Chapter 1. Epizootiological background
Chapter 2. Clinical signs
Chapter 3. Clinical pathology
Chapter 4. Post-mortem findings
The causative virus
Natural host range
From time immemorial into the twentieth century, waves of rinderpest have regularly devastated buffalo and cattle in Asia and Europe and have occasionally caused havoc in North Africa. Animals in sub-Saharan Africa were hit severely, perhaps for the first time, when rinderpest was unwittingly introduced into the Horn of Africa in 1887. The resulting panzootic swept north to the Mediterranean, west to the Atlantic and south to the Cape of Good Hope, permanently changing the flora and fauna of the continent. It burnt itself out in southern Africa in the early 1900s, but lingered on in northern equatorial Africa until very recently.
Today, Europe and most of Asia are free of the disease except for a pocket of infection that exists in southern India affecting buffalo, cattle, goats, sheep, pigs and wildlife. In Africa, a focus persists north of Lake Turkana in the borderlands of Ethiopia, Kenya, the Sudan and Uganda, an area of civil unrest. At the time of writing, rinderpest is known to be active in the northern part of the Awash Valley in Ethiopia as well as in Pakistan and Sri Lanka. Three disquieting episodes have occurred in recent years in the former Union of Soviet Socialist Republics. In 1990 rinderpest was diagnosed in cattle in Georgia, the first penetration of the disease into Europe since 1949. Fortunately it was quickly recognized and stamped out. The source of the outbreak was not identified, but Georgia and its neighbours were and are still embroiled in civil wars, a proven seed bed for rinderpest to flourish. The second episode occurred on Mongolia' s northeastern border with Russia in 1991, when transhumant Russian cattle grazing in Mongolia developed clinical signs of rinderpest; 64 percent of those affected died. Several months later the third episode occurred on the Russian side of Mongolia's northwestern border with that country in which 265 out of the 389 yaks affected died. Tissue samples were forwarded to the Institute for Animal Health, Pirbright Laboratory, Surrey, United Kingdom, and the presence of two distinct rinderpest strains of rinderpest virus was demonstrated, one related to Plowright's cell-cultured vaccine virus and the other related to virulent Asiatic field strains (Barrett et al., 1993a).
Historically, the Near East has experienced occasional invasions of rinderpest imported with slaughter stock from Africa and the Indian subcontinent. In September 1991, there was a major outbreak in Turkey, the first since 1971. The disease spread rapidly, affecting 516 herds in 44 localities within two months, but prompt action by the Turkish veterinary authorities eradicated the disease within four months. In the end, 2 700 cattle died, 12 000 were slaughtered and 12.5 million were vaccinated (Sahal, 1992). During March/April 1994, outbreaks of rinderpest were reported from eastern Turkey, northern Iraq and northwestern Iran. This raised the possibility of an endemic focus in the Kurdish areas of Iraq and Turkey. Emergency efforts quickly eliminated infection from Iran and similar action taken in Turkey and Iraq seems to have been effective. Kuwait, Saudi Arabia, Bahrain, Qatar and the United Arab Emirates continue to be exposed to periodic invasion of rinderpest with live animals imported from South Asia. Thanks to constant vaccinations, recent outbreaks in this area have been of limited spread.
Recovery from an attack of rinderpest has long been known to confer lifelong immunity to the disease. Early attempts to immunize cattle artificially were unpredictable and often disastrous. In the pre-Jennerian manner, used to protect humans against smallpox, cloth setons soaked in "matter" from a sick animal were inserted into the subject's skin. The discovery in Russia in the late nineteenth century of the protective powers of serum drawn from a recovered animal (Semmer, 1893) led shortly thereafter to the development in South Africa of the serum-virus simultaneous immunization method (Kolle and Turner, 1897). The method was in vogue for nearly 35 years. As the source of the virus for immunization was the blood of a reacting ox, the risk of inadvertently injecting other bovine pathogens was high. Edwards (1928) attempted to obviate the risk by passaging the virus serially in goats and, in me process, fortuitously developed an attenuated goat-adapted virus that could be injected alone into cattle without serum. This vaccine, together with the development of lyophilization (freeze-drying) techniques in the late 1930s, revolutionized the control of rinderpest. Mass national and continental campaigns followed. The global prevalence of rinderpest reached its lowest level in 1976, when its presence was reported from only three countries. There has since been a resurgence in Africa, India and the Near East. Vigorous application of multinational eradication campaigns has curbed the resurgence so successfully, however, that active disease is restricted to defined pockets in Africa and Asia. The incidence today is the lowest it has ever been.
