The diseases of the African camel have not been very extensively researched in comparison with those of other domesticated species, probably owing partly to the non-sedentary nature of the herds, constantly moving in search of grazing and water. It is only in a few places, where the animals are found in favourable environments, often alongside other species, that attempts have been made to study camel pathology. In such areas, e.g. Borana, Bale and Harar in Ethiopia, the camel herders may even request veterinary attention for their dromedaries. Available literature indicates that dromedaries suffer from fewer diseases than other domestic livestock (Leupold, 1968a) and epidemic are rare. For further details on disease the reader should consult the works of Leese (1927 and 1969), Gatt-Rutter (1967), Curasson (1947), Castagnera (1957), Bares (1968), Cauvet (1925), Burgemeister (1975), Burgemeister et al (1975), Blaizot-Bouvier (1975), Ferry (1961) and Richard (1979). The present review is by no means exhaustive.
Fluctuations are commonly observed in the body temperature of the camel, which is able to adjust its own body temperature. Leese (1969) indicates that the temperature is lowest at dawn and gradually increases until sunset before dropping during the night. It may vary from day to day. He gives the normal temperature at 6 a.m. as 36.4° C and at 6 p.m. as 38.1° C. Schmidt-Nielsen (1959) gives a morning temperature of 33.9° C and asserts that the higher limit is never above 40.5°C. Altman and Ditmer (1968) give the intramuscular neck temperature of the dromedary as 35.1–39.1° C and the rectal temperature as 34.5–38.5° C. Mason (1917) gave a range of 35–38.6° C.
Leese (1927 and 1969) showed that the pulse of the camel can be taken from' the posterior tibial artery, with the animal in a sitting position. The medial sacral artery, near the root of the tail, could also be used. He estimated the pulse rate of a resting camel as 45–50. He observed that the normal respiration rate of the camel at rest is 5–12 per minute. A higher respiration rate is often indicative of a febrile reaction. Like the pulse rate, respiratory rates tend to be higher at noon than in the early morning.
The camel is capable of closing its nostrils and breathing through its mouth. At such times the lower lip tends to become pendulous. Occasionally the animal will puff out its cheeks during mouth breathing.
Vomiting occasionally occurs in the dromedary and is not necessarily a sign of disease. Camels are nervous animals and may vomit and spit when handled. When vomiting occurs in an undisturbed animal, however, it should be regarded as a symptom of disease.
Among camels, trypanosomiasis is sometimes also referred to as surra. It has received much attention, being extensively discussed or investigated by almost everyone involved in camel medicine. It is caused by Trypanosoma evansi, present in most areas where camels are found. Bremaud (1969) also lists T. congolense as a possible cause of the disease. The organism is transmitted by Tabanus, Stomoxys, Lyperosaa and Haematobia flies (Scott, 1973), which are prevalent around river banks and watering points in the arid zones. Tsetse flies, the main vectors of bovine trypanosomiasis, are not involved in the transmission of T. evansi to camels.
Through blood samples and smear examination it was estimated by Richard (1976) that about 15% of camels in Borana (Ethiopia) were infected. An extensive account of the disease is given by Curasson (1947), but it would appear that trypanosomiasis mainly occurs as a chronic (subacute) debilitating ailment. The acute form is rare.
Fazil (1977) confirmed that camel trypanosomiasis is a slow, wasting disease. The animal becomes thin, weak, prostrate and eventually dies. The first signs of the disease are a drop in production (milk yield) and the tendency of pregnant females to abort. There is loss of appetite and the animals become very emaciated. Leese (1969) discusses the acute and subacute forms of camel trypanosomiasis at some length, indicating that the latter form may last 3 to 4 years before the animal finally succumbs. Recovery may occur in 20% of animals which are well fed, rested and managed. These animals subsequently become immune. The death of chronically affected animals is often triggered off by secondary infections, e.g. bronchopneumonia.
A tentative diagnosis of trypanosomiasis may be made on the basis of clinical signs, after which camel herders are often able to summon help or rest the affected animals. Thick blood smears taken from the tip of the ear to detect the organisms are useful in confirming the disease.
The best way of controlling the disease is by treatment with drugs. Two drugs have proved useful: Naganol (Suramin, Moranyl) and Anthrycide. It is necessary to give the correct dosage since underdosing may create resistant trypanosomes. Scott (1973) reported strains of T. evansi which were resistant to Suramin in Ethiopia and recommended the use of Anthrycide sulphate. Fazil (1977) reported good results with Anthrycide sulphate injected subcutaneously at a dosage of 4.4 mg/kg body weight, 2 g being sufficient for a 500 kg animal. He cautions against the use of Berenil, however, which may be toxic to camels. Other drugs have also been employed, but with less efficiency. Balis and Richard (1977) used 0.5–1 mg/kg of Isometamidium chloride hydrochlorate (intravenous or intramuscular) and recommended its use only in the absence of the more effective drugs. Dosages higher than 1 mg/kg are very poorly tolerated by the camel, according to Balis (1977).
