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La myxomatose en France.


- Vue d'ensemble:

Après la diffusion dramatique de la myxomatose en Australie au début de l'année 1951, une introduction illégale en vu de contrôler la population de lapins a été faite sur un domaine près de Paris [ Maillebois ] en juin 1952. Le type du virus utilisée (' Lausanne ') avait été récemment prélevé sur Sylvilagus [ Lapins d'Amérique ] au Brésil. Elle a mené à l'établissement de la maladie en France. Au cours de la décennie suivante la myxomatose s'est étendue à la plupart des pays d'Europe parmi les populations de lapins, qui subirent une mortalité très élevées.
La réaction publique à la myxomatose en France a été dominée par le souci profond des éleveurs pour la sauvegarde de leurs lapins domestiques et des chasseurs contre la destruction d'un animal important pour la chasse, le lapin sauvage. D'autre part, les forestiers et la plupart des fermiers ont fait bon accueil à la destruction d'un parasite important. La vaccination des lapins domestiques et sauvages a été pratiquée sur une grande échelle.
La souche virale de Lausanne était fortement mortelle et les lésions de peau étaient beaucoup plus protubérantes que celles produites par le virus utilisé pour l'introduction australienne. Des souches moins virulentes ont été identifiées deux ans après son introduction, et les testes réalisés neuf et quinze ans après ont prouvé qu'une souche de virulence différente étaient présente, le pourcentage des souches fortement virulentes a décru progressivement pour atteindre 2% en 1962. En 1980 on a observé une forme « non-myxomateuse » ou « respiratoire" de myxomatose dans les élevages de lapins; c'est bientôt devenu la forme la plus commune et considérée comme transmise par contact étroit. Au début les populations de lapins sauvages ont été décimées. En dépit de la réduction de la virulence du virus et de la plus grande résistance des lapins, dans les années 90 la myxomatose semble avoir ramenés les populations sauvages de lapins à un nombre légèrement inférieur à la moitié de celui constaté avant 1953.

- Introduction en France:

L’éruption dramatique de la myxomatose parmi des lapins d’Australie en 1951 a immédiatement reçu une importante couverture médiatique en Europe. Les premières réponses internationales à cette démonstration d’efficacité pour la régulation des populations de lapins se sont produites en France.
Enquêtes de l'Institut Pasteur, Paris, janvier 1952.
Le 22 janvier 1952 DR G. Remaudière, du service de Parasitologie végétale de l'Institut Pasteur, a écrit à Francis Ratcliffe, à la tête de la Wildlife Survey Section of CSIRO, demandant des réimpressions sur la myxomatose, un spécimen du virus et des détails sur sa culture, et indiquant, entre autres choses :
Les lapins constituant dans certaines parties de la France, un véritable fléau, l’Institut Pasteur désirerait entreprendre la lutte biologique contre ce Rongeur et essayer de développer une épidémie de myxomatose en Sologne. Cette région infestée de lapins semble, à priori, favorable à l’expansion de la maladie, car les Culicidés et Simulides sont abondants.

Ratcliffe a transmis la lettre à son collègue Fenner, qui a envoyé le 15 février 1952 à Remaudière deux fioles de virus myxoma lyophilisé et tous les détails de la méthode de préparation pour de grandes quantités en vue des campagnes d'inoculation. La réception de la lettre et du virus a été attestée le 29 février, mais aucune information supplémentaire sur l'utilisation du virus n'a été reçue en Australie ou n’a pu être trouvée dans une recherche récente parmi les archives en France.
Dissémination du virus myxoma sur le domaine de Maillebois, juin 1952.
DR P.F. Armand Delille (fig. 9.1) était un médecin et un bactériologiste distingué qui avait 77 ans quand il apprit, par les journaux de Paris, la grande épizootie de myxomatose en Australie en 1950-51, et a conçu l'idée d'éliminer les lapins sauvages de son domaine au château de Maillebois (Eure-et-Loir) par l'utilisation de ce virus. Lockley décrit sa visite à Maillebois en décembre 1953 dans les termes suivants (Lockley, 1964):
À ce moment le Dr Delille était un homme très inquiet; des poursuites contre lui avaient été entamées par les représentants de la chasse sportive en France, et il a entrepris avec ses conseillers juridiques à Paris de préparer sa défense auprès des tribunaux. Une action a été intentée contre lui, avec l'aide financière des clubs de chasse français, par le propriétaire local d'un élevage dont tous les lapins étaient morts de la myxomatose. ...

