Clinical reactions in buffalo and cattle are similar and may be peracute, acute, subacute and 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, and sometimes even before mucosal erosions develop. Fortunately, peracute reactions are not common, occurring most frequently in young calves and certain species of wildlife.
The classic syndrome is divided into five phases: an incubation period, a prodromal fever, an erosive-mucosal phase, a diarrhoeic phase and death or convalescence.
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 depressed, standing apart from others in the herd. Respiration is shallow and rapid. The coat hairs stand erect, the muzzle is dry, and tearing, as well as nasal discharges are common. 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 surface of the mucosal membranes lining the mouth, nasal passages and urogenital tract. These are readily abraded to expose a haemorrhagic layer of basal cells. 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 infected animal experiences diarrhoea as soon as the fever falls, usually 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 dark blood. The smell of the diarrhoea 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.
In fatal cases the diarrhoea progressively worsens, causing rapid loss of contition and dehydration. Affected animals visibly waste away; they have sunken eyes and stand with lowered heads and arched backs. Most collapse and die six to twelve 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 will likely 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 fifteen 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. Therefore clinical suspicions of rinderpest are often not aroused.
Rinderpest virus selectively destroys T- and B-lymphocytes, but not memory cells. Thus, latent pathogens are commonly activated and suprainfection is encouraged. Both processes induce clinical signs that mask even those of the classical rinderpest syndrome. 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 signs 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.
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 twelve days in pigs that survive. Pregnant sows abort. Subacute reactions are non-fatal fevers with partial inappetence and fleeting cutaneous eruptions.