Rinderpest

P B ROSSITER

GENERAL INTRODUCTION: PARAMYXOVIRIDAE AND PNEUMOVIRIDAE

Introduction

Classical rinderpest is an acute to subacute, highly contagious viral disease of cattle and other artiodactyles. The main gross pathological changes are necrosis and erosion throughout the gastrointestinal tract, which can cause diarrhoea, dehydration, and death. Epidemics of the severe ‘cattle plague’ form of the disease may have morbidity and mortality rates exceeding 90 per cent. However, mild and virtually inapparent infections with very low mortality rates also occur and are perhaps the more typical form in endemic areas.

The decimation of cattle and wildlife populations by rinderpest has influenced human history,^{119, 180, 235} and the ecology of large areas of southern and central Africa.^{369, 376} So serious were the effects of the disease that its control and eradication were major stimuli for the establishment of the first veterinary schools in Europe during the eighteenth century.

Historically, the disease invaded Europe with armies from the Orient, encouraging the view that the disease originated in Asia. Antigenic comparison between morbilliviruses has suggested that rinderpest may be the archetypal morbillivirus from which measles and distemper evolved five thousand or more years ago, possibly in the river civilizations of south-west Asia where the domestication of cattle is thought to have occurred.^{109, 233}

Introductions of rinderpest into Europe, usually as a sequel to wars, were often followed by major epidemics. By the end of the nineteenth century other forms of transport began to replace oxen as the main source of military draught power, effectively removing this source of infection. Strict application of slaughter and quarantine eradicated rinderpest from most of Europe, though a series of outbreaks occurred during and immediately after the First World War, most notably in Poland. The last reported outbreaks in Europe were in Belgium in 1920 and Rome zoo in 1949, both of which were caused by the importation of live infected animals from high-risk areas.^{15, 79} The only recorded outbreaks in the New World, in Brazil in 1920 and Australia in 1923, were also due to the importation of live infected animals. ^{294, 295, 407}

After the eradication of the disease from Europe the scientific study of rinderpest continued in Asia where the disease was widespread in the first quarter of the twentieth century. The first vaccine that allowed large-scale prophylactic immunization of rinderpest was developed in India in 1925 by Edwards,¹⁰⁶ allowing the possibility of mass control and even eradication of the disease in countries where strict control of animal movement or even slaughter were unfeasible. The vast and comparatively unconfined cattle population and even larger goat and sheep populations of India continued to pose an almost insuperable problem for vaccination and control, even with the advent of improved vaccines.

Finally, after focused programmes in the 1980s and 1990s, rinderpest was eradicated from the country in the mid-1990s, setting the example for the rest of Asia and for Africa. Unfortunately, in Asia, at the time of writing, Pakistan remains endemically infected and, although the prevalence of the disease has decreased significantly in the past decade, widespread traffic in live animals still poses a threat to southern Asia and the Middle East.^{219, 304} Effective control in the Near and Middle East decreased during the 1980s because of reduced vaccination and increased movement of cattle resulting from civil and military disturbances. Fortunately, the 1990s saw renewed control and it is increasingly likely that there are no endemic foci in this region.^{1, 20}

In Africa the disease was introduced to North Africa, especially Egypt, and possibly to West Africa on a number of occasions before 1887.^{87, 112, 211} If it reached West Africa it apparently failed to establish itself there, and if it persisted in Egypt it was effectively isolated from the rest of Africa’s cattle. For most historians the history of rinderpest on the continent begins with the ‘Great African Pandemic’ of 1887 to 1897, which was widely described in southern Africa and Ethiopia.^{135, 147, 202, 387, 388} Although the source of the virus that started the pandemic is still unknown, there are several possibilities, all classically associated with military campaigns. The most frequently quoted possibility is the introduction of infected Indian or Arabian cattle to Massawa in Eritrea by the Italian army in either 1887, 1888 or 1889.^{194, 424} The inefficient attempts to use prophylactic and therapeutic control rather than slaughter and quarantine, ⁴²⁴ made it easier for the disease to establish itself. Infection was then transported throughout Ethiopia and into the Nile Valley in Sudan in 1890. Alternatively, the virus may have moved slowly up the Nile from Egypt in cattle used by British military campaigns, which reputedly brought rinderpest to Khartoum in 1884 and 1885. Whichever is true, it seems likely that the disease was not present in this area before the 1880s when the American adventurer James¹³⁷ encountered numerous herds of healthy African buffalo (Syncerus caffer) as he travelled between the Nile and Massawa in 1881. All subsequent work has shown that the African buffalo is probably the most susceptible species to rinderpest. Another possible origin of the pandemic was suggested by Littlewood,¹⁹⁴ who reported that in late 1889 a German military expedition brought cattle from Aden and Bombay against his advice, instigating a severe outbreak of rinderpest on the coast of what is today Kenya and Tanzania. It may have been virus from this outbreak, carried in cattle which the Maasai say were brought back to Kilimanjaro from the coast by their warriors in late 1890, that was responsible for the outbreak at Oloitokitok in early 1891. Suggestions^{202, 323} that Joseph Thompson encountered rinderpest among the Laikipia Maasai in 1883 overlook the author’s description of the severe epidemic disease he saw in cattle. His book records, as Theiler also noted,³⁷⁶ a convincing post-mortem description of contagious bovine pleuropneumonia, which was widespread in the area some six to seven years before the outbreak of rinderpest.¹³³

Whatever its source, the pandemic was raging in Kenya, Uganda and Tanzania in 1891. Moving south in 1892, it had reached Karonga on Lake Nyasa by July and the Luapala River in Zambia by October. Very high mortality was reported not only in cattle but also in wildlife, though alcelaphines and waterbuck (Kobus ellipsiprymnus) seem to have been relatively insusceptible. The southerly spread of the virus was halted by the Zambezi River, where the disease, which had not yet been fully confirmed as rinderpest, came to be called Zambezi cattle fever. During this period of southerly advance the virus also may have spread westward into Angola and Zaire, whilst further north the western extension of the pandemic had penetrated right through sub- Saharan West Africa to the Atlantic Ocean.

Eventually the virus was transported across the Zambezi River. Disease was reported south of the river in February 1896 and appeared at Bulawayo in Zimbabwe in March, where it was confirmed by Gray and Theiler, and in the same month at Palapye in Botswana. Soon afterwards the mostnorthern provinces of South Africa were infected via the transport routes (Figure 49.1). stretching through Botswana and Mafikeng, and in October the disease spread south through Kimberley in the Cape Colony to the Orange (now the Gariep) River by December. There it was temporarily halted not only by the river, but by a 1 600-kilometre-long fence and rigorous quarantine measures (Figure 49.2). Unfortunately, in March 1897, a drover crossed the river reputedly wearing a pair of trousers he had found in a sack containing meat. Within a few days his cattle developed rinderpest and so the virus moved swiftly southwards. During 1897 the disease also infected the Natal Colony (present-day KwaZulu-Natal), Lesotho and the region of present-day Namibia.

Wild ungulates were reputedly also a factor in the spread of the disease. President Paul Kruger of the then Zuid Afrikaansche Republiek (now comprising the four most northerly provinces of South Africa) was of the opinion that game were the most important spreaders of infection, with bushbuck (Tragelaphus scriptus), impala (Aepycerosmelampus) and kudu (Tragelaphus strepsiceros) being the main culprits.¹⁸⁰

Energetic control campaigns which included newly developed prophylactic inoculations eventually contained the disease and it was briefly eradicated from South Africa in 1899. A re-introduction from Namibia in 1901 was milder and easier to control, and southern Africa was reported to be free of rinderpest in 1905.³⁸³

It was the losses incurred during the pandemic — 5,25 million cattle and innumerable wildlife south of the Zambezi River — which have most dramatically illustrated the killing power of rinderpest. In the Zuid Afrikaansche Republiek alone there were 1 556 760 cattle prior to the rinderpest, of which 1 002 297 (66,5 per cent) died from or were killed as a result of the disease. A total of 205 801 (13,2 per cent) was said to have recovered from the infection while the rest (20,3 per cent) was unaffected. The direct financial losses were estimated to total 3 006 891 pounds sterling.¹⁸⁰ In the Natal Colony, 46 per cent of the cattle population was lost, but the highest mortality rate in southern Africa occurred in Matabeleland (Zimbabwe), where it reached 90 per cent.¹⁸⁰

The pandemic also left its mark on the continent in other ways. In East Africa dominant cattle-keeping tribes such as the Maasai were irrevocably weakened and replaced politically and economically by agricultural tribes. Further south, the disease and the stern measures that were used to fight it provoked rebellions in Matabeleland and Lesotho. In South Africa not only were stock owners, both black and white, ruined financially, but the whole transport system virtually collapsed, further contributing to the impoverishment and resultant urbanization of the Afrikaners.¹⁸⁰

The decimation of wildlife and cattle led to the apparent disappearance of Glossina spp. from many areas of southern Africa. The comparatively swift eradication of rinderpest from the subcontinent allowed wildlife in the region to recover their numbers and distribution, whereas the persistence of the virus further north may have contributed to the formation of isolated ‘island’ communities of species such as sable (Hippotragus niger) and greater kudu (T. strepsiceros).