Gatt-Rutter (1967) discussed the prevalence of protozoal infections in the camel. In some cases, however, the mere demonstration of an organism in the blood or faeces was used to establish the presence of a disease. Typical of the uncertainty surrounding these diseases are the results of Sharma and Gautam (1974), who found that 13.08% of 191 camels randomly sampled were serologically positive when tested for Toxoplasma gondii in the Hissar area of India. The animals were otherwise healthy, showing no clinical signs of the disease. No extensive accounts of protozoal diseases are available and only a brief list of the diseases treated by various authors (Gatt-Rutter, 1967; Richard, 1979, etc) is given here: leishmaniasis, coccidiosis, theileriosis, anaplasmosis, sarcrosopridiosis and toxoplasmosis.
On the basis of faecal (1,500 samples) and postmortem examination, Richard (1976) estimated that 92% of the animals examined in various parts of Ethiopia were to some degree infested with internal parasites (80% with Strongyloides ova, 10% with Strongyloides larvae and 16% with Trichuris ova). Fourteen helminth species were identified on postmortem examination, the main ones being Monezia spp., Stilesia vittata, Avitellina centripunctata, Trichuris globosus, Haemonchus contortus, Trichostrongylus spp. and Impalaia somaliensis. Cysticercosis and hydatidiosis were also found in a few cases. Additionally, Leese (1969) listed the frequent occurrence of Oestrus cameli (the camel bot), Haemonchus longistipes, Nematodirus spathiger and Ostertagia mentulata, while Trichocephalus echinopbyllus, T. centripunctata, T. globipunctata, Distoma hepaticum, D. lanceolatum and Taenia expanse were found in smaller numbers. He added that echinococcosis was common among camels but is of little consequence, and recorded the presence of Linguata larvae cysts in the mesenteric glands of camels in India. Leese also went on to describe husk as a disease of camels in the Nile delta caused by Strongylus filaria. Blaizot-Bouvier (1975) found, on the basis of faecal sample examinations, that Ethiopian camels were infected with parasites such as Monezia expansa, Stilesia vittata, Avitellina centripunctata, Strongyloides papillosus, Trichuris ovis and T. globosus. In a survey of camels at a government camel breeding farm in India, Lodha et al (1977) found that 64.7% of the faecal samples examined contained Tricburis globosa, while 13% contained Haemonchus longistipes.
Richard (1976) wrote that acute helminthiasis in dromedaries (gastro-intestinal parasitism) is generally associated with diarrhoea and weakness. The frequently encountered form is the chronic one with sporadic bouts of diarrhoea, constipation and emaciation. There is disturbed absorption of nutrients with a resultant drop in production. Animals with chronic gastro-intestinal parasites also tend to succumb very easily to other diseases.
The presence of echinococcosis (caused by Ecbinococcus granulosus) in Nigerian camels was established and investigated by Dada (1978): Out of 3,410 slaughtered animals examined, 1,952 (57.2%) were found to be infected with the disease. Hydatid cysts were found in the lungs, liver and spleen of infected animals (but not in the heart), and losses of what would otherwise have been parts for human consumption were considerable. El-Khawad et al (1979) found recently that 35% of the camels surveyed in central Sudan were infected with hydatidosis.
Magzoub and Kasim (1978) reported Fasciola gigantica and F. hepatica among camels in Saudi Arabia. They found a higher incidence of fascioliasis (liver fluke) in animals from the eastern region and associated this with the higher rainfall and irrigation schemes in the area, conditions which are conducive to the survival of the intermediate snail hosts. A very high percentage (14.2%) of camels imported for slaughter from Sudan were infected with fascioliasis.
Filariasis has recently attracted attention as an important camel disease caused by Dipetalonema evansi, which inhabits the arteries, especially the spermatic artery, but sometimes also the pulmonary and diaphragmatic arteries. Michael and Saleh (1977) developed a slide agglutination test for the diagnosis of camel filariasis, a method found to be 86% accurate.
It is clear that the helminth parasites and the extent of infestation vary with location and management system. As with helminthic infestations in other domestic species, the disease picture varies with the burden. An individual account of the disease picture for each of the above-named parasites is beyond the scope of this review. Suffice it to say that good management practices should be coupled with regular deworming of the camels.
