Appearance and development of diseases
Other disorders of the rabbit
Reproductive diseases and disorders
It would be inappropriate here to insert a treatise on rabbit diseases. A disease cannot be described without reference to medical data with which the user of this book is in all likelihood not familiar. In addition, the pathogenic agents of many rabbit diseases are known and in some cases well described, but their presence does not necessarily imply the existence of a disease. Disease is almost always the result of poor husbandry and environment coupled with the onslaught of a pathogenic agent - microbe, virus or parasite.
This chapter therefore starts with a general discussion of the pathology of the rabbit before it goes into more detailed descriptions of the principal diseases.
The animal has multiple and interlinking defences for countering attacks from the outside environment. These can be classified arbitrarily and briefly as:
· non-specific defences, which can be mobilized very rapidly or even instantly (such as adrenalin discharge), and which bring into play all the major body metabolisms (mobilization of sugars and fats), and all the major functions (blood circulation, breathing, etc.);
· specific defences, including immunity, which is how the organism recognizes a hostile foreign body (microbe, parasite, virus, protein) and sometimes, though not always, eliminates it.
The body does not have an infinite capacity for non-specific or specific defence. So the producer's main job is to rear the animal in conditions where it does not have to engage in a permanent struggle for survival.
When it does, the physiologically exhausted animal eventually can no longer defend itself and disease will break out -which disease will depend on the climate, the environment and the type of rabbitry. Not all animal species are equally sensitive to the same kinds of attack. The major known environmental conditions that are unfavourable to rabbit health are described later in this chapter.
The influence of germplasm is unquestionably one element in resistance or vulnerability to disease. In terms of species evolution, however, the rabbit was introduced outside the Mediterranean basin only fairly recently, and new European progenitors have constantly been reintroduced. The concept of "local breed" needs to be viewed with some circumspection.
The environment is everything that surrounds the animal: its habitat, its congeners, its solid and liquid feed, microbial contamination, temperature, air and noise. The concept of environment can be extended to the farm, village, region and even the country. How far the environment extends is no longer an abstract concept when the number of animals per square metre, hectare or square kilometre grows without a parallel upgrading of hygiene and health standards. An infinity of examples for every species of plant and animal shows that the larger a population grows, the more it becomes imperative that rules of hygiene be respected.
A point that agricultural officials have all too often ignored is that this basic notion is as true at the production-unit level as it is at the village, region or country level. In traditional French rabbitries, for example, pasteurellosis was once a lethal respiratory disease that could decimate the rabbit population of a whole village within a few weeks. Today, the drop in the numbers of these traditional units has led to a marked reduction in the epizootic and lethal properties of this disease.
Myxomatosis decimated the rabbit population in Western Europe in a few months, not only because the virus had been introduced but mainly because the environment as a whole was favourable; the main factor was the overpopulation of wild and domestic rabbits in France at that time. An increase in the number of large rabbitries, combined with expanded trading in France, Spain and Italy, fostered the appearance and simultaneous spread throughout these three countries of three hitherto sporadic diseases: dermatomycosis, staphylococcis and colibacilli O103.
Microflora is also a component of the environment. This chapter devotes special attention to microbial contaminations because they are a major, inevitable form of attack in all rabbitries.
Microbial contamination refers to the polluting of air, objects and soil by bacteria, parasites, viruses or fungi. Most often, these microscopic organisms are not intrinsically pathogenic. They become pathogenic when pollution reaches a high, continuous threshold. Ambient microflora is present from the start of production in a unit and inevitably expands as time goes by. One of the breeder's basic tasks is to slow this inevitable increase as much as possible. This is done by respecting the rules of hygiene and by limiting stock to the number of animals that can be maintained and nourished properly. A small, properly run rabbitry is more productive in the long term than a large one that is poorly run. It is also less of a menace to neighbouring rabbitries.
Farmers everywhere know how important and beneficial fallow periods and crop rotation are for the soil they till. One reason these methods are so beneficial is that they reduce local microbial infections specific to each crop. Plant species, like animal species, are each surrounded by their own microbial environment. No matter how capable a breeder is, the day will come when the rabbitry will have to be cleared, thoroughly cleaned and disinfected in order to lower ambient microbial contamination to a safe level.
Management (husbandry) is also part of the production-unit environment, but the impact of management on disease is often forgotten. The way breeding and husbandry methods have evolved in different countries shows that any method can have both positive and negative consequences. Age at weaning is undoubtedly the most important variable. Weaning at 28 days does limit or even eliminate the transmission of certain disease agents, such as Pasteurella and Escherichia coli, but stopping the mother's milk somewhat curtails the passive immunity of young rabbits and unquestionably favours E. coli. Weaning much later wears out the dams. Intensified production has led some breeders to opt for a highly accelerated mating calendar (mating following kindling the same day) or for moving the females very often. These choices mean a shorter life for breeding females. Raising rabbits in groups, as is done in the big European producer countries, considerably modifies rabbit pathology.
Breeders need to remind themselves, in deciding how to manage their stock, that the theoretical advantages they see may be accompanied by disease repercussions. As for pathologists, they will need to consider the production methods and not simply the disease agents and symptoms they have identified. Health-care interventions are contingent upon knowledge of these methods.
It would be wrong to think that the following sections will do more than elaborate on the foregoing, for the heart of the matter has already been discussed. The producer's best ally for healthy rabbits is the animals' own capacity to ward off disease. An organism's defence against outside attacks is basically a global, non-specific response which is fundamentally dependent on good hygiene standards in the rabbitry. The rules of hygiene are easier to apply and to respect in small rabbitries with simple equipment that is easy to maintain. Daily preventive cleaning will keep the contamination and pollution levels down and make the rabbitry viable and productive for a longer period. Preventive hygiene is the key to a clean, well-run rabbitry in which the producer can more effectively control any disease which might break out.
This chapter will deal with disease not as a function of the pathogenic agents specific to the rabbit, but as a function of syndromes or combinations of disease manifestations which share common or closely related symptoms and are important in economic terms. Unquestionably, intestinal diseases are most costly to rabbit breeders and the major obstacle to expanded rabbit production. Diarrhoea is a serious economic threat, primarily in young weaned rabbits (four to 10 weeks). It is rare before weaning and can in any case easily be prevented by elementary sanitary and feeding hygiene. It should be noted that diarrhoea appears later in young rabbits than in other young domes tic mammals such as piglets, calves, lambs or even young hares. Among these species diarrhoea strikes in the very first days after birth. The fact that young rabbits do not suffer from neonatal diarrhoea is probably due to their being born hairless and blind, and thus confined for weeks to their nests, sheltered from outside attacks. Diarrhoea is also rare among adult rabbits. It is usually the final consequence of some other ailment.
The first point to make clear is that the rabbit's reaction to disease, whatever the nature of the attack, takes the form of intestinal disturbance, which nearly always expresses itself as diarrhoea. This response can be traced to several features peculiar to the rabbit.
The first has to do wish a rabbit's mental reactions. The rabbit is an excitable animal. Its relatively recent domestication has undoubtedly not yet conditioned it to adjust its alarm reactions (discharge of adrenalin) according to the gravity of the attack.
The second peculiarity is the complexity of the rabbit's intestinal physiology. Caecotrophy is one manifestation of this. The hormone reactions governing the alarm reaction directly affect the nervous system of the intestine, halting or slowing peristalsis, which slows the passage of food through the intestine and halts caecotrophy.
A third feature of the rabbit's post-attack reactions is the alkalinization of the contents of the caecum. The increased pH is linked with the slowed passage of food which modifies the intestinal environment, particularly the flora. Escherichia coli, usually few in the healthy rabbit, become dominant. The fact that the soft pellets are no longer ingested also helps to modify the intestinal milieu, particularly the volatile fatty acid balance.
The last peculiar feature of the rabbit is that the appearance of clinical symptoms is delayed after an attack. In animal species that seem to be very excitable (pigs, horses) the symptoms appear most often within a few hours (ulcer, colic, diarrhoea). In the rabbit, an ordinary change of habitat, a scare or a journey have no immediate consequences. Diarrhoea appears only some five to seven days afterwards.
General symptoms of digestive problems
The symptomatology of rabbit enteritis is relatively simple and constant and rarely permits an aetiological diagnosis of the disease. The first signs, scarcely noticed by the breeder, last one to three days, and take the form of a decrease in feed intake (especially solid feed) and in growth. Next, diarrhoea appears, sometimes preceded by complete constipation or production of soft pellets which are not eaten.
Diarrhoea is moderate, consisting of a small quantity of fairly liquid faeces which soil the animal's hindquarters. Death can occur at this stage, sometimes even before the appearance of diarrhoea. Skin dehydration also appears at this time.
Two or three days later the acute phase of the illness starts. It involves an almost total stop in both solid and liquid intake, extensive diarrhoea and high mortality; grinding of the teeth is a symptom of severe intestinal pain. Death follows after several hours of agitated coma with spasmodic twitching. If the animal survives a full day in coma it may recover fully within a few days.
Recovery is in fact remarkably swift. Diarrhoea often gives way to constipation. The pellets are small, hard and malformed. In a rabbit two or three months old, the constipation phase is often the only symptom. Physiologically, however, diarrhoea will have occurred and can be perceived by palpating the abdomen: during the acute phase the breeder can feel that the caecum contents are liquid.
A post-mortem examination shows lesions, usually atypical. During the acute phase the intestinal contents are very liquid, sometimes discoloured. The caecum often fills with gas and contains little food matter.
The intestine is sometimes congested or bruised. The walls of the caecum are most striking, congested and streaked with red, like brush strokes. The colon may be filled with a translucent jelly. There will usually be no fibrin in the abdominal cavity, an indication of the acute stage of this disease.
Non-specific causes. It has been seen that very different factors can cause outbreaks of diarrhoea. Rabbits seem to react negatively to: transport, especially during the postweaning period; being put in a new hutch or cage; the presence of unusual visitors (people or animals); and sounds not identifiable by the animal and lasting for hours or days, such as work in progress near the rabbitry.
Feeding is unquestionably a prime factor in the occurrence of diarrhoea. Not enough crude fibre, too much protein and meal which has been too finely ground are all unfavourable. Also to be remembered is the fact that the rabbit regulates its intake according to the energy in the feed. Too much energy in the feed can lower the intake too far and vice versa. These are all factors which can favour the onset of intestinal problems. Feed changes are all too often blamed for diarrhoea. Even when feed is the obvious cause, more often the problem is the composition of the feed rather than the change itself. On the other hand, when the animals do not always have good feed available, at least the daily timetable of feeding should be respected. There have been many instances of diarrhoea "epidemics" in rabbitries where a change in timetable was the suspected culprit. This is easily explained by the rabbit's complex intestinal physiology (caecotrophy).
