Toxoplasmosis. 91. 5. Coccidiosis. 94. Ectoparasites. 1. Mange. 97. 2. Ticks. 103. 3 ...... There is no effective treatment that can neutralize the tick paralysis toxin.
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WƌĞĨĂĐĞ The camel (Dromedary or Bactrian) has been serving millions of people living in the driest (hot or cold) areas of the World for centuries. It provides food, fiber, transportation and social status.Because presence a very few numbers of books about an infectious diseases in camel, so that this book was written. However, during the last two decades there has been a tremendous increase in the number of scientific papers in the world literature. It is now known that infectious diseases cause 50% of fatalities in New World camelids (NWC) and 65% in Old World camelids (OWC). Parasitic, viral, fungal and bacterial diseases are the main causes in NWC. Due to presence of many publication in different journals, these helped us in write our book. We hope this has been successful endeavor. Pray that Allah "All mighty" may give us strength to complete this work.
0XVWDID6DODK+DVDQ BVM,MSc.& PhD.
List of Contents Subject
Pages
Introduction 1
Introduction Chapter One : Bacterial diseases 1
Brucellosis:
5
2
Tuberculosis
13
3
Anthrax
20
4
Pasteurellosis (Hemorrhagic septicemia)
28
5
Camel Plague
32
6
Enterotoxemia
33
Chapter Two : Viral diseases 1
Camel pox
46
2
Contagious ecthyma (ORF)
49
3
Rabies
50
4
Rift Valley Fever
54
Chapter Three: Parasitic diseases 1
Haemonchus longistipes
59
2
Chabertia ovina
62
3
Trichostrongylus spp. (Hair worms)
64
4
Nematodirus
65
5
Trichuris spp.
66
6
Capillaria spp.
67
7
Stilesia spp.
67
8
Dictyocaulus spp.
68
9
Onchocerca spp.
71
10
Dipetalonema evansi
73
11
Moniezia spp.
74
12
Echinococcus spp.
75 Protozoal diseases
1
Trypanosomiasis
79
2
Anaplasmosis
86
3
Sarcocystosis
88
4
Toxoplasmosis
91
5
Coccidiosis
94 Ectoparasites
1
Mange
97
2
Ticks
103
3
Lice
107 Chapter four: Fungal diseases
1
Ring Worm (Dermatophytosis)
120
2
Aspergillosis
124
,QWURGXFWLRQ
ŝƐĞĂƐĞƐŽĨĂŵĞů Domesticated representatives of the family Camelidae are an important part of the national livestock populations of numerous countries in arid and semi-arid regions of Asia and Africa, as well as the high mountains of the Andes in South America. The family Camelidae comprises two genera: - The genus Camelus (Linnaeus, 1758), includes two species. The first species is C. dromedarius, the dromedary or one-humped camel, the world population of which is estimated to be 15,368,000, with approximately 80% in Africa and 20% in Asia. The second species is C. bactrianus (Linnaeus), the bactrian or two-humped camel, of which there are some 1.7 million in their natural habitat in Asia. - The genus Lama comprises Lama glama (the llama), Lama pacos (the alpaca),
Lama guanicoe (the guanaco), and Vicugna vicugna (the
vicugna). Only the first two have been domesticated. They are raised in herds in the Andes at altitudes above
2,500 m. Their population is
estimated to be 7,165,000. Well adapted to severe environmental conditions, the Camelidae are bred as working animals and for the production of meat and milk. Their hair and hide is used by craftsmen. Camels are better adapted than any other domestic animal to the very hot and very dry desert or sub desert regions. By contrast they are poorly adapted to moist climates and marshland. Although camels are hardy animals and can tolerate the harsh conditions of arid regions because of their unique adaptive physiological characteristics, these animals face a wide variety of diseases Dromedaries and bactrian camels feed on a natural vegetation composed of grass and spiny plants (e.g. acacia, cactus) which are not eaten by sheep,
goats or cattle. Camels are raised in herds which range in size from a few head to many dozens (ranging from 12 to 24 in Saudi Arabia, 50-80 in Oman, 60-70 in Iran, 100-150 in Mongolia and Kazakhstan); in Somalia and Ethiopia a herd may comprise several hundred animals.