Fig. 9.1
Fig. 9.1. Paul F. Armand Delille (1874-1963). Né à Fourchambault (Nièvre) en 1874. Delille reçu un diplôme de médecine et est devenu l'un des principaux pédiatres à Paris, il effectua une recherche distinguée sur la tuberculose et les maladies infectieuses des enfants. Il a été nommé professeur à l'école de médecine de Paris et a été vice président de la Société de Biologie. Pendant la première guerre mondiale, il a servi comme chef de la bactériologie de l'Armée d'Orient et conduisit des travaux sur la malaria pour lesquels il a été fait commandeur dans l’ordre de la légion d'honneur. Il s'est retiré sur un domaine muré de 300 hectares situé à Maillebois, aux environs de Paris. Sa relation avec cet ouvrage découle du fait qu'en 1952, à l'âge de 78, il a introduit la myxomatose en France, et de là à toute l'Europe, en inoculant deux lapins sur son domaine avec un virus issu d'une collection de culture conservée à Lausanne. Un acte pour lequel il était réprouvé par les éleveurs, les fourreurs et les chasseurs de lapins mais félicité par les fermiers et les forestiers.


Le château Maillebois est une habitation médiévale flanquée de tours se situant dans un beau domaine boisé de 600 acres avec une ferme et une petite rivière, le tout clos d’un haut mur en pierres. Ce mur est interrompu seulement par quelques portes d'entrée qui avaient été rendues hermétiques aux passages de lapins avant l'introduction du virus. Les milliers de lapins sauvages dévoraient les récoltes de ferme et tuaient les jeunes arbres forestiers, le fils du Dr Delille nous a dit que, qu’en juin 1952, deux lapins sauvage capturé ont été inoculés avec le virus myxoma. En six semaines environ 98% des lapins sauvages étaient morts, mais aucun des lapins domestiques dans les clapiers du domaine n'a été affecté.
En octobre 1952, la maladie a été identifiée sur cadavre ramassé à proximité de Rambuoillet, non loin de la résidence du président de la République Française, à cinquante kilomètres de Maillebois.

Tandis que les agriculteurs et particulièrement les forestiers soutenaient Delille, et devaient finalement lui attribuer une médaille d'or (fig. 9.2), il a été vigoureusement dénoncé par les puissants organismes de chasse. Le ministère de l'agriculture était en position difficile, parce qu'en plus de ses fonctions par rapport à l'agriculture et à la sylviculture, il était responsable du Conseil Supérieure de La Chasse, dont les revenus provenaient des permis payés par les chasseurs qui étaient principalement intéressés les lapins.

Fig. 9.2
fig. 9.2
Fig. 9.2. médaille présentée à Dr P.F. Armand Delille par les agronomes et les forestiers français, à une cérémonie organisée par M. Chavet, Secrétaire général de la Fédération nationale des Producteurs de Bois et Reboiseurs français.


Des propositions de lois ont été présentées à l'Assemblée française pour rendre l'introduction et l'utilisation de la myxomatose illégales, mais il était trop tard - la maladie s’était propagée et établie. Avec l'aide financière des clubs de chasse français, une procédure à été intentée contre Delille par le propriétaire d'un élevage domestique local, tous les lapins étaient morts de la myxomatose. Echouant sur un point de procédure ; il ne pouvait pas montrer que le virus avait été introduit directement dans l'élevage affecté par Delille (il ne l'avait d’ailleurs pas été).
Le virus que Delille avait employé différait de ceux a employé précédemment pour des introductions dans les lapins européens, qui ont été dérivés de la souche Moïse et avaient été intensivement introduite chez des lapins de laboratoire. Il a été envoyé à Delille par son ami le professeur Hauduroy, directeur du centre de Collection de Types microbien à Lausanne, Switzerland². DR G. Bouvier, directeur d'Institut Galli-Valerio à Lausanne, a décrit l'origine de cette souche (Bouvier, 1954), qui a été dérivée du réservoir que constituait Sylvilagus au Brésil, avec tout au plus six passages chez les lapins domestiques avant d'être envoyé à Delille. Il s'est appelé 'Lausanne' dans les journaux scientifiques depuis une description de ses propriétés par Fenner et Maréchal (1957).

