Rinderpest

Last updated March 26, 2003

Agent
Hosts
Epidemiology
Rinderpest As a Biological Weapon
Clinical Features
Differential Diagnosis
Laboratory Diagnosis
Treatment
Prevention and Control
Public Health Issues
References

Agent

Rinderpest, also referred to as cattle plague, is a viral disease caused by rinderpest virus (RPV). The virus predominantly affects cattle, domestic buffalo, and some species of wildlife. Key features of the virus are outlined below (see References: Mebus 1998).

Viral classification:

Family: Paramyxoviridae
Genus: Morbillivirus

Virion morphology:

Helical
Enveloped
150+ nm

Genetic composition:

Negative-sense, single-stranded RNA virus
Only one serotype (although field strains vary in pathogenicity)
Immunologically related to peste des petits ruminants virus, canine distemper virus, and human measles virus

Environmental survival:

Stable within pH range of 4.0 to 10.0; optimal pH between 6.5 and 7
Killed by sunlight and/or heat
Sensitive to different levels of humidity
Susceptible to glycerol and lipid solvents as well as most disinfectants
Viable in chilled or frozen tissue samples for long periods

Hosts

Rinderpest is a disease mainly of cattle and domestic buffalo, including water buffalo. The disease is of great concern to livestock producers because of its communicability and high morbidity and mortality rates. There is no age or gender predisposition, and transmission to humans does not occur.

Most wild and domestic cloven-footed animals can become infected. Animal hosts other than cattle and buffalo include the following:

Zebus
Wild ungulates in contact with cattle (eg, African buffalo, elands, kudus, wildebeests, antelopes, bushpigs, warthogs, giraffes, hippopotamuses)
Sheep and goats
Pigs (Asian pigs appear to be more susceptible than African or European pigs)

Epidemiology

Occurrence

Ancient reports place cattle plague at the siege of Troy in 1184 BC. It has continued to devastate cattle operations for centuries, warranting establishment of the first veterinary school in 1792. Cattle plague often followed war movements as cattle traveled with troops and refugees.

Up to the 1860s: Rinderpest outbreaks in Africa were localized and self-limited; however, in 1885 the "Great African Pandemic" broke out, decimating 90% of cattle herds and making rinderpest a highly dreaded disease.
1920s: Rinderpest spread from India to Belgium and Brazil. The disease was also reported in Australia.
Late 1960s1970s: The disease spread from Lebanon to Israel and Syria.
1979-1983: A resurgence in Africa, killing more than a million cattle, prompted the Pan African Rinderpest Campaign (PARC) to develop control programs in an attempt to limit the disease.

Currently, only two main wildlife reservoirs of rinderpest are thought to exist: the Indus River buffalo tract in Pakistan (in which elimination of the virus is thought to be near) and the Somali pastoral ecosystem of southern Somalia and northern Kenya (see References: Roeder 2002)

Endemic areas of rinderpest have produced a cattle population with inherited innate resistance. Therefore, outbreaks in these areas often affect only young and immunocompromised animals (see References: FAO1996).
Nomadic cattle herds are a major means of dispersing RPV.
The presence of the virus in wildlife populations is thought to be one reason for the decline in some wildlife species in the African endemic area (see References: Roeder 2002).

RPV has never been established in the Americas or in Australia/New Zealand. However, significant concern for introduction exists in these areas. These areas' national cattle herds are naive to RPV and, as a result, disease could rapidly infect entire populations, affecting all ages of livestock and consequently annihilating cattle production (see References: FAO 1996).

Transmission

Transmission occurs predominantly between animals, although the disease can be spread through several additional routes as well (see References: Mebus 1998, Aiello 1998, OIE:

Direct or close contact with infected animals or infected animal discharge/secretions

Urine
Feces
Saliva
Blood
Tears
Nasal secretions

Contaminated water or food
Aerosolization (only over very short distances)
Contaminated equipment/fomites (not a major source of disease spread)
Viremia and subsequent dissemination (follows infection via attachment to mononuclear cells); multiplication occurs in tonsilar and lymph tissues

Vertical transmission does not occur, and transmission via arthropod vectors has not been recognized. Disease in wild reservoir populations does not persist without the presence of susceptible cattle. Therefore, the disease is essentially eradicated when domestic herds are rinderpest-free (see References: FAO: Global Rinderpest Eradication Program; Aiello 1998).