Rinderpest was one of the first diseases to be recognized as being caused by a filterable virus. It is now classified as a paramyxovirus in the genus Morbillivirus, whose terrestrial members - bovine rinderpest, canine distemper and human measles viruses - have been chronicled for centuries as virulent plagues of their host species.
In contrast, the fourth terrestrial morbillivirus - peste des petits ruminants (PPR) virus - was only recognized in the 1940s. At first the PPR virus was thought to be a variant of rinderpest virus, but it has now been identified as a distinct member of the genus (Gibbs et al., 1979). Since 1987 a clutch of previously unknown morbilliviruses has emerged and plagued populations of marine mammals such as seals, porpoises and dolphins in the Northern Hemisphere. More recently, morbillivirus antibodies - although not disease - have been detected in the sera of Atlantic pinniped and many cetacean species (Duignan et al., 1994). The relationships between these newly discovered viruses are shown in Figure 1.
The most-studied and best-known morbilliviruses not only look alike but they also have similar physico-chemical properties, produce similar cytopathic effects in cell cultures and share antigens. They are all negative single-stranded, non-segmented ribonucleic acid (RNA) viruses possessing six structural proteins and two non-structural proteins (Diallo, 1990). Sequence analyses of parts of the F protein gene of rinderpest virus have revealed distinct lineages of the virus that reflect the geographical location of then-isolation in Africa and Asia (see Figure 2).
Morbilliviruses are pleomorphic. The common shape is an enveloped spheroid, 100 to 300 nm in diameter, while less common are enveloped filaments up to 1 m m long. The serrated nucleocapsids are tightly coiled in the spherical particles and regularly coiled along the length of the filamentous virions. The envelopes are covered with minute projections, which are the surface glycoproteins (H and F proteins) responsible for cell attachment and fusion. Only these proteins stimulate the virus neutralizing antibody response.
FIGURE 1. Phylogenetic relationships between the differed morbilliviruses
Rinderpest virus is not robust. Outside its hosts it survives best at low or high relative humidities and is readily destroyed when the relative humidity lies between 50 and 60 percent. It is sensitive to heat, light and ultrasonic waves. High and low hydrogen-ion concentrations (pH) denature the virus; consequently, rinderpest-infected carcasses are rendered safe relatively quickly by the hydrogen-ion changes that follow autolysis and putrefaction, together with the inactivating effect of high ambient temperatures. Being enveloped, rinderpest virus is destroyed by lipid solvents; lipophilic disinfectants, therefore, are recommended for cleansing contaminated premises. In the presence of organic matter, the most effective disinfectants are 5 percent sodium hydroxide and 50 percent lysol (Wamwayi ,1989).
The stability of viral suspensions is enhanced by the addition of salt. For example, a molar concentration of magnesium sulphate heptahydrate (25 g in 100 ml) will slow down inactivation of the virus in water at 50°C by a factor of 3 to 4.
The 1981 checklist (Scott, 1981) of natural hosts of rinderpest virus requires updating. Although strains of the virus vary widely in their host affinities and in their virulences for particular hosts, natural infections are restricted to the even-toed ungulates belonging to the order Artiodactyla. It should be emphasized, however, that rinderpest virus may not attack all the susceptible species at risk. Moreover, host preferences have been known to change with time; in the great African panzootic, wildebeest was the last species to sicken, with none dying until after all the cattle were dead.