Suite du document à traduire:

- Attitude to Rabbits in France

Myxomatosis was a subject of great public interest in France, because there was a large commercial rabbit­breeding industry, many people had back­yard hutches (‘clapiers’) and there was a large and influential hunting fraternity for whom the wild rabbit was an important resource. On the other hand, foresters and farmers were very much aware of the importance of rabbits as an agricultural pest (Fig. 9.3). They shared with wild boars the distinction of being regarded as the major vertebrate pest, and in 1952, before the advent of myxomatosis, rabbit damage to agriculture and forestry had reached an estimated annual cost of 1000 million francs and 88 of the 90 départmentes in France had declared the rabbit a pest (Siriez, 1957).

 Fig 9.3.
Fig. 9.3. The place of the rabbit (wild and domestic) in France as it was before myxomatosis. (From Fenner and Ratcliffe, 1965; modified from Barthélémy, 1953.)

The French Game Act of 1844, with later amendments, protects wild rabbits as game; predators which attack rabbits or game birds, such as foxes, stoats and weasels, are regarded as vermin. There is an open season for hunting rabbits between early September and early January, with possible
extension to 31 March. In 1952, the year before the introduction of myxomatosis, 1,850,000 shooting permits were issued, of which some 80% were held by persons who were primarily rabbit hunters. The importance of adequate numbers of wild rabbits to these enthusiastic chasseurs is obvious (see Table 9.1, below), as well as their significance for the supporting industries indicated in Fig. 9.3. The major hunting organizations, the Conseil Supérieur de la Chasse and the St Hubert Club de France, made prolonged and vigorous protests about the destruction of rabbits by myxomatosis, and supported such counter­measures as the vaccination of wild rabbits with fibroma virus, the introduction of cottontails from the United States, and the introduction of resistant rabbits from Australia, all to no avail.
Besides the importance of wild rabbits for hunters, there was a large domestic rabbit industry. In 1950 some 140 million domestic rabbits were produced and consumed annually in France, and many retired workers were partly dependent upon rabbit raising for their livelihood. Because mosquitoes were major vectors and myxomatosis was sweeping through the wild rabbit population, many outbreaks of the disease occurred among domestic rabbits in the early 1950s. Short books on myxomatosis soon appeared (Radot and Lépine, 1953; Virat­Pilet, 1954) and a comprehensive two­ volume monograph was published in 1972–73 (Joubert et al., 1972, 1973). The spread of myxomatosis in France prompted the organization of an International Symposium on Myxomatosis by l’Office Internationale des Epizooties in Paris in November 1953, and there were special sections on myxomatosis at the International Veterinary Congress in Stockholm in August 1953 and at the International Congress of Microbiology in Rome in September 1953.

- Official Action on Myxomatosis

A Central Service for the Fight Against Myxomatosis was set up by the Conseil Superiéur de la Chasse on 16 July 1953, responsible to Dr F. Barthélémy, Engineer in Charge of Water and Forestry. It worked in close collaboration with the Veterinary Service, the Laboratory of Veterinary Research and the Institut Pasteur. Details of legislation providing for the control of myxomatosis are set out in the monograph by Joubert et al. (1973). The French Rural Code (RC) and Penal Code (PC) severely penalize deliberate importation and spread of infectious diseases of domestic and wild animals (PC articles 452, 454–1, 31 October 1955). Some articles of the Rural Code authorize the destruction of animal pests (RC articles 393–395) and specify the methods that can be used. Rabbits can be shot, trapped or poisoned. Sanitary regulations of rabbit farms are strictly policed, and farmers are required to maintain a register containing all information on diseases of their stock and vaccinations carried out.
No immediate official action was taken when myxomatosis was first recognized in October 1952. However, after the rapid spread of the disease in Spring 1953, decrees were published by the Ministry of Agriculture on 27 May 1953 and 27 June 1953. These made myxomatosis a notifiable disease and prohibited the movement of rabbits in an infected area. Appropriate measures were specified for the isolation and disinfection of domestic rabbitries, dead animals being incinerated and their remains buried in quicklime. It was further required that the sanitary status of rabbit farms had to be published fortnightly in the National Sanitary Bulletin (Ministerial decree of 9 July 1953). Persons guilty of ‘the voluntary propagation of an epizootic’ were liable to imprisonment for a period of one to five years. In the case of wild rabbits, areas at risk had to be indicated by notices bearing the words ‘Myxomatose, maladie contagieuse du lapin’, and all rabbits within the area were supposed to be destroyed.
However, strict as these regulations seem to be, it was impossible to eliminate the disease, and periodically outbreaks continue to occur among wild rabbits, and sometimes spread from them to domestic rabbits which are not protected by vaccination or insect-proof screening.