Improper watering is very common in farm rabbitries. It is probably one of the major causes of mucoid enteritis. Rabbits must have clean water available at all times.
It is worth repeating here that the nonspecific causes favouring the appearance of diarrhoea can be defined as anything which forces the animal to spend too much time defending itself against its surroundings.
Specific causes. Theoretically, these include any cause which, alone, allows the disease to manifest itself. In fact, the state of health is almost always the main factor.
Chemical agents. Administration of some antibiotics invariably provokes diarrhoea: ampicillin, lyncomycin and clyndamycin. Antibiotics should always be used very sparingly with rabbits, especially penicillin. It also seems that drinking-water with a high nitrate content causes the chronic diarrhoea observed in some areas.
Mouldy feed (pellets, domestic waste, bread, vegetable peels) can very quickly cause diarrhoea even in a healthy rabbit.
Viruses and bacteria. There has been little work on enteropathogenic rabbit viruses but they are known to exist. It is very likely, however, that as with most other animal species the condition of the animal itself is a decisive factor in the occurrence of viral diarrhoea. The presence of rotaviruses is a good example of the important role of management. These viruses appear in group rearing (all animals in the rabbitry being the same age), with weaning at 35 days (suppression of passive immunity) and after the animals have been grouped (stress) at 42 days.
Much the same is true of bacteria. Salmonella are rarely isolated in sick rabbits but this is not true of Corynebacteria, Clostridium, Pasteurella and, especially, Escherichia coli. Apart from some Clostridium species and a few serotypes of E. coli, healthy rabbits carrying these bacteria do not contract the relevant disease. Nevertheless they must be regarded as specific pathogenic agents even if they express their pathogenicity only in a random manner. For example:
· the most pathogenic among them (Clostridium, certain serotypes of E. coli) can, above a certain pollution threshold in the rabbitry, be the direct cause of diarrhoea and its persistence;
· very often, if not always, they constitute a secondary complication of enteritis which, although not serious at the outset, does become serious and then lethal;
· with both Clostridium and E. coli, pathogenicity depends in part on toxins which rapidly provoke irreversible and incurable lesions.
Intestinal parasites. All the major parasite families are found in rabbits: trematodes (flukes), cestodes (tapeworms), nematodes (intestinal worms) and protozoa (coccidia). Coccidia are the major specific agents of diarrhoea in the rabbit. In view of their importance the following section is concerned solely with them. The other parasitic diseases will be dealt with as a whole after coccidiosis and bacterial enteritis.
Coccidia and coccidiosis
Coccidia. Coccidia are protozoa, the most primitive phylum of the animal kingdom. They are sporozoa, i.e. parasites with no cilia and no flagella, which reproduce both sexually and asexually. A large number of families are represented. The Eimeriidae family is typified by the independent development of male and female gametes.
Almost all coccidia belong to the genus Eimeria - they include four sporocysts containing two sporozoites. Typically they form oocysts, a parasite mechanism for dispersal and defence in an external environment.
The coccidia cycle. Eimeria are monoxenous and have very high host specificity. The rabbit therefore cannot be infested by the coccidia of other animal species, nor can they be infested by rabbit coccidia. Eimeria develop in the epithelial cells of the digestive apparatus (intestine, liver). Eggs (oocysts) are found in the intestine and faeces. After maturing (sporulation), the oocysts contain eight "embryos" (sporozoites).
The Eimeria cycle includes two distinct phases:
· an internal phase (schizogony + gamogony) in which the parasite multiplies and the oocysts are eliminated in the faeces;
· an external phase (sporogony) during which the oocyst becomes able to infest if it finds favourable conditions of humidity, heat and oxygenation.
The internal part of the cycle begins with ingestion of the sporulated oocyst and the excretion of the sporozoites. The parasite then multiplies. This may entail one, two or more schizogonies (asexual reproduction) according to the species (E. media, two schizogonies; E. irresidua, three or four schizogonies). It can take place in different parts of the digestive system (E. stiedai in the liver; E. magna in the small intestine; E. flavescens in the caecum). The final schizogony leads to the formation of gametes.
The next step, gamogony (sexual reproduction), ends in the formation of oocysts that are excreted with the faeces; the total duration of the internal phase of the cycle also varies with the species (e.g. E. stiedai, 14 days; E. perforans, four days).
The external part of the cycle (sporogony) is typified by the extraordinary resistance of the oocysts to the outside environment. Their resistance to chemical agents is particularly striking. In the right conditions of humidity, heat and oxygenation the oocysts become able to infest. They sporulate. Hatching time varies: at 26°C, E. stiedai takes three days and E. perforans one day.
Coudert (1981) in France and many others have studied this part of the cycle, as the oocyst is the agent to be destroyed. In practice, oocyst resistance is hard to overcome, particularly in disinfecting rabbitries. Chemical disinfection is pointless as oocysts can only be destroyed by heating and drying.
Species. At least 11 coccidia species are rabbit parasites. One infests the liver, the other ten the intestine.
· Eimeria stiedai, the liver coccidiosis, causes no economic losses in Europe except at the slaughterhouse. It is relatively easy to eliminate this parasitosis by a few weeks of very strict health and hygiene measures and preventive medicine. A four- to six-week treatment with conventional anticoccidia products (Decox, Pancoxin, formosulfathia-zole) in the feed at preventive doses virtually eliminates the disease. In climates less clement than Europe's and in countries where it is not so easy to get the right medicines, liver coccidiosis can have more serious consequences. As the liver is an organ basic to every process involving homeostasis, chronic liver attacks cannot fail to diminish the animal's resistance capacity.
Intestinal coccidia can be classified in four categories (Table 48):
· Eimeria coecicola and E. exigua are apathogenic. No clinical sign is detectable even with an inoculum containing several million oocysts.
· E. perforans is very slightly pathogenic. Alone, it never causes diarrhoea or mortality. Massive infestations (106 oocysts) are needed before there is a slight and very brief decrease in growth.
· E. irresidua, E. magna, E. media and E. piriformis are pathogenic species that cause diarrhoea and growth retardation of as much as 15 to 20 percent of live weight for infestations with between 0.5 and 1 × 105 oocysts. When they occur alone these coccidia are not usually lethal, even in a relatively heavy infestation.
· E. intestinalis and E. flavescens are the most pathogenic coccidia. They cause diarrhoea and mortality, even at very low dose rates (upwards of 103 oocysts).
TABLE 48 Comparative pathogenic strengths of different intestinal coccidia of the rabbit
Non-pathogenic or slightly pathogenic
No sign of disease or slight drop in DWG
Drop in DWG
Little or no mortality
Severe drop in DWG
Note: DWG = daily live-weight gain.
Pathogenic effect has been judged here solely on the basis of retarded growth and mortality. But it must not be forgotten that coccidiosis, like all diseases, can have certain after-effects on the kidneys or liver in particular, which in turn have repercussions on fattening status at slaughter or on the animal's future if it is to be kept as a breeding animal.
Often one disease is also complicated by other diseases. In fact, the above results were obtained with rabbits reared under especially favourable conditions, which means there were practically no bacterial side-infections. It is not known, for example, whether in an unfavourable environment coccidia of the second group (E. media, etc.) might not have a more severe impact.
Lesions. There are two kinds of lesions: macroscopic and histological.
· Macroscopic. Every coccidium has a preferential place to develop where it causes a reaction of the intestinal epithelium varying in visibility according to the bacterial species. The duodenum and the jejunum are parasitized by E. perforans, E. media and E. irresidua. The latter species is the only one which, at high concentrations, causes macroscopic lesions visible at autopsy. E. magna, E. vejdovskyi and E. intestinalis multiply in the ileum. E. intestinalis causes the most spectacular macroscopic lesions. The ileum becomes bruised and whitens; segmentation appears very clearly, especially in the part nearest the caecum. The appearance of the lesions is the same with high concentrations of E. magna. The caecum is the domain of E. flavescens, which at medium dose levels produces lesions on the colon. The caecum wall thickens and changes appearance according to whether there is microbial infection or not. It may look whitish in heavy infestations with no complications, but very frequently reddish striations, necrotic plaques or generalized congestion appear. The most constant factor is the emptiness of the caecum. Lesions can be caused in the colon by E. flavescens and above all by E. piriformis, the only rabbit coccidium capable of causing enterorrhagia in the Fusus coli at medium dose levels (30 000 to 50 000 oocysts).
· Histological. There are two points to stress here: lesions, both macroscopic and histological, are relatively short-lived. They appear towards the eighth or ninth day and disappear by the 12th or 13th day, despite their sometimes spectacular appearance (E. intestinalis, E. flavescens and E. piriformis). Histologically, hypertrophy can only be observed in the epithelial cells of the intestine. Cell structure remains intact. Moreover, the number of cells parasitized is extremely low in proportion to the number of cells of the epithelium, but all the cells, whether parasitized or not, look the same. Only a few cell clusters deep in the crypts of Lieberkühn will be destroyed.
Coccidiosis. Coccidia are specific pathogenic agents. When inoculated into rabbits pathogenic coccidia cause the same lesions and the same symptoms (diarrhoea, loss of weight, death) in all the animals tested.
Clinical signs. Most of these are not specific to intestinal coccidiosis. The main symptoms are: diarrhoea, weight loss, low intake of feed and water, contagion and death.
The clinical evolution of an intestinal coccidiosis is illustrated in Figure 22.
Depending on the coccidia species, diarrhoea appears between the fourth and the sixth day after infestation. The peak is from the eighth to the tenth day. It then declines in three or four days. Diarrhoea is the first visible symptom, together with cutaneous dehydration, clinically demonstrated by the persistence of skin folds.
Weight gain and feed intake evolve in a sequence that faithfully follows the evolution of the diarrhoea. For two or three days growth and feed intake are low. Between the seventh and tenth day after infestation there is weight loss, perhaps as much as 20 percent of live weight in two or three days. Recovery is equally rapid. Two weeks after inoculation the animals may resume their initial growth.
Mortality occurs during a relatively short period (three or four days), starting abruptly on the ninth day after infestation.
The intensity of these general symptoms naturally varies according to the Eimeria species involved (see above), the degree of infestation and the animal's general condition. Identical effects can be obtained by using different dose levels of different species of Eimeria.
Few data are available on simultaneous infestations, but there appears to be no synergistic action among the various species except with E. piriformis, which seems to augment considerably the pathogenicity of other species. This is rather easily explained by its locus of implantation and the fundamental role of the colon (see physio-pathology, below).
It is common for bacterial flora to develop at the same time as coccidiosis, complicating and aggravating the symptoms of the disease.
