Appearance and development of diseases

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The animal has multiple and interlinking defences for countering attacks from the outside environment. These can be classed arbitrarily and briefly as:

The body does not have an infinite capacity for nonspecific or specific defence. So the producer's main job is to keep 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 unfavourable to rabbit health are described later in this chapter.


The environment is everything that surrounds the animal: its habitat, its congeners, its solid and liquid feed, microbial infection, temperature, air, 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 show 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 seen fit to ignore 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 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.

As another example, 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 3 countries of a hitherto sporadic disease-dermatomycosis.


Microflora is also a component of the environment. This chapter devotes special attention to microbial infections because they arc a major, inevitable form of attack in all rabbitries.

Microbial infection refers to the polluting of air, objects and soil by bacteria, parasites, viruses or fungi. Most often, these microscopic flora or fauna 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 he will do by respecting the rules of hygiene (discussed later) and by limiting stock to the number of animals he can maintain and nourish 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.

No matter how capable a breeder is, the day will arrive when his rabbitry will have to be cleared, thoroughly cleaned and disinfected in order to lower ambient microbial infection to a safe level. 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 cut down on the local microbial infections specific to each crop. Plant species, like animal species, are each surrounded by their own microbial environment.

The producer's best ally in keeping his rabbits healthy is the animals' own capacity to defend themselves from disease. An organism's defense against outside attacks is basically a global, nonspecific response which is fundamentally dependent on good hygiene standards in the rabbitry. The rules of hygiene are easier to apply and respect in small rabbitries with simple, easy to maintain equipment. Daily preventive cleaning will keep the infection and pollution level 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 hut as a function of syndromes or combinations of disease manifestations which share common or closely related symptoms, and which are important in economic terms.

Intestinal diseases

Unquestionably this is the disease order most costly to rabbit breeders and the major obstacle to expanded rabbit production.

Diarrhoea is a serious economic threat primarily in young weaned rabbits (4-10 weeks). It is rare before weaning and can in any case easily he prevented by elementary sanitary and feeding hygiene. It should be noted that diarrhoea appears later in young rabbits than in other young domestic 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 with 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 slow the passage of food through the intestine and halt 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, men) 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 5-7 days afterwards.


The symptomatology of rabbit enteritis is relatively simple and constant and rarely permits an etiological diagnosis of the disease. The first signs, scarcely noticed by the breeder, last 1-3 days, and take the form of a decrease in feed intake (especially solid feed) and 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 troth 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 2-3 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 content is liquid.

A post-mortem examination shows Iesions, usually atypical. During the acute phase the intestinal content is very liquid, sometimes discolored. 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 brushstrokes. 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.


There are many causes of diarrhoea. Specific and nonspecific causes should be distinguished.

It has been seen that very different kinds of attack can cause outbreaks of diarrhoea. Rabbits seem to react negatively to: transport, especially during the post-weaning period; being put in a new hutch or cage; the presence of unusual visitors (people or animals); unusual sounds not identifiable by the animal, 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.

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 feed distribution 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 can bear 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.

Theoretically, these include any cause which, alone, allows the disease to multiply. In fact, the state of health is almost always the main factor.

Chemical agents. Various antibiotics invariably provoke diarrhoea: ampicillin, Iyncomycin and clyndamycin. Antibiotics should always be used very sparingly with rabbits, especially penicillin.

It seems that drinking water with a high nitrate count causes the chronic diarrhoea noted in some areas.

Mouldy feed (pellets, domestic waste, bread, vegetable peels) can very quickly give even a healthy rabbit diarrhoea.

Viruses and bacteria. There is 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 outbreak of viral diarrhoea.

Much the same is true of bacteria. Salmonella bacteria are rarely isolated in sick rabbits, but this is not true of Corynebacteria, Clostridia, Pasteurella and, especially, Escherichia coli. Apart from some Clostridia 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 an aleatory manner. For example:

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 are protozoa, the most primitive phylum of the animal kingdom. They are sporozoa, ie, 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 4 sporocysts containing 2 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 they 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 8 "embryos" (sporozoites).