A rinderpest outbreak in wild ruminants in Kenya confirmed the importance of wildlife as sentinels but showed that the wildlife did not act as a reservoir for the domestic population. Although the exposed cattle were only mildly infected and the mortality rate in buffalo was nearly 80%, the cattle were thought to be the source of the virus for the wild ruminants (see References: Kock 1999).

Communicability

Infection is transmitted via the conjunctiva, mucous membranes, epithelium of the nasopharynx, and upper and lower respiratory tracts.
Secretions and discharges are infective 1 to 2 days prior to the onset of clinical signs and contain a high viral load for 8 to 9 days following illness onset.
Maternal antibodies provide immunity to offspring until 6 to 11 months of age (see References: Aiello 1998).
RPV is highly communicable and often spreads rapidly throughout an entire herd.
Recovered animals are not contagious, and no chronic carrier state exists.

Rinderpest As a Biological Weapon

Rinderpest is of concern as a biological weapon for the following reasons:

The disease has high rates of morbidity and mortality.
The disease is highly communicable and spreads rapidly once introduced into nonimmune herds.
Cattle herds in the United States and other developed countries are not routinely immunized against RPV and therefore are susceptible to infection.

Clinical Features

Cattle and Domestic Buffalo

Clinical features of the disease in cattle and buffalo are outlined in the table below.

Clinical Features of Rinderpest in Cattle and Domestic Buffalo*
*Feature*	*Characteristics*
Incubation period	3-15 days Varies depending on strain, dosage, and route of infection
Peracute form	Particularly important in young animals High fever, congested mucous membranes Death often occurs within 2-3 days
Acute (classical) form	Fever, constipation followed by diarrhea (watery-hemorrhagic), anorexia, tenesmus, serous-mucopurulent nasal/ocular discharge, leukopenia, ptyalism, necrotic-hemorrhagic oral erosions (see Figure DEFRA 2005]), enlarged lymph nodes, tachycardia, decreased rumination, dehydration Death often occurs within 6-12 days On necropsy, necrotic lesions throughout gastrointestinal tract, especially in lymphoid rich areas Rarely, clinical signs regress about 10 days after onset and recovery occurs within 25 days; these naturally exposed and recovered animals are immune for several years, maybe life-long
Subacute form	Mild clinical signs combined with low mortality rates
Atypical form	Irregular pyrexia and mild or no diarrhea Immunosuppression due to virus's lymphotropic tendency can lead to secondary infections as well as emergence of latent infection
Morbidity rate	Often 100%
Mortality rate	Up to 90%
Extent and severity of lesions will vary depending on strain, route, and duration of exposure and on susceptibility of herd. See References: Aiello 1998. Adapted from Mebus 1998; OIE (see References).*

Goats and sheep

Major signs:

Variable pyrexia
Anorexia
Intermittent diarrhea

African goats and sheep generally have subclinical infection (demonstrated by seroconversion in the absence of clinical findings) and do not transmit the disease to cattle.
Indian sheep and goats that have been inoculated by a low-passage goat vaccine have demonstrated passage of the virus to domestic buffalo.

Pigs

Major signs:

Pyrexia
Prostration
Conjunctivitis
Buccal erosions
Death

Infected European pigs may transmit virus to other pigs as well as to cattle

Differential Diagnosis

The following agents and conditions should be considered in differential diagnosis:

Viral Agents

Bovine viral diarrhea (BVD) virus (closely resembles RPV)

BVD generally is a disease of animals between 4 and 24 months of age, which can be a major factor in differentiating it from RPV.
Rinderpest should be considered and differentiated from BVD in all cases of rapidly spreading, acutely febrile disease accompanied by oral erosions.

Foot-and-mouth disease (picornavirus)
Infectious bovine rhinotracheitis (alpha herpesvirus)
Malignant catarrhal fever (gamma herpesvirus)
Vesicular stomatitis (rhabdovirus)
Peste des petits ruminants (small ruminants; paramyxovirus)
Bluetongue (small ruminants; reovirus)

Bacterial Agents

Salmonellosis (Salmonella species)
Necrobacillosis (Fusobacterium necrophorum)
Paratuberculosis (Mycobacterium paratuberculosis)

Dietary Factors

Arsenic poisoning

Sources: Mebus 1998, OIE, Kirk (see References).