The pandemic set the stage for one of the keenest competitions medical science has ever seen. The southern African republics and colonies each set about finding a method of curing or preventing the disease. The race became even more significant when the Russian government offered a prize of one million roubles for the winner. Drs Arnold Theiler of the Zuid Afrikaansche Republiek and Herbert Watkins-Pitchford of the Natal Colony collaborated from October 1886 to March 1887 in developing a technique for immunizing cattle with simultaneous but separate inoculations of immune serum and infectious virus (which was used until the advent of attenuated vaccines in the 1930s). In December 1886 Dr Robert Koch, the eminent German microbiologist, arrived at the request of the government of the Cape Colony to begin work at Kimberley.

Figure 49.1 A trek ox affected by rinderpest

Figure 49.2 Many cattle were slaughtered during the rinderpest epidemic at the end of the nineteenth century in South Africa in an attempt to control the spread of the disease

He lost no time in evaluating, among other things, the Boer farmers’ preventive remedy of inoculating bile from dead cattle into healthy animals. Koch refined the technique to a stage where it was successful in experienced hands at the laboratory, at which point it was hastily introduced throughout the affected areas. With hindsight it is easy to criticize the bile method for being a poor way of immunizing cattle and for spreading the virus, but the experiments of Theiler and Watkins-Pitchford were barely complete and immune serum was in desperately short supply and time-consuming to produce. Undoubtedly the bile method helped to reduce the mortality in the later stages of the pandemic.

The Zuid Afrikaansche Republiek government also obtained the services of the distinguished French microbiologists, Drs Jean Danysz and Jules Bordet, who arrived to begin work in January 1897. Theiler was ordered to join them and they eventually reported jointly to the government on the success of the serum-virus method of immunization, which then gradually replaced the bile method. Watkins-Pitchford was less fortunate: the government of the Natal Colony largely ignored his results and his data were destroyed in a fire at Pietermaritzburg town hall. The million roubles were never officially awarded.

Elsewhere in Africa rinderpest persisted wherever nomadic or semi-nomadic pastoralism was common. Such husbandry involves keeping large herds of cattle that may range over thousands of square kilometres and are frequently inaccessible for vaccination. Southern Africa has been under constant potential threat from the north, but the threat has assumed real proportions only occasionally. Usually the danger has arisen from a southerly spread of the disease through Tanzania along natural stock routes towards the gap between Lakes Tanganyika and Malawi. This occurred during the First and Second World Wars,^{59, 89, 126, 135, 196} but was contained by vigorous control of cattle movement and vaccination of all stock in the belt between the lakes. Implementation of a ‘cordon sanitaire’ involving, to varying degrees, the elimination of all domestic stock and susceptible species of wildlife from a 6- to 40-kilometre-wide strip and the erection of game-proof fencing was also carried out.³⁷⁹ In 1983 and 1984, this same region was again the target of co-ordinated vaccination campaigns by the governments of Tanzania, Zambia and Malawi. Their aim was to generate a cordon of immune animals that would halt the passage of disease from what can now be regarded as the second Great African Pandemic. Fortunately the effectiveness of this immune belt was never tested as the virus did not spread south of the central railway line in Tanzania, and southern Africa escaped the losses and disruption experienced by less fortunate countries further north.

The progress of the second Africanpandemic(1979 to 1984) attracted considerable attention, though accurate details of the origin of primary outbreaks and subsequent dissemination of the virus were often as elusive as they had been in the first pandemic 90 years earlier.^{128, 132, 228, 230, 271, 310, 314} The underlying causes, however, were easy to discern. The outstanding success of vaccination campaigns using cell-culture attenuated rinderpest virus led to an impressive fall in the number of outbreaks of rinderpest in Africa in the mid-1970s (Figure 49.3). Joint Project 15 (JP15) of the Organization of African Unity, Food and Agriculture Organization of the United Nations, and the European Community, assisted by individual donor countries including African states such as Nigeria, was especially instrumental in this control.²¹ The virus was eradicated throughout vast areas of the continent and by 1976 was apparently restricted to two zones where access and animal movement control had always been difficult: one in West Africa between the Mali/Mauritania border and the internal delta of the Niger, and the other in East Africa including Ethiopia and Sudan (Figure 49.3).

When JP15 ceased in 1976, it left behind a strong sense of security but no funds to maintain the high levels of herd immunity it had induced. Coinciding with rising fuel prices, the effects of a recession in the world economy on the emergent African nations were particularly hard. With rinderpest having been eradicated from many countries for over a decade, cutting back vaccination against the virus was an obvious way to save money for more pressing matters. Some countries ceased vaccination completely while others covered only a small proportion of their cattle.

The outcome was that the number of susceptible cattle started to increase as soon as JP15 ceased and, despite warnings, ^{271, 336} the virus began to spread from its endemic strongholds. Motor transport facilitated rapid spread of infection, and civil and military strife in many parts of the continent hindered control. The virus rapidly regained most of the territory it had lost during JP15 (Figure 49.3). Fortunately, in one of the most successful emergency campaigns ever seen, this second pandemic was controlled by vaccination carried out by national veterinary departments supported by international funds totalling well over US$ 20 million. The emergency provoked renewed calls for a campaign to eradicate rinderpest from Africa completely.^{19, 152, 228} From 1986 until 1999, the Pan African Rinderpest Campaign (PARC), funded by the European Community, and advised and assisted by various other donors and agencies, attempted this. Building on the successes of the national campaigns of the 1980s this regional programme facilitated further eradication in several parts of the continent, most notably Ethiopia. Unfortunately, inaccessibility of cattle populations in some of Africa’s chronically unstable, insecure and most inhospitable areas, especially southern Sudan and the southern Somali pastoral ecosystem in Somalia and Kenya (Figure 49.3), prevented PARC from achieving its objective.^{78, 189} New campaigns are now attempting to eradicate these remaining African foci of infection, and the one remaining Asian focus in Pakistan.

Extensive descriptions of the history and all aspects of rinderpest are covered in numerous reviews.^{18, 87, 119, 135, 159, 206, 252, 333, 334, 337, 338}

Aetiology

In 1902 Nicolle and Adil Bey showed that rinderpest was caused by a filterable agent. It was grown in whole blood cultures by Boynton,⁵⁵ and Takematsu and Morimoto³⁶⁷ detected increased amounts of infectivity in cultured leukocytes derived from infected animals. After earlier unsuccessful attempts to grow the agent in cell culture,⁷⁶ Plowright and Ferris^258–260 demonstrated cytopathic effects and new infectivity in bovine cell monolayers. Subsequent studies revealed the close antigenic relationship of rinderpest virus (RPV) to canine distemper^{267, 409} and measles viruses,^{153, 259, 404} and led to RPV being included in the measles-rinderpest-distemper subgroup of the Paramyxoviridae. This subgroup, reclassified as the genus Morbillivirus, ¹⁷⁵ also includes the viruses that cause peste des petits ruminants (PPR) in sheep and goats, phocine and cetacean distemper,^{85, 203} and hedgehog distemper.³⁸⁶

Figure 49.3 Recent distribution of rinderpest in Africa

Figure 49.4 Dendrogram of rinderpest virus. (By kind permission of T. Barrett, 2001. Morbilliviruses: dangers of old and new. In: Smith, G.L., McCauley, J.W. & Rowlands, D.J. (eds). New Challenges to Health: The Threat of Virus Infections. Society for General Microbiology. Cambridge: Cambridge University Press)

The virus is pleomorphic with roughly spherical (100 to 300 nm in diameter) and tubular forms (up to 1 × 103 nm in length).^{60, 257} The enveloped virus is readily inactivated by lipid solvents and is sensitive to light, ultraviolet radiation, heat and extremes of pH.^{252, 328, 329} Infectivity is destroyed by most disinfectants and chemicals such as β-propiolactone. ^{158, 363, 399} Glycerol also destroys RPV and must not be used in transport media for diagnostic samples.^{169, 178}

The virus contains a negative strand of ribonucleic acid, approximately 15 kilo base pairs long, which codes for eight polypeptides.^{38, 43, 104, 127, 182, 324} The viral envelope contains the H protein (a haemagglutinin in other morbilliviruses), which binds to cell receptors, and the fusion (F) protein that induces the formation of syncytia, and is underlain by the matrix (M) protein. Within the virion the RNA is protected by a nucleocapsid (N) protein. Transcription in infected cells is mediated by polymerase (L) and polymerase- associated (P) proteins. A non-structural polypeptide (C) is translated by modification from the P polypeptide mRNA.³⁸