- Clinical Features of Myxomatosis as Seen in France

Myxomatosis in France was initiated by the inoculation of two wild rabbits with the Lausanne strain of myxoma virus; no further inoculations of virulent virus were ever made in the field. Laboratory studies in Australia showed that the Lausanne strain produced a disease (Fig. 9.4A) with more protuberant lesions than those caused by the Standard Laboratory Strain, initially used in Australia for rabbit control. In experiments conducted in Australia, challenge infections of rabbits with increased innate resistance showed that the Lausanne strain was also more virulent than the Standard Laboratory Strain, in that the case-fatality rate was about 99% when the Standard Laboratory Strain was associated with a case-fatality rate of 60–80%3.
Attenuated strains of myxoma virus were first recognized in 1955, in the département of Loiret (Jacotot et al., 1955; Fig. 9.5). The lesions produced by this strain (‘Loiret 55’) retained the protuberance characteristic of the Lausanne strain lesions (Fig. 9.4B) but the disease evolved more slowly. In more extensive tests the case-fatality rate was 65% and the mean survival time 33.1 days, with a range of 19 days to recovery. It was later designated as the prototype European strain of Grade IV virulence.

 Fig 9.4.A.  Fig 9.4.B.
Fig. 9.4. Clinical signs of myxomatosis caused by strains of myxoma virus found in France during the early stages of the epizootic in France. (A) Lesions produced by the Lausanne strain. Rabbit photographed 10 days after inoculation; it died on the twelfth day. The primary lesion on the flank was very large, protuberant and deep purple in colour. The head was oedematous (‘leonine facies’) and the eyes completely closed with a profuse conjunctival discharge. The secondary lesions were also raised, purple in colour and not demarcated from the surrounding skin. (B) Lesions produced by the Loiret 55 strain. The photograph was taken on the 25th day and the rabbit died next day. About one-third of rabbits inoculated with this strain recovered. The primary lesion was very large and exuded serum. There were numerous secondary lesions all over the body, the eyes were completely closed and the ears hung down because of numerous lesions on the pinnae. From Fenner and Marshall (1957), with permission.

Respiratory or non-myxomatous myxomatosis
In addition to the increase in the occurrence of attenuated strains characterized by the usual protuberant skin lesions but lower case-fatality rates (see below), in 1980 French scientists observed for the first time a ‘respiratory or non-myxomatous’ form of the disease (Brun et al., 1981b; Joubert et al., 1982). This syndrome was characterized by a longer incubation period (1–3 weeks), swelling of the eyelids accompanied by severe purulent conjunctivitis, genital lesions, and prominent nasal lesions accompanied by lacrimation and a mucopurulent nasal discharge (Fig. 9.6). There were often pink or red spots on the ears, but no nodular skin lesions (Arthur and Louzis, 1988). Its epidemiology is described below (p. 220).
Although initially described in domestic rabbits raised by intensive husbandry and vaccinated with the SG33 attenuated myxoma virus vaccine (Chantal, 1981), this syndrome was also seen among rabbits kept under traditional husbandry and sometimes in wild rabbits. It was often accompanied by sterility and the abandonment of litters by farmed does.