If there has been no contact with coccidia (non-immune rabbits), then age is not a major factor in susceptibility in rabbits. The disease is briefer in animals 10 to 11 weeks old and diarrhoea less severe, but weight loss and mortality are often more pronounced than in younger rabbits. However, the early contact does confer relative immunity.
Physiopathology of diarrhoea of coccidian origin. The main symptom of intestinal disease in young rabbits is diarrhoea. Rabbit enteritis following cocciodiosis has been studied with reference to calves and human infants, in whom episodes of diarrhoea are essentially linked with hydromineral perturbations. In calves and infants diarrhoea seems to be dominated by three main phenomena. There is, of course, considerable loss of faecal matter. The usual impact on the metabolism is extracellular dehydration and metabolic acidosis. Rabbits suffering from diarrhoea, like calves and infants, certainly have more watery faeces, but sick animals produce a smaller quantity of faeces than healthy ones. Calves and infants urinate little or not at all with diarrhoea and there is haemoconcentration associated with extracellular dehydration. In young rabbits, diuresis is not altered during diarrhoea and there is haemodilution. The distribution of water in the organism is unmodified except that the skin is heavily dehydrated. Blood pH is normal. The most marked modification of the blood plasma is severe hypokalemia.
FIGURE 22 The clinical evolution of coccidiosis
The pathogenesis of diarrhoea in the young rabbit thus appears to differ from the more conventional diarrhoea of the calf or infant, but the prime mover at the intestinal level seems to be common to all. In diarrhoea of calves due to E. coli, for example, the small intestine secretes water and minerals, especially sodium, which will be lost by the animals.
In the young rabbit there is also a lack of reabsorption - indeed an actual secretion -of sodium and water in the loci where the parasites multiply. Unlike calves, however, rabbits can compensate for these disturbances in the distal colon and, most important, they can initiate an Na-K exchange which limits sodium losses to a minimum. Potassium losses are replaced from body reserves. These parameters evolve at the same time as the symptoms described earlier. Peak intensity of symptoms occurs at about the tenth day after infestation. Certain elements are generally described as constants in rabbit enteritis: lengthening of the retention time of the ingesta in the intestine, high levels of colibacilli and intestinal pH tending towards basicity.
This suggests that the basic phenomena of the pathogenesis of diarrhoea are independent of the aetiology (infectious agents or non-specific causes) and that the diarrhoea syndrome is a complex process. It may lead to a single response but several elements are involved - digestion, flora, motility, absorption and secretion.
It could, likewise, be tempting to attribute the sometimes spectacular lesions to the pathogenicity of the coccidia. But this would overlook the fact that these modifications in hydromineral metabolism and pH are delayed manifestations of an attack that took place days before.
Coccidiosis and field conditions. All production units are parasitized, usually by several species of coccidia. Investigations show that the least pathogenic species are the most numerous (Eimeria perforans, E. media). E. magna is also very common and of ten found in great numbers. E. intestinalis, E. flavescens and E. Irresidua are less common. This is a good thing, because their mere presence is a real menace to the rabbitry. E. piriformis is rare in Europe and E. intestinalis has not been identified in Benin.
It must not be forgotten that a single pellet from a healthy rabbit raised in a sound, clean rabbitry usually contains enough coccidia to cause diarrhoea if the same number were inoculated into the animal. Yet not all rabbits contract clinical coccidiosis. It almost always depends on conditions in the rabbitry. If conditions are good only a few animals will die of diarrhoea. If conditions are bad there will be a chronic mortality rate of 10 to 15 percent. Indeed, this is the usual situation.
Whether the environment is good or bad, any stress can set off coccidiosis, whatever the animal's age. It is curious to note that diarrhoea strikes not only young, newly weaned rabbits, but also older animals which have been in contact with the parasites for several weeks. Naturally acquired specific immunity is always very weak.
The outbreak of coccidiosis, the progress of which is summarized in Figure 23, can therefore be attributed mostly to stress.
Non-specific stress occurring singly cannot cause diarrhoea in a rabbitry where sanitary standards and physiological comfort are good. In such an environment the animal is able to marshal fully its nonspecific defence potential. On the other hand, a simple change of feed in a rabbitry with a poor environment is enough to set off diarrhoea. The mere fact of raising five or six rabbits together in a cage one-third of a square metre in a room with 100 or 1 000 other cages acts as a sort of sounding board to amplify all these phenomena.
Finally, non-specific factors cannot be discussed without mentioning their intensity - five minutes of transport does not constitute the same amount of stress as does four hours. These upsets are the root cause of outbreaks and it is only later, in most cases, that specific disease agents intervene (viruses, bacteria, coccidia). Each agent, merely by its permanent presence at low or average level, can also help undermine the rabbit's defence mechanisms without there necessarily being any permanent clinical disease.
The same is true of the other specific chronic diseases such as respiratory ailments and myxomatosis which by the very process of sapping the organism's defence capacities will become the indirect agents of outbreaks of coccidiosis and diarrhoea. Cases of primary coccidiosis are therefore probably rare. They can nevertheless occur, in particular when animals which are carriers of pathogenic species are introduced to the rabbitry.
Diagnosis. Coccidiosis is often extremely difficult to diagnose. It can only be done in the laboratory, by counting coccidia per gram of excrement and examining the viscera. Counts must be made on several animals for several days running to diagnose coccidiosis properly. The specific coccidia species and their pathogenic potential also need to be identified.
FIGURE 23 Development of coccidiosis
For coproscopic investigations, examination of excreta several days old taken from under a cage where there are several animals is preferable to and far more reliable than a caecum contents examination. At any given moment (death or slaughter of the animal) there may be:
· no trace of coccidia and coccidiosis: this is the not uncommon case in animals that die before the completion of the coccidial cycle;
· few coccidia and little coccidiosis: as above, with mortality occurring a little later. This happens mainly with very pathogenic coccidia which kill rapidly (E. intestinalis, E. flavescens) even at low concentrations;
· many coccidia and no clinical coccidiosis in the case of infestations with not very pathogenic coccidia (E. coecicola, E. perforans, E. media). The multiplication of the parasite will none the less be a negative factor.
Despite these difficulties it can be stated categorically that the presence of E. intestinalis, E. flavescens and even E. irresidua or E. piriformis is a serious circumstance and, for the first two, a definite menace. A post-mortem examination is often disappointing. The typical coccidiosis lesions appear only with massive infestations and persist for only two or three days. The presence of whitish spots on the intestine is an indication, but not a proof, of coccidiosis. In any case, it is recommended that an autopsy be carried out on all dead animals. A combination of observed factors, even if observed hastily, is far preferable to an isolated finding.
Liver coccidiosis, on the contrary, is very easy to diagnose. The presence of small whitish-yellow patches or small nodules on the surface or inside the liver is typical of this disease. But only massive coccidiosis, which sometimes provokes spectacular liver hypertrophy and considerable weight loss, can account for mortality.
Prognosis. A coccidiosis prognosis will not be of much use unless the expert also diagnoses why there has been an outbreak. All rabbits are coccidia carriers so it cannot be attributed to the parasites alone (they were already present). Conditions in the rabbitry and the animals' resistance being such as to produce a multiplication of Eimeria, the environment must also be examined and treated. This is why the prognosis is often quite bleak.
Control. Treatment is often disappointing and always expensive. There are basically two reasons for this:
· medical treatment is not really appropriate unless the cause of the disease is known. In the rabbit, the disease most often begins through a combination of several non-specific factors. The environment thus needs to be dealt with first;
· anticoccidiosis treatment is feasible for animals that have been infected for only a few days (five or six), but it is not effective otherwise. Even after successful treatment it should be realized that mortality and diarrhoea will continue in the rabbitry for a few more days. The most disappointing thing is that an improvement lasting one or two weeks is often followed by a relapse. It must be understood that a few days of diarrhoea in a rabbitry breeds thousands of millions of coccidia, only a few hundred of the most pathogenic of which are enough to kill an individual rabbit.
Sulpha drug treatment. The most common drugs are nitrofurans and sulpha drugs. The former have been used non-stop for nearly 30 years in feed. This may be one reason why present-day coccidia control is so ineffective. Nonetheless, the bacterio-static activity of these drugs probably favours recovery or avoids problems. Bifuran (50 percent furazolidane, 50 percent furoxone) at rates of 200 mg/kg of feed is now used only as a preventive measure.
Sulpha drugs are most effective in treatment, not in prevention. Sulfadimethoxine is the most effective sulpha drug and the one best tolerated by nursing or pregnant does:
· curative dose: 0.5 to 0.7 g/litre drinking-water;
· preventive dose: 0.25 g/litre drinking-water.
The bacteriostatic activity of this drug, especially on pasteurellosis, makes it one of the best rabbit medicines. It should not be overused.
Sulfaquinoxaline is commonly used, but at higher doses:
· curative dose: 1 g/litre drinking-water;
· preventive dose: 0.50 g/litre drinking-water.
Sulfadimerazine, at 2 g/litre, is less effective.
These sulpha drugs can be boosted by antifolics, such as pyrimethamine or diaveridine, which allows the dose to be reduced considerably, but this increases their toxicity, especially for pregnant does. The use of sulpha drugs for pregnant does must be systematically avoided.
Formosulfathiazole is another excellent coccidiostatic drug at rates of 0.5 to 0.8 g/kg of feed as a curative measure, or 0.3 to 0.5 g/kg as a preventive measure. Unfortunately it is not water-soluble.
Curative treatments should always be applied to all growing animals for four or five consecutive days followed by a therapeutic rest. Treatment is then resumed for a further four or five days. If the medicine is given in the drinking-water care must be taken that the water is constantly clear. Where animals are fed watery forage such as roots and greens, these should be replaced by dry feeds or the animals will not drink enough water. Drug concentrations as generally indicated correspond roughly to a water intake of 100 to 150 g water per kg of live weight. When water intake exceeds this normal quantity (nursing does, very hot weather) the drug should be further diluted. Stepping up the concentration is not really possible - the rabbit would then probably refuse to drink the water.
Treatment with antibiotics. Antibiotics do not cure coccidiosis. They may, however, be used in cases of persistent diarrhoea or to prevent secondary bacterial complications. The most common antibiotics used for rabbits are neomycin (0.1 to 0.4 kg/litre of drinking-water), colimycin (3 to 4.105 IU/litre) and the tetracycline group (0.2 to 0.3 g/litre). Once treatment with antibiotics is started it must be continued for three or four days at steady doses if it is to have any chance of being effective.
Antibiotics must be used cautiously in treating rabbits. Some that basically act on gram-positive flora are toxic to rabbits (ampicillin, lyncomycin, clyndamycin), while others should not be administered orally (chloramphenicol, penicillin, erythromycin, tylosin). With the possible exception of neomycin and the tetracyclines, antibiotics always entail the risk of digestive troubles.