Laboratory Diagnosis

Although eventual definitive diagnosis is appropriate, it is essential that RPV be assumed during a clinically apparent disease outbreak in endemic areas so that control measures can be implemented immediately. However, where sporadic foci are concerned, confirmation of the virus is essential in order for compensation to be awarded (see References: FAO).

There are several ways to confirm a rinderpest diagnosis (see References: OIE):

Viral isolation (the "gold standard" for definitive diagnosis of rinderpest in a previously disease-free area)
Antigen detection

Agar gel immunodiffusion test
Direct and indirect immunoperoxidase tests
Counter-immunoelectrophoresis
Immunohistopathology

Paired serology

Enzyme-linked immunosorbent assay (ELISA)
Virus neutralization

Detection of virus RNA (recent)

Rinderpest-specific cDNA probes
Polymerase chain reaction (PCR) amplification

A new rapid pen-side chromatographic strip test using ocular secretions was useful in a 2000 outbreak of subacute rinderpest in three Pakistani herds. In the past, field diagnosis was based on clinical signs of an acute outbreak, but improved immunity in dairy herds (cattle and buffalo) has resulted in subacute forms of the disease that are more difficult to diagnose. The pen-side test allowed veterinarians to make a diagnosis at the farm. Without the test, the milder outbreak may not have been identified (see References: Hussain 2001).

Specimen Collection

It is crucial to select appropriate sample donors, ideally multiple animals, to confirm the presence of RPV (see References: Mebus 1998):

Animals showing early-onset diarrhea (best)
Febrile animals with oral lesions
Dead animals if death occurred during the febrile phase from cardiogenic shock, since viral load would still be high (specimen collection from dead animals as a confirmatory diagnosis should be avoided, as death usually occurs after viral titers recede)

The following table outlines collection of laboratory specimens for the diagnosis of rinderpest.

Collection of Laboratory Specimens for the Diagnosis of Rinderpest
*Donors/Samples*	Specimen collection*
Live, febrile animals	Sterile whole blood in heparin (10 IU/mL) or EDTA (0.5 mg/mL) Lacrimal and/or nasal swabs (150 mcL PBSA) Tissue samples of oral erosions Gum debris (in 0.5-1 mL PBSA) Aspiration biopsy of superficial lymph node
Sacrificed, slaughtered febrile animals	Spleen Lymph node Tonsil Place tissue sample in 10% formalin
Tissue from dead animals	Splenic, prescapular, or mesenteric lymph nodes Chill to subzero temperatures
Abbreviations: EDTA, ethylenediamine tetra-acetic acid; PBSA, Poisson Boltzmann surface area. Transported samples should be kept on wet ice, never frozen. Biopsy samples destined for long-term storage should be stored at -700C, whereas serum samples should be maintained at -200C. Adapted from Mebus 1998 (see References).*

Treatment

There is no prescribed treatment for RPV infection; this fact,combined with high morbidity rates, accounts for the devastating nature of the disease.
Often a diagnosis of rinderpest means slaughter of the affected animal(s) and significant economic loss. In rare cases, supportive care and antibiotic therapy can help in the treatment of especially valuable animals.
Because of the lack of effective treatment, preventive measures are of key importance.

Prevention and Control

RPV has only one serotype, making it a good candidate for control and eradication programs. Furthermore, recovered animals have lasting immunity, with some reports suggesting a life-long response (see References: Aiello 1998).

Vaccination Programs

Vaccine protocols must take into consideration the environmental stability of the virus (see References: Mebus 1998, Aiello 1998):

Sunlight quickly inactivates the virus; therefore, vaccine must be stored in protective brown bottles.
Because RPV is heat-labile, special considerations must be taken to ensure vaccine effectiveness in tropical areas. Vaccines derived from heat-stable attenuated strains or constituted in molar concentrations of sulfate ions can better maintain viability.

Excellent vaccines exist to help combat RPV, as outlined below. Many of them confer life-long immunity.

Vaccines Used in the Control of Rinderpest
*Geographic Area*	*Vaccine Type*
Middle East, India, Africa	Cell cultureadapted*
India	Goat-adapted*
China and Korea	Lapinized
Korea	Avianized-lapinized
Experimental	Vaccinia-vectored (has shown experimental protection)
Only partially attenuated. Should not be used in immunosuppressed animals, animals with latent infections, or animals with low innate immunity. Also, this version of the vaccine will kill goats and sheep. Nonetheless, immunity is life-long in cattle. Most commonly used. Imperative in the eradication effort, since it eliminates the use of a live virus. Adapted from* Mebus 1998 (see References).