FIGURE 2 Geographical grouping of isolates by sequence data
Disease is most commonly observed in domestic ungulates, particularly buffaloes and cattle. Sheep are reported to contract mortal rinderpest in India, but elsewhere the disease has been recognized in this species only sporadically; the common rinderpest-like disease of sheep in southern India may be PPR. In contrast, in northern equatorial Africa and the Near East, overt disease from PPR is more frequently observed in goats. The Asian domestic sway-backed pig suffers from and succumbs to rinderpest, while European pigs experience inapparent infections when exposed experimentally. The first demonstration of natural infection in European-type pigs was belatedly reported from Egypt in 1991; blood samples were collected from 128 pigs slaughtered in 1982, when severe outbreaks of rinderpest were affecting Egyptian buffaloes and cattle. Rinderpest neutralizing antibodies were detected in the sera of 36 (28 percent) pigs (Youssef et al., 1991).
Fulminating peracute infections occur in free-ranging African buffalo, eland, kudu and warthog. Acute infections that usually end fatally have been observed in Africa in bongo, bushbuck, bush pig, chevrotain, dik-dik, duiker, giant forest hog, giraffe, sitatunga and wildebeest, and in Asia in banteng, blackbuck, gaur, nilgai and sambar.
Inherited innate resistance to rinderpest markedly influences the epizootiological character of the disease. In countries where the disease has long been enzootic, cattle possess a high innate resistance that slows the spread of the disease, lessens the clinical response and ensures the survival of most of the afflicted animals. In contrast, in countries long free of the disease, introduction of an apparently a virulent strain from an enzootic area often results in a fast- moving, explosive epizootic with many deaths. Nevertheless, on occasion, virgin-soil epizootics have failed to explode. For example, the 1920 epizootic in Belgium that provided the stimulus to found the international office of Epizootics (OIE) was relatively benign, delaying diagnosis for three to four weeks (Curasson, 1932).
Attacks in enzootic areas tend to be restricted to immature and young adult stock since the mature adults are immune either as a result of disease recovery or vaccination and the sucking young are protected through the ingestion of antibodies in their dam's colostrum. Attacks in previously disease-free areas affect livestock of all ages.
Rinderpest virus spreads when healthy, susceptible animals are exposed to infected droplets, either in the breath of a sick animal or in its virus-rich secretions or excretions. As the droplets are large and short-lived, the contact between sick and healthy animals must be close for transmission to occur.
Attenuated vaccine strains of rinderpest virus do not spread because they are not released into the expired air or in the faeces, having lost their epitheliotrophism.
On rare occasions, transmission has allegedly occurred through indirect contact with contaminated bedding, fodder or water. An analysis of valid records of virgin-soil epizootics from 1851 to 1950, however, clearly revealed that all instances were traceable to the importation of live animals. In short, the most likely source of a fresh focus is a newly arrived live animal.
Controlled experiments have shown that pigs also acquire infection through eating uncooked infected meat scraps. The practical significance of this mode of transmission, however, is not clear and warrants investigation.
Buffalo and cattle infections
Goat and sheep infections
Domestic pig infections
Many authors have described the clinical signs of rinderpest, the most comprehensive description being that given by Curasson (1932) in his book La peste bovine. Most of the descriptions, however, are misleadingly dramatic, having been based on observations made during virgin-soil panzootics. The classic syndrome is manifested by an incubation period of three to nine days, a short sharp fever, erosive stomatitis, gastroenteritis, fetid odour, dehydration and death. The enzootic disease in livestock with a high inherited innate resistance is much less dramatic and less typical, often with one or more of the cardinal features of the classic syndrome modified or absent.
Clinical reactions in buffalo and cattle are similar and may be peracute, acute, subacute or even inapparent.
The onset of a peracute reaction is sudden and unexpected. It is manifested by inappetence, high fever, depression, deep congestion of visible mucosae, severe panting and racing pulse. Death supervenes within two or three days, even before mucosal erosions develop. Fortunately, peracute reactions are not common, occurring most frequently in young calves and exotic animals.