In treating undiagnosed diarrhoea the proper treatment of coccidia alone is often enough to reverse the situation. Many French and other authors stress the importance of intestinal coccidiosis as a factor in the outbreak of enteritis and the benefit of treating coccidia. It should be remembered that giving medicine is not in itself sufficient treatment.
Prevention. Non-specific attacks and coccidiosis are the basic causes of diarrhoea. Diarrhoea prevention therefore consists of controlling these two factors. Good hygiene is the proper way to prevent the first. Preventive medicine should be added to combat coccidiosis.
There are two kinds of preventive medicine: vaccination and chemopreventive treatment. There is no anticoccidiosis vaccine (as of 1996). Active research is ongoing and hopefully short-cycle attenuated strains may soon be seen (early strains). Doses of sulpha drugs (see preceding pages) given to the young rabbits at weaning for eight to ten days are a good preventive measure in problem rabbitries.
Anticoccidial drugs administered as a preventive measure in balanced pelleted feeds are without doubt the most popular control method. A certain number of products can be used for rabbits (Figure 20). Robenidine has been used as a food additive in Europe since 1982 (66 mg/kg) and is very effective and well tolerated by rabbits. But ten years of use in the region have produced chemoresistance (E. media and E. magna). Others are effective (Lerbek) or highly effective (Salinomycin, Diclazuril, Toltrazuril-hydrosoluble), but had not been used for rabbits as of 1993. Anticoccidial products of the ionophore family used in poultry husbandry are usually very toxic to rabbits: Narasin, Monensin, Maduramycin. Some are well tolerated (Salinomycin 20 ppm; Lasalocid 50 ppm), but overdosage must be avoided. Anticoccidial products much in use in poultry husbandry, such as Amprolium and Coyden (methylchlorpindol), have little, if any, effect on rabbits. Coudert (1981) has made an exhaustive bibliographic review of these products. The disadvantage of such drugs is that they are not water-soluble, which means they can only be administered in balanced pelleted feeds. Antibiotics added to feed in constant low doses are strongly warned against as ineffective and dangerous.
Preventive hygiene is the keystone of coccidiosis control and successful rabbit production. It is far more important than any other anticoccidiosis measures and for this reason the last section of this chapter deals solely with preventive hygiene.
Acquired immunity to coccidia is species-specific. Coccidia cannot develop in young rabbits before 21 to 25 days, i.e. while lactation is the principal source of nourishment. The presence of coccidia before the age of 28 days is a sign of insufficient milk or poor hygiene. After weaning, in the presence of contamination, immunity is acquired in 10 to 12 days and lasts to adulthood. Acquired resistance is weakened, however, by the immunodepressive effect of major stress.
Apart from coccidiosis there are two other classic types of rabbit diarrhoea. Renault (1975) has published a detailed description of the mechanism of these diseases.
Mucoid enteritis. A special kind of diarrhoea sometimes affects growing rabbits and nursing does: very soft pellets are mixed with a translucent, gelatinous substance called mucus. Autopsy shows the colon and rectum filled with considerable amounts of this mucus, which somewhat resembles egg white. All sorts of hypotheses have been put forward to explain this type of diarrhoea. It is now universally considered a particular expression of enteritis which can have many varied causes: bacterial (E. coli, etc.) or nutritional (not enough water and/or not enough roughage).
Enterotoxaemia, colibacillosis, typhlitis.
These various names, like mucoid enteritis, refer in fact to types of enteritis which may have different causes but are very similar clinically and necroscopically. The diseases often develop rapidly (three or four days). Death can intervene before diarrhoea appears. When developing enzootically in a rabbitry there are phases of mucoid diarrhoea or constipation.
The autopsy shows lesions not dissimilar to those described for coccidiosis. There is more gas in the caecum, which is frequently mottled with red striations. The liver and kidneys sometimes look abnormal (crumbly liver, discoloured kidneys). The bacteria most often blamed are Clostridium spp. and Escherichia coli.
Clostridia (C. perfringens, C. welchii, C. septicum) are hardly ever isolated in growing rabbits after weaning. Perhaps this is partly because these are anaerobic germs which require a battery of special techniques for isolation and identification. Clostridium spiroforme has often been described in rabbits in recent years. This type of enteritis is common, mostly in well-fed animals (perhaps due to excess protein?). Both young and breeding animals may be affected. The diarrhoea is often very liquid and characteristically quick to putrefy. The corpses are blown up and the autopsy reveals greenish viscera. Treatment aimed specifically at anaerobic bacteria can be effective (Dimetridazol, Tetracycline + Imidazol, etc.).
E. coli, on the other hand, occur systematically in very large numbers in rabbits with diarrhoea or even with coccidiosis. It should be remembered that a healthy rabbit, unlike all other animal species, hosts very few colibacilla (102 to 103/g faeces). Some authors have isolated nearly 200 different strains in sick rabbits. Fortunately, not all are pathogenic and the number of serotypes (strains) involved is relatively small. Serotype O103 is virtually the only one considered specifically pathogenic in France. Licois (1992) and Peeters (1993) have done wrap-up studies.
The enteropathogenicity of these strains comes from toxins they secrete. However, diarrhoea has rarely been produced experimentally using these enteropathogenic strains alone (O103). For these E. coli to cause diarrhoea the animal has to be under some other stress at the same time (unbalanced feeding, coccidia, thermal shock, etc.).
Strictly speaking, colibacillosis is mainly a postweaning disease. Diarrhoea in unweaned rabbits is usually a consequence of poor maternal health. Since the young drink only milk, to treat neonatal diarrhoea one treats the mother. There has to be enough antibiotic in the milk. Because antibiotics are held back and rapidly broken down by the intestinal wall, the drug administered in the dam's feed must be supplemented by parenteral administration. Rabbits are less susceptible to diarrhoea after seven to eight weeks. Broad-spectrum antibiotics (colistin, flumequin) plus general hygiene can redress the situation where there is no other major primary cause, e.g. feed, population density or maternal health.
Some antibiotics are very toxic to rabbits, particularly penicillins, ampicillins, amoxillins and other betalactamins, virginiamycin, lyncomydn and oxolinic add (toxic embryo).
Conclusion. While the clinical and necroscopic appearance of these diarrhoeas of non-parasitic origin differs somewhat from that of coccidiosis, the conditions governing their occurrence are the same. First and foremost the field conditions must lend themselves to the spread of the infectious agent (E. coli or coccidia). Some factors perhaps more specifically favouring this type of diarrhoea are excess protein in the diet (over 18 percent) combined with insufficient roughage (under 10 percent indigestible crude fibre). Such enterotoxaemia, often associated with coccidiosis, is frequently reported from farm rabbitries where the rabbits are fed fresh-cut forage which is strewn on the ground.
Curative treatment is always too late, given the acute nature of this kind of enteritis. Antibiotics and sulpha drugs will prevent the spread of the disease and very often it is enough to replace the feed (pellets or green forage) by some good dry hay to cut losses. But if nothing is changed in the general conditions of the rabbitry, the same problems will soon recur. Chronic pasteurellosis, particularly during fattening, is also a direct or indirect cause of diarrhoea and mortality in rabbits.
Other gastrointestinal parasites
Glancing through a book on parasitology the reader soon discovers that several dozen different sorts of parasite can be found in the rabbit's digestive tract. They will not all be dealt with here as most are either very rare or only pathogenic under exceptional circumstances, or else little known or unknown in domestic rabbits. But in the farm rabbitry context, especially in the tropics, it is useful to have a basic grasp of the biological conditions that favour the development of such parasites.
Only two intestinal parasitic diseases are found in rational rabbit production in Europe: coccidiosis and oxyurosis. Wild rabbits living in the same regions, however, have many other parasites. The main reason for this has to do with the various parasite cycles. Many are heteroxenous (multihost): to multiply and develop they must live successively on several hosts. For example, the little liver fluke shifts from mammal to snail to ant to mammal. Others are monoxenous (single host) but the larval or adult form develops only in the outside environment under certain conditions (wet grassland, stagnant water, etc.). This explains why rational production, by breaking the life cycle of these parasites, has eliminated the parasitic diseases they cause.
Intestinal parasites found in farm rabbitries.
Cysticercosis (tapeworm). This common parasite produces fine, white streaks on the liver and translucent cysts, alone or in bunches, on the peritoneum and viscera. The cysts are produced by the larvae of dog and cat tapeworms. Rabbits are contaminated by eating feed that has been in contact with excrement. The terminal hosts (dog, cat, fox) become carriers by eating rabbit viscera. Symptoms are few - sometimes diarrhoea -except with heavy infestations (not uncommon) when growth rate slows. There is no curative treatment. The other domestic animals have to be treated. Tapeworm larvae of other species of animals (pig, rat, etc.) can also infest rabbits. It is worth mentioning here that the larvae of some dog and cat tapeworms can infest not only rabbits but people as well (echinococcosis, coenurosis). The lesions are cyst clusters forming translucent "tumours" on the viscera or in the brain.
Taeniasis (tapeworm). Half a dozen tapeworm varieties can infest rabbits which become contaminated by eating mites in wet grass. Clinical symptoms are slight: mild diarrhoea, sometimes weight loss, very rarely mortality from intestinal perforation. A necropsy reveals flat worms, a few millimetres wide, varying in length by species from 1 cm to 1 m.
Tapeworms are seldom found in domestic rabbits. Treatments applicable to other animal species may be used.
Fasciola spp. and Dicrocoelium spp. (trematodes). Liver fluke (Fasciola hepatica) and little fluke (Dicrocoelium lanceolatum) are also very rare in rabbits. The conditions of infestation are the same as for ruminants. The intermediate hosts are certain snails found in grass from marshy areas (Fasciola spp.) or other types of snails and ants (Dicrocoelium spp.). Usually the only symptom is slowed growth. Treatment is pointless.
Trichostrongylus (nematodes). These are also small round worms (called round-worms), measuring 4 to 16 mm in length. The Graphidium (stomach worm) is rare in Europe but Trichostrongylus is very common in farm rabbitries. Rabbits become infested by eating green forage contaminated by larvae. The intrinsic pathogenic strength of these parasites is relatively weak, but they do greatly aggravate other rabbit ailments, particularly diarrhoea. Massive infestations can cause extreme inflammation of various parts of the intestinal tract (stomach, small intestine, caecum). The conventional anthelmintics (thiabendazole, phenothiazine, tetramisole) can be used for rabbits. It is recommended that regular treatments be applied every month or two in contaminated farm rabbitries.
Two other small roundworms are frequently found in rabbit caeca and colons: Passalurus (oxyuris) and Trichuris. These do not appear to be pathogenic except with massive infestations.