Maternal immunity is present in offspring between 6 to 11 months of age; therefore, vaccination programs should be designed to avoid the period when colostral immunity could interfere with vaccination. It is suggested that calves be vaccinated annually for 3 years.

In endemic countries, vaccination is often performed annually at the national herd level. Where spot epidemics arise, slaughter of affected animals is coupled with a ring-vaccination program. This involves vaccination and quarantine of animals in the area surrounding the outbreak (see References: Aiello 1998).

Control Following Outbreaks

Rinderpest outbreaks are considered quite serious, and immediate steps have been designed to eliminate the virus:

Quarantine and slaughter of infected and exposed animals
Ring vaccination of surrounding areas

Strategies for the prevention of future outbreaks:

Quarantine, testing, and vaccination of introduced animals
Prevention via sanitary prophylaxis (see References: OIE)

Appropriate destruction of cadavers
Disinfection of equipment and facilities

Serologic monitoring of wild ungulates, sheep, and goats. When monitoring small ruminants, the use of a rinderpest vaccine must be taken into consideration. (The vaccine is often used to protect against peste des pestis ruminant because it provides cross-protection against this virus [see References: Mebus 1998]).
Heightened awareness of and surveillance for RPV and restricted movement of animals and meat into rinderpest-free zones.

The Global Rinderpest Eradication Programme (GREP)

Currently, rinderpest is limited to a few foci in east Africa and the Indian subcontinent. GREP is designed to respond to and address all rinderpest outbreaks in order to reach the goal of complete global eradication by the year 2010 (see References: FAO: Global Rinderpest Eradication Program).

The immediate challenges stated by GREP are:

To define, contain, and eliminate the last foci or rinderpest persistence
To remove doubts about rinderpest persistence
To persuade uncommitted countries to endorse GREP
To strengthen rinderpest surveillance and emergency preparedness
To ensure cessation of unnecessary mass vaccination

Current US Policies

In the United States, rinderpest is a reportable disease and, as such, policy restricts the importation of live animals and meat products from known rinderpest- positive countries.

Public Health Issues

RPV does not cause infection in humans; therefore, there are no public health issues to be considered.

References

Aeillo S, ed. Rinderpest: Introduction. In: Merck veterinary manual. Ed 8. Whitehouse Station, NJ: Merck & Co, 1998:542-4 [Full text]

Anderson J, Barrett T, Scott GR. Collection of specimens. In: Manual of the diagnosis of rinderpest. Ed 2. Part II, Chap 5. Rome, Italy: Food and Agriculture Organization of the United Nations, 1996 [Full text]

DEFRA (Department for Environment Food and Rural Affairs). Animal health and welfare. Rinderpest: pictures. May 24, 2005 [Web page]

FAO (Food and Agriculture Organization of the United Nations). Global Rinderpest Eradication Program (GREP) [Web page]

FAO (Food and Agriculture Organization of the United Nations). Rinderpestthe toll and treatment of a plague. Aug 6, 1996 [Full text]

Hussain M, Iqbal M, Taylor WP, et al. Pen-side test for the diagnosis of rinderpest in Pakistan. Vet Rec 2001 Sep 8;149(10):300-2

International Food Safety Consultancy. Global Rinderpest Eradication Programme: the GREP strategy

Kirk J, Moeller R. BVD . . . or is it rinderpest? University of California, Davis, and California Animal Health and Food Safety System, Veterinary Medicine Extension [Web page]

Kock RA, Wambua JM, et al. Rinderpest epidemic in wild ruminants in Kenya: 1993-1997. Vet Rec 1999 Sep 4;145(10):275-83 [Abstract]

Mebus CA. Rinderpest. In: US Animal Health Association, Committee on Foreign Animal Disease. Foreign animal diseases: the gray book. Ed 6. Part IV. Richmond, VA: US Animal Health Assoc, 1998 [Full text]

OIE (Office International des Epizooties/World Organization for Animal Health). Rinderpest. Technical disease card database [Full text]

Roeder PL,Taylor WP. Rinderpest. Vet Clin North Am Food Anim Pract 2002 Nov;18(3):515-47, ix [Abstract]


Home	Mission & Activities	About Us	Center Support	Contact Us