A few chemotherapeutic agents have been evaluated for the treatment and control of camel helminths. Recently, Lodha et al (1977) found that a 90% Methyridine injectable solution at 1 ml/4.5 kg and 4% Morantel tartrate at 1 ml/4 kg liveweight were very effective in the treatment of mixed infestations of Trichuris, Haemoncbus, Nematodirus and Strongyloides in camels. Tetramisole hydrochloride (Nilverm) 3% w/v oral drench at 0.5 ml/kg liveweight was the next best treatment, whereas Thiabendazole, even at 90 mg/kg liveweight, did not produce encouraging results.
Camel mange is sometimes considered the most important disease of dromedaries after trypanosomiasis. The only mite that infects camels is Sarcoptes scabiei var. cameli (Richard, 1976). Mange is a highly contagious disease which can spread to herdsmen or others associated with infected animals. The mite may be transmitted directly by contact or indirectly through objects such as saddles, harnesses, utensils, bedding and even tree trunks. It tends to spread more quickly during cold weather, when animal coats usually grow long and the animals huddle together more often.
Sarcoptic mange affects animals of all ages and sexes and is certainly more common and severe than was previously thought (Lodha, 1966). The organism, which is just visible to the naked eye, requires 2 or 3 weeks to multiply, after which the population explodes, spreading very rapidly all over the animal body and through the herd. Infection generally starts in the head region, extending through the neck to other areas with thin skin, such as the penile sheath and the udder. The whole body may become infested within a month. Affected areas become swollen, hardened, hairless and wrinkled, especially in the hindquarter, thigh and hock joint areas. Infected foci are highly irritating, forcing the animals to scratch themselves and rub against one another, or against other objects such as trees, thereby spreading the infection even further. The infection leads to a loss in feeding and grazing time, with a subsequent loss in condition and productivity. Seriously affected animals are often unsightly and blood may be seen oozing out of areas traumatized by scratching and rubbing.
Once the disease has been diagnosed (which should not be difficult since sarcoptic mange is the only type affecting camels), the infected animals should be isolated. Their living quarters should be disinfected with 5–10% phenol and then exposed to the sun for 2 weeks. Treatment should aim at killing the mites, promoting healing of affected areas and restoring the normal health and productivity of the animals. Thus it is common practice to clip around the infected areas, which are then scrubbed, preferably with a brush, and washed with soap.
After drying an acaricidal dressing is applied, e.g. Gammexane or any of the hydrocarbon or organophosphorous insecticides. Dipping is the most efficient method of application, but the camel's large size limits its extensive use, and hand dressing and spraying are the more commonly employed methods. Lodha (1966) studied the efficacy of DDT, Lindane, and Co-Ral, and concluded that Lindane at 0.05% concentration was the most effective. Three applications at weekly intervals are generally used, irrespective of the acaricide. A power sprayer was used in this particular study and with a pressure of about 500 g/cm2 it took approximately 3 minutes to cover one animal completely, requiring 9 litres of the solution.
Camels do not suffer greatly from tick-borne diseases. Nonetheless, a few species of ticks have been isolated, including Amblyomma gemma, A. variegatum, Hyaloma truncatum, H. excavatum, Ripecephalus pulchellus, R. pravus and R. simus (Bremaud, 1969; Richard, 1979). Spraying by hand pump with any of the dipping or spraying compounds usually used for cattle or sheep appears to be effective.
Leese (1969) recommended that riding camels should be deticked as a matter of normal routine and observed that camels tend to accumulate ticks just below the anus, which if unattended may result in severe ulceration. Ticks generally cause consistent irritation, leading to rubbing. When located around the eyelids they may force the animal to rub against trees or other objects, often resulting in conjunctivitis.
Camel pox is an ailment mainly of young camels (6 months to 2 years) caused by a virus closely related to other variola poxes (Fazil, 1977), which was only recently isolated in Iran (Richard, 1976). Camel pox is an infection of the skin which can also infect man. It is a typical pox disease showing the four usual stages of pox lesions: papules, vesicles, pustules and crusts. These lesions are commonly observed on the head and other areas of the body with fine skin. The incubation period of the disease is about 2 weeks. In young camels there may be associated diarrhoea and subsequent death of the animals. Animals recovering are immune for life, and nursing calves attain some degree of immunity through colostrum for the first few months of life.