Strongyloïdes (nematodes). These are small roundworms, a few millimetres long, that are able to migrate throughout all organs and reach the intestine. The aetiology and epizootiology are identical to those in ruminants and pigs. Some massive infestations have been described in rabbits living in dark, damp, poorly kept hutches.
Preventive hygiene and intestinal parasites.
Intestinal parasitism is very common in wild rabbits. It is frequent and not of great economic importance in farm-bred domestic rabbits if overall sanitary and health conditions are satisfactory. In poorly kept hutches, or where infestation is massive, these parasites enhance all other ailments, both intestinal and other, making them acute, enzootic and lethal.
Rational rabbit production has done away with all these intestinal worms. Control is easy; it is only necessary to break the parasite's life cycle. Essentially this means taking the following measures regarding forage:
· it should not be gathered in areas where there are large numbers of dogs, cats or wild rabbits;
· it should be stored out of reach of these animals;
· it should be gathered at midday when the dew is gone (avoiding marshy areas) and not be cut too near the ground, because many of these parasites avoid dry surroundings and strong light;
· it should be sun-dried before it is given to rabbits - drying kills most of the worms and their larvae;
· it should be distributed on feed racks where animals are unable to soil it with their faeces or urine.
Parasitism can be considerably cut back by frequent changing of the straw litter, which should always be dry. Late slaughter of fattening rabbits (three months or more) is a negative factor, as some parasites (oxyuris) have a rather long life cycle. This is interrupted by earlier slaughter. Regular treatment can also include broad-spectrum anthelmintics or copper sulphate-based preparations in drinking-water (1 percent) for one or two days.
Respiratory ailments are common among domestic rabbits. In rational production they essentially strike breeding adults. In a farm rabbitry young rabbits can also be affected. Where such ailments are endemic, losses are especially to be feared among the females, in which the disease becomes chronic, leading to production stoppages and mortality among the nursing young. Respiratory diseases usually remain endemic, but abrupt epidemics, which can decimate the stock in a few weeks, sometimes break out in farm rabbitries.
The first symptoms are a clear, fluid nasal discharge and frequent sneezing. The rabbit often rubs its nose with its forepaws, the fur of which becomes matted and dirty. This is the first stage, or common coryza, which affects the upper respiratory tract.
Later the discharge turns yellowish, thick and purulent. Sneezing is less frequent but coughing may begin. Purulent coryza can remain stationary or develop into pneumonia, either spontaneously or from other specific or non-specific causes (enteritis, lactation, malnutrition, etc.). With pneumonia, coryza, sneezing, even coughing and snuffling may disappear. The only symptoms will be slower respiratory movements, clearly visible in the nostrils, and difficulty in breathing in. In young rabbits, growth slows or stops. Complications are frequent: diarrhoea, ophthalmia, sinusitis, torticollis (wryneck) and abscesses. Females can die suddenly during lactation or gestation.
At autopsy, coryza is manifested by the presence of pus in the nasal cavities and atrophy of the mucous membranes. The lungs may be congested and parts may have a liver-like appearance. Very often there are lung abscesses with abundant yellowish-white caseous pus filling most of the chest cavity.
As with diarrhoea, respiratory infections are due to an association of non-specific contributing causes with infectious agents.
Many of the non-specific attacks mentioned in the previous sections are decisive for the development of respiratory ailments. Control of chronic enteritis in fattening units, in particular, will reduce the incidence of coryza. Other contributing causes are directly linked with rabbit respiratory physiology. The lungs are protected by the rabbit's very developed, very complex nasal cavities. These cavities are covered by the pituitary membrane which acts as a filter to stop dust and airborne microbes. It is therefore essential to protect this mucous membrane and keep it intact. The pituitary membrane is particularly sensitive, which may explain many of the following observations:
· abrupt cooling of the air can be the sole cause of common coryza, which may clear up spontaneously and quickly in a healthy environment;
· dust (crumbly granulated feed, pollen, dust in the air from dry sweeping or a nearby dirt road) can cause common coryza through the reflex action of the pituitary membrane, but may also clear up quickly;
· air flow, humidity and temperature are three very closely linked environmental factors that are instrumental in triggering respiratory ailments. At lower temperatures the air must be correspondingly drier and move more slowly. Rabbits seem to be very sensitive to draughts. Air flow should not exceed 0.30 m/second unless the humidity is more than 75 percent. Ventilation errors in closed buildings are the chief cause of chronic pneumonia;
· ammonia and gases forming from decomposing, urine-soaked straw litters may quickly break down the pituitary membrane and gain direct access to the lungs.
Infectious agents. Three constants of disease agents are the randomness of their pathogenic strength, their numbers and the fact that they are interchangeable. In other words, only some alteration in the mucous membranes of the upper respiratory tract will allow the germs present to develop to their specific pathogenic strength.
Bacteria. Pasteurellosis is the disease most often cited, because rodents and lagomorphs are particularly susceptible to this germ. Pasteurellosis may take many forms in the rabbit: abscesses, mastitis, diarrhoea, metritis, wryneck or septicaemia. The rabbitry can easily become thoroughly infested, to the point where pasteurellosis can become endemic. Some pasteurella strains are more pathogenic than others. Pathogenicity can be acquired during the endemic stage, provoking an epizootic outbreak in the rabbitry or even in the entire region (Rideau et al., 1992). While pasteurella is the worst and most common of the germs isolated from the respiratory apparatus of a sick rabbit, there are others: e.g. klebsiella, staphylococci, streptococci, bordetella, E. coli, salmonella and listeria. These are usually secondary infections or associations such as streptococci and bordetella.
All production units are contaminated with pasteurella and, while there may not be respiratory pasteurellosis, the constant threat is there, and varies with the pathogenic strength of the strain.
Viruses. Apart from myxomatosis, which now seems more and more likely to cause pneumonia, no respiratory virus has been described in the literature. Viruses certainly do exist, however, and in rabbits as in other animal species, the problem is the bacterial complications which follow viral infections.
Parasites. There are several species which can develop in the lungs (Protostrongylus spp., linguatulids, etc.). They are relatively uncommon in domestic rabbits because, as with intestinal worms, an intermediate host such as a snail or dog is required. Only a laboratory analysis can reveal the presence of respiratory parasites.
Epidemiological and physiopathological elements
Pasteurella are basically transmitted through direct contact such as mother to progeny, male to female, or via a vehicle such as the drinker, the trough or the breeder's hands. These bacteria cannot live very long outside the body, making sanitary isolation effective. Airborne transmission is infrequent and only effective if the air is full of dust or water particles.
In a healthy production unit, young rabbits are unlikely to be contaminated before the age of 21 to 25 days. Most adults are silent carriers. The sites most commonly colonized are the sinuses, vagina and middle ear. Autopsies show that more than 60 percent of female rabbits have asymptomatic pasteurella-associated otitis of the middle ear. Pasteurella are carried into the inner and middle ear by the lymphatic system in a two-way direction.
Other pasteurella affections are frequent: cutaneous abscess, mastitis, vaginitis and metritis; the last two more frequent in units where artificial insemination is practised with unsterilized implements. All these external suppurative forms are incurable and affected animals must be culled immediately.
Respiratory disease control
Chemotherapy. Tetracyclines are pneumotropic antibiotics well tolerated by rabbits. Chloramphenicol and sulfadimethoxine are also often effective. Dosages vary according to the preparation but treatment should always be for three to four days. The medicine is best injected intramuscularly. Whenever a bacterium is isolated in the laboratory it is strongly recommended that an antibiogram be made immediately. Although antibioresistance is rare in rabbit pasteurellosis, resistance to streptomycin, spiramycin and the sulphonamides is reported. Systematic preventive antibiotic treatments are both useless and dangerous.
Vaccination. The numerous vaccines on the market are of very uneven effectiveness. Most of them are pasteurella-based and sometimes bordetella-based. It is difficult to immunize rabbits against these two germs, whatever the quality of the vaccine. The main point is that bacteria are only exceptionally the direct cause of the disease, so that even if the rabbit is protected against pasteurella, it can still catch pneumonia from streptococci or staphylococci.
Given the large number of pasteurella strains and their variable pathogenicity, autovaccines are always preferable. Furthermore, to be at all effective, vaccination must be performed on healthy animals just after weaning and repeated one month later. Action is generally taken during the course of the disease only. Vaccination and chemotherapy are merely temporary measures to back up preventive hygiene.
Preventive hygiene. Preventive hygiene is the sine qua non of successful respiratory disease control, even more so than for digestive disorders. Where pasteurellosis is endemic in a nursery, the breeder needs to know that a long battle lies ahead for which the following strategy is proposed. Where possible, the first action, before administering antibiotic treatment, is to remove two or three sick rabbits to identify the germ, make an autobiogram and perhaps prepare an autovaccine. Successful control depends on culling sick animals, which the breeder will need to be able to replace. Pasteurellosis control should be preceded by the preparation of new breeding females from the youngest (newly weaned) animals which have been isolated, treated and perhaps even vaccinated.
The first stage of pasteurellosis control is the elimination of all clinically diseased animals: i.e. those with signs of suppurating coryza, sniffling, breathing problems, abscesses, mastitis, vaginal discharge, etc. The second stage is to analyse the nursery environment: i.e. air flow, ammonia, humidity, temperature, dust content. No specific control is possible unless the environmental problems are identified and solved. The third stage (and hopefully not the first) is antibiotic treatment with tetracyclin, chloramphenicol, etc.; it is particularly effective if administered for long enough and by parenteral injection.
The bacteriological clean-out of the unit should be supplemented by extra-rigorous cleaning of the floors, walls and all equipment and implements.
Culling of the sick is to be followed by the removal of healthy carriers such as old females, non-productive females, females that refuse mating or that abort, females with coryza in the late stages of pregnancy, etc. Male rabbits are formidable healthy carriers.
New females should not be brought in until the situation has improved, i.e. several weeks after the start of the operations. This must not signal a slackening of vigilance in either maintenance of a sound environment or good hygiene. Culling of the breeding animals retained should continue.
There are many rabbit diseases other than digestive and respiratory ailments. Most have disappeared from intensive rabbit production without the reason always being known. Others are still found in farm rabbitries but are rarely of economic importance. The following is a brief review of diseases that are not uncommon.
This is a viral disease (Sanarelli virus) which decimated rabbits in Europe for more than 20 years after being introduced into France in 1952. The Sanarelli virus develops in certain American rabbits, Sylvilagus (cottontails), without causing the disease, thus making them dangerous carriers.
Myxomatosis is extremely contagious and can be transmitted in many ways. Biting or stinging insects such as mosquitoes and fleas are the main vectors because of the rapidity with which they can inoculate animals and the distances they are able to fly. Spread by animal-to-animal contact or from contaminated equipment is also common. It now appears certain that pulmonary contamination is possible in confined rearing. This virus is very resistant to weather and physical changes (cold, dryness, heat) and disinfectants. Formol, however, is very effective and is recommended for disinfecting equipment.