Camelus dromedaries
Camelus bactrianus
Lama glama (the llama)
Lama pacos (the alpaca)
&KDSWHURQH %DFWHULDOLQIHFWLRQ
Bacterial infection 1. Brucellosis: Brucellosis is a serious zoonotic disease affecting man and all domestic animals including camels. It is recognized as a major cause of heavy economic losses to the livestock industry and poses serious human health hazard. Human infection due to Brucella from camels is known to occur mostly through the consumption of unheated milk. Brucellosis was reported in camels as early as 1931; since then, the disease has been reported from all camel-keeping countries. Camels are not known to be primary hosts of Brucella, but they are susceptible to both B. abortus and B. melitensis. Etiology Brucellosis is an infectious bacterial disease caused by the genus Brucella, affecting a number of animal species. Brucella bacteria are Gram-negative coccobacilli that are non-motile and nonspore-forming. They grow anaerobically and certain strains need a 5% to 10% carbon dioxide atmosphere. Brucella organisms grow slowly, but can be enhanced by using enriched media. The genus Brucella is divided into ten classified species and subdivided into biovars. The disease in dromedary camels iscaused by Brucella abortus and Brucella melitensis. Public health importance of brucellosis Human brucellosis is a potentially life-threatening multisystem disease with a broad spectrum of nonspecific symptoms. Brucellosis in humans is a major public health hazard which affects social and economic development in various countries due to acute and chronic illness, physical
incapacity and loss of manpower. Occupational acquired brucellosis is of special concern for public health because of the high risk of direct transmission from infected animals to persons being employed in animal husbandry. This exposed group includes slaughter men, dairymen, herdsmen and veterinary clinicians. Herdsmen are at the highest risk. The occupational exposure is high especially in countries where herding of animals is still traditional and unscientific. Camels¶ milk is increasingly becoming a delicacy, as in Arab nations camel milk is consumed raw by camel keeper. Isolation of B. melitensis from camels¶ milk and seropositivity to B. abortus and B. melitensis indicate that brucellosis is a hazard to public health. Therefore, pasteurization is adequate for public health assurance especially the pasteurization does not affect the chemical composition of camel milk. Human infection due to Brucella from camels is known to occur mostly through the consumption of raw milk. Malta fever due to B. melitensis was diagnosed in 30% of the camel handlers and milkers on large camel farm in Riyadh, Saudia Arabia. The abortion rate in the farm reaching 12% and B. melitensis biovars 1, 2 and 3 were isolated from aborted camel fetuses. Therefore, there is a real need for cooperation between public health officials and veterinary officers to reduce the circulation of human brucellosis in endemic areas. Transmission: The infection occurs via the mucous membranes, including oralnasopharyngeal, conjunctival and genital mucosa, and also through cutaneous abrasions. Animals become infected through feed, water, colostrum, contaminated milk and, especially, by licking or sniffing at placentas and aborted fetuses. The spread of brucellosis during sexual
activity plays a subordinate role. The primary shedding routes of Brucella organisms remain uterine fluids (lochia) and placenta expelled from infected animals. In cattle it is known that abortion is associated with the shedding of 1012 to 1013 Brucella bacteria. Survival of the organisms in the environment is enhanced by cool temperatures and humidity; however, it was proven that two dromedaries in a Brucella-negative dromedary herd were infected with B. melitensis through contaminated dust particles from aborted camel fetuses 500 m apart, indicating that organisms can also survive in a hot desert environment. Many
placental
mammals,
including
herbivores,
participate
in
placentophagy, with camelids as a noted exception, which may contribute to the spread of Brucella bacteria through wind. In human, The main modes of transmission are contact through skin with animal tissues, blood, urine, vaginal discharge, aborted fetuses and, especially, placentas, and consumption of raw milk and other unheated dairy products. Airborne infections occur in animal pens, stables, laboratories and abattoirs. Some cases have also occurred from accidental self-inoculation with live vaccines. Moreover, it was also shown that Rev 1 vaccine strain can cause human infections. In their study humans became infected after consuming milk from vaccinated adult pregnant animals which excreted the vaccine strain in milk for a long period of time. Clinical signs: Camels of both species (C. dromedarius and C. bactrianus) are frequently infected with Brucella organisms, especially when they are in contact with infected large and small ruminants. Serological evidence for Brucella infection in camels has been reported from Asia and Africa. Non pregnant
dromedaries experimentally infected with a field strain of B. abortus developed only mild, transient clinical symptoms including reduced appetite, slight lameness and bilateral lacrimation.