The classic syndrome is divided into five phases: an incubation period, a prodromal fever, an erosive-mucosa phase, a diarrhoeic phase and convalescence in surviving animals (see Figure 3).
Although the onset of the prodromal fever is sudden, it is frequently missed because other clinical signs are minimal, except in lactating cows whose milk yield falls. Overt illness is clearly evident 24 to 48 hours later, when the animal becomes restless and then stands depressed, apart and alone. Respirations are shallow and rapid. The coat hairs stand erect, the muzzle dries, tears are wept and the nose runs. Appetite is impaired, rumination is retarded and defecation stops. Visible mucous membranes are congested but intact.
The first suggestive sign of rinderpest occurs two to five days after the onset of the prodromal fever, when raised pinheads of necrotic epithelium emerge from the surfaces of the mucous membranes lining the mouth, nasal passages and urogenital tracts. These are readily abraded to expose a haemorrhagic layer of basal cells (see Figure 4). Salivation is profuse. The erosions enlarge and coalesce. Thick yellow patches of necrotic cells begin to coat the nasal passages and mix with the nasal secretions, producing a fetid mucopurulent discharge. Lacrimal secretions likewise become mucopurulent. Thirst is intense but the appetite is lost. Soft faeces are voided frequently.
The diarrhoea proper begins as the fever falls, two to three days after the first appearance of the mucosal erosions. The dark, fluid faeces contain excess mucus and shreds of epithelium and necrotic debris streaked with blood. The smell is memorably sweet, fetid and offensive. Affected animals arch their backs and strain frequently, exposing congested and eroded rectal mucosae. Respirations are laboured and painful, characterized by an audible grunt when exhaling.
FIGURE 3 The clinical phases of classic rinderpest
In fatal cases the diarrhoea worsens progressively, causing rapid dehydration. Affected animals waste visibly; they have sunken eyes and stand with lowered heads and arched backs. Most collapse and die six to 12 days after the onset of the prodromal fever. Some, however, linger on for three weeks.
In surviving cases, the diarrhoea stops within a week of its onset. Pregnant animals, however, will abort during convalescence, which is prolonged, and a return to full health will take many weeks.
Subacute reactions are encountered in immature and young adult stock indigenous to a country where the disease is enzootic. The incubation period tends to be longer than that of the acute syndrome and may even last 15 days .The clinical signs are muted and often one or more of the cardinal features of the classic disease, such as fever, mucosal erosions, mucopurulent nasal and ocular discharges or diarrhoea, are absent. Most affected animals survive. Diagnostic suspicions of rinderpest, therefore, are often not aroused.
FIGURE 4 Rinderpest erosive stomatitis
Rinderpest virus selectively destroys T- and B-lymphocytes, but not memory cells. Thus, latent pathogens are commonly activated and supra-infection is encouraged. Both processes induce clinical signs that mask even those of the classical rinderpest syndrome (see Figure 5). However, it is in areas where subacute rinderpest is encountered that activated latent infections and suprainfections create the greatest diagnostic confusion.
Acute, subacute and inapparent rinderpest reactions occur in goats and sheep. Many of the clinical signs mimic those evident in cattle, but the course of the disease is shorter and pneumonic symptoms are more prominent. Affected animals develop high fevers and, almost concurrently, mucosal erosions. Sometimes, however, the erosive stomatitis is fleeting or even absent. Inappetence and depression quickly follow and the animals stand, hair-on-end, with their heads thrust forwards and downwards and their backs arched. They pant and cough. Serous nasal and lacrimal secretions increase in volume and induce sneezing but soon become mucopurulent. The nasal discharges tend to encrust and block the nasal passages, causing oral breathing. Auscultation reveals pleurisy and partial consolidation of the lungs. At first the faeces are hard, well formed and dark, but they quickly turn soft and pasty before becoming fluid and fetid. Acute cases die six to seven days after the onset of illness, whereas survivors show signs of recovery within two weeks.