Pasteurellosis eradication plan: order of operations
1. Cull live animals for laboratory examination (antibiogram and autovaccine).
2. Prepare a stock of future breeders to replace animals culled, isolate them, treat them and vaccinate them if possible.
3. Cull sick females, including those with suppurating coryza, sniffling, breathing problems, abscesses, etc.
4. Check and modify the environment (air flow, ammonia).
5. Administer appropriate antibiotic treatment to the remaining stock.
6. Wash and disinfect cages, hoppers, drinkers, floors and walls.
7. Continue to eliminate healthy carriers for several weeks or even several months, i.e. cull females which are not productive, refuse the male, do not get pregnant or abort.
8. When the situation improves, renew stock with young vaccinated females and continue the accelerated renewal of the entire stock.
The first symptoms are inflammation of the mucous membranes (eyelids, genital area) which thicken and form small tumours. These tumorous nodules are found first on the tips of the ears and then all over the body. The tumours adhere closely to the skin and grow until they filially deform the whole head. Numerous nodules can be felt under the skin on the back.
Respiratory forms of the disease with no other symptoms also seem to be common. Clinical diagnosis is then impossible. Recovery is rare but not unheard of when the animal can eat and there is no secondary infection; however, the rabbit then becomes a healthy carrier of the virus.
There is no treatment, nor should there be. Vaccination is effective and can be done with a heterologous virus such as the Shope virus, which causes a small benign nodule in rabbits, or with a weakened form of the myxomatosis virus. In Western Europe the first is more popular, in Hungary the second. Prevention requires good hygiene and insect control, especially of lice and fleas in farm rabbitries.
Breeders or countries buying rabbits should ensure that the animals have been vaccinated for more than three weeks but less than two months before purchase, and that they come from a healthy rabbitry where regular vaccination is the rule.
Viral haemorrhagic disease (VHD)
There are many synonyms: RVHD (rabbit VHD), viral hepatitis, haemorrhagic hepatitis, X disease, etc.
Epidemiology. The epizootic form of this disease appeared in China in 1984 and spread rapidly throughout the world. By 1988, it had reached all of Europe and the American continent (Mexico, Venezuela, etc.).
The epizootic disease is most spectacular where farm rabbitries or wild rabbits are heavily concentrated. (In Italy, for instance, an estimated 80 percent or more of the farm rabbitries were entirely decimated within a few months.) One or two years later these epizootic forms appear less frequently and are less widespread, but the disease remains endemic.
However, when VHD hits a previously unaffected country, as in Cuba in 1993, the extent and evolution of the disease are dramatic. In general, animals over eight weeks old, particularly adults, are the most susceptible to VHD.
Frozen Chinese rabbit meat was the original source of contamination in Western Europe and Mexico. All producer countries of meat, by-products, breeding animals, etc. are now contaminated. Even though rabbit VHD spreads very quickly, few industrial production units in Europe except Spain were affected since they use only granulated feed. The forage collected by breeders is often suspected of being the principal vector of the virus.
Symptoms and lesions. When the disease appears in a rabbit production unit, it spreads immediately. Death occurs within three days after exposure and, in the chronic form, survivors recover in one week. The clinical symptoms are straightforward: fever, sudden death, sometimes preceded by convulsions and cries. Ante-mortem epistaxis is spectacular but not frequent. The disease is fairly easy to diagnose thanks to the dramatic mortality throughout the rabbitry (20 to 40 percent per day), particularly in adult rabbits.
The characteristic post-mortem lesions are:
· haemorrhagic syndrome throughout the respiratory apparatus, liver and intestine;
· congestion of the kidneys, spleen and thymus;
· frequently major enlargement of thymus and liver, the liver showing the most constant lesions, discoloration, a "cooked" appearance, very marked lobular patterns;
· clear failure of coagulation revealed by incision of the organs in fresh cadavers;
· necrotic hepatitis and general intravascular clotting in all organs, the most typical lesions revealed by histo-pathology.
Causes. Although the RNA virus which causes VHD has never been cultivated, most authors now agree that it should be classified in the family of the Caliciviridae. It is very resistant to freezing, ether, chloroform and proleolitic enzymes. It can be inactivated by formol or beta-propiolactone. It is destroyed by bleach, soda and the phenols.
The first target cells in the organism are those in the reticulo-endothelial system. The virus can subsequently be found in all cells, particularly the hepatocytes. Indeed, the purified virus used to produce inactivated-virus vaccines is taken from the liver.
Prevention and treatment. There is no treatment. Preventive hygiene measures have proved inefficient except in industrial-scale rabbitries. Several vaccines have been made from the inactivated viruses. They act very swiftly (two to five days) and confer six months of protection. In areas where the disease is endemic, vaccination is essential and effective. When an epidemic breaks out in a rabbitry in a region, immediate vaccination following the first fatality can save a production unit. The major problem in contaminated countries is having enough vaccine on hand to intervene immediately.
Two different policies are recommended for imported or new breeding animals (in addition to the standard measures such as quarantine): they are prior negative sero-logical test or vaccination. Neither is entirely reliable because the specificity of the test is low, and the disease has a very short incubation period. Vaccination would be the method of choice as the virus apparently does not multiply in vaccinated animals, but formal confirmation of this point is still pending.
Finally, despite the numerous similarities (virus, symptom, epidemiology), the disease European brown hare syndrome (EBHS) is not transmissible to rabbits and vice versa.
Foot pad abscesses
Foot pad abscesses are a very common complaint, familiar to all breeders. Chronic abscesses are far more frequent under the hind paws. They start as a barely visible swelling which can be felt by palpation. They may be limited to the cutaneous and conjunctive tissues. The skin becomes thick (parakeratosis) and scabby. Infection is latent and the sores may bleed. Poor cage floor hygiene can cause heavy secondary infection. The abscess then covers the whole metatarsus and becomes purulent.
These abscesses are found in farm rabbitries and in intensive production where mesh floors are used. Breeding animals are especially prone to this disorder. In farm rabbitries the main cause is poor upkeep of the straw litter, which becomes damp and rots. Various infections can follow (staphy-lococci, fungi) but the worst is a Corynebacterium (Schmorl bacillus) which gives rise to an evil-smelling necrotic gangrene which can spread to the head and the whole body and then to other animals (necrobacillosis).
This disease is rare where rabbits are raised on wire-mesh floors, but sore hocks (caused by staphylococcus) are much more common than in rabbitries where straw litter is used. Poor quality, rough or twisted wires, wrong mesh size (too wide) and rust are the main culprits, all fostering the development of foot pad abscesses. It is difficult to raise heavy rabbit breeds on wire mesh.
The control of foot and hock diseases is primarily preventive and consists of the following:
· choice of medium-weight breeds and animals whose foot pads are well furred to protect the skin, such as the New Zealand White and the Californian;
· use of thick, galvanized, welded wire mesh (mesh size 13 to 15 mm); it should not irritate the palm of the hand when rubbed;
· straw litter always kept dry and clean;
· frequent washing and disinfecting of cages.
Treatment is difficult. When there is no obvious suppuration the sores may be treated every day and then every two days with strong disinfectants such as iodine, Fehling liquor, paraffin oil and permanganate. The antifungoid action of iodine and permanganate is useful too in units using the litter system, which fosters complications with fungi. Antibiotic ointments are not recommended because the treatment is long and expensive and the ointments soften the skin. When the abscesses become purulent or the forepaws are affected the infection is then incurable and the animals should be culled. If other abscesses are noted, especially on the head (necrobacillosis), the bodies should be burned or buried deep. Foot pad abscesses make it practically impossible for males to mate.
Buck-teeth prevent the upper and lower incisors from touching and so they do not wear down. The incisors keep growing and eventually prevent the rabbit from eating. Buck-teeth may be hereditary (jaw malformation), or the result of injury (teeth broken against wire mesh). There is no connection with the type of feed - forage, hard granulated feeds and so on. The only prevention is breeding. Teeth should be carefully examined when buying or choosing a breeding animal. Treatment consists of cutting the teeth with sharp pliers right down to the gums every 15 to 21 days.
Ear and skin mange
Ear canker or mange is very common. It is a parasitic disease caused by a mite (Psoroptes or Chorioptes) and frequently complicated by bacterial infection. The symptoms are external otitis and yellow or brown scabs in the ear canal. The course of the disease can be very long. The scabs become waxy and invade the whole ear. The inside of the ear becomes scaly. The middle ear may then be affected, causing wryneck (the rabbit's head is held constantly to one side).
Treatment can be effective if the disease is caught in the very early stages, that is, as soon as small yellow-brown deposits are noticed in the ear. Insecticides are applied locally in the ear. Organophosphates such as malathion are preferable to organochlorines (DDT, lindane) which, although very active, are dangerous to humans. Glycerine, iodized oil or cresyl oil are also effective when applied frequently.
Prevention involves culling rabbits whose external ears are severely affected, and treating all other rabbits for several days running and then every fortnight. Throughout the treatment the straw litter must be changed frequently as the parasites can stay alive in the litter for a long time.
Ivermectine is unquestionably the drug of choice; two 200 mg injections per kilogram of live weight every eight hours provides a spectacular cure. The product is very persistent and if the stock is carefully treated at the same time and the rabbitry cleaned out, it will be effective for several months. This is a very strong medicine and should be reserved for breeders, for animals treated with it cannot be eaten for several months.
Skin mange is much less common. Today it is only found in poorly managed rabbitries. Lesions start at the edge of the lips, nostrils and eyes, spreading to the head and forepaws as rabbits frequently rub their heads. The skin dries, the hair falls out and the skin becomes scaly and finally scabby. The skin mange mites, Sarcoptes and Notoedres, are not of the same family as ear canker mites. Treatment is the same, but prevention measures (culling diseased rabbits, cleaning cages) must be stricter.
Ringworm. Also called dermatomycosis or trichophytosis, ringworm is a skin and hair disorder. Not very common in farm rabbitries, it is widespread in intensive rabbit production. It starts with circular bald patches, usually on the nose. The hair looks clipped and the skin is irritated and inflamed. More small patches appear on the head, ears and forepaws and then over the whole body. On the oldest lesions the hair can be seen growing again in the centre.
It is a very contagious infestation that can sometimes be transmitted to humans, although it is more commonly transmitted to other domestic animals such as dogs and cats. Ringworm is caused by microscopic fungi that can belong to different genera (Trichophyton, Microsporum, Achorion) and are not specific to rabbits. There is no economic loss as long as infestation is light.
