Rinderpest or cattle plague

Rinderpest virus is a Morbillivirus, closely related to the viruses causing peste des petits ruminants, canine distemper and measles.Rinderpest virus is shed in nasal and ocular secretions and can be transmitted during the incubation period (1–2 days before onset of fever). Transmission required direct or close indirect contact between susceptible animals and sick animals shedding the virus.

1. RINDERPEST CATTLE PLAGUE Submitted by Ranjini M anuel

2. INTRODUCTION Acute, highly contagious, viral disease of cattle, domesticated buffalo and other ruminants Characterized by   Fever Necrotic stomatitis Oral erosions Diarrhoea Lymphoid necrosis High mortality

3. HISTORY O riginated in Asia   The Mongol invasions of Europe by Genghis Khan and his successors were associated with pandemics of rinderpest in 1222,1233,1238 They hit Europe especially hard in the 18th century, with three long panzootics   P eriods of 1709–1720 1742–1760 1768–1786

4. In 1889, cattle shipped from India carried the rinderpest virus to Africa- Epidemic 90% of the cattle in sub-Saharan Africa and many sheep and goats died –Mass starvation- most catastrophic disaster ever to affect Africa A more recent rinderpest outbreak in Africa in 1982–1984 resulting in an estimated US$2 billion in stock losses R inderpest in South Africa

5. RINDERPEST IN INDIA RP 1st introduced in to India- Mid 18th century 1st Report – Assam (1722) Madras (1848 ) Calcutta (1864) Varanasi (1869) Case fatality rates – 60 % Last confirmed report – North Arcot district of T.N (1995).

6. ETIOLOGY Family: Paramyxoviridae Genus : Morbillivirus Negative sense, Single stranded RNA virus Only 1 serotype of this virus Three genetically distinct lineages African Lineages 1 and 2 Asian Lineage 3 All are immunologically identical Antigenically related to PPR, CD & measles

7. EPIDEMIOLOGY Rinderpest was eradicated from Europe early in the 20th century Lineage 1 has been reported only in Africa and the Middle East, and was last seen in 2001 Lineage 3 (the “Asian lineage”) was found in Russia, Turkey, and parts of Asia and the Middle East This lineage has not been seen since 2000 Lineage 2 was once reported from many parts of Africa

8. HOST Most cloven-hooved animals (order Artiodactyla ) are susceptible to rinderpest virus to some degree Cattle, water buffalo, yaks, African buffalo, giraffes, warthogs and Tragelaphinae (spiral-horned antelope) are particularly susceptible to disease Gazelles, sheep and goats - mildly susceptible Rinderpest is rare in camelids

9. TRANSMISSION By direct or close indirect contact between infected and susceptible animals Virus is excreted by the infected host in their urine, feces , nasal discharge Airborne transmission is limited but possible Feed and water contaminated with the secretions of infected host RPV is sensitive to direct sunlight thus fomites are not a viable means of transmission Failure of the virus to persist outside the body – easy to control

10. Because rinderpest virus is inactivated quickly by autolysis and putrefaction, this virus is destroyed within 24 hours in carcasses F reezing or chilling of the carcass in some climates could slow these processes and allow the virus to survive longer High morbidity and mortality

11. SOURCE OF VIRUS Incubation period is around – 1 to 2 weeks 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 During periods of clinical disease, high levels of RPV can be found in expired air, nasal and ocular discharges, saliva, faeces, semen, vaginal discharges, urine and milk Infection is via the epithelium of the upper or lower respiratory tract No carrier state

12. VIRUS- URT,tonsilslymphnode VIREMIA Lymphocytes Apoptosis & necrosis Lymphopenia Replication in epithelial cells of alimentary tract Focal, necrotic stomatitis & enteritis Severe dehydration Parasitic or bacterial D eath PATHOGENESIS

13. CLINICAL SIGNS Classical acute or epizootic form Clinical disease is characterised by an acute febrile attack within which prodromal and erosive phases can be distinguished

14. PRODROMAL PHASE Lasts approximately 3 days Pyrexia of between 40 and 41.5°c Partial anorexia Depression Reduction of rumination Constipation Lowered milk production , Increase of respiratory and cardiac rate Congestion of visible mucosae Serous to mucopurulent ocular and nasal discharges Drying of the muzzle

