by high
fever, sores, diarrhea and pneumonia.
 Death rate in neonates are high.
 Synonyms - Kata, stomatitis-pneumoenteritis
complex, goat plague & pseudo rinderpest
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3. AETIOLOGY
 Agent-Paramyxoviridae-Morbillivirus-PPRV.
 Epitheliotropic & lymphotropic
 Antigenically related to CD virus of dogs, RP
virus of cattle and measles virus of humans.
 Secondary Bacterial infection increases the
death rate in neonates.
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4. Susceptible Hosts
 Primarily affects goats and sheep. More severe in
goats.
 Sometimes, camels and wild small ruminants are also
affected.
 Cattle and buffaloes are sub-clinically infected.
 Have 80–100% mortality rate in acute cases .
 Morbidity is high in case of neonates.
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5. TRANSMISSION & ROUTE OF
INFECTION
 Secretions and excretions of sick animals are the
sources of infection in all Paramyxovirus
infection.
 Close contact with infected animals –Inhalation,
Ingestion of contaminated feed and water.
 Through conjunctiva
 Carrier state is not accepted here.
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6. INCUBATION PERIOD
• OIE recognized –21 Days.
• The incubation period is usually 4–5 days.
• But it varies according to load, strain, nature and
health status of animal.
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7. PATHOGENESIS
 The virus gain entry into the animals body
through nasal passage or by ingestion.
 After entering into the host, it multiplies first in
the retropharyngeal mucosa and local lymphoid
tissues and pharyngeal and laryngeal tonsils.
 Then they drained into lymphatics and then to
venous system and get into systemic blood flow.
 The virus specifically targets the alimentary and
respiratory mucosa along with lymphoid tissues .
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8. PATHOGENESIS
• Infected cells undergo necrosis (Lymphoid tissues,
alimentary tract)
• In respiratory mucosal epithelium there is proliferation of
cells.
• Young goats may suffer from severe diarrhea before
respiratory signs and they die of dehydration and
electrolytic imbalances.
• Death can also be occurred due to secondary infection.
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9. CLINICAL SIGNS
 Pyrexia (104°–106°F ) due to viremia. Leukopenia
 Restlessness, a dull coat, dry muzzle, congested mucous
membranes, and depressed appetite.
 Nasal and ocular discharges – initially serous later become
mucopurulent and exudate dries up & forms crusts in the
regions of nares and mouth.
 Matting of the eyelids and occlusion of the nostrils.
 Dyspnea and coughing develop later.
 Secondary bacterial complications aggravate respiratory signs.
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10. CLINICAL SIGNS
 Necrotic and erosive lesions with bran like
diphtheritic deposits on the oral mucosa,
Pronounced halitosis, Swollen lips.
 Necrotic stomatitis affects the lower lip, gum dental
pad, palate, cheeks and their papillae, and the tongue.
 Diarrhea after 3-4 days of fever, profuse and watery
later blood tinged.
 Dehydration and emaciation; hypothermia and death
follow, usually after 5–10 days.
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11. CLINICAL SIGNS
 Morbidity and mortality rates are higher in
young animals than in adults.
 Death within a week, if not properly treated.
 Pregnant animals may abort.
 Pipe Stream Diarrhea present.
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12. Stepwise clinical manifestations in goats infected with PPR virus. a Congestion of
conjunctiva on 5 days post-infection (dpi); b mucoid ocular and nasal discharge on 7 dpi (cited
from FAO web); c oral (gum) lesions on 7 dpi; d and e tongue lesions and deposit of fibrins
on
8dpi; f diarrhoea on 10 dpi; g progressive weight loss and dull on 10 dpi and h death on 10dpi
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13. Gross post mortem lesions
GI TRACT LESIONS
 Necrotic & erosive stomatitis.
 Necrotic lesions inside the lower lip and on the
adjacent gum, the cheeks near the commissures,
and on the ventral surface of the tongue.
 In severe cases, the lesions may extend to the
hard palate, pharynx and upper esophagus.
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14. GI TRACT LESIONS
 The erosions are shallow, with a red, raw base
and later get deposited with diphtheritic material.
 The rumen, reticulum, and omasum are rarely
involved.
 The abomasum exhibits regularly outlined
erosions that have red, raw floors and ooze
blood.
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15. GI TRACT LESIONS
 Severe lesions are less common in the small intestines
 Streaks of hemorrhages, and less frequently erosions, may be present
in the first portion of the duodenum and terminal ileum
 Peyer’s patches are severely affected; entire patches of lymphoid tissue
may be sloughed.
 Necrosis & haemorrhage of mesenteric lymph nodes.
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16. GI TRACT LESIONS
 Large intestine - severely affected, with
lesions developing around the ileocecal valve
and at the cecocolic junction and rectum.
 Cecocolic junction and rectum exhibits
streaks of congestion along the folds of the
mucosa, resulting in the characteristic “zebra-
striped” appearance.
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17. LESIONS IN THE
RESPIRATORY TRACT
 Petechiae in the turbinate's, larynx, and trachea.
 Interstitial pneumonia.
 Bacterial complications lead to Broncho interstitial
fibrinous pneumonia and pleuritis.
 Severe congestion, hemorrhages ,fluid in bronchial
region.
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18. Other Gross lesions
• Liver – hemorrhages on surface
• Serosanguinous fluid in pericardial sac of heart
• Minor hemorrhages on cortico-medullary junction of kidney
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19. Congestion, hemorrhages, and consolidation
in lungHemorrhages in trachea
Hemorrhagic stripes in mucosal
surface of intestine
Presence of serosengunious
fluid in pericardial sac of
heart

20. Microscopic lesions
• GI tract- Similar to RP- Necrosis of mucosal
epithelial cells & formation of multinucleate syncytial
cells with inclusion bodies, necrosis of lymphocytes
in peyer’s patches.
• Respiratory tract – Proliferative rhino tracheitis,
bronchitis, bronchiolitis, proliferation of type II
pneumonocytes and formation of multinucleated
syncytial giant cells with intranuclear and
intracytoplasmic inclusion bodies.
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21. Micoscopic lesions
• Spleen & LN -haemorrhages & depletion of
lymphoid cells in cortex & medullary cords.
• Kidney-degenerative changes, desquamation of
tubular epithelium, haemorrhage, mild glomerular
atrophy, interstitial nephritis.
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22. DIAGNOSIS
• Virus isolation
• Serological tests-AGID, CIEP, etc
• Virus neutralization tests, immunocapture ELISA, sandwich ELISA, etc
• RT-PCR routine diagnostic tool
• PCR in combination with nucleotide sequencing
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23. DIFFERENTIAL DIAGNOSIS
• FMD
• RP
• BLUE TONGUE
• CONTAGIOUS ECTHYMA
• PASTEURELLOSIS
• MYCOPLASMOSIS
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24. Extra Points
• 1.Not Zoonotic
• 2.Vaccine strain-Live Attenuated Vaccine -SUNGRI 96
• 3.Z-stripes /Zebra stripes are also found in some cases like
that of Rinderpest, in intestine colon and caecum.
• 4.Frequency of vaccination is-Once a year.
• 5.Other vaccines-PPR Vac.
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26. THANK YOU