Adult camels are generally resistant. Those that become infected usually develop a benign form manifesting as oedema of the head, associated with swollen lips that may become blistered. However, Leese (1969) indicated that camel pox may become malignant, its lesions spreading to any part of the body, especially the areas with thin skin. Occasionally the disease is fatal.
Saddles which are not well fitted or loads which are improperly balanced are often associated with skin bruises and saddle burns. Such areas become infected, ulcerate and may lead to skin necrosis. Raw areas of flesh may be seen on the back or hump after the loss of the top skin, and Richard (1976) isolated a wide variety of pyogenic organisms from these necrotic areas.
Fazil (1977) indicates that skin necrosis among camels may be associated with salt deficiency. Once established, the ulcers spread to surrounding areas, and there is little spontaneous healing. Fazil suggests that cleaning with antiseptic solutions, e.g. 1:100 Acriflavine, together with the supplementary feeding of salt should be able to control the lesions.
Domenech et al (1977) studied the various pyogenic skin conditions of the dromedary in Ethiopia. Besides the type of skin necrosis described above (locally known as maha) they found that camel skins could also be affected by localized abscesses known as mala. Mala is a typical infection of the lymph nodes, caused by Corynebactenium pseudotuberculosis and Streptococcus of the Lancefield type B group. A mixed infection may occur and sometimes the abscesses may be due to Staphylococcus or C. pyogenes organisms. It is a chronic infection which often affects the lymph nodes at the base of the neck and around the rump. The abscesses are usually closed, cold and painless.
Camel herders do not generally slaughter their animals for meat, but sometimes consume the meat of those that die of disease. Anthrax is thus a disease of major public health importance, although its incidence in the camel may not be very high.
Camel anthrax is an acute or peracute disease caused by Bacillus anthracis. In Ethiopia, Richard (1976) reported serious outbreaks of anthrax in camels, with some grazing areas being notorious for the disease. Bacillus anthracis spores may remain alive in the ground for 60 years. Fazil (1977) indicated that the disease in camels is similar to that in other species but Leese (1969) is more specific, observing that camel anthrax is similar to the form observed in horses and pigs. Bremaud (1969) wrote that anthrax was particularly rampant in the Wajir camel herding area of eastern Kenya.
Major signs observed include oedematous swelling of the head, throat, neck and body. Involvement of the throat may lead to difficult breathing and swallowing. It is possible for death to occur without septicaemia, and apoplectic and diarrhoeic forms may also be observed.
The diagnosis and treatment of the disease should follow the lines recommended for other species, and it is possible to protect camels with the same type of vaccine as used for cattle, e.g. Blanthax, which also protects against blackquarter.
Salmonellosis among camels of the Sudan has been reported by Curasson (1947). Cheyne et al (1977) also described an outbreak of the disease in Somalia.
The disease is caused by Salmonella choleraesuis bacteria and may be peracute with death occurring in a few days. It may also become protracted. In the acute form, affected animals have a high temperature (39° C) and a pulse rate of 50 per minute. In the observations made by Cheyne et al (1977), the prescapular and submaxillary lymph nodes were swollen, muscle twitches were observed on the head and neck regions, and there was diarrhoea. Protracted cases (5 to 6 days) exhibited a thready pulse, congested mucous membranes and black, liquid, foul-smelling faeces. The mortality rate in this particular outbreak was under 10%.
Like anthrax, salmonellosis is of great public health importance. Cheyne et al reported salmonella food poisoning caused by the consumption of infected camel meat. They also quoted work which showed the presence of Salmonella spp. in the faeces of healthy animals, and that up to 3% of the carcasses at one camel abattoir in Egypt contained Salmonella typhimurium in their viscera.
As regards treatment, favourable results have been obtained by combining antibiotics with sulfonamides.
Camel tuberculosis is generally sporadic. Leese (1969) reported that it is frequently found in Egyptian camels, while Mason (1917) indicated that at one Cairo abattoir the incidence of tuberculous carcasses was 2.8%. Tubercular lesions were found to affect the liver and lungs, or the lungs alone, or were sometimes generalized throughout the body. Mason concluded that camel tuberculosis was caused by the same bacilli as cause the bovine type (Mycobacterium bovis). He indicated that the close confinement of camels and cattle together may be the source of cross-infection, since no lesions were found in the carcasses of animals originating from purely camel herding regions. Although the camel is thus susceptible to bovine tuberculosis, it would appear that the disease is not an important one. In spite of their susceptibility to infection, camels are very resistant to the effects of the disease, and a long period elapses before they become cachectic and emaciated. Trypanosomiasis, with which this disease can be confused, is a far more common and debilitating illness.