The main advance in rinderpest research since the first edition of this book has been the molecular dissection of the viral genome and the benefits this has brought. The nucleotide sequences of all the genes have now been sequenced and most have been compared to their equivalents in other morbilliviruses.^{30, 31, 35, 37, 111, 192, 382, 414, 415} The P, N, and L genes appear to be more conserved amongst the morbilliviruses and the F andHgenes more variable. Comparison of a region of the F gene can distinguish between different strains of the virus, which has allowed the virus to be ‘taxonomically’ classified into a number of subtypes or lineages. The main contemporary lineages (Figure 49.4). are Asia, Africa-1 and Africa-2, and there are a number of ancestral lines that have been maintained in vaccines.^{9, 41, 400} Refined subtyping within these lineages is now allowing molecular epidemiology to make significant contributions to the understanding of the persistence and distribution of different clades of the virus in Africa and Asia.^{39, 41, 400} However, most of the differences are small; for instance, the difference in the sequences of the complete genome of the modified live cell culture vaccine and its highly virulent parent stock, Kabete O strain, is only 87 base pairs or 0,55 per cent.¹⁸ Fortunately, the antigenic differences between the different lineages and clades are also very small and the immunity induced by the vaccine protects against all known isolates of the virus. Determination of the gene sequences has facilitated the construction of new experimental recombinant vaccines and diagnostic reagents.^{40, 44, 49, 123, 155, 168, 231, 299, 364, 417, 420, 421} Most of the earlier recombinant vaccines inserted rinderpest genes into larger DNA vectors such as pox viruses. The recovery of viable virus from cloned cDNA copies of the RNA genome has facilitated the development of a new generation of RPV recombinants in which foreign genes can be introduced into the virus genome.^{32, 121, 122}

In vitro, RPV grows relatively slowly in cells derived from bovine tissues and in cell lines such as Hela and Vero, producing titres of cell-free virus of 10⁵ to 10⁶ (occasionally 10⁷) log₁₀ tissue culture infectious doses (TCID₅₀) per millilitre of fluid.^{212, 259} Cytopathic effects comprise rounding of cells which become refractive, cytomegaly, cytoplasmic stranding, the formation of small and large syncytia and eventual degeneration of the cell sheet. In culture the virus is capable of producing plaques and induces interferon.^{28, 145, 371, 423}

Individual strains of virus vary in their pathogenicity for various host species. Experimentally this has been best shown by attenuation studies whereby adaptation of a strain to produce disease in one species can often bring about a concomitant reduction in the severity of clinical diseases for some but not all other species.⁷⁰ This was the basis for the production of many early live vaccines.^{107, 156, 163, 224, 253, 333, 362}

In contrast to the measles virus, the haemagglutinin equivalent of RPV does not readily agglutinate erythrocytes;^{148 328, 329} some haemagglutinating activity has been demonstrated in special circumstances,¹⁸⁷ but the specificity of the reaction was not established. However, since RPV induces the development of antibodies which react with measles virus haemagglutinin,^{54, 406} it is likely that RPV bears a similar envelope antigen in a more sequestered site.

Epidemiology

Rinderpest virus infects a wide variety of vertebrates. Some of these, including rabbits, hamsters, mice, giant rats (Cricetomys gambianus), ferrets, and susliks (Citellus mongoliscus ramosus) usually are only infected experimentally, and often only by using strains of virus adapted to them.^{88, 154, 226, 252, 333, 346} In the field, only artiodactyles are naturally infected, although dogs fed infected meat may develop antibodies to the virus, suggesting subclinical infection.²⁶⁷ Amongst domestic stock, cattle and water buffaloes (Bubalus bubalis) are especially susceptible and are more frequently infected than other species. Sheep, goats and pigs are also susceptible and may develop clinical disease.^{56, 125, 143, 284, 326} European breeds of pigs undergo subclinical infection with African strains of virus.^{98, 342} Although some early reports indicated that camels are susceptible to clinical disease,^{101, 129, 193, 232} more recent experimental studies have shown only mild or subclinical disease in this species. ^{356, 368} Contact transmission from cattle to camels occurs under experimental conditions³⁶⁸ but is probably rare in the field.³⁴³

Infection of wild artiodactyls with strains largely maintained in cattle causes a wide spectrum of clinical disease ranging from very severe in African buffalo, giraffe (Giraffa camelopardalis), eland (Taurotragus oryx) and kudu (Tragelaphus strepsiceros and T. imberbis) through increasingly less severe syndromes in other antelopes to mild or atypical in impala³⁴¹ and subclinical in hippopotami (Hippopotamus amphibius).²⁶³ There is also variation in susceptibility to clinical disease between breeds or races of a species, especially cattle.^{138, 171, 322, 332, 384} Most European cattle breeds (Bos taurus) are more susceptible than Bos indicus breeds. African humpless cattle, such as the Ankole in East Africa, are notoriously susceptible in comparison to East African zebus.^{62, 71, 83, 135, 216, 332} Japanese black cattle reacted so severely to goat-adapted vaccines, which were sufficiently attenuated for other cattle, that the virus had to be further attenuated in rabbits and embryonated chicken eggs.^{225, 226}

Infected animals excrete virus in their ocular, nasal, oral and vaginal secretions and faeces.^{87, 130, 139, 333} Excretion begins one or two days before the onset of fever (the first clinical sign) and continues for up to 9 to 10 days after the start of pyrexia.^{113, 188} Highest titres of virus are excreted during the early stages of clinical disease when epithelial lesions, especially those in the mouth, are developing to their maximum extent. Subsequently, the titres of excreted virus wane as antibody develops.^{188, 340} Recovered cows may abort an infected foetus some weeks after apparent recovery, with virus excretion in their uterine and vaginal discharges. ^{87, 157, 390}

The fragility of the virus ensures that most infectivity survives for only a few hours outside the host, though some may persist under favourable conditions for up to two to four days.^{353, 380} Carcass decomposition inactivates the virus within one to three days.⁸⁷

The spread of RPV is effected almost exclusively by contact between infected and susceptible animals. Airborne transmission by infected aerosols probably only occurs under ideal conditions of close proximity and gentle air currents, for example among housed animals.¹⁵¹ Nevertheless, experimentation has proved that airborne transmission is a theoretical possibility over several hundred metres,¹⁵⁰ and circumstantial evidence for such transmission occurred during the 1980s’ epidemics in Nigeria.

The high levels of antibody that are maintained in recovered animals for years after infection, usually for life, suggest persistent infection with RPV. A preliminary study went some way to confirming this by demonstrating viral RNA in the peripheral blood lymphocytes of cattle for up to three months after the cessation of viraemia and recovery from clinical disease.³⁸ As a rule there is no carrier state in rinderpest and recovered animals do not excrete infectious RPV and are not involved in the maintenance and transmission of the disease. The handful of reports of chronic cases of rinderpest^{87, 92, 99, 124} are exceptions to the rule. The virus is not transmitted by arthropods³⁴⁷ and the potential for transmission through abortion³⁹⁰ is limited.

Consequently, RPV has a short and direct cycle of infection and is spread by close contact. Even under experimental conditions regular contact transmission can be difficult to achieve.^{82, 151, 373} As originally observed by Lowe,¹⁹⁶ the spread of rinderpest is like a bushfire; it continually moves on to new uninfected animals (unburnt bush) leaving behind dead or immune animals (burnt bush). The disease stops when it runs out of susceptibles (firebreaks) and vaccination is a technique of rendering animals non-susceptible (backburning). As a result, rinderpest is maintained by large, heterogeneous populations of animals with a sufficient supply of susceptible animals. In Africa in recent times the endemic areas have been those with large cattle populations belonging to nomadic or semi-nomadic people, which ensures good mixing of the population, especially when restricted by the availability of water during dry seasons. One of the most important epidemiological features of rinderpest was summarized byHuytra et al.:¹⁴⁹

Rinderpest causes enormous losses among cattle in regions previously free from infection and may lead to the almost complete extinction of animals in large areas. On the other hand, in permanently infected regions it may assume a milder form and cause only a slight loss.

In populations consisting mainly of susceptible animals rinderpest behaves in epidemic fashion with the virus infecting virtually all the susceptibles and causing severe clinical disease in most age groups. Endemic rinderpest, however, is much milder and is maintained by young animals usually less than two years old that have lost their maternal immunity. Intermediate patterns also exist. Examples in Africa were the enormous losses reported in southern Africa during the first Great Pandemic^{135, 147} compared with the mild and frequently subclinical infections seen in endemic areas such as Maasailand in the 1950s and early 1960s and the Somali pastoral ecosystem today. ^{197, 250, 297} Undoubtedly the selection of resistant animals in the wake of epidemics plays a part in this.^{135, 216, 332} Selection of milder strains of the virus, however, may be an equally or more important mechanism, particularly as the generation time of virus is so much shorter than that of cattle. Computer modelling provided insight as to how this might occur through the selection of strains with differing transmissibility.^{161, 305} The model showed that during an epidemicRPVis transmitted rapidly to susceptible animals and the most transmissible strains eventually predominate. For a strain to be highly transmissible it must cause the release of large quantities of infectivity from damaged epithelia. Hence transmissibility and virulence are directly related and the selection of increasingly transmissible strains in an epidemic involves an increase in virulence. In endemic areas such highly transmissible strains tend to die out because of the lack of susceptibles. However, milder, less transmissible strains of virus which are continually produced, presumably through mutation, can persist for longer in the limited supply of susceptible individuals, thus being given the opportunity to become dominant strains.³⁰⁵ A limited experimental study supported this hypothesis.⁵² When the less transmissible strain is reintroduced to an unconfined supply of susceptibles it will again transmit freely and revert to virulence. This ability of the virus to render itself less clinically obvious in endemic areas may explain those outbreaks of disease that have occurred in areas long thought to have been free of the virus.^{184, 197, 369, 374}

Other domestic species such as small ruminants play only an accessory role in the maintenance of the disease by helping it to ‘smoulder’ for a while after epidemics have occurred in the cattle population.^{426, 427} They are, however, insufficiently susceptible to maintain endemic strains of RPV. In India it was thought that certain strains of RPV have become established in sheep and goats, which could pass the disease back to bovine animals.^{45, 96, 227, 242, 265} The origin of such strains is unknown, though the use of insufficiently attenuated goat-adapted vaccines has been implied.⁸⁶ Fortunately, these viruses, if truly rinderpest and not PPR virus, appear not to have been maintained in small ruminants because rinderpest has now been eradicated from India.