The Eimeria cycle includes 2 distinct phases:

The internal part of the cycle begins with ingestion of the sporulated oocyst and the exit of the sporozoites. The parasite then multiplies. This may entail 1, 2 or more schizogonies (asexual reproduction) according to the species (E. media, 2 schizogonies; E. irresidua, 3 or 4 schizogonies). It can take place in different parts of the digestive apparatus (E. stiedal 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 into the outside environment. The total duration of the internal phase of the cycle also varies with the species (eg, E. stiedai, 14 days; E. perforans, 4 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 26C, E. stiedai takes 3 days and E. perforans 1 day.

Numerous studies, especially those of Coudert (1981) in France, have dealt with this part of the cycle, as the oocyst is the contaminant 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 9 coccidia species are rabbit parasites. One infests the liver, the other 8 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 4-6 week treatment with conventional anticoccidia products (Decox, Pancoxin, formosulfathiazole) 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 4 categories (Table 45).

E. coecicola is apathogenic. No clinical sign is detectable even in an inoculum containing several million oocysts.

E. perforans and E. media are very slightly or slightly pathogenic. Alone, they never cause diarrhoea or mortality. Massive infestations ( 106 oocysts) are needed before there is a slight and very brief decrease in growth.

E. irresidua, E. magna and E. piriformis are pathogenic species that cause extensive diarrhoea and retarded growth-as much as 15-20 percent of liveweight-for infestations between 0.5 and 1 x 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 concentrations (upwards of 103 oocysts).


Pathogenicity Eimeria Simptoms
Nonpathogenic coecicola No sign of disease
Slightly pathogenic perforans Slight drop in DWG
media No diarrhoea
Pathogenic magna Drop in DWG
irresidua Diarrhoea
piriformis Little or no mortality
Very pathogenic investnalis Severe drop in DWG
flavescens Considerable diarrhoea
  High mortality

DWG = Daily liveweight 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 a 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 coccidia of the second group (E. media, etc) might not in an unfavourable environment have a more severe impact.

Lesions. There are two kinds of lesions: macroscopic and histologic. Both are relatively short-lived. They appear towards the 8th or 9th day and disappear by the 12th or 13th day, despite their sometimes spectacular appearance.

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 causes macroscopic lesions visible in an autopsy at high concentrations.

E. magna 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 lesional appearance is the same with high concentrations of E. magna.

The caecum is the domain of E. flavescens, which at medium concentrations produces lesions on the colon. The caecum wall thickens and changes appearance according to whether there is microbial side 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 cold at medium concentrations (30 000 to 50 000 oocysts).

Histology: Hystologically, 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 Lieberkuhn will be destroyed.

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:

The clinical evolution of an intestinal coccidiosis is illustrated in Figure 18.

Depending on the coccidia species, diarrhoea appears between the 4th and the 6th day after infestation. The peak is from the 8th to the 10th day. It then declines in 3 or 4 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 2 or 3 days growth and feed intake are low. Between the 7th and 10th day after infestation there is weight loss, perhaps as much as 20 percent of liveweight in 2 or 3 days. Recovery is equally rapid. Two weeks after inoculation the animals may resume their initial growth.

Mortality rages for a relatively short period (3-4 days). It starts abruptly on the 9th 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 concentrations 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 physiopathology, below).

It is common for bacterial flora to develop at the same time as coccidiosis, complicating and aggravating the symptoms of the disease.

FIGURE 18.-The clinical evolution of coccidiosis

Rabbit age is not a major factor in susceptibility to coccidia. The disease is briefer in animals 10-11 weeks old and diarrhoea less severe, but weight loss and mortality are often more extensive than in younger rabbits.

Physiopathology of diarrhoea of coccidian origin. The main symptom of intestinal disease in young rabbits is diarrhoea.

Rabbit enteritis following coccidiosis 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 3 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.

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 the diarrhoea of calves due to E. coli, for example, the small intestine secrete water and minerals, especially sodium, which will be lost by the animal

In the young rabbit there is also a lack of reabsorption-indeed a' actual secretion-of sodium and water in the loci where the parasite multiply. Unlike calves, however' rabbits can compensate for tines' disturbances in the distal colon and, most importantly, they can initiate an Na-K exchange which limits sodium losses to a minimum. Potassium losses are replaced from body reserves.