15. EROSIVE PHASE Development of necrotic mouth lesions at height of fever: flecks of necrotic epithelium appear on the lower lip and gum In rapid succession may appear on the upper gum and dental pad Underside of the tongue Cheeks and cheek papillae Hard palate; erosions or blunting of the cheek papillae

16. Bovine, oral mucosa. There is severe diffuse necrosis ulceration of the dental pad; mandibular mucosa contains smaller erosions

17. Bovine, hard palate. Palate erosion .

18. Bovine, hard palate. The mucosa contains many small, coalescing, pale to dark red erosions or foci of necrosis .

19. Bovine, oral mucosa. There are numerous erosions on and between the buccal papillae.

20. GASTROINTESTINAL SIGNS Appear when the fever drops or about 1–2 days after the onset of mouth lesions Diarrhoea is usually copious and watery at first later may contain mucus, blood and shreds of epithelium; accompanied, in severe cases, by tenesmus Diarrhoea or dysentery leads to dehydration, abdominal pain, abdominal respiration, and weakness Terminal stages of the illness, animals may become recumbent for 24–48 hours prior to death

21. Shooting Diarrhoea

22. The mucosa is hyperemic and covered by abundant mucopurulent exudate . BOVINE TRACHEA

23. The mucosa is hemorrhagic and edematous, and the Peyer's patch is depressed (necrosis). BOVINE ILEUM

24. The mucosa is edematous and contains many small hemorrhages and shallow erosions. BOVINE COLON There are many petechiae on the crests of the mucosal folds, and there are several small blood clots on the mucosal surface.

25. The mucosa contains multiple longitudinal linear hemorrhages BOVINE COLON

26. Erosions with ulceration; dark areas of mucosal necrosis and hemorrhage zebra striping’ - haemorrhages of the longitudinal folds of the large intestine

27. Some animals die while showing severe necrotic lesions High fever and diarrhoea Others after a sharp fall in body temperature Often to subnormal values In rare cases, clinical signs regress by day 10 and recovery occurs by day 20–25

28. PERACUTE FORM No prodromal signs except high fever (>40–42°C ) sometimes congested mucous membranes death within 2–3 days This form occurs in highly susceptible young and new born animals

29. MILD SUBACUTE OR ENDEMIC FORM Clinical signs limited to one or more of the classic signs Usually no associated diarrhoea May show a slight, serous, ocular or nasal secretion Fever: variable, short-lived (3–4 days) and low (38–40°C) No actual depression; animals may continue to graze, water and trek Low or no mortality; except in highly susceptible species

30. ATYPICAL FORM Irregular pyrexia and mild or no diarrhoea Fever may remit slightly in the middle of the erosive period, and 2–3 days later, return rapidly to normal accompanied by a quick resolution of the mouth lesions, a halt to the diarrhoea and an uncomplicated convalescence The lymphotropic nature of RPV leads to immunosuppression and favours recrudescence of latent infections and/or increased susceptibility to other infectious agents

31. SHEEP AND GOAT Variable signs; some pyrexia, anorexia and minor ocular discharge Sometimes diarrhoea Asian RPV strains can be transmitted to cattle by contact with infected small ruminants

32. DIFFERENTIAL DIAGNOSIS Bovine viral diarrhoea/mucosal disease Malignant catarrhal fever Infectious bovine rhinotracheitis Foot and mouth disease Papular stomatitis Vesicular stomatitis Contagious bovine pleuropneumonia Theileriosis Salmonellosis Necrobacillosis Paratuberculosis Arsenic poisoning

33. LABORATORY DIAGNOSIS SAMPLES pyrexia - blood Spleen, prescapular or mesenteric lymph nodes of dead animals chilled to sub-zero temperatures for virus isolation base of the tongue, retropharyngeal lymph node and third eyelid - histopathology and immunohistochemistry Ocular and nasal secretions – prodromal phase