Clinical rinderpest in pigs was also common in southern India before the virus was eradicated from cattle.²⁸⁴ European pigs can be infected by diseased cattle and by eating contaminated meat. Although clinical disease has been reported, ¹²⁵ mild or subclinical infection is more common, especially with African strains of virus, making pigs a potential source of infection for other pigs and cattle.^{97, 342}

In Asia wildlife have been described with clinical disease, and such infected animals can transmit infection to other susceptible species, including domestic stock.^{27, 92, 193, 245, 357, 385} However, the sizes and densities of these wildlife populations are low and they are not considered to be involved in the maintenance of the virus in Asia.

The role of wildlife in Africa has received much closer attention due to the greater population sizes and densities, the larger number of susceptible species, and the frequency with which the disease has been reported in wildlife.^{5, 75, 84,410} Until the 1960s a widely held view in East Africa was that wildlife, particularly the vast populations of plains game in Maasailand, could maintain the virus independently of cattle,^{191, 196, 249, 292} though some authorities considered cattle to be the main reservoir of infection.^{94, 140} However, when cell-culture attenuated vaccine led to the eradication of the disease from cattle in Maasailand in the early 1960s, clinical disease also disappeared from wildlife.³⁶¹ The absence of antibodies in wildebeest and other species born after 1963 supported this,^{256, 264, 374} and considered opinion changed to the view that wildlife could not maintain the virus.²⁵⁴

Nevertheless, the virus may persist for months, perhaps years, during prolonged epidemics in wildlife. In a study of wildlife sera collected in Kenya between 1970 and 1981 significant levels of specific antibody to RPV were detected in 8 per cent of the samples.³¹¹ Whilst acknowledging that these infected animals may have been sentinels for RPV in nearby cattle or that other morbilliviruses might be responsible, it was suggested that certain strains of RPV might be maintained independently of cattle for variable periods of time.^{272, 311} Coincidentally, rinderpest was diagnosed in African buffalo in the Serengeti National Park in 1982, which was the first confirmation of the disease in Tanzania since 1965. A re-evaluation of mortalities in wildlife during the preceding two to three years in Tanzania attributed many of these to rinderpest.²³⁴ The 1982 outbreak then expanded to involve wildlife and cattle throughout a large area of Tanzania north of the central railway line before being controlled by the vaccination of cattle in 1983 and subsequent years.¹³⁵

Subsequent serological surveillance showed that most of the African buffalo population in the area of Kenya immediately north of the Serengeti also had high levels of antibody to RPV, despite having shown no signs of clinical disease. Analysis of the birth dates of sampled animals indicated that new seroconversions had occurred during a two- to threeyear period³¹⁴ but, unfortunately, no virus was recovered. Since no rinderpest was reported in cattle in this area, it appeared that the wildlife may have assisted in maintaining RPV for a period of years and that the infections were inapparent or mild enough to escape notice by wildlife authorities. Between 1994 and 1997, and again in 2001, similar outbreaks occurred in wildlife in Kenya’s national parks with only limited evidence of infection in nearby cattle.¹⁷⁹ Fortunately, virus was isolated from these outbreaks and shown in experimental infections to cause only very mild or subclinical disease in cattle. Molecular typing revealed that the virus involved was the Africa lineage-2 virus, which had not been isolated in Africa for over 30 years.⁴¹ Since this previous isolation was from a giraffe,²³⁰ this encouraged renewed debate on the role of wildlife. At present all evidence indicates that wildlife do not maintain RPV indefinitely, though it is possible that sufficiently large populations may occasionally maintain mild or subclinical RPV for periods of a few months to perhaps one or two years. Nevertheless, wildlife do play a very important role in rinderpest. Rather than being permanent reservoirs of infection they act as sensitive sentinels for mild rinderpest in nearby cattle populations. All recent confirmed outbreaks of Africa lineage-2 virus have been detected first in wildlife. Even when rinderpest is proved to have been eradicated from cattle it is likely that final acceptance of the eradication of rinderpest from Africa will come from clinical and serological surveillance of wildlife.

Pathogenesis

Experimental infections can be established by all routes of parenteral inoculation and, more variably, by intranasal or conjunctival installation. Natural infection usually occurs via the upper respiratory tract following inhalation of virus containing aerosols, or the oropharynx after ingestion of infected material.^{87, 130, 139, 251, 252, 333, 380} Primary multiplication of RPV has not been demonstrated in the invaded epithelium,³⁷³ but following intranasal and contact challenge, the virus can be recovered within 24 hours from the pharyngeal lymph nodes and tonsils and, to a lesser degree, from other lymph nodes draining the head and upper respiratory tract.^{251, 373} In vivo infectivity is closely associated with mononuclear leukocytes and is not readily detected in plasma and other body fluids.^{93, 252, 325, 380}

Primary multiplication in lymph nodes draining the site of entry of the virus leads to viraemia, which enables the virus to infect and replicate in lymphoid tissues throughout the body, and eventually in epithelial tissues, especially those of the alimentary tract. There, virus-induced cytopathic effects produce the typical lesions of the disease, some of which may also be due to infection of small lymphoid aggregates in the lamina propria.²⁵²

There is a direct relationship between attenuation and the degree of viral multiplication in lymph nodes of cattle.^{333, 418} Virulent strains of RPV have a greater ability to infect lymphoid cells and mononuclear phagocytes and may grow to higher titres in these cells than do strains which induce mild disease.³¹⁷ The cell-culture attenuated variant of the Kabete ‘O’ strain of RPV, which is the most commonly used vaccine, only produces low levels of infectivity in lymphoid tissues and is barely detectable in the blood.³⁷² These low levels of viraemia are probably one reason why attenuated and mild strains cause so little epithelial damage. The virus has a predilection for T lymphocytes and attains higher titres in the T4 and T8 subsets of T cells than in lymphoblasts of B or null cell origin.^{301, 312, 315, 317} Rinderpest virus grows more readily than PPR virus in bovine lymphoblasts, whereas the reverse is true in sheep and goat lymphoblasts. ³⁴⁷

During disease the virus is also found in non-lymphoid organs, such as the lungs, liver and kidneys.^{54, 57, 93, 188, 372, 373} Immunocytochemistry has shown that antigen-bearing cells in these organs are usually associated with reticuloendothelial and perivascular connective tissue.^{38, 73, 412, 413}

Virulent strains of RPV are excreted from epithelial tissues one or two days before the appearance of fever or lesions, ¹⁸⁸ but the amount of excreted virus increases considerably as the lesions develop and only starts to decline when the immune response becomes detectable some four to six days after the start of fever. The virus is usually undetectable by 12 to 14 days after the start of fever. At the height of virus excretion, three to six days after the start of pyrexia, virus titres of up to 105 tissue culture infectious doses (TCID₅₀)/nasal swab and up to 10⁶ TCID₅₀/g of faeces can be recovered from cattle infected with virulent strains.¹⁸⁸ This copious output explains why the disease can be so contagious despite the fragility of the virus.

The diarrhoea and oculonasal discharge probably help to increase the transmissibility of the virus by forming infectious aerosols, and by contaminating the environment.