FIGURE 5 Activation of latent babesiosis by rinderpest virus
Subacute reactions in goats and sheep are common and may be the norm. In spite of transitory fever, systemic disturbance is not obvious and affected animals continue to feed. Rinderpest is seldom suspected unless frank clinical cases occur simultaneously.
Clinical disease has only been observed in Asiatic sway-backed domestic pigs. Peracute reactions are characterized by sudden sharp fevers and death before other premonitory signs develop. Acute cases have a similar sudden onset, manifested by fever, inappetence and depression. Within a further 48 hours, affected pigs are shivering, vomiting and bleeding from the nose. Shallow erosions emerge in the oral mucosa while vesicles erupt in the perineal skin. Diarrhoea soon supervenes, the fluid faeces being fetid and heavily streaked with blood. Dehydration and emaciation thereafter are rapid and progressive .The diarrhoea persists until death - five to nine days after the onset of illness - or for ten to 12 days in pigs that survive. Pregnant sows abort. Subacute reactions are non-fatal fevers with partial inappetence and fleeting cutaneous eruptions.
The study of the clinical pathology of rinderpest has been neglected and its potential role in aiding the formulation of a presumptive diagnosis by the clinician has been largely ignored. Both the haematological and biochemical changes are characteristic, although not pathognomonic.
The selective destruction of lymphocytes by rinderpest virus induces significant haematological changes, and the severity of the changes appears to be linked to the degree of virulence of the virus strain involved. All infected species react in a similar manner.
FIGURE 6 Total leucocyte counts in cattle infected with rinderpest virus
A transient leucocytosis often precedes the onset of fever but immediately thereafter there is a dramatic and profound leucopenia (see Figure 6). The lowest level, reached during the erosive-mucosa phase of the clinical reaction, is followed by a gradual return over several weeks to normal levels in survivors. The count does not rise significantly in fatal cases.
The total leucocyte pattern is attributable almost entirely to changes in lymphocyte numbers .These increase towards the end of the incubation period, fall precipitously during the prodromal fever and slowly return to normal levels in survivors (see Figure 7). Both T-and B-lymphocytes are affected. Recent studies of the growth of strains of rinderpest virus in cloned lymphoblastoid cell lines transformed by infection with Theileria parva revealed that the virus grew readily in B cells, CD4+ and CD8+ alpha/betaT cells, and gamma/delta T cells. The virus had no apparent predilection for particular phenotypes of lymphoblasts (Rossiter et al., 1992).
Changes in numbers of monocytes are not significant.
In contrast to the changes in lymphocyte numbers, the number of neutrophils in surviving cases remains within the normal range (see Figure 8). In fatal cases, however, there is a terminal degenerative shift to the left. In other words, an excessive number of immature neutrophils - the so-called Band cells - indicates a poor prognosis.
FIGURE 7 Lymphocyte counts in cattle infected with rinderpest virus
Eosinophil numbers fall with lymphocyte numbers and disappear during the erosive-mucosa phase to re-emerge in survivors during convalescence (see Figure 9).
In cattle that die from rinderpest, basophils disappear shortly after the onset of fever.
In surviving animals the erythrocyte count fluctuates within the normal range, but in fatal cases there is an apparent increase, terminally attributable to the effects of dehydration. This terminal change is manifested also by a 40 to 65 percent increase in the packed cell volume (PCV). As a result, the loss of body water approaches 40 percent and the blood at death is dark, thick and slow to coagulate. Serum separation is poor.
FIGURE 8 Neutrophil counts in cattle infected with rinderpest virus
FIGURE 9 Eosinophil counts in cattle infected with rinderpest virus
Animals suffering from a transient or a mild diarrhoea survive infection with rinderpest virus. Animals that develop severe diarrhoea die because of the loss of body water and essential electrolytes. The significant biochemical changes, therefore, reflect this loss.