 Fig 9.5. Fig. 9.5. Henri Jacotot (1896–1991). Born in Dijon in 1896, Jacotot served in France in the 1914–1918 war and was decorated with the Military Cross. Subsequently he graduated in veterinary science and was posted to the Pasteur Institute at Nhatrang, in Indo-China, in 1922, initially as chief assistant to Alexandre Yersin. In 1927 he was appointed Director of that institute. In 1948 he returned to the Pasteur Institute in Paris as head of the service of animal microbiology, a post which he occupied until he retired in 1965 as a Professor Emeritus. In Indo-China he studied the many veterinary and zoonotic diseases found in that country and was responsible for the construction of the building currently used by the Pasteur Institute at Nharang. After returning to Paris he took a leading role in the investigations of myxomatosis in France, describing the first recognized case in 1953, experimenting with insect transmission and studying the changes in virulence of the virus. A highly respected scientist and recipient of many prizes, he was a member of the Academies of Veterinary Science and of Medicine and served as President of the former.


- The Spread of Myxomatosis in France

As commonly occurs when a dramatic ‘emerging’ disease breaks out, a number of fantastic stories about its mode of spread circulated during the early days of the French epizootic (Lockley, 1953).

 Fig 9.6.
Fig. 9.6. Hutch rabbit showing signs of the ‘respiratory’ form of myxomatosis. Courtesy Dr A. Brun.

The consumption of grass that might have been contaminated by myxomatous wild rabbits was thought to transfer myxomatosis to hutch rabbits, and motor cars which ran over infected rabbits were blamed for moving the disease to new districts. It was commonly reported that there was a black market for myxomatous rabbits, up to 5000 francs being paid by landholders anxious to get rid of a pest. However, it soon became apparent that mosquitoes were important vectors in France, and the presence of such a highly mobile and efficient vector provided an explanation for the movement of the disease to new areas (Fig. 9.7) and from wild to domestic rabbits. In the early days of the outbreak, there was often inadvertant transfer of disease between rabbit farms via infected rabbits still incubating the disease. Rabbit fleas are as common amongst wild rabbits in France as they are in Britain and undoubtedly contribute greatly to maintenance of enzootic myxomatosis throughout the year.

 Fig 9.7.
Fig. 9.7. The spread of myxomatosis in France between January and September, 1953. From Rogers et al. (1994), after Joubert et al. (1972), with permission.

Epidemiology
With the knowledge that mosquitoes had been important vectors in Australia, it was soon shown that the prime suspect for transmission in the early epizootics in France, Anopheles maculipennis atroparvus, was an effective vector (Jacotot et al., 1954). Subsequently, quiescent rabbit fleas were recovered from soil scrapings from deep burrows that had been abandoned by rabbits ten weeks earlier, following autumn epizootics of myxomatosis, and myxoma virus was recovered from these fleas (Joubert et al., 1969). Arthur and Louzis (1988) postulated that eventually an enzootic–epizootic cycle involving reservoirs, vectors and susceptible rabbits developed. They suggested that the virus might overwinter in fleas in the soil of the burrow, in rabbits convalescing from infection, and in hibernating mosquitoes that might be contaminated with the virus. With the onset of warm weather, sharp mosquito-borne epizootics occurred among wild rabbits, rising to a peak in mid-summer and extending into autumn. These spread into domestic rabbits housed in non-mosquito-proof shelters.
Sightings of diseased rabbits fell when the wild rabbit population became greatly depleted in the mid-1950s, but after the attenuation of the virus and growing innate resistance in the rabbits in the late 1960s, the numbers of rabbits increased again. The seasonal and annual variations in myxomatosis then seen resulted from the interaction of the abundance of rabbits, their immune status (which was influenced by the age structure of the population) and the abundance of vectors. The occurrence of epizootics in southern France during summer and autumn was due to the concurrence of large numbers of aggressive mosquitoes and the presence of non-immune young rabbits. If there had been no myxomatosis the previous year, out-breaks often occurred in the spring and simulids and ceratopogonids were often involved (Joubert and Monnet, 1975). Spring outbreaks affected mainly young rabbits that had not been infected the previous summer, the resulting decrease in breeding females greatly depressing reproduction. Infection is maintained by rabbit fleas during autumn, winter and early spring, spread then being slow. Overwintering in the absence of obvious disease may be due to the persistence of virus on the mouth parts of fleas, which can remain in a quiescent state for some time in uninhabited burrows.
Impact on wild rabbits
Myxomatosis clearly had a major impact on the number of wild rabbits that were available for hunting, and the bag did not reach even 20% of its pre-myxomatosis level until the 1961–62 season, although the recorded figures may partly reflect the paucity of hunters as well as of rabbits (Table 9.1). In the Sologne, a favoured département for rabbit hunting, the mean numbers shot per season (compared with pre-myxomatosis figures) increased from 1.5% in 1953–58 to 13.5% in 1967–72 and 17.6% in 1972–77 (Arthur et al., 1980). However, after rabbits began to build up in numbers due to the presence of attenuated strains of virus and greater innate resistance, variations in the timing of major outbreaks of myxomatosis in relation to the hunting season caused large fluctuations in the numbers of rabbits shot. National surveys in France in 1977 and 1978 (Arthur et al., 1980) showed that rabbit density varied from place to place depending on environmental factors, such as type of soil and agricultural practice, and was also affected by hunting pressure and predation. At that time rabbits were most abundant in north-western France and much less common in the south and west, where in contrast to pre-myxomatosis times they often lived only in isolated pockets. Twenty years later (1997) the picture has not changed.