Infected animals mount a vigorous response against the virus. Interferon is produced within two days of infection, enabling attenuated vaccines to protect cattle very rapidly against challenge by virulent virus.^{146, 405, 411} Viral antigens are produced in large amounts throughout the lymphoid tissues and affected epithelia^{224, 306, 335, 340, 418} and stimulate an effective antibody response which begins two to five days after the onset of clinical disease in virulent infections, and some 6 to 10 days after infection with mild or avirulent strains.^{164, 223, 260, 339, 394} The early response consists predominantly of IgM antibodies^{14, 241} which can be detected by virus neutralization (VN), enzyme-linked immunosorbent assay (ELISA) and also, for a period of a few months, by immunoprecipitation, complement fixation and measles virus haemagglutination inhibition.^{316, 345} At the same time IgG antibodies are produced, but these persist for much longer, usually for life,^{255, 261, 320} and are usually measured by VN or ELISA tests.^{13, 293, 307, 308, 339, 351} Generally, high titres (10² to 10³ log₁₀ VN₅₀) of neutralizing antibodies are produced within two to three weeks of infection and remain high for several months, after which they may decline slowly, but usually remain at easily detectable levels (in excess of 10¹log₁₀ VN₅₀) for the rest of the animal’s life.^{255, 261, 266} Rarely, neutralizing antibodies may decline to very low or undetectable levels but such animals are clinically immune, although limited replication of the virus may occur in tissues such as the tonsils before the stimulation of an anamnestic response.^{255, 266, 281, 320, 425} The antibody responses of naturally infected cattle and those vaccinated with live tissue culture virus vaccine are indistinguishable.

A study using ELISA showed the development of serum IgA antibodies in cattle after vaccination.¹⁴ However, one other study using an indirect immunoperoxidase technique failed to detect IgA antibodies and, in contrast to most other studies in cattle, ascribed most of the IgG antibodies to the IgG₂ subclass.³⁵⁰ Secretory antibody is found in nasal secretions of convalescent cattle²⁶⁹ but its persistence is presumably limited to only a few months after recovery, and the role it plays in preventing reinfection is unknown. Cell-mediated immunity to vaccine and infectious virus has received very limited study and its role is still uncertain though undoubtedly important.^{198, 199, 237, 238}

The severity of the cytopathology caused by the virus before the onset of antibody development influences the course of the disease. Virulent strains cause severe lesions before being constrained by the immune response, and such animals, if sufficiently damaged, will still die despite high titres of antibody and low or undetectable amounts of virus.^{328, 340} The persistence of immunity in recovered animals and those given live virus vaccines contrasts with the short-lived immunity induced by inactivated vaccines,^{158, 339} thus implying that recovered animals may be immunologically re-stimulated by RPV antigen throughout their lives.

Immunohistological techniques have shown that the necrotic changes in the lymphoid tissues, epithelia and other organs are associated with large quantities of RPV antigen. ^{73, 85, 239, 365, 412, 418} Cells containing RPV antigen are widespread in lymphoid tissues and are also prevalent in cells in the loose connective tissue surrounding blood vessels in most tissues.^{85, 307, 412}

Circulating immune complexes have been demonstrated in rabbits recovering from rinderpest,²⁸⁸ associated with the rapid elimination of the mass of viral antigen by the specific humoral response. There is a transient autoimmune response in infected rabbits which produce an IgM (19S) haemagglutinin to homologous erythrocytes and an IgG (7S) anti-nuclear antibody.^{116, 287}

The massive destruction of lymphocytes causes immunosuppression. In rabbits, cell-mediated and humoral immunity is suppressed through the loss of both T and B lymphocytes.^{176, 239, 240, 416} In cattle, lymphoid necrosis is first seen in the germinal centres which are populated with B cells.³⁷⁸ However, in vitro, RPV grows readily in bovine T and B lymphocytes.³⁰³ Immunosuppression in cattle therefore probably involves both cell-mediated and humoral immune responses.

Possible immunosuppression by the cell-culture attenuated vaccine has been investigated experimentally by simultaneous inoculation of RPV with other immunogens such as vaccines against foot-and-mouth disease and contagious bovine pleuropneumonia. Most experimental studies have shown no diminished responses to RPV or the other immunogens, ^{72, 105, 134, 169, 201, 277, 278} although there is still some doubt, especially with regard to bivalent vaccines incorporating live Mycoplasma mycoides¹⁶² or inactivated foot-andmouth disease virus.¹⁷⁰ One report also describes the development of severe bovine virus diarrhoea virus (BVDV) infection in cattle given live attenuated RPV in conjunction with live attenuated BVDV,²⁷⁶ another lymphotropic and known immunosuppressive agent.

There are some reports that the vaccine may exacerbate trypanosomosis or that trypanosomosis reduces the antibody response to the vaccine.³⁵⁶ The overwhelming evidence from the field, where several hundred million cattle have been vaccinated in the past 40 years, many of which would have had intercurrent infections, is that rinderpest vaccine does not reactivate or exacerbate trypanosomosis or other diseases as experimental studies show.³⁶⁰ Even when suffering from severe but non-fatal rinderpest, cattle develop a rapid and full humoral response to the virus despite the changes in their lymphoid tissues. Admittedly, the early vaccines prepared from caprinized, lapinized and avianized virus often did produce mild clinical signs and occasional flare-ups of latent or subclinical infection,^{65, 71, 332, 362} but they produced no lasting check on the growth rate of healthy cattle⁶⁷ and did not increase the severity of a concurrent outbreak of East Coast fever.¹⁶

Rabbits inoculated with lapinized virus show depressed and delayed hypersensitivity skin responses and impaired lymphocyte responses to mitogenic stimulation.⁴¹⁹

Clinical signs

The clinical signs of rinderpest have been extensively described. ^{25, 87, 88, 119, 135, 252, 274, 322, 335, 336} The following description gives the basic signs in the sequence in which they usually occur in severely affected cattle.

Acute natural infections and those induced by parenteral inoculation of RPV have an incubation period of three to five days. Incubation periods following experimental contact infection are longer, from 8 to 15 days,^{188, 250, 297, 373} and there are reports of extended incubation periods in natural outbreaks. ⁸⁷

Pyrexia heralds the onset of clinical disease. The rectal temperature rises rapidly to 40 to 41,5 °C and this can be maintained for up to one week before gradually returning to normal. During the first one or two days of fever there may be depression or restlessness, inappetence and reduced milk yield. The visible mucosae are congested and a serous oculonasal discharge (Figure 49.5), one of the characteristic signs of rinderpest, becomes apparent. Between the second and fifth days of fever the mucosal lesions become obvious,initially as pin-point white foci on the gums (Figure 49.6) and lips, which spread rapidly to involve the buccal mucosa and ventral and lateral aspects of the tongue (Figure 49.7) and muzzle (Figure 49.8 and 49.9).

The foci enlarge and coalesce into plaques of caseous necrotic debris, which desquamate easily, leaving circumscribed erosions. The halitosis is memorable. Similar lesions may be seen on the palate, posterior dorsum of the tongue, pharynx and in the nares and vagina. Severe cases often drool foetid saliva, presumably because of the discomfort in their mouths and pharynges when swallowing.

Figure 49.5 Serous to mucoid oculonasal discharge in a calf

Figure 49.6 Marked necrosis and erosions in the buccal mucosa

Figure 49.7 Focal necrosis of the ventral aspect of a bovine tongue

In cattle infected with strains of high virulence, diarrhoea, sometimes preceded by an absence of defaecation (there are usually no signs of constipation), starts four to five days after the onset of pyrexia, usually one to three days after mouth lesions become visible. The faeces are initially thin and dark, but may progress to contain blood, mucus and shreds of necrotic epithelium. The hindquarters are fouled (Figure 49.10 and 49.11) and tenesmus with eversion of the rectal mucosa is frequent. The diarrhoea causes dehydration (Figure 49.12), weakness and prostration, and in severe cases abdominal pain is evident. Recumbent animals face their flanks in typical ‘milk fever’ posture. The oculonasal discharge becomes increasingly purulent during the course of the disease and conjunctivitis causes photophobia. Corneal opacity is rare in cattle, but has been recorded in some species of wildlife such as giraffe, kudu (Figure 49.13 and Figure 49.14) and buffalo.^{179, 349} Epiphora may be evident below the medial canthus.¹³⁵

Early descriptions of rinderpest frequently made mention of skin lesions.^{232, 322} Most recent accounts^{88, 252, 333} regard these as rare, though they are sometimes present in water buffaloes, sheep and goats. The lesions appear as a maculo-papular rash on areas of soft skin such as the axillae and groin, where the hair may become matted when the rash eventually becomes pustular and breaks open.^{25, 87, 165, 215, 218}

Although respiration may be laboured during acute clinical disease, pulmonary lesions are uncommon and are mainly due to secondary bacterial infection. Emphysema of the lungs may occur terminally. Lymphadenopathy is not usually evident even on palpation of the superficial lymph nodes. Milk may become watery or dry up. Pregnant animals frequently abort, occasionally weeks or months after clinical disease.^{87, 157, 232, 390} Most animals that succumb to rinderpest die 5 to 14 days after the onset of pyrexia.

Convalescence is marked by the rapid healing, within two to six days of oral mucosal lesions, starting some three to six days after their appearance. In cases of mild disease the mouth lesions may only be visible for one or two days. Diarrhoea diminishes more slowly and may persist, in a less severe form, for up to two weeks. Complete recovery from severe rinderpest takes one to two months or more, depending on how much condition the animal has lost and the quality of nursing.

