RINDERPEST (CAT TLE PLAG UE)
ETIOLOGYRinderpest is associated with a morbillivirus (family Paramyxoviridae)
there are many strains with considerable variation in virulence between them but all are immunologically identical.
Consequently, the immunity which develops after infection or vaccination with one strain protects against all other strains or isolates.
Three genetically distinct lineages of the virus are now recognized, with lineages 1 and 2 being of African origin and lineage 3 of Asian origin, 1 but the differences between lineages are small and do not affect the immunity induced.
Rinderpest virus is quite fragile and is antigenically related to the other members of the morbillivirus group including the viruses causing peste des petits ruminants (PPR) in sheep and goats, canine distemper in dogs, measles in humans, phocine distemper in seals and hedgehog distemper.
EPIDEMIOLOGY
Historically, rinderpest (cattle plague) was a most devastating disease spread from Asia to Europe, the Middle East and Africa, usually as a sequel to wars.
Rinderpest was eradicated from southern Afri ca, Europe and China by the middle of that century.
In the 1960s, the disease was cleared from West Africa and most of East Africa, but there was a dangerous resurgence less than 10 years later and again in the 1990s.
Occurrence
Most countries today claim to be free of rinderpest. At the end of the last century, the disease was still endemic in parts of Asia and in a small area bordering on Kenya and Somalia.
In the 1980s, outbreaks occurred over much of tropical Africa and Asia. The most recent outbreaks occurred in Kenya and Tanzania (1993-97, 2003) and in Pakistan (2000-2002).
The disease has never appeared in North America but there have been single outbreaks which were quickly eradicated in Brazil and Australia.
All ruminants and pigs are susceptible to infection with rinderpest virus.
Natural infection occurs commonly only in domestic cattle, buffalo and yak but in some outbreaks, sheep and goats do become infected and show clinical signs.
European pigs are susceptible to infection but only show a mild transient fever and do not spread the disease.
Pigs indigenous to Thailand and Malaysia are highly susceptible and natural spread of the clinical disease can occur.
Similarly, clinical disease is common in Asian sheep and goats and they contribute to the persistence of the virus in the region.
There is the belief that rinderpest became prevalent in small ruminants in Africa and Asia only after the introduction of goat adapted rinderpest vaccine from which the vin.Js of PPR probably mutated.
One humped camels become infected, but show no clinical signs.
Wildlife (especially buffalo and eland, giraffe, kudu, deer and wildebeest.) are often affected during outbreaks and the infection usually spreads to them from infected cattle.
wildlife did not appear to act as reservoirs but as fully susceptible hosts during the Kenyan epidemic of 1993-1997 involving the lineage 2 virus in national parks.
Prevalence In the absence of an outbreak, the prevalence of the disease in endemic countries is low.
Morbidity and case fatality When epidemics occur in highly susceptible populations, the morbidity and case-fatality rates approximate 100% and 50% (25-90%) respectively, ? and large numbers of in-contact animals may have to be destroyed.
In endemic areas, most of the cattle population have some degree of immunity and case-fatality rates rarely exceed 30%.
Methods of transmission
Close contact between infected and non infected animals is usually necessary for spread of the disease to occur because the virus does not survive for long outside the host.
The virus is excreted by infected animals in urine, feces, nasal discharges, and perspiration.
Transmission occurs through contaminated feed or by inhalation of aerosol.
Survival of aerosolized virus depends particularly on humidity and it may last for more than 30 min at relatively low humidity.
Ingestion of food contaminated by discharges of clinical cases, animals in the incubation stage, or animals with subclinical infections, may also be important modes of infection, especially in pigs.
Aborted bovine fetuses may contain live virus.
Insects, many of which have been shown to contain the virus, are unlikely to act as vectors.
Other species, including European breeds of pigs in particular, and sheep, goats, camels and wild ruminants may serve as a source of the virus for cattle.
recovered animals act as carriers for more than a few days.
Because of the failure of the virus to persist outside the body, rinderpest can be controlled by interrupting its transrnission.
Risk factors
Host factors
Cattle and buffalo of all ages are susceptible to rinderpest, unless they have been vaccinated or have recovered from a previous infection or, in the case of calves, they have received colostral antibodies.
European breeds of cattle are believed to be more susceptible than zebu cattle, but zebu cattle without antibodies from previous exposure or vaccination are fully susceptible.
Herds that seasonally migrate over long distances in search of pasture and water. Any other legal or illegal movement of animals incubating the disease could be a mode of spread.
Cattle raids and communal grazing can be risk factors.
Other ruminants and pigs in contact with infected cattle or buffalo may develop the disease.
Environmental and pathogen factors.
The virus is present in the blood, tissues, secretions and excretions of infected animals, reaching its peak of concentration at about the height of the temperature reaction and subsiding gradually to disappear about a week after the temperature returns to normal in those animals that recover.
The risk of transmission is therefore greatest during the febrile stage.
The virus does not persist outside the host for more than a few hours at normal temperatures. It is inactivated in cadavers within 24 h as a result of pH changes and putrefaction, and it is readily destroyed by heat, drying and most disinfectants.