Table 9.1. Numbers of rabbits killed each hunting season in 25 hunts in France, before and after the
introduction of myxomatosis. (Data from Giban (1956) and personal communication to Fenner (1963).

1950–51 -> 64,439,000
1951–52 -> 37,723,000
1952–53 -> 55,133,000
1953–54 --> 6,721,000 : of which 80% were from two unaffected hunts
1954–55 --> 2,750,000 : of which 87% were from one unaffected hunt
1955–56 --> 2,404,000 : of which 50% were from one hunt
1956–57 --> 1,293,000
1957–58 --> 3,357,000
1958–59 --> 2,043,000
1959–60 --> 4,074,000
1960–61 --> 5,491,000
1961–62 -> 10,906,000

After the first disastrous epidemics, a variety of measures were undertaken by hunting organizations to mitigate the impact of myxomatosis. Vaccination with fibroma virus was carried out in an attempt to preserve some rabbits for shooting and hopefully to build up ‘barriers’ to the movement of myxomatosis. Later it was suggested that, as with domestic rabbits, wild rabbits should first be injected with fibroma virus followed 6–8 weeks later by SG33, both being administered by jet injector (Joubert et al., 1982; Fig. 9.8). Other early and unsuccessful methods for preserving rabbits as game animals included the introduction of cottontails (Sylvilagus floridanus), both as game animals and to hybridize with Oryctolagus, and a proposal to import rabbits from regions of Australia where innate resistance was high.

 Fig 9.8. Fig. 9.8. Louis Joubert (1922–1989). Born in Grenoble in 1922, Joubert enrolled in the National Veterinary School at Toulouse in 1939, graduating with honours in 1945 and becoming assistant to the Professor of Infectious Diseases. He continued his studies in veterinary medicine and in pharmacy, and in 1948 was appointed project director at the Veterinary School in Lyon, where he advanced to become a professor in 1962. His early research was focused on the epidemiology of zoonotic diseases, and after Jacotot had retired he became the leading expert on myxomatosis in France, showing particular interest in unusual insect vectors and especially in the ‘respiratory’ or ‘amyxomatous’ form of the disease. He was the senior author of a major book on myxomatosis, published in Paris in 1972–1973.