A number of minor bacterial organisms have been isolated from camel tissues. Further bacterial diseases have been suspected on the basis of personal interviews with camel herders. The list of such diseases includes pneumococcosis (Kamel, 1939), pasteurellosis, brucellosis, blackquarter, paratuberculosis (Johne's disease), pneumonia and tetanus (Leese, 1969). Burgemeister et al (1975) demonstrated antibodies against Brucella obortus, B. melitensis, Listeria monocytogenes type 1, Mycobacterium tuberculosis and Leptospira from the sera of 52 camels from southern Tunisia. Richard (1979) also lists rickettsiosis, tetanus, plague, glanders and infectious pustulo-dermatitis.
Leese (1969) indicated that rabies is not infrequently found in African camels. Infection often follows attacks and bites from wild animals. Affected camels become violent and aggressive and should be restrained or destroyed to avoid spreading the disease to other animals. Sometimes, sick animals simply become noisy and terror-stricken. They may also develop paralysis of the tongue.
Rinderpest and FMD are two diseases which are suspected to occur in camels, but as yet no classical cases have been recorded. The suspicion probably arises from the prevalence of the diseases among cattle.
Fazil (1977) comments that camels are slightly susceptible to rinderpest and that there might be an occasional death. Curasson (1947) reported outbreaks of rinderpest among camels in West Africa. Richard (1976), while reporting rare occurrences of FMD in Ethiopian camels, confessed that his attempts to detect the virus (types A, O and C) in camels herded with cattle experiencing a severe outbreak of FMD were negative. The current problem is to establish whether the dromedary is capable of acting as a carrier for the rinderpest and FMD viruses.
Burgemeister et al (1975) isolated antibodies against infectious bovine rhinotracheitis, bovine virus diarrhoea and para-influenza type 3 virus in Tunisian camels. Both Chlamydia and Coxiella burnetti were also demonstrated.
Traumatic wounds may result from the use of nosepegs or rings. If the tears are observed fresh, they should be stitched or handled like fresh wounds. Caution should be taken against subsequent fly infestation of the wounds.
The camel is capable of protruding its soft palate beyond the lips. This balloon-like structure may sometimes be traumatized by sharp objects or during fighting, and infections may result. The throat of affected animals becomes swollen and the camel may be unable to swallow. Breathing becomes laboured and the neck may be extended. Palatal inflammations of the camel tend to be chronic and often ulcerative. Leese (1969) recommended that the best corrective measure is to amputate the inflamed portion of the palate at the level of the first grinders. Little haemorrhage is encountered and the animals show almost instantaneous relief.
Bloat or gas tympany occurs in camels under similar circumstances as in cattle, and is handled in a similar manner. However, when a trocar is used to relieve the gas, a finer type than the cattle trocar is recommended. It is often unnecessary to use a trocar, since drugs may be just as effective. Fazil (1977) shows that the use of 0.85–1.14 litres of linseed oil or any of the commercial anti-bloat drugs is effective.
The camel differs from the cow in that its third and fourth stomachs are not clearly demarcated. The common opening between these two chambers is also very patent. The contents of these stomachs are always more fluid than in cattle. It is thus rare for impaction to occur in camels, but when it does so it often involves both stomachs. Common causes of impaction include extreme dehydration and chemical poisoning. A lack of faeces is observed. Vomiting may occur, rumenal movements become suppressed, while excitement and other nervous signs may also be exhibited. If untreated, the camel may die in 2 to 3 weeks, most of which time is spent in a recumbent position.
Treatment of impaction in camels consists of giving 2.27 litres of linseed oil or 0.68–1.38 kg of magnesium sulphate (the exact amount being proportional to size and age), with the subsequent administration of plenty of water. If the treatment is repeated the dosage has to be reduced.
Mason (1920) reported a high rate of mortality in the Indian Camel Corps. Indian camels, which are not used to working in a sandy terrain, failed to adopt proper grazing habits and consumed too much sand. The Sudanese and Egyptian animals in the group, which were accustomed to the habitat, were not affected. Signs before death included profuse vomiting, diarrhoea, tympany, colic and pain, although the temperature generally remained normal. Mason recommended the administration of oil to affected camels, the application of muzzles when animals were not grazing, and feeding 42.53 gm of salt per day. It would, however, appear dangerous to use animals which are unaccustomed to sand on work in the desert.
For a review of surgical diseases, lameness and other sporadic diseases of the camel, the reader is recommended to consult the work of Leese (1969). Curasson (1947) continues to serve as a standard reference work on camel helminthology and general medicine.