Even in untreated premises, it survives for only a few days. However, it is relatively resistant to cold and may survive for as long as 1 month in blood kept under refrigeration.
The risk of transmission can therefore be greatly minimized by applying appropriate sanitary and other control measures.
Immune mechanism
Immunity after a natural infection or by vaccination is long and for all practical purposes, persists for life.
The protection is associated with the induction of humoral antibodies, first IgM and later, IgG and IgA, which are detectable by enzyme immunoassay.
The disease is also associated with immunosuppression because the virus causes extensive necrosis of lymphocytes throughout the body.
Older live vaccines can also cause immunosuppression.
However, the newer tissue culture vaccine does not and can be simultaneously administered with other vaccines, for example, FMD and contagious bovine pleuropneumonia vaccines, without any diminished responses to any of the immunogens used.
Economic importance
Rinderpest has been one of the major diseases of cattle that occur in the form of epidemics.
It is a List A diseases by OlE classification. Under extensive systems of management as practised in many African and Asian countries, the disease easily spreads across national boundaries and can involve most of the national herds of cattle and buffalo.
Losses can be colossal and are due to deaths, loss of productivity and cost of effective prevention and control.
The virus of rinderpest is not pathogenic to humans.
Although rinderpest is not highly contagious, the mortality rate can be so high that care should be taken in handling diagnostic specimens to avoid accidental spread.
Under intensive system of management, any accidental infection can be easily curtailed and eradicated.
PATHOGEN ESIS
The virus is inhaled in infected droplets; it penetrates through the epithelium of the upper respiratory track and multiplies in tonsils and regional lymph nodes.
From these sites, the virus enters the blood in mononuclear cells and is disseminated throughout the body, intimately associated with leukocytes and only a small proportion free in plasma.
The virus has a high degree of affinity for lymphoid tissues and alimentary mucosa and replicates in monocytes, lymphocytes and epithelial cells.
There is a striking destruction of lymphocytes in tissues resulting in marked leukopenia.
Lymphocytes are destroyed by apoptosis as well as necrosis. The focal, necrotic stomatitis and enteritis which are characteristic of the disease are the direct result of viral infection and replication in epithelial cells in the alimentary tract.
However, because the virus induces a strong antibody response shortly after infection, there is a rapid decline and elimination of virus from the body as clinical signs and lesions become manifest.
Death is usually from severe dehydration, but in less acute cases, death may be from activated latent parasitic or bacterial infections which are exacerbated because the animal is immunosuppressed as a result of the destruction of lymphoid organs by the virus.
CLINICAL FINDINGS
Most outbreaks reported recently have been usually mild in cattle.
In general, clinical signs may be peracute, acute, subacute or inapparent (in species other than cattle and buffalo).
The peracute form is not common except after experimental administration
of the virus. It is characterized by characterized by alimentary tract signs 239
high fever, congested mucous membranes, respiratory distress and death
1-3 d later.
Acute cases may be seen in naive cattle in areas or countries that were previously
free of the disease.
An incubation period of 6-9 d is usual.
The first stage of the disease is several days of high fever (40.5-41, 105-107°F), without mucosal lesions (phase of prodromal fever).
Anorexia, a fall in milk yield, lacrimation and a harsh, staring coat accompany the fever and this corresponds to the period of peak virus production in tissues.
This is followed by the mucosal phase characterized by inflammation of buccal, nasal and conjunctival mucosae and, in some cases, hyperemia of vaginal mucosa and swelling of vulva. The lacrimation becomes more profuse and then purulent and is accompanied by blepharospasm. Bubbly salivation of clear blood -stained saliva is followed by purulent saliva and halitosis.
A serous nasal discharge similarly becomes purulent. Discrete, grayish, raised necrotic lesions (1-5 mm in diameter) develop, appearing first on the inside of the lower lip and adjacent gum, on the cheek mucosa at the commissures, and on the lower surface of the tongue.
Later they become general in the mouth, including the dorsum of the tongue, and may become so extensive that they coalesce.
Similar lesions are common on nasal, vulval and vaginal mucosae. The necrotic material sloughs, leaving raw, red areas with sharp edges and these may coalesce to form shallow ulcers. Vesicles are not present.
Severe diarrhea, and sometimes dysentery with tenesmus, appear as lesions develop in abomasum and intestines.
Skin lesions affecting the perineum, scrotum, flanks, inner aspects of thighs and the neck are less common.
The skin becomes moist and reddened and later overed with scabs.
After a period of illness lasting from 3-5 d, there is a sudden fall in temperahIre, accompanied by exacerbation of the mucosal lesions.
Other signs include dyspnea, cough, diarrhea, severe dehydration and sometimes abdominal pain.
Prostration and a further fall in body temperature to subnormal levels occur on days 6-12, after which death usually occurs within 24 h. A few animals may survive and go into a convalescent phase during which the mucosal lesions heal rapidly, the diarrhea eventually stops and recovery of body condition takes several weeks.