Treatment is long and costly. An antimycotic, Griseofulvin, is administered in the feed for about ten days. During treatment all equipment should be frequently cleaned and disinfected in a 5 percent formol solution. Many producers, successfully it seems, sprinkle powdered sulphur (sulphur flowers) on the ground, cages and nesting boxes. In small rabbitries local treatment can be applied with antimycotics in powder or liquid (tincture of iodine and other dyes), but preventive hygiene should accompany the treatment. Badly afflicted animals should be culled and domestic animals treated.
Ectoparasites and trichophagy. As well as the lice and fleas that are specific to rabbits, ectoparasites of other animal species, particularly poultry, can also bother rabbits. Not found in intensive rabbit production, these farm rabbitry ectoparasites can harm production and, worst of all, they are the vectors of many disease agents, including the myxomatosis virus. With good hygiene and external antiparasitic preparations they can be rapidly eliminated.
Trichophagy or fur-eating occurs both in farm rabbitries and in units using wire-mesh floors. The animals eat each other's fur and end up with bare backs and flanks. All sorts of diagnoses have been advanced: unbalanced rations, behavioural problems, unsuitable environment, amount of light, overpopulation, genetics and so forth. It was very widespread when wire-mesh cages were first used extensively, but seems to be declining with the general improvement in production conditions (equipment, feed, strain). There is no exact preventive measure and no specific treatment.
Zoonoses are diseases shared by many animal species and humans. Most have no special feature peculiar to rabbits and are rarely contracted by them (rabies, tetanus, etc.). Therefore only a few are mentioned here, either because they can be dangerous to people or because the appearance of the disease in the rabbit reveals its existence on the farm or in the village.
This disease is very rarely reported in rabbits. Nevertheless it does exist and may be of avian, bovine or human origin, in decreasing order of frequency. The rabbit is very resistant to tuberculosis, so the disease evolves very slowly. The lesions, which are the sole indication of tuberculosis, can only be seen in breeding animals. The main organs affected are the lungs and less frequently the liver, intestine and kidneys. The spleen is very rarely affected. The classic tubercular nodules are found in the parenchyma of these organs, often containing an almost solid cheese-like pus.
This is more common in guinea-pigs, wild rabbits and hares than in domestic rabbits reared on straw litter. It has almost disappeared with modern wire-mesh cage production. Pseudotuberculosis is one cause of synovial arthritis in humans. The germ Yersinia pseudotuberculosis provokes numerous whitish nodular lesions on the intestinal viscera, especially the spleen, which become enlarged. These nodules, ranging in size from a lentil to a chickpea, are sometimes amalgamated. They are scattered throughout the abdominal cavity but are rarely found in the lungs. Apart from steady weight loss there are no symptoms to diagnose. The disease can easily be recognized by post-mortem examination.
Tularaemia (rabbit fever)
This very contagious disease is common in hares, but rabbits seldom contract it. Its significance is the danger it represents for humans. A bacterial disease caused by Francisella tularensis, it gives rise to high fever, leaving the animals in a semicomatose state. Lesions are enlargement and congestion of the spleen. The liver is often dotted with numerous tiny greyish-white spots (miliary necrosis) about the size of a grain of millet.
This disease is less rare than tularaemia, and still appears sporadically in farm rabbitries. A septicaemic disease caused by Listeria monocytogenes, it is very difficult to diagnose clinically. Listeriosis should be suspected when the following symptoms appear on the farm:
· nervous upsets: photophobia, spasms, wryneck;
· abortions in does or ewes;
· miliary necrosis of the liver and spleen (without enlargement).
This disease is unquestionably more common in farm rabbitries than is generally believed. It is caused by the intermediary stage of an internal cat and dog parasite, Isospora. The course of the disease does not usually produce symptoms, although there may be jerky nervous reactions. The lesions are translucent cysts in the brain and in muscles or viscera. Often the spleen is enlarged.
Zoonoses are infrequent in farm rabbitries and have apparently never been identified in intensive rabbit production. This is because contamination is usually spread by forages polluted by other animal species. Zoonoses are also usually diseases of adult animals; the early slaughter of animals (10 to 12 weeks) limits their spread. When these diseases are suspected the dead animals should be burned or buried and human hygiene intensified. Although antibiotic treatment may be effective in certain cases it is best not to treat but to cull the entire stock. Good hygiene is the only prevention. Apart from the usual rules of cleanliness, forage must be cut and stored with special care. Rats and mice are formidable propagators of these diseases. Rat extermination around rabbitries is fundamental.
There are few data on this disease. Various findings from Africa on the subject, while not contradictory, are not uniform. It has been demonstrated that rabbits can contract trypanosomiasis experimentally or in special circumstances. They are particularly susceptible to Trypanosoma brucei.
There are reportedly some rabbitries in tsetse fly areas, for instance in Côte d'Ivoire, with no recorded cases of spontaneous outbreaks of trypanosomiasis in rabbits. Trypanosomiasis has caused some problems in Mozambique, however. It has been reported that its symptoms are oddly like those of myxomatosis.
Note: Other diseases that are transmissible from rabbits to humans, or common to both, have already been mentioned. By contrast, neither rabbit variola (pox virus) nor rabbit syphilis (Treponema cuniculi) can be transmitted to humans.
A doe can produce over 60 young in one year, but few breeders are in a position or context to exploit this potential fully. Rabbit maternities are the source of many disease problems. The breeder should focus efforts on the nursery and on maternal health, the prime guarantee of obtaining healthy young rabbits at weaning. Productivity factors in the rabbitry (frequency of mating, litter size, age at weaning) depend at least as much on the breeder, equipment, feed quality and quantity as on the female rabbit's potential.
Maternal health determines the survival of the offspring
All the diseases mentioned above can affect breeding females. Only a few points peculiar to reproduction will be mentioned in the following paragraphs and the relative importance of the major diseases of females will be discussed in order of importance.
Respiratory ailments are the main disorders affecting pregnant rabbits in closed rearing. In intensive production, apart from the environmental causes described earlier, lactation must be added as a contributing cause. In young nursing does, hard-to-diagnose ailments can be complicated by acute or subacute pneumonia. The doe may die before weaning her litter or she may have to be culled shortly afterwards.
Digestive disorders and enterotoxaemia
Digestive diseases are far less serious in adult animals than in growing rabbits. The classic coccidiosis-type diarrhoea is rare in adults. Intestinal parasitism (coccidiosis, strongylosis) will be latent or chronic, fostering the appearance of other diseases.
Enterotoxaemia is more common, especially in farm rabbitries. It can develop very rapidly (one to seven days) with or without mucoid enteritis. Most often it occurs in late pregnancy or mid-lactation, sometimes in association with symptoms of acute pneumonia. In traditional rabbitries, complications of paresis or paraplegia are common, especially in fat, overfed does working at low-intensity breeding rates. Control in this case involves adapting the reproduction rate to the feeding capacities of the production unit. There is no treatment.
Some 25 to 30 percent of does in intensive production die, usually with no warning symptoms. Mortality occurs in mid-lactation in young first- and second-litter females and in the latter stages of pregnancy in older does. Often called enterotoxaemia, this illness is certainly not of infectious origin, although bacterial complications are common. It is rather more like a metabolic disorder, such as milk fever in ruminants or eclampsia in women. Its aetiology is still not clear. There is no curative treatment. Mortality can sometimes be reduced by preventive doses of calcium in drinking-water or parenteral injections (Ca gluconate) just before kindling.
Abscesses and mastitis
Abscesses are very common in rabbits. They sometimes grow to enormous size, and develop very quickly without any apparent change in the animal's health. There are two preferential sites in does: the sub-maxillary area and the teats. These and foot abscesses are the main reasons for culling breeding does.
Most often the cause is Staphylococcus aureus, but other germs may be present. The worst are pasteurella, which can make the disease epizootic and lead to numerous complications (pneumonia, septicaemia, abortion). Mastitis is common in units with mesh floors and is probably fostered by congestion caused by chilling. When mastitis is in the congestive stage (hard, reddened mammary gland but no pus) the disease may be staved off by a three-day antibiotic treatment and the local application of astringents (vinegar) twice daily to aid decongestion. It is uneconomical to treat abscesses or purulent mastitis.
Clamydia psittaci is found in rabbits. The clinical symptoms are many: refusal of the male, early miscarriage, peri-partum haemorrhage, hydrocephalus and poor viability of newborn rabbits. Tetracycline as a preventive measure for the entire rabbitry is efficient but there may be relapses.
External genital organs. The external genital organs (vulva, penis, scrotum) can be the site of specific venereal diseases. The best known is rabbit syphilis or vent disease, caused by a spirochete (Treponema cuniculi). It has never been reported in intensive rabbit production, but vent disease is not exceptional in rural rabbitries. Inflamed lesions become ulcerated. Bucks are often affected (orchitis, balanitis) and transmit the disease, which can turn enzootic. This is a benign disease which impedes mating; it can easily be treated with antibiotics (penicillin, tetracycline).
This disease can be confused with the onset of myxomatosis!
Internal genital organs. The internal genital organs can also become infected. These, far more serious, far more common infections make reproduction impossible.
Metritis or white discharge, a uterine infection, is often associated with mastitis and respiratory complaints. It is a major rabbit disease. One symptom of metritis is an abnormal frequency of sterile does and mastitis in the rabbitry. Abortion, which is usually rare, may become more common. Metritis shows up at post mortem: the uterus is thickened and poorly retracted and there may be abscesses at the last embryo implantation site, sometimes covering the whole uterus (pyometra).
Aetiology is complex. Gestation and kindling are obviously contributing causes, but hygiene is a determining factor, and a chronic pasteurellosis in the rabbitry could be the culprit. The most common germs are non-specific: staphylococci, pasteurella. The specific germs such as toxoplasm, Listeria and Salmonella are much less common. Specific infections are likely if there is widespread abortion.
Antibiotics can be given, especially at the onset of the disease. But they will not be effective unless the most advanced cases, such as very thin does, or does with purulent mastitis or symptoms of pneumonia or purulent coryza, are culled. Preventive medicine, in this case vaccination, is only valid for pasteurellosis (see section on respiratory diseases). Preventive hygiene is decisive in controlling internal genital diseases.
Non-infectious reproduction problems
Sterility. Absolute sterility is relatively rare. "Sterility epidemics" are usually seasonal and can often be traced to insufficient light (less than 14 to 16 hours). Sterility otherwise occurs after one or several kindlings (see previous chapter). Does serviced three times with no results should be culled for both hygiene and economy.
Twisted uterus. Cases of twisted uterus are not uncommon. This is discovered during post mortems on does that died during gestation. The causes are not clear. Overcrowding of the uterus and disturbance of does are frequent explanations.