Heuschele and Barber (1966) found that serum chloride levels fell terminally below normal in cattle dying after infection with the highly virulent Pendik strain of rinderpest virus. Other electrolyte serum levels remained constant or rose slightly, indicating, in fact, a net loss because of the haemoconcentration. The total serum proteins also decreased, but in surviving animals increased serum globulin levels were detected (French, 1936).
Total, direct and indirect bilirubin values rose terminally in Heuschele and Barber's fatal cases and were linked to an unexpected terminal jaundice. Extensive cell and tissue damage was also manifested by a terminal increase in serum glutamic oxalacetate transaminase levels and an increase in serum urea nitrogen. In contrast, serum creatinine levels remained essentially normal, suggesting that kidney function was not impaired.
Recently, Al-Ani (1992) detected metabolic acidosis, haemoconcentration, hypoglycaemia, hypochloraemia, hyponatraemia and hyper-calcaemia in calves affected with rinderpest.
Buffalo and cattle deaths
Goat and sheep deaths
Rinderpest virus has a core affinity for lymphoid tissues and a secondary affinity for the epithelium of the alimentary, upper respiratory and urogenital tracts. The latter tropism is well developed in highly contagious strains of the virus but is muted or absent in strains serially passaged experimentally by parenteral injection of suspensions of infected tissues .The virulent Kabete "O" bovine strain, for example, seldom induces mucosal erosions, and contact transmission between cattle is rare. Similarly, the Nakamura III lapinized strain does not provoke epithelial lesions. Most natural cases of rinderpest, however, exhibit grossly more pronounced changes in epithelial linings than in lymphoid organs. Microscopic examination reveals the opposite.
Most buffaloes and cattle die six to 12 days after the onset of illness and, typically, the carcass is dehydrated, emaciated, fetid and soiled (Maurer et al., 1956). The eyes are sunken, with the tear tracts scalded by a profuse mucopurulent discharge. The conjunctivas are congested and oedematous. Corneal ulceration occurs occasionally and bilateral corneal opacity rarely. The external nares and muzzle are encrusted with mucopurulent discharge. The hindquarters and flanks are soiled with the fetid fluid faeces.
In contrast, the carcasses of buffaloes and cattle that die early in the course of the disease, before the onset of profuse diarrhoea, are often in good condition, unsoiled and free of mucopurulent crusts and discharges.
The spectacular changes observed post mortem involve the alimentary tract. At death, the characteristic erosions of the oral mucosa have usually coalesced, causing extensive desquamation of all surfaces of the mouth. The edges of the desquamated areas, like those of individual erosions, are sharply demarcated from the surrounding healthy epithelium. The desquamation often extends into the pharynx and sometimes into the upper portion of the oesophagus.
Readily visible lesions are rare in the fore stomach; if present, they are sited on the pillars of the rumen and on the surfaces of the omasal leaves. If affected, the abomasal folds are congested, oedematous and have linear erosions along the margin. The pyloric region of the abomasum is nearly always affected with necrotic patches of epithelium that slough to form bleeding ulcers, some of which contain black clots of blood. The underlying lamina propria is thickened by oedema and streaked by congestion and haemorrhage.
Lesions of the epithelium of the small intestine are similar but much less intense. They are usually restricted to the initial portion of the duodenum and the terminal part of the ileum. In contrast, Peyer's patches, like other gut-associated lymphoid tissues, are severely affected. They are swollen, black from haemorrhage and friable from necrosis.
Striking changes are observed in the large intestine. The chief sites of the lesions are the ileocaecal valve, the caecal tonsil and the crests of the folds of the caecal, colonic and rectal mucosae. The superficial impression is that of numerous stripes of haemorrhage extending from the blind sac of the caecum to the anus, the so-called zebra stripes. In fresh carcasses of animals that die early in the course of the disease the stripes are bright red, but in the carcasses of animals that die later and in decomposed carcasses the stripes are greenish-black. The stripes are neither haemorrhages nor petechiae but greatly distended capillaries packed with erythrocytes in the lamina propria. In addition, the severely eroded mucosa oozes blood into the lumen of the gut, which fills with dark, partially coagulated fluid.