Pregnant cattle may abort at this stage, discharging infective virus in the fetus and vaginal secretions for up to 24 h.
In enzootic areas, both a subacute form and a skin form occur with lower morbidity and mortality.
In the subacute form, the temperature reaction is mild and the accompanying anorexia and malaise are not marked.
The inflammation of the mucosae is catarrhal only and there is no dysentery.
In the skin form, the systemic reaction is absent and small pustules develop on the neck, over the withers, inside the thighs and on the scrotum.
Most affected animals recover and convalescence is short.
However, because of the severe lymphocytolysis, latent pathogens, particularly Anaplasma marginale, are often activated and the resulting disease may overshadow the primary rinderpest.
Signs and lesions similar to those which occur in cattle develop in sheep and goats and in Asian pigs.
The disease in European pigs is clinically inapparent and wild ungulates exhibit a wide range of clinical signs, from severe to mild. Keratoconjunctivitis has been described in buffaloes and kudus affected with lineage 2 virus.
CLINICAL PATHOLOGY AND LABORATORY DIAGNOSIS
A marked leucopenia occurs at the height of the infection and after vaccination in cattle and in experimentally infected sheep and pigs.
The total count usually falls to below 4000 /L and is due to a precipitous drop in lymphocytes.
With diarrhea, animals also become severely dehydrated.
Later, they may show neutrophilia.
Various methods for diagnosing rinderpest have been described and basically
involve identification of the agent and serological tests.
A rapid chromatographic strip test (Penside test) that can detect rinderpest antigen in lachrymal fluid is a useful tool for field personnel.
In areas where there had been recent outbreaks, a presumptive diagnosis also can be made on the basis of the history, clinical signs and postmortem findings.
Since the prevalence of the disease is decreasing, it is recommended that for each outbreak, the virus should be isolated, its lineage identified and its virulence in cattle assessed.
Antibody detection in paired serum samples is not recommended during an outbreak because of the length of time required to confirm a diagnosis but it is used for disease surveillance and vaccine evaluation.
For antigen detection and virus isolation, the key to diagnostic success is the collection of suitable samples at the optimum time (3-5 d after fever commences) from many animals rather than many samples from one sick or dead animal.
The proportion of positive reactors falls sharply after diarrhea commences and in moribund or dead animals.
A technique suitable for laboratory and field use is the agar gel diffusion (AGID) technique in which needle biopsy samples
NECROPSY FINDINGS
The important necropsy findings are in the alimentary and upper respiratory
tracts and in the external genitalia in females.
The carcass is dehydrated, emaciated emaciated and soiled with fetid feces. Small, discrete, necrotic areas develop on the oral mucosa and separation of the necrotic material leaves sharply walled, deep erosions with a red floor which maycoalesce to form large erosions or ulcers.
These lesions extend to the pharynx, upper esophagus and abomasum, particularly the pyloric region.
The forestomachs are spared and lesions are mild in the small intestine except at the Peyer's patches which are swollen, hemorrhagic and necrotic.
Severe changes occur in the mucosa and lymphoid nodules in the large intestine, particularly at the cecocolic junction.
Zones of hemorrhage and erythema running transversely across the colonic mucosa produce a characteristic striped appearance, the so-called 'zebra stripes'.
The nasal turbinates and septa are coated with a tenacious mucopurulent exudate beneath which is an eroded and lcerated surface.
Lesions may extend to the upper trachea but not beyond and the lungs are usually not affected. Congestion, swelling and erosion of the vulval and vaginal mucosae may occur.
Materials sent for laboratory examination should include fixed sections of lymph node, tonsil and alimentary tract lesions, as well as fresh spleen, blood and alimentary tract for antigen detection or virus isolation.
----- Differential diagnosis list
Bovine virus diarrhea
Foot-and-mouth disease
Malignant catarrhal fever
Peste des petits ruminants.
Treatment None
Control
Surveillance and annual vaccination with tissue culture vaccine in endemic areas, eradication by slaughter and rigid quarantine during outbreaks in non-endemic areas ---
--- PESTE DES PETITS RUMI NANTS
(PPR, GOAT PLAG UE OR KATA)Etiology Peste des petits ruminants virus, a morbillivirus
Epidemiology Contagious disease of goats and sheep; endemic in west and central Africa, outbreaks in northeastern Africa, Middle East and Asia, high mortality in goats
Pathogenesis Inhaled/ingested virus upper respiratory infection viremia
target cells (lymphocytes, alimentary and respiratory mucosae) signs and lesions
Signs Fever, oculonasal purulent discharge, necrotic stomatitis, diarrhea and
respiratory distress
Clinical pathology Marked leukopenia
Diagnostic confirmation
Virus neutralization test and immunohistochemistry
Differential diagnosis list
• Rinderpest
• Contagious ecthyma
• Bacterial pneumonias
• Coccidiosis
Treatment Hyperimmune serum and symptomatic treatment for valuable animals
Control Segregation of new stock, vaccination with tissue culture or other vaccines ----------------------