Figure 49.8 Severe necrotic stomatitis, encrusted muzzle, salivation, conjunctivitis and evidence of photophobia

Figure 49.9 Desquamating lesion on the muzzle of a cow

Figures 49.10 (top) and 49.11 (right) Severe faecal soiling of the hindquarters as a result of diarrhoea

Since RPV destroys lymphoid tissues, infected animals suffer from a variable degree of immunosuppression. In Africa this frequently leads to the reactivation of a variety of chronic or latent diseases, especially those caused by haemoparasites such as anaplasmosis, which, if not treated therapeutically, increase the mortality caused by RPV.^{87, 120, 138, 141, 275, 291, 333, 335}

In endemic areas the disease is milder: most of the signs are much reduced in severity and some may be absent.^{87, 197, 250, 274, 297} Experimental infections with virus strains recovered from these areas may cause no deaths, no diarrhoea, transient mouth lesions in only a proportion of infected Bos taurus cattle, and only transient pyrexia in Bos indicus cattle.^{250, 297, 369}

Clinical signs vary in sheep and goats. Disease was seen in sheep during the British epidemics of 1865 to 1866³²² and in the first Great African Pandemic.¹⁴⁷ Clinical signs in naturally infected small ruminants have occasionally been reported in Africa^{47, 191, 200, 326, 340, 388} but experimental infections with African strains of RPV have produced only transient fever, sometimes accompanied by slight oculonasal discharges.^{4, 110, 248, 331, 388, 393} Sero-conversion is usually the only evidence that sheep and goats have been infected.^{71, 72, 309, 428}

In contrast, clinical rinderpest occurred frequently in sheep and goats in India before its eradication.^{8, 108, 285, 286, 348, 358} The duration of the incubation period is similar to that in cattle, with fever being the first clinical sign although its onset may be more gradual than in cattle. Diarrhoea starts two to three days later and, if severe enough, causes dehydration and death. The tail and hindquarters are soiled by faeces. Sero-mucoid, oculonasal discharges that rapidly become purulent are seen within 24 hours of fever. Mouth lesions are less obvious than in cattle. Inappetence is usual. Pneumonia is commoner in small ruminants than in cattle, but is also probably due to secondary bacterial infections.⁹⁵

Figure 49.12 Sunken eyes as a result of severe dehydration in a calf

Figure 49.13 Corneal opacity and lachrymation in a kudu (Tragelaphus strepsiceros)

Figure 49.14 Severe keratitis in a kudu (T. strepsiceros)

Figure 49.15 Severe watery diarrhoea in a buffalo (Syncerus caffer) calf

Figure 49.16 Severe haemorrhagic/necrotic abomasitis

In Asia, both local and European pig breeds develop clinical disease.¹⁵³ The signs are typical: pyrexia, inappetence and depression, and prostration.^{56, 81, 143} Typical mouth lesions develop in one to two days, and diarrhoea within two to three days after the onset of fever. The diarrhoea lasts 5 to 10 days and in severe cases leads to dehydration and death. Pregnant sows may abort. Erythematous skin lesions may be seen. Transient low fever is all that may develop in European pigs inoculated with African strains of virus, most infections being totally inapparent.³⁴²

Mouth lesions, diarrhoea^{129, 19} and deaths101 have been reported in camels, but generally, in areas where rinderpest is prevalent in other species, camels do not show clinical signs^{194, 246} or develop antibodies which would indicate inapparent infection.³⁴³ Most of the reports of clinical disease were based only on clinical evidence without other diagnostic confirmation. Experimental infection of dromedaries (Camelus dromedarius) with cattle strains of RPV resulted in subclinical infection.^{280, 368}

Disease in water buffalo is frequently severe, with clinical signs being the same as those in cattle, although skin lesions are reputedly more common.^{25, 87}

Wild ungulates exhibit a wide range of clinical signs, from typical erosive stomatitis, gastroenteritis and death in African buffalo (Figure 49.15), eland (Taurotragus oryx), giraffe and warthog (Phacocoerus aethiopicus)^{247, 379} to mild or nonspecific signs in impala.³⁴¹ As a generalization, the more bovine- like species amongst the Bovidae suffer more severe clinical disease than do the caprine-like species. Corneal opacity and skin lesions have often been described for rinderpest in wildlife such as giraffe, Grant’s gazelle (Gazella granti) and African buffalo, though not all of these outbreaks wereconfirmed in a laboratory.^{254, 349, 354, 379} During the 1994 to 1997 and 2001 wildlife epidemics in Kenya these same signs were seen in animals in which the disease was confirmed by laboratory tests. Corneal opacity and blindness were such regular features in these outbreaks that reports of blindness in some species such as kudu (Figure 49.13 and Figure 49.14) should always be treated as possible rinderpest.²²⁰ Affected wildlife often exhibit behavioural changes. Dehydration forces thirsty animals to migrate long distances for water, while discomfort makes them more aggressive, especially African buffalo.^{58, 75} In the Kenyan outbreaks, sick animals such as eland fell behind their herds and were closely approached by inquisitive members of other species, thereby providing a greater chance for interspecies transmission.

Pathology

A proportion of infected cattle shows slight lymphocytosis before the onset of pyrexia. This is followed by marked lymphopenia, caused by lymphoid necrosis, which in most cases lasts throughout the acute clinical stage of the disease. ^{24, 136, 208, 290, 296, 378} During convalescence, lymphocyte levels slowly return to normal over a period of days to weeks. The number of neutrophils remains relatively unaltered, though juvenile forms are not infrequent during the terminal stages of fatal infection. However, a degree of neutropenia that parallels the decline in lymphocyte levels has been reported.³⁷⁸

Eosinophils may also disappear from the blood during the early stages of clinical disease, returning to normal levels some two to three weeks later. In severe cases the excessive loss of water causes haemoconcentration.²⁴

Serum aspartate transaminase and blood urea nitrogen levels increase during severe cases of disease.^{51, 137} Serum chloride levels fall markedly in terminal illness, and other electrolytes may decrease in absolute terms although this can be masked by haemoconcentration. Blood clotting may be impaired in severely affected animals. Serum protein levels may be lowered, especially in fatally infected animals.^{87, 102, 115} In cattle recovering from experimental infections a rise in serum globulins was attributed to the specific humoral response to the virus,¹¹⁵ but since the challenge material was citrated blood, this may need reinterpretation in the light of known responses to heterologous tissue antigens.

The lesions of rinderpest are a direct result of virus-induced cytopathology. There are many descriptions of the gross pathology,^{25, 61, 87, 119, 159, 333} but those of Maurer et al.^{207, 208} are especially valuable. Generally, the severity of the lesions is directly related to the virulence of the strain of virus involved.^{377, 418} Complications may arise during convalescence through reactivation of latent pathogens, especially protozoa.^{87, 138, 335}

The overall appearance at necropsy is similar for most species that die of typical severe rinderpest. The carcass is dehydrated, sometimes emaciated, and usually soiled with fluid faeces. The eyes are sunken and often encrusted with mucopurulent discharge and the cheeks may show signs of epiphora.

Erosions with or without necrotic material may be found throughout the mouth but predilection sites are the gums, lips, buccal papillae, dorsal and ventral aspects of the tongue and the soft palate. The erosions often extend into the pharynx, cranial part of the oesophagus, rumen (especially the pillars), reticulum and omasum. Necrotic areas, some of which may penetrate the leaves of the omasum, are sometimes present.

The folds of the abomasum are congested and oedematous and often show necrosis, erosions and haemorrhage along the edges (Figure 49.16). The fundus of the abomasum may have small discrete erosions that increase in size towards the pylorus where whole areas of mucosa may become desquamated. The early necrotic lesions are palegreyish, whereas the erosions are often red as a result of congestion of the underlying lamina propria. Haemorrhage may occur from the raw surfaces. The abomasum is almost invariably severely affected, whereas the small intestine frequently shows less involvement. Congestion, oedema and erosions may occur on the margins of mucosal folds of the cranial part of the duodenum and terminal ileum. The Peyer’s patches, being lymphoid tissue, are often severely affected and may be swollen, dark red to almost black as a result of haemorrhage, and may slough completely leaving deep ulcer-like areas. Large erosions are commonly found on the ileocaecal valve. In the large intestine, marked oedema and congestion accompanied by petechiae or larger haemorrhages occur, particularly along the crests of longitudinal folds of the mucosa. This can be very striking in the colon and rectum, meriting the description ‘zebra striping’. In acute cases, the gut contains little other than desquamated necrotic epithelium, blood, and fibrin exuding from exposed lamina propria.

The urinary and gall bladders are sometimes congested and haemorrhagic with occasional erosions. The vaginal mucosa may be congested and have small erosions.

The mucosa of the nasal passages, sinuses and larynx may be congested and is usually covered with mucopurulent exudate. Petechiae are frequent and necrotic; erosive lesions may extend from the nares to the larynx. The tracheal mucosa is frequently congested. Congestion and emphysema may be seen in the lungs while secondary bronchopneumonia may complicate chronic cases.