Liver and gall-bladder
The liver is not a target organ of the rinderpest virus and is therefore affected only secondarily. It usually appears normal. Occasionally, chronic passive congestion is evident. Latent hepatic pathogens are often activated by rinderpest, however, producing a striking hepatitis at death.
The mucosa of the gall-bladder reacts like that of the lower alimentary tract. Scattered petechiae and blotches of haemorrhage are evident with, on occasion, free bleeding into the lumen. Erosions are rare.
Marked changes also affect the upper respiratory tract where the turbinates and nasal septa are coated with a thick, tenacious mucopurulent exudate. The mucosae are congested, contain petechiae and are sometimes eroded, with lesions that extend into the larynx. Narrow longitudinal streaks of congestion and rusty red haemorrhage invariably mark the trachea. The lungs are often normal except in lingering cases when the animal dies after suffering severe respiratory distress. The lungs of such animals reveal spectacular alveolar and interlobular emphysema accompanied by congestion, haemorrhage and small patches of consolidation. The interlobular septa, in particular, are conspicuously filled with grossly visible air bubbles. The emphysema also often involves the pleura and even the fascia of the thorax.
Changes in the kidneys are limited to congestion in the medulla, especially at the corticomedullary junction. In contrast, the epithelium of the urinary bladder is usually severely desquamated, the underlying stroma being so heavily infiltrated by erythrocytes that the surface appears mottled with different shades of red. The urine, however, appears normal. The mucosae of the lower genital tract exhibit changes similar in character and sequence to those in the mouth.
The selective destruction of lymphocytes is the characteristic lesion of a rinderpest virus infection. All lymphoid organs are affected, with the severest damage occurring in the mesenteric lymph nodes and the gut-associated lymphoid tissues .The nodes are enlarged, soft and oedematous except in animals that die late in convalescence, when the nodes are shrunken, greyish and show radial streaks in the cortex.
The spleen usually appears normal. Occasionally, however, striking ecchymoses occur on the serosa, especially along the splenic borders. The gut-associated lymphoid tissues exhibit changes similar to those affecting the lymph nodes but their anatomical sites enable sloughing of the necrotic debris, creating deep craters in the intestinal wall that ooze blood.
The heart is usually grossly normal except in animals that die early in the course of the disease from cardiogenic shock. The lesions, however, are non-specific and consist of a variable degree of subendocardial haemorrhage in the left ventricle, rarely in the right ventricle, and subepicardial petechiae on the base of the heart. Petechiae occasionally occur on the apex and along the coronary grooves. The myocardium tends to be flabby.
In the past, cutaneous rinderpest eruptions were often reported and, in fact, many vernacular names in Africa and Asia for the disease mean "pox". Today, however, skin lesions are seldom seen. The lesions allegedly emerge first as discrete macules that rapidly become papules, then vesicles and finally pustules. The exudate mats the hair into tufts. The common sites are the fine-skinned areas of the body around the anus, on the perineum, udder or scrotum and between the legs. Buffaloes are alleged to be particularly prone to rinderpest skin lesions. Microscopic and ultramicroscopic examinations reveal either Dermatophilus congolensis or a pox virus or both.
In countries where the disease is enzootic, cases of rinderpest in goats and sheep tend to be subacute and most survive. Lesions in slaughtered animals are vague and far from suggestive. Lesions in acutely ill goats and sheep that die mimic those seen in cattle but tend to be less intense. Pulmonary involvement, however, is more frequent than in cattle.
The carcass is emaciated, fetid and soiled. The eyelids are matted with mucopurulent exudate and the nostrils are encrusted and often blocked with a mucopurulent nasal discharge.
The lips are hyperaemic. Stomatitis may or may not be evident; if present, it may range from a few sharply demarcated erosions to extensive desquamation of the oral epithelium that may extend into the congested pharynx.