These different parameters evolve at the same time as the symptoms described earlier. Peak intensity occurs about the 10th 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 the basic phenomena of the pathogenesis of diarrhoea are independent of the etiology (infectious agents or nonspecific 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.

One might likewise be tempted 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.

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 often 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 far rarer, at least in Europe.

It must never 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 amount 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 10-15 percent. Indeed, this is the usual figure.

Whether the environment is good or bad, any attack 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 19, can therefore be attributed mostly to stress.

Nonspecific attacks 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 56 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.

Lastly, nonspecific factors cannot be discussed without mentioning their intensity-5 minutes' transport does not constitute the same aggression as 4 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 concentrations, can also help undermine the organism'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 outside 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 strength also need to be identified.

FIGURE 19.-Development of coccidiosis

For coproscopic investigations, a stool examination of excrete several days old taken from under a cage where there are several animals is preferable to and far more reliable than a caecum content examination. At any given moment (death or slaughter of the animal) there may be:

Despite these difficulties it can be stated categorically that the sole presence of E. intestinalis, E. flavescens, and even E. irresidua or E. piriformis is a serious circumstance and with 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 2 or 3 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 where the prognosis is often quite bleak.

This section is always eagerly awaited, because people still hope for miracles. There is no miracle available in coccidiosis 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 nonspecific factors. The environment, then, needs to be dealt with first;

-anticoccidiosis treatment is feasible for animals that have been infected for only a few days (5 or 6), 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 1 or 2 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 nonstop for nearly 30 years in feed. This may be one reason why present-day coccidia control is so ineffective. Nonetheless, the bacteriostatic activity of these drugs probably favours recovery or avoids problems. Bifuran (50% furazolidane, 50% 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 0.5-0.8 g/kg of feed as a curative measure, or 0.3-0.5 g/kg as a preventive measure. Unfortunately it is not water soluble.

Curative treatments should always be applied to all growing animals for 45 consecutive days followed by a therapeutic rest. Treatment is then resumed for a further 4-5 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 100-150 g water per kg of liveweight. 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 (0.1-0.4 mg/litre of drinking water), colimycin (34.105 lU/litre) and the tetracycline group (0.2-0.3 g/litre). Once treatment with antibiotics is started it must be continued for 3-4 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, Iyncomycin, 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 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. Nonspecific 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 and vaccination against intestinal bacterial diseases has proven nearly 100 percent ineffective.

Doses of sulpha drugs (see preceding pages) given to the young rabbits at weaning for 8-10 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 is today the most effective and best tolerated product. Others, such as Salinomycin and Narasin, are just as effective against coccidia but the conditions under which they should be used have not yet been worked out. 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 these 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.


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.

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 above all not enough roughage).

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 (3-4 days). Death can intervene before diarrhoea appears. When developing enzootically in a rabbitry there are phases of mucoid diarrhoea or constipation.

FIGURE 20.-Comparative evaluation of 10 drugs used against 2 serious forms of rabbit coccidiosis



Infestation with 5 • 104 oocysts of E. intestinalis

Infestation with 5 • 104 oocysts of E. flavescens





100 Robenidine            
100 Decoquinate            
750 Formosulfathiazole            
200 Lerbek            
200 Pancoxin            
175 D.O.T.            
200 Nicarbazine            
200 Bifuran            
50 Monenzin            
400 Framycetine            
  Relatively effective
  Insufficiently effective or ineffective

WG - Effect on weight gain
FC - Effect on feed consumption
- Effect on mortality

The autopsy shows lesions not very dissimilar from those described for coccidiosis. At most 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 Clostridia 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 their isolation and identification. 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 (102-103/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.

The enteropathogenicity of these strains comes from toxins they secrete. However, diarrhoea has hardly ever been produced experimentally using these enteropathogenic strains alone. For these E. cold to cause diarrhoea the animal has to undergo some other attack at the same time (unbalanced feeding, coccidia, thermal shock, etc).

While the clinical and necroscopic appearance of these diarrhoeas of nonparasitic 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. cold 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). This 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.


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