Although regularly described in early reports, skin lesions are now rarely seen, although they are reputedly still common in water buffalo. The exudative dermatitis would seem to develop from macular to pustular lesions, but the role of secondary bacterial infections such as Dermatophilus congolensis needs clarification.^{141, 196, 218}

Although RPV has a predilection for lymphoid tissues, there are usually few visible changes in the superficial and visceral lymph nodes. These may show congestion, oedema, and a few petechiae. The nodes of animals that die after a prolonged clinical course may be shrunken and show greyish radial streaks in the cortex, presumably due to haemorrhage.²⁵ The spleen and haemolymph nodes appear normal or slightly enlarged.

The necropsy findings in goats inoculated with caprinized virus are similar to those in cattle, although they may be less marked.

The lymphotropism of the virus is perhaps best shown in rabbits inoculated with lapinized virus. Although there are no observable epithelial lesions, white, pin-head sized foci of necrosis are easily seen in the gut-associated lymphoid tissues.^{117, 159}

Histopathological lesions become more easily detectable with increasing severity of clinical disease, implying that the pathology is directly related to the ability of a strain to multiply rapidly in the tissues.^{378, 418}

The essential histopathology of rinderpest was first described in infected rabbits.^{62, 117} Widespread necrosis of lymphocytes is apparent throughout the lymphoid tissues, together with syncytia and intracytoplasmic and, less frequently, intranuclear inclusion bodies. The histology in cattle is similar^{172, 208, 377} with lytic destruction of lymphoid tissues that is most evident in the germinal centres, sometimes accompanied by an increase in the numbers of macrophages. In acute cases lymph nodes are virtually devoid of cells, with just a reticular stroma containing eosinophilic material remaining.

The early epithelial lesions in the squamous epithelium of the digestive tract are associated with the formation of syncytia and eosinophilic intracytoplasmic inclusions in the stratum spinosum.¹⁷³ Infected epithelial cells become necrotic and slough off, leaving clearly demarcated erosions. The erosions heal rapidly unless complicated by secondary infections which may rarely cause them to ulcerate.

Changes in other tissues are not remarkable, although small foci of necrosis in the liver have been described.¹⁷⁴

Ultrastructurally, infected cells contain large parallel arrays of tubular nucleocapsid material which are probably the intranuclear and intracytoplasmic inclusion bodies seen by light microscopy.^{60, 282, 366} Virus is released from cells by some of the tubular strands budding through the cell membrane. Similar changes were described in lymphoid cells from two Japanese black cattle infected with the virulent Fusan strain of RPV,¹⁷⁷ and in persistently infected Vero cells.¹⁷⁷

Diagnosis

The clinical and laboratory diagnosis of rinderpest is described in detail in many handbooks and reports.^{6, 25, 29, 270, 279, 335, 345} A presumptive diagnosis can be made on the basis of the clinical signs and gross pathology. However, in countries where rinderpest is not prevalent it is essential to obtain laboratory confirmation of the diagnosis as soon as possible. Countries where rinderpest is either endemic or a high risk should treat any syndrome resembling rinderpest as such until proven otherwise. This will allow immediate steps to be taken to control the disease and restrict losses.

The collection of adequate quantities of appropriate specimens greatly increases the chances of an accurate laboratory diagnosis. A thorough clinical examination should be made of animals in suspected herds and six or seven animals in the early acute stage of the disease with fever, mouth lesions and lachrymation should be selected for sampling. Animals that are dead, moribund or have had diarrhoea and mucopurulent discharges for more than three days are less reliable sources of virus or antigen as the levels of these decline with the onset of antibody development. ³³⁵

From each selected animal the following specimens should be collected: whole blood for serum antibody assay, and in anticoagulant for virus isolation from leukocytes, a biopsy from a superficial lymph node, debris from oral lesions, and ocular and nasal swabs for virus isolation and antigen or nucleic acid detection. If possible, two or more animals should be killed for necropsy examination and collection of up to three universal bottles of splenic tissue and mesenteric lymph nodes. All specimens should be collected and bottled aseptically, kept cool on ice (but not frozen) and transported as rapidly as possible to a diagnostic laboratory. ^{335, 345, 389}

Glycerol should not be used as a preservative because it inactivates RPV. The use of anti-proteases increases the survival of RPV antigens in tissue suspensions³⁰¹ and reduces the degradation of RNA.

At the laboratory, suspensions of solid tissues are prepared in physiological saline or cell-culture medium, the buffy coat is removed from the whole blood and the serum separated from the clotted blood. Thirty per cent tissue suspensions (w/v) for antigen detection can be prepared by most techniques, including grinding with sand in a mortar, but 10 per cent suspensions for attempted virus isolation can best be prepared in Ten Broeck or similar grinders.

The first procedure usually carried out is to detect viral antigen using specific rabbit hyperimmune serum against RPV. The most commonly used assay is the agar-gel immunodiffusion test (AGID)^{340, 408} which is simple, easy to read, and highly specific. Moreover, it can be used in the field with swabs and gum debris and can give a result within two hours, especially if micro-versions are used.¹¹³ Counterimmunoelectrophoresis is quicker and more sensitive than AGID but requires more sophisticated equipment.^{3, 313} Immunofluorescence and immunoperoxidase staining methods are very sensitive but also need more equipment than AGID.^{22, 118, 269, 306, 352} Although once widely used, complement fixation and conglutinating complement absorption tests are too complicated in comparison with more recently developed tests. Various haemagglutination assays are sensitive but not widely applied,^{27, 355} though latex bead agglutination tests have given encouraging preliminary results²¹³ and, if combined with monoclonal antibodies, could prove very sensitive. Recently, a monoclonal antibody-based rapid chromatographic strip test has proved useful under penside conditions.^{74, 144, 398} If classically prepared rabbit hyperimmune serum³³⁵ is unavailable, serum can be prepared using other immunizing techniques in rabbits^{214, 220, 301} or in goats or cattle.^{330, 344} A positive test result in any of these antigen detection tests confirms rinderpest.

Where cell-culture facilities are available, attempts should be made to isolate the virus. Suspensions prepared from swabs, gum debris, buffy coats or lymphoid tissues are inoculated onto growing monolayers of primary or secondary bovine kidney cells in tubes.^{258, 262} Vero cells and lymphoblastoid cell lines^{160, 212} are also suitable, while culture systems such as microplates can also be used⁴⁰³ but may be less sensitive. After 12 to 24 hours adsorption the tubes are washed, refed with maintenance medium and rolled at 37 °C. Typical cytopathic effects develop within 3 to 14 days, occasionally longer, and consist initially of foci of round and refractile cells with cytoplasmic processes and small syncytia, followed by generalization throughout the monolayer with distinct syncytium formation. Negative test cultures should be passaged at least once. The virus can be identified by inoculating sample materials into tubes containing antiserum to RPV or by examining fixed monolayers using immunofluorescent or immunoperoxidase techniques.^{181, 186, 268} Where cell cultures are not unavailable, the specimens can be inoculated into known immune and susceptible cattle, as long as these are isolated from other susceptible animals.

If antigen detection and virus isolation are negative, then convalescent animals should be bled again two to four weeks later. Assays for serum antibodies should demonstrate a four-fold or greater increase in antibody titre in recovered cases. Virus neutralization in microplates was most commonly used for this,^{12, 293, 307} although several other techniques such as measles virus haemagglutination inhibition, indirect immunofluorescence, ELISA and counterimmuno- electrophoresis are alternatives.¹⁶⁶ A number of ELISA tests have been developed. Original indirect tests based upon whole virus antigens^{12, 13, 14, 308} have largely been replaced by competition ELISAs that use monoclonal antibodies to different viral antigens such as the H or N protein, and may also use purified or recombinant antigens.^{11, 190, 321} The ELISA has the advantage that laboratories without cell-culture can test thousands of sera, which is often required in current eradication programmes, and the sensitivity and specificity of these new tests is under validation at present. During the early antibody response, serum contains significant levels of IgM to RPV,^{14, 241} the detection of which confirms the diagnosis, though this approach is rarely used.

Histopathology is not sufficiently specific to confirm a diagnosis of rinderpest, but demonstration of syncytia and viral inclusions is supportive.

Nucleic acid techniques including hybridization with probes and polymerase chain reactions (PCR) are capable of detecting minute quantities of RPV RNA in tissues and secretions,^{38, 244} and are now often a routine choice for confirmation in reference laboratories. The PCR offers the advantage of providing amplified viral RNA for nucleotide sequencing in order to establish the virus subtype or lineage for epidemiological purposes.¹¹⁴

Differential diagnosis

All conditions that cause stomatitis and/or enteritis in domestic stock can be clinically confused with rinderpest. In cattle, difficulties may occasionally arise in distinguishing rinderpest from mucosal disease (MD), malignant catarrhal fever,³⁷⁶ infectious bovine rhinotracheitis (particularly when caused by strains that induce diarrhoea),^{131, 132} papular stomatitis,²²² Jembrana disease³⁷⁵ and foot-and-mouth disease. In small ruminants, PPR and Nairobi sheep disease can resemble rinderpest. Infection with Campylobacter spp.,Brachyspira hyodysenteriae and Salmonella serovars needs to be considered when investigating possible rinderpest in pigs.