Obvious changes in the oesophagus and fore stomach have not been described, although it has been noted that the ingesta in the omasum are often liquid. The mucosa of the abomasum is invariably involved, although the intensity of the lesions varies enormously. Sometimes the mucosa is merely diffusely congested, at other times it is also petechiated and eroded. The pyloric portion of the abomasum is usually ulcerated and the ulcers are often coated with a tenacious grey pseudomembrane.
Severe congestion and erosion may extend throughout the length of the small and large intestines but usually the gross changes are limited to the duodenum, the terminal ileum, the caecum and upper colon. The ileocaecal valve is a prominent site of congestion and may ooze blood. Zebra stripes mark the crests of the folds of the caecal, colonic and rectal mucosae. Erosions and ulcerations are usually restricted, however, to the mucosae of the caecum and rectum.
Liver and gall-bladder
Both the liver and gall-bladder appear grossly normal. Most observers are struck by the absence of changes in the mucosa of the gall-bladder and in the character of the bile.
Secondary purulent bronchopneumonia is a conspicuous lesion and usually affects the apical and cardiac lobes of the lungs. It is attributable to activated pasteurellas. Emphysema is not common. The mucosae of the upper respiratory tract are congested, eroded and coated with a thick mucopurulent exudate. Congestion lines the upper trachea.
Congestion and erosion of the mucosa of the urogenital tract occur occasionally. The kidneys are usually normal, with any changes being considered non-specific.
Lymph nodes are conspicuous, being oedematous and soft. Congestion, in addition, has been observed in the retropharyngeal lymph nodes. Spleens are usually normal but occasionally may be swollen. Capsular blood vessels are sometimes engorged. The gut-associated lymphoid tissues are all attacked, the large Peyer's patch in the terminal ileum in particular being obviously affected. The necrosis leads to sloughing, which produces craters that ooze poorly clotting blood.
Subepicardial petechiae sometimes occur in the coronary grooves, but otherwise the heart usually appears grossly normal.
Cutaneous lesions, pock-like in character, have been described as affecting the skin without hair or wool.
Rinderpest virus kills Asian domestic pigs but not European-type domestic pigs. Fatal infections also occur in African wild pigs such as the warthog, bush pig and giant forest hog.
The carcass is in poor condition, soiled with fluid faeces and fetid (Hudson and Wongsongsarn, 1950).
The stomatitis ranges in severity from cyanosis at the back of the tongue and in the pharynx to extensive diphtheresis involving all the oral surfaces. The gastritis likewise varies from mild hyperaemia in the pyloric region to an overall, diffuse, deep congestion with necrosis, desquamation and ulceration of the epithelium. The ulcers are often covered by diphtheritic pseudomembranes. Lesions in the small intestine are usually limited to the Peyer's patches, but, on occasion, a haemorrhagic enteritis extends from the duodenum to the rectum. Lesions are usually prominent in the caecum and include congestion, ulceration and diphtheria; in pigs that die late in the disease, the necrotic ulcers in the caecum may be the sole lesions. The colonic mucosa has irregular blotches of congestion along its length.
Liver and gall-bladder
The liver is not affected. The lesions in the gallbladder, however, range from mild vascular arborescence to diffuse congestion of the mucosa.
Gross changes in the respiratory tract are common and consist of cyanosis of the larynx, haemorrhagic streaks in the upper trachea, pulmonary congestion and patches of secondary bronchopneumonia.
Opinions clash regarding the frequency of pulmonary emphysema.
The kidneys and the mucosa of the urinary bladder are both congested, but the intensity of the congestion varies.
Lymphoid organs exhibit a variety of necrotic lesions that are particularly conspicuous in the gut-associated lymphoid tissues. The spleen is usually grossly normal although it may be swollen on occasion.
The heart, at most, shows pale, dry areas in the myocardium. Subendocardial and subepicardial haemorrhages have not been described .The blood is dark but clots promptly.
Changes in the skin are common, ranging from discrete areas of congestion and cyanosis on the abdomen and legs to extensive purple blotching and subcutaneous ecchymoses. Eczematous eruptions may occur around the anus and on the perineum.