Impact on domestic rabbits
Myxomatosis was spread by mosquitoes from wild to domestic rabbits and initially it devastated the rabbit-breeding industry; it was estimated in 1954 that 30–40% of the industry had been destroyed. Vaccination afforded some protection, and with the reduction of the size of the wild rabbit reservoir of myxomatosis in the late 1950s new outbreaks in rabbitries became less common. Initially fibroma vaccine was used on a very large scale, amounting to tens of millions of doses annually; later it was used on a smaller scale, primarily to protect breeding animals. It was only moderately effective, and after limited trials with an attenuated myxoma virus vaccine developed in California (Saito et al., 1964), another attenuated vaccine (SG33) was developed in France (Saurat et al., 1978). Given to rabbits at 2–3 months of age, it was effective for about a year after vaccination. However, the use of the SG33 vaccine was found to have an immuno-suppressive effect, which among rabbits housed under conditions of poor hygiene led to a variety of secondary bacterial infections (Brun et al., 1981; Godard, 1980). In such circumstances it was recommended that fibroma virus should be used for primary vaccination, followed by SG33 vaccine a month later.
The epidemiological cycle as seen in the 1980s differed according to the type of husbandry (Arthur and Louzis, 1988). Under conditions of traditional husbandry, in animal quarters with open contact with the outside world, the strains of virus were usually of the traditional nodular type, and were usually more lethal among the (genetically) unselected domestic rabbits than they were for wild rabbits. Outbreaks usually occurred in the autumn; there was a delay of 6–8 weeks between epizootic peaks in wild and domestic rabbits, the domestic rabbit peak coinciding with the arrival of mosquitoes within farm buildings (Puech, 1980). This form of myxomatosis could be prevented by efficient protection against the entry of mosquitoes by netting, unless animals harbouring the virus were brought in during the purchase of breeding animals.
Respiratory or non-myxomatous myxomatosis
Under intensive husbandry within closed mosquito-proof buildings, a non-myxomatous, pulmonary form of the disease, in which respiratory signs predominated, was most common (Brun et al., 1981a; see p. 216). It appeared to be transmitted by the inhalation of infective particles, both experimentally (Chantal, 1981) and in the rabbit farms. The incubation period varied between one and three weeks, and infection was manifested by swelling of the eyelids, genital and nasal lesions, lacrimation and a mucopurulent nasal discharge. This occurred primarily in premises in which there was poor ventilation and a high frequency of respiratory disease, and episodes of this form of myxomatosis were likely to occur at any time of the year. Most outbreaks occurred after recent introductions of rabbits from farms which had experienced infection during the previous 2–3 months. Such animals may have been incubating the disease for a longer period than usual, or, it has been suggested, they were asymptomatic carriers, in which reactivation occurred after the stress of transfer to new premises.

- Changes in the Virulence of the Virus

Attenuated strains of myxoma virus were first recognized in 1955, in the département of Loiret (see Fig. 9.4B). Other strains with a similar degree of attenuation were soon found elsewhere in France (Fenner and Marshall, 1955; Siriez, 1960); the virulence of these strains was not altered by several serial passages in the rabbit testis (Jacotot et al., 1956). Of ten French strains recovered in 1960–63, three were classified as of Grade IIIA virulence, three of Grade IIIB, three of Grade IV and one of grade V (Fenner and Ratcliffe, 1965). More recent data (Table 9.2) suggested that 15 years after the introduction of the virus a few highly virulent strains were still circulating, although the majority of strains were moderately or highly attenuated.

Table 9.2. The virulence of field strains of myxoma virus in France in 1953, 1962, and 1968, calculated on
the basis of mean survival times and expressed as percentages(a).
Virulence grade II IIIA IIIB IV V
Mean survival time (days) 9–13 17–22 14–16 23–28 29–50
Presumed case-fatality rate (%) >99 95–99 90–95 70–90 50–70 <50
Year
1953(b) >99
1962 11 19.3 34.6 20.8 13.5 0.8
1968 2.0 4.1 14.4 20.7 58.8 4.3

(a) From Joubert et al. (1972), p. 132.
(b) From field observations.


Endnotes:

1Basser Library Archives, MS143/25/5A. Letters; G. Remaudière to F.N. Ratcliffe (22 January 1952),
F. Fenner to Remaudière (15 February 1952) and reply (19 February 1952).
2Basser Library Archives, MS143/25/5A. Correspondence between G. Bouvier and Fenner about ori-
gins of ‘Lausanne’ strain, used to introduce myxomatosis into Europe.
3G.W. Douglas, personal communication to Fenner (1978), J.W. Edmonds and R.C.H. Shepherd, per-
sonal communication to Fenner (1982), published in Fenner, F. (1983). The Florey Lecture, 1983.
Proceedings of the Royal Society B218, p. 268.
4In a communication to Jacotot et al. (1954), M.E. Roubaud, an entomologist with special knowledge
of mosquitoes, commented: ‘Au point de vue de la transmission de la myxomatose dans le milieu des
clapiers, c’est cet anophèle A. maculipennis s. lat. qui apparait sans nul doute, en Europe, comme
devant jouer le rôle principal. Dans les bois, dans les garennes, parmi les lapins sauvage, ce sont
d’autres espèces culicidiennes qu’il convient d’incriminer, parmi lesquelles de nombreux Aedes,
l’Anopheles claviger (bifurcatus) et surtout l’A. plumbeus’.

References:

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