In practice, onlyMDin cattle and PPR in small ruminants present a problem.^{69, 334} The clinical signs and gross pathology in cattle with MD can be indistinguishable from rinderpest and diagnosis requires laboratory confirmation. However, MD usually affects very few animals in a herd, whereas morbidity rates in rinderpest are much higher. Agar-gel immunodiffusion applied to tissue suspensions can rapidly differentiate the two diseases.⁹⁰ Immunohistochemical techniques can be used on frozen sections of mesenteric lymph node or on formalin-fixed tissues to distinguish between rinderpest and MD.¹¹⁸ Failing this, virus isolation with subsequent virus identification must be attempted, with follow-up studies to detect rising antibody titres. Nucleic acid-based techniques may also be used.

The differentiation of PPR from rinderpest is more difficult. Useful epidemiological evidence is provided by the absence of disease in cattle. The virus cross-reacts serologically with RPV and is difficult to differentiate with hyperimmune polyclonal sera. Fortunately, contemporary studies have produced monoclonal antibodies and nucleic acid techniques that clearly distinguish between PPR virus and RPV, at least for the limited number of strains tested to date.^{10, 103, 209, 210} In African countries that have previously been free of PPR it is unwise to assume that a rinderpest-like syndrome in small ruminants is not PPR.

Control

In countries where rinderpest is exotic, confirmed outbreaks are controlled by the slaughter and disposal of all affected and in-contact animals, as well as by appropriate quarantine and animal-movement controls. Such measures eradicated the only outbreak of rinderpest in Australia within two months⁴⁰⁷ and halted the 1866 outbreak of rinderpest in Britain within six months.³⁸³

Virtually all outbreaks of rinderpest in virgin areas have been due to the importation of live infected animals.³²⁷ Prevention in such areas is therefore largely dependent upon vigilant control of the introduction of live animals from potentially infected areas. Importation of fresh carcasses and meat products constitutes a minimal threat, although at least one epidemic has been attributed to this source^{2, 80, 88} and outbreaks in endemic areas have been traced to fresh infected meat. During the first Great Pandemic, the virus is reputed to have crossed the Orange River in South Africa in this way. In frozen meat the virus persists for much longer than in fresh meat and is therefore a risk to swill-fed pigs.^{289, 327, 329} Infectivity disappears rapidly from adequately dried infected hides⁴⁸ and from decomposing carcasses held at ambient temperatures in tropical regions for more than two or three days.^{87, 106} A limited number of outbreaks have also been associated with the spread of the virus from laboratories. ⁴²²

Contaminated areas should be physically cleaned of all animal waste and soiled bedding and treated with disinfectant solutions of high (>10) or low (<3) pH containing solvents to destroy the virus envelope. Most disinfectants have some activity against RPV, but it has been shown that solutions of caustic soda and lysol have the highest virucidal activity against virus contaminated with organic matter.³⁹⁹ Such premises could be restocked after a week but the customary caution of veterinary authorities usually results in the period being longer.

Control is more difficult in endemic areas. Clinical diagnosis should be sufficient to instigate control procedures and all outbreaks of rinderpest-like disease should be treated as rinderpest until proven otherwise. Slaughter of affected and in-contact animals removes the source of virus, but may be counter-productive where owners have either a close cultural bond with their animals or are unlikely to receive compensation. In such areas, quarantine and strict movement control must be enforced immediately and the support of local cattle owners (which is usually forthcoming) is essential in this. Countries bordering high-risk zones must channel the import of domestic animals through border quarantine stations for vaccination and three weeks of observation.¹⁹¹

All susceptible animals in affected herds should be vaccinated immediately with subsequent ‘ring’ vaccination of herds in the surrounding districts.

The importance of vaccination in the control of rinderpest in endemic areas cannot be overemphasized, and most early research concentrated on the development of effective vaccines.^{87, 217, 333}

Initial ‘vaccines’ in South Africa included the inoculation of infected bile, developed by Koch,¹⁷⁸ and the simultaneous administration of convalescent serum and virulent virus developed by Danysz and Bordet, Theiler and Watkins Pitchford, and Kolle and Turner.¹⁴⁷ Neither of these was entirely satisfactory, and Kakizaki¹⁶⁷ subsequently developed a glycerol inactivated tissue vaccine. The immunity it induced was solid but short-lived. This encouraged the development of many other inactivated vaccines, but these required frequent administration. It was known that, where it could be produced, immunity following techniques that used live virus persisted much longer, perhaps for life. Continuing research led to the development of a series of increasingly attenuated vaccines that were produced by passage in hosts other than cattle (caprinized, lapinized, and avianized vaccines).^{107, 163, 226, 362}

Finally, repeated passage of the virulent Kabete ‘O’ strain of RPV in bovine kidney cells produced a totally safe and effective attenuated virus,^{164, 261} which has been the principal vaccine used to combat rinderpest throughout the world during the past 40 years. It is inexpensive and simple to produce and test, stable in freeze-dried form,²⁵³ and highly effective even in animals with severe infections such as East Coast fever and trypanosomosis.^{318, 392}

It induces life-long immunity. The only drawback of the vaccine is that after reconstitution in normal saline it has a working life of only a few hours in the hot climates where rinderpest still occurs, ^{253, 338} and there is some evidence that it should not be used more than one hour after reconstitution at ambient temperatures around or above 37 °C.²⁸³ Nevertheless, this vaccine has produced strikingly successful results such as those of the JP15 campaign in northern Tanzania where vaccination often produced herd antibody prevalences in excess of 90 per cent. The thermostability of the vaccine has been improved through more stringent freeze-drying procedures. ^{185, 204, 205, 275, 338} This product, ‘Thermovax’, is very stable at high ambient temperatures and is now the vaccine of choice in areas with little or no ‘cold-chain’ facilities and where it is often administered by community-based animal health workers. The vaccine is, however, still sensitive to heat and light when reconstituted.

Several laboratories have attempted to address this problem by genetically engineering recombinant vaccines in which genes expressing RPV-immunizing antigen are incorporated into more thermostable poxviruses.^{142, 231, 381, 382} These recombinants have proved effective against experimental challenge in the short-term, but preliminary results from most longer term studies indicate that immunity is not as long lasting as with cell-culture vaccine,^{49, 231, 298, 300, 417, 420, 421} though one recent study claims that lasting immunity can be achieved even after a single inoculation.²³⁶ One advantage these vaccines do possess is the possibility of distinguishing vaccinated from naturally infected animals, which could be valuable in eradicating outbreaks. Another and perhaps more promising approach has been the recent development of recombinants of RPV itself. These new chimaeras and antigenically marked rinderpest viruses also offer the potential for serological differentiation between vaccinated and unvaccinated animals but without losing the known benefits of the homologous vaccine.^{33, 34, 91, 396, 397}

The use of dry vaccine in subcutaneous implants⁶⁶ or powder for application to mucosal surfaces⁷ could remove the ‘diluent problem’ in hot, isolated areas.

Prevention of rinderpest in endemic areas requires annual vaccination of all calves up to two years of age. Maternal antibodies from immune dams interfere with active immunization and may persist for 9 to 10 months.^{63, 64} In practice, however, few animals over six months of age have antibody and it is sensible to immunize the 6- to 12-month-old animals rather than only those over a year old in an effort to economize on vaccine. Where vaccination is difficult, infrequent or inefficient, and where cattle populations are continually mobile, annual vaccination of all cattle will produce the highest levels of herd immunity.^{265, 305} In such areas some serological monitoring of herd antibody levels is also advisable to assess whether mass vaccination campaigns have been successful or need to be repeated. The successful eradication of endemic rinderpest from Maasailand in 1962 and 1963 was accomplished by very efficient vaccination campaigns which raised overall herd immunity levels to 90 per cent or more. Values in excess of this have been calculated to be necessary for the eradication of measles virus from human populations and rinderpest from cattle.^{4, 305} Lower levels of vaccination coverage may also stop virus transmission on occasion, especially milder strains.³⁰⁵

In endemic areas sero-surveillance of unvaccinated animals such as small ruminants and wildlife is also important. These species are sentinels, as any antibody they possess must have been induced by field strains of RPV or related agents such as PPRV.

The development of the cell-culture vaccine opened the door to a world free from rinderpest. The Global Rinderpest Eradication Programme (GREP) has set the year 2010 as the target for complete eradication of the disease from the world, and very significant progress has been made in Africa and Asia in the last decade and a half. In Africa in 1999 the virus was restricted to southern Sudan and to the southern Somali pastoral ecosystem, neither of which has ever been completely under government administration, and both of which are now effectively war zones; and in Asia to parts of southern Pakistan. The challenge now faced is to safely access the cattle populations in these remaining foci using conventional and community-based techniques, which have proved successful elsewhere, including the Afar area of Ethiopia. If human and financial resources can be maintained, ³⁹⁵ the goal of global freedom from rinderpest could become a reality.^{17, 229, 319, 333, 370}

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