PPR in goats and sheeps

Introduction

PPR in animals refers to Peste des Petits Ruminants (PPR), commonly known as sheep and goat plague. This highly contagious viral disease primarily affects small ruminants, especially sheep and goats. The causative agent, the PPR virus, is classified under the genus Morbillivirus within the family Paramyxoviridae. It shares a close genetic relationship with the rinderpest virus, which has been successfully eradicated worldwide.

Etiology

PPR  is usually caused by Peste des petits ruminants virus (PPRV) an RNA virus.

Serotypes and Lineages

PPRV has only one serotype but four genetically distinct lineages that are based on the sequence analysis of the F and N genes of various strains of the virus originally isolated from Africa and Asia. Lineage I and II viruses were first isolated from West Africa, lineage III from East Africa, and lineage IV from Asia. Whereas lineages I and II viruses are still largely confined to West Africa, the lineage III virus appears to have spread from East Africa to Sudan, Yemen, and Oman; the lineage IV (Asian) virus has recently been introduced to some African countries including Cameroon, Gabon, Central African Republic, Uganda, Sudan, Egypt, Algeria, and Morocco. In Asia, this lineage has been identified in the Middle East and in many South Asian countries, including Pakistan, India, Nepal, Bangladesh, and Tibet/China.

Epidemiology

The disease occurs mostly in goats and sheep and has spread extensively across national and continental boundaries in the last few decades. Outbreaks were first described in West Africa in 1942, but the disease is now endemic in many African countries as well as in the Middle East and South Asia, and there is concern that it could spread to Europe. In Africa, outbreaks have been reported as far north as Morocco, Algeria, and Egypt and as far south as Cameroon, Gabon, Uganda, and Tanzania.5 Since the 1990s, outbreaks have been reported from the Arabian Peninsula as far north as Turkey and extending through Pakistan and India to Nepal, Bangladesh, and China where the disease is now endemic.

Morbidity

Infection rates in enzootic areas are generally high (above 50%) and can be up to 90% of the flock during outbreaks. The percentage of sheep and goats with antibodies rises with age. Furthermore, PPR was diagnosed in samples from 24.5% of 592 sheep and in 38.2% of 912 goats. The disease is generally more severe in goats than in sheep and is rapidly fatal in young animals.

Case fatality

Case–fatality rates are also much higher in goats (55%-85%) than in sheep (less than 10%). An exception to the rule was the recent (2011) outbreak in Gabon in which the case fatality in sheep was 98.9% (91 of 92 sheep) and only 18.2% in goats (2 of 11 goats).

Seasonal variation

There is no significant seasonal variation
in the prevalence of the disease but because maternal antibodies are lost at about 4 months of age, the number of susceptible animals is likely to increase 3 to 4 months after peak kidding and lambing seasons. In India, there are more outbreaks during the summer and in September and October corresponding to the wet season.

Mode of transmission

PPRV is transmitted by the way of aerosols when animals live in close contact. Large amounts of the virus are present in exhaled air and in all body excretions and secretions including feces, saliva, ocular and nasal discharges, and urine that can contaminate fomites. Diarrheic feces are especially infectious. Infection is mainly by inhalation but could also occur through the conjunctiva and oral mucosa. Goats experimentally infected with PPRV can shed the virus for a few days during the incubation period.19 Naturally infected goats can continue to shed virus in feces up to 1 month after vaccination and for 2 months without vaccination. Transmission can occur during the incubation period.PPR is transmitted by close contact, and confinement favors outbreaks.

Risk factor

Age
Kids over 4 months and under 1 year of age are most susceptible to the disease, corresponding to waning maternal antibodies from immune dams.

Zoonotic importance

The virus of PPR does not affect humans.

Pathogenesis

The initial site of virus multiplication is not within epithelial cells of the respiratory mucosa, as had been previously reported for PPRV and RPV, but is within macrophages and dendritic cells and is transported to local lymph nodes for multiplication before the virus enters the circulation and causes a viremia (like the viruses of measles and canine distemper).

Viremic

Following viremia, the virus specifically damages epithelial cells of the alimentary and respiratory systems as well as lymphocytes in the lymphoid system. Infected cells may undergo proliferation and formation of syncytial giant cells before they undergo necrosis/ apoptosis.

Clinical signs

Signs generally appear 3 to 6 days after being in contact with an infected animal. A high fever (above 40°C) is accompanied by dullness, sneezing, and serious discharge from the eyes and nostrils. A day or two later, discrete necrotic lesions develop in the mouth and extend over the entire oral mucosa, forming diphtheritic plaques. There is profound halitosis and the animal is unable to eat because of a sore mouth and swollen lips. Nasal and ocular discharges become mucopurulent and the exudate dries up, matting the eyelids and partially occluding the external nares. Diarrhea develops 3 to 4 days after the onset of fever. It is profuse, and feces may be mucoid and blood-tinged. Dyspnea and coughing occur later, and the respiratory signs are aggravated when there is secondary bacterial pneumonia.

Lab test

Lab test usually is RT-PCR.

Differential diagnosis

1. Heartwater
2. Pneumonic Pasteurellosis
3. Contagious Caprine Pleuropneumonia (CCPP)
4. Contagious Bovine Pleuropneumonia (CBPP)
5. Helminthiasis
6. Coccidiosis
7. Contagious Ecthyma (Orf)
8. Foot-and-mouth disease (FMD)

At necropsy findings

Necropsy, the following specimens should be collected for histopathology and virology, including PCR detection:

•  Oral mucosa
• Tonsil
• Mesenteric lymph nodes
• Lungs
• Small and large intestines

TREATMENT AND CONTROL

There is no specific treatment for food animals.

Supportive and symptomatic treatment is recommended

• Antibiotics Gentamycin, Tylosin
• NSAIDS Flunixin meglumine, Ketoprofen
• Multivitamin Amivicam
• KMNO4 for oral lesion washing
• IV infusion for dehydration
• Hyperimmune serum (valuable animals) (R-2)

Control

The disease can be prevented through vaccination and by avoiding the introduction of new stock from unknown sources, particularly animals purchased at livestock markets. Additionally, farmers should segregate animals that return unsold from markets unless they have vaccinated the entire herd or flock. Mortality rates in affected flocks or herds can be high. A live, attenuated PPR vaccine prepared in Vero cell culture affords protection from natural diseases.

Note

PPR is also a Transboundary Animal disease. As can cross borders and can spread from one country to another.

FAQ’s

1. What is PPR?
   A highly contagious viral disease affecting small ruminants (goats and sheep), caused by the Morbillivirus.
2. Which animals are affected?
   Primarily goats and sheep; wild small ruminants can also be infected.
3. How is PPR transmitted?
   Through direct contact with infected animals, contaminated feed, water, or equipment.
4. What are the symptoms?
   Fever, mouth sores, diarrhea, pneumonia, and high mortality rates, especially in young animals.
5. Is PPR zoonotic?
   No, PPR does not infect humans