Delayed birth. Delayed birth often occurs with small litters (one to three). Foetal retention is common in this case, invalidating the doe economically. In modern production, birth is systematically induced by injections of oxytocin on day 33 of pregnancy (servicing on day zero).
Parturition outside the nest box. Young first-litter females are the usual offenders. Disturbances, or mice in the nesting box, are possible causes.
Prolapsus of the vagina. There is no treatment for prolapsus of the vagina.
Cannibalism. Real cannibalism caused by abnormal behaviour in the doe is exceptional. The female usually eats only those young which are already virtually dead but still warm. This may happen a few hours or days after parturition. Insufficient drinking-water after parturition is considered a cause in farm rabbitries, and this could well be the true reason.
Abandonment of the litter. This is most often done by young females whose milk has not let down, or has let down too late. A doe that abandons two litters should be culled.
The nest and young rabbit mortality
Compared with other domestic animals, rabbits are still virtually in the foetal stage at birth. The survival of newborn rabbits, and hence the success of the rabbitry, is closely related to the quality and hygiene of the litter's immediate environment.
If the amount and type of materials used for the nest (straw, wood shavings, hay, etc.) are inadequate during the first few days, the newborn rabbits will get cold and death is then inevitable. The doe does little to intervene. She pulls fur to help make the nest; she nurses her young once a day and sometimes she will defend access to the nest, but she does not care directly for the young. If the nest box is poorly designed and the young are able to get out after the first few days, the doe will not put them back.
If nest hygiene is poor (droppings, dampness) or if the mother is sick (mastitis, coryza) the young will develop a nostril-blocking rhinitis which will impair their sense of smell within a few hours. Their sense of smell is crucial as it guides them to the mother's teats. Small staphylococcic abscesses can quickly develop on the young rabbits' bodies (belly, groin, tarsus) under these conditions.
In modern French rabbitries with highly prolific does, an intensive reproduction system and adequate environmental conditions, an estimated 5 to 7 percent of the young are still-born and another 16 to 20 percent normally die before weaning. About a third of this mortality is accounted for by precocious dam mortality. Some of the young can be saved by fostering two or three to another nursing doe with young of the same age. The remainder of the losses take place during the first two weeks of lactation. Occasionally an entire litter is lost during the first four or five days.
The aetiology of these mortalities is not known, but it seems to have more to do with the doe's state (lactation?) than with any particular disease of the newborn rabbits. The above figures indicate that a mortality rate of less than 15 to 20 percent should not be considered catastrophic. On the other hand, after the first 15 to 20 days of lactation young rabbit mortality should be very low. If it is not, the dam should be examined for mastitis or coryza. Cage and nest-box hygiene should be checked. Pre-weaning diarrhoea (30 to 35 days) is a sign of inadequate hygiene. Coccidiosis indicates very poor hygiene.
The word prevention has been constantly repeated throughout this chapter as essential for successful rabbit production. Careful hygiene is usually enough to prevent major disease crises. Preventive medicines (vaccinations, anticoccidiosis treatments, etc.) have been described. They are not widely used in rabbit production. The basic rules of preventive hygiene are now set down in detail.
Location and design of the rabbitry
It has been emphasized from the outset that rabbits must have an environment in which they do not constantly have to withstand external disturbances and aggression. The rabbitry should be located whenever possible far from such nuisances as noise and dust (dust carries microbes), sheltered from the prevailing winds and, in hot countries, shaded from the sun. Rat and mice extermination should be considered, as both are formidable healthy carriers of diseases to which rabbits are susceptible.
Cleaning should be constantly kept in mind in the designing and building of a rabbitry. Nothing that cannot easily be cleaned and disinfected should be allowed. The rabbit's immediate surroundings (cage, feeding racks and drinkers in particular) should be portable, so they can be regularly removed, cleaned, dried and disinfected. In completely closed buildings the ventilation system should be carefully designed for flow without draught. Where ventilation is used, forced-air ventilation is preferable, as it keeps insects out and makes it possible to control the air flow by adding or removing vents.
Some authors insist that in tropical countries the interior of the building should be sufficiently protected to act as a buffer against extremes in temperature and humidity, especially during the rainy season, to cut down the incidence of pulmonary diseases. As an example, a rabbitry in Burkina Faso built with local materials (laterite bricks, palm framework, straw roofing) recorded a much lower range in temperature variations than did a "strong" building made of construction blocks with a tin roof. Where possible, metal should be used for the wire-mesh hutch and accessories as it is the easiest material to clean and disinfect.
Preventive hygiene. The rabbit's excitability is a contributing factor in illness. Casual visitors such as feed suppliers, rabbit buyers and other breeders (who are vectors of diseases from other rabbitries) should be barred. Rabbits should be protected against dogs, cats and small wild carnivores.
Feed and water hygiene is basic as both can carry numerous agents of rabbit diseases (e.g. coccidiosis and worms). Feed should be stored out of the reach of domestic animals. It should be distributed in troughs or racks, but never on the ground. Drinkers should never be set on the ground. Rabbits drink a lot of water, but they will not drink dirty water. Water is the ideal medium for coccidia sporulation. Accordingly it should be changed and drinkers cleaned often.
Cage and nest hygiene is particularly important while the does are nursing. In wire-mesh hutches the cage must be removed and cleaned after each kindling. In farm rabbitries the straw litter must be renewed often. After kindling, any stillborn young should be removed from the nest and the nest remade if necessary. Contrary to widespread belief, a doe will not abandon her young if they have been touched. It is only necessary to keep the doe out of the nest during the cleaning operation.
After weaning, if straw litter is used, it should be kept clean and dry. The more animals per cage, the more difficult this is. In every type of production system weaning demands scrupulously clean, disinfected, dry cages. Weaning is one of the crucial moments in rabbit production. Transporting the animals, mixing up litters and using questionable cages should be avoided. Successful production depends on these details.
Microbial infection. It is also necessary to work constantly against any buildup of microbial infection. Chronically sick animals (with coryza, pneumonia, mastitis, abscesses), especially breeding animals, must be culled. One sick breeding animal in a rabbitry is of small value in relation to the danger it represents for the rest of the stock, the cost and uncertain outcome of treatment and the possibility of its quick replacement (sexual maturity at four months).
In completely closed buildings the control of microbial contamination should include the maintenance of walls, ceilings and especially floors. Damp or dusty floors are a permanent source of air pollution.
Early slaughter. Early slaughter (10 to 12 weeks) of animals for market is also a form of preventive hygiene. Many diseases take several months to develop before becoming contagious, especially in small or farm rabbitries.
Human factor. People are the most dangerous permanent vector of disease. They can bring in contaminants from the outside and so should wash their hands before entering and don footgear and a smock which always remain inside the rabbitry. Only a human being can palpate a doe suffering from mastitis and then systematically go on to infect all the mammary glands of the females to be palpated that day. Clean hands are extremely important, especially when handling animals and distributing feed and forage.
Preventive medicines to control parasitic diseases also help to maintain a healthy environment. Many parasites undermine the animals' state of health without causing directly perceptible losses and pave the way for a great variety of infections. However, the systematic use of antibiotics as a preventive measure is definitely not recommended. The abuse of antiparasitic drugs, especially of sulpha drugs, does far more harm than good. All drugs, at a certain dose, are poisons and must be used with caution.
Disinfecting. The literature covers this topic extensively, so the following will be brief. Disinfecting the rabbitry should be a routine matter, following some simple rules regarding cleanliness, dryness and disinfection. Dirty equipment cannot be disinfected. It must be washed first or, if water is short, carefully scraped and brushed. It must then be thoroughly dried as a first step towards disinfecting equipment. It should not be forgotten in this context that sun-drying well-cleaned equipment for several days is a simple, cost-free and very efficient means of disinfecting. The only preconditions are a storage area off limits to domestic animals and a reserve supply of extra equipment so that cleaning and disinfecting time will not cut into production time. In industrial production, pressurized steam-cleaning equipment is indispensable.
Occasional measure: sanitary isolation
No matter what precautions are taken, after one, two or three years health problems will become less and less easy to control. Imperceptibly, productivity will decrease despite an increase in hygiene and care and in the experience of the breeder. This has to do with the buildup of bacterial contamination in the rabbitry, coupled with the irreversible presence of harmful micro-flora and microfauna in the animals.
Sanitary isolation becomes essential at this point. All rabbits in the affected section of the rabbitry must be culled. All equipment must be cleaned, repaired and disinfected. After this is done the area must be left vacant for some time (one or two weeks) before introducing new rabbits. Some small farm rabbitries have two premises which they alternate every year. This is a kind of one-year sanitary isolation which has proved very effective.
1 New Zealand White rabbit (Foto Saleil)
2 Bouscat Giant White rabbit (Foto Saleil)
3 French Belier rabbit (Foto Saleil)
4 Californian rabbit (Foto Saleil)
5 Dutch Belted rabbit (Foto Saleil)
6 French Giant Papillon rabbit (Foto Saleil)
7 Vienna Blue rabbit (Foto Saleil)
8 Flemish Giant rabbit (Foto Weber)
9 Creole (Guadeloupe) rabbits (Foto Lebas)
10 A "family package" of bucks and breeding does supplied by a Mexican programme (Foto Lebas)
11 Wooden hutches with mesh floors arranged in a two-storey system (Guadeloupe) (Foto Lebas)
12 Open drinkers supplied semi-automatically from a fitted bucket (Guadeloupe) (Foto Lebas)
13 Fattening cages built entirely in wire mesh, placed outside in superimposed rows (France) (Foto Lebas)
14 Cages arranged in a plastic greenhouse, protected with a reed lattice (France) (Foto Lebas)
15 Exterior of the same greenhouse, photographed in winter (Foto Tudela)
16 Fattening cages for rabbits in a greenhouse with a makeshift floor (Foto Saleil INRA)
17 Italian system for arrangement of fattening cages (Foto Lebas)
18 Mesh cages arranged by the Californian system (France) (Foto Lebas)
19 Breeding cages with forward nest box in a modern French rabbitry (Foto Cuniculture)
20 Cages for the collection and transport of rabbits to the abattoir (Hungary) (Foto Lebas)
21 Plastic cages for trucking rabbits from the rabbitry to the abattoir (Foto Cuniculture)
22 Rabbitry in Cameroon. Recycling cages for laying hens in a semi-Californian arrangement (Foto Solambe)
23 Health-care room at the Solambé Demonstration Centre, Yaoundé, Cameroon (Foto Solambe)
24 Rabbitry with semi-underground cages: overall view (Foto Finzi)
25 Rabbitry with semi-underground cages: unit (Foto Finzi)
26 Faeces from rabbits receiving feed with a normal proportion of roughage, slightly deficient and deficient in roughage but without diarrhoea (Foto Colin)