34. VIRUS ISOLATION RPV virus can be cultured from the leukocyte fraction of whole blood (heparin or EDTA) or uncoagulated blood Virus can also be isolated from samples of the spleen, prescapular or mesenteric lymph nodes of dead animals presence of syncytial cell formation, and cells with intranuclear viral inclusion bodies R inderpest antigens can be demonstrated in the formalin-fixed tissues by immunoperoxidase staining

35. DIAGNOSIS For rapid differentiation between rinderpest and PPR Antigen detection by agar gel immunodiffusion Differential immunocapture ELISA Lineage identification using the reverse-transcription PCR VIRUS NEUTRALIZATION TEST –Gold standard ELISA CHROMATOGRAPHIC STRIP TEST Developed for assisting field personnel in investigating suspected outbreaks of rinderpest Any positive result should be treated as indicating a highly suspicious rinderpest case that must be immediately be subjected to a thorough investigation

36. TREATMENT Treatment is ineffective Vaccines are of no value in treating already infected animals

37. CONTROL AND ERADICATION S laughter and rigid quarantine measures In endemic areas, control used to be by annual vaccination and surveillance vaccine prepared from one strain will protect against all other strains Rinderpest vaccine protects goats against infection with the virus of PPR Prevention of the introduction of ruminants from known infected areas

38. DISINFECTION Rinderpest virus can be killed by most common disinfectants including phenol, cresol, sodium hydroxide (2% for 24 hours) and lipid solvents The FAO recommends that premises, equipment and clothing be cleaned, then decontaminated with oxidizing agents such as sodium or calcium hypochlorite, or alkalies such as sodium hydroxide or sodium carbonate Faeces and effluents should be treated with sodium carbonate, before they are burned or buried Pasteurization or heat treatment can inactivate the virus in milk.

39. MILE STONE 1920s : J.T. Edwards made a breakthrough by discovering that animals given attenuated rinderpest virus preparation were protected from rinderpest for their whole life. 1957 : Walter Plowright developed a rinderpest vaccine which was stable, safe and cheap to produce Walter Plowright

40. Plowright tissue culture rinderpest vaccine ( TCRV) TCRV was one of the finest vaccines ever developed in human or veterinary medicine It protected against all clades of rinderpest virus provided lifelong immunity to cattle never associated with any adverse reactions a single tissue culture infectious dose was immunogenic The vaccine benefited hundreds of millions of livestock-dependent people The principal limitation of the vaccine was that it required a strict cold-chain The production process using primary bovine kidney cells was a potential source of contaminants and a constraint to large-scale manufacturing.

41. ThermoVax The new vaccine, named ThermoVax , shelf life of 30 days outside the cold-chain and it was required to hold the minimum titre for 14 days at 45°C, sufficient to dramatically extend the reach of field vaccination programmes The transfer of technology to African production facilities led to the commercial availability of ThermoVax in quantities sufficient for rinderpest eradication by 1992.

42. NPRE Rinderpest Control Programme was launched in India during the year 1952 The 100 % centrally sponsored National Project for Rinderpest Eradication was launched - May, 1992 The main objective of this project was total eradication of Rinderpest from the country as a whole National ceremony on Rinderpest eradication

43. The need to combat rinderpest provided the impetus for the establishment of the first modern veterinary school in Lyon (France) in 1762

44. GLOBAL FREEDOM FROM RPV After several decades of success in eradicating rinderpest from Europe, the disease recurred unexpectedly in Belgium in 1920, which resulted in the creation of the World Organization for Animal Health (OIE) in 1924 & Food and Agriculture Organization (FAO) 1946 The last confirmed case of rinderpest was reported in Kenya   in 2001  The final vaccinations were administered in 2006 The last surveillance operations took place in 2009, failing to find any evidence of the disease

45. Eradication was confirmed by the World Organization for Animal Health on 25 May 2011 On 28 June 2011, FAO and its members countries officially recognized global freedom from the deadly cattle virus Rinderpest is the first worldwide eradication of an animal pathogen; only one other virus, human smallpox, has ever been completely eliminated from nature. Rinderpest virus is biologically similar to the virus of peste des petits ruminants which has been targeted by the OIE and FAO as the next animal disease for global eradication.

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