Bilateral lacrimation in Camel due to brucellosis Orchitis and epididymitis have also been associated with brucellosis caused by B. abortus and B. meletensis. Other conditions caused by the disease were retention of placenta, placentitis, uterine infections, fetal death and mummification, delayed maturity and infertility; it also caused arthritis and hygroma. As previously mentioned, abortion has been reported in pregnant camels and B. mel-Infections may cause stillborn calves, retained placenta, fetal death, mummification and reduced milk yield. Also, delayed service age and fertility have been reported. Pathology Little is known about the pathological changes caused by Brucella organisms in camelids.
These bacteria have a predilection for the pregnant uterus, udders, testicles, accessory male sex glands, lymph nodes, joint capsules and bursae. Lesions may be found in these tissues. Many authors described lesions in non-pregnant dromedaries. They found inflammation of the uterus lining with reddening, oedema and necrotic foci in the uterus epithelium, as well as fibrosis of the endometrium and atrophy of the uterine glands. The authors also observed an increased number of ovariobursal adhesions and hydrobursae. The adhesions occurred between the bursa ovarica and the ovary and in several cases also between the bursa ovarica and the salpinges, causing a severe induration of the latter. Hydrobursitis was often observed in brucellosis-positive dromedaries causing an enlargement of the bursa, which was then filled with a clear amber-coloured fluid. No lesions have been described so far in aborted camelids and in brucellosis-positive camelid males except orchitis and epididymitis. The testes and epididymis of 360 dromedaries were examined for gross and histopathological lesions. Around 12% of the tested organs originated from seropositive camel bulls. From the investigations it is not clear if the epididymitis, orchitis or testicular degeneration was caused by Brucella infection or was a normal pathological feature. A pregnant llama was experimentally infected by inoculating viable B. abortus bacteria into the conjunctival sac. Forty-three days post inoculation, the llama aborted an eight-month-old fetus. Brucella abortus was isolated from the placenta and all fetal specimens, including the brain, small and large intestines, spleen, kidney, liver, stomach fluid, heart blood and lung.
Bacteria were also isolated from numerous mammary gland lymph nodes in the dams. Histologically there was a moderate, multifocal, lymphocytic and histiocytic, subacute placentitis, with a marked loss of trophoblastic epithelial cells. The chorioallantoic stroma contained abundant necrotic and mineralized debris and the swollen capillaries. Other authors showed the followings -lymph node (especially supramammary): oedema, enlargement, lymphoid hyperplasia, granulomatous reaction in the cortical area of the lymphoid follicle ± Spleen: enlargement with granular surface in some cases, depletion of some lymphoid follicles, proliferation of fibrous tissue, histiocytosis ± Mammary gland: granulomastitis in some cases, proliferation of interlobular fibrous connective tissue ± Uterus: moderate amount of mucus and ulceration of endometrial mucosa, endometrial stroma showed oedema and diffuse and heavy infiltration (mainly of macrophages and lymphocytes in the lamina propia) blood vessels were dilated and congested.
Aborted Fetus
Diagnosis: - Brucella spp could be identified by isolated using plain or selective media by culture from uterine discharges, aborted fetuses, blood, udder secretions or selected tissues, such as lymph nodes and male and female reproductive organs. Polymerase chain reaction (PCR) can provide both a complementary and biotyping method based on specific genomic sequences. Serological Methods: -None of the serological brucellosis tests are validated for use in camels yet. However, it was found that a combination of different serological tests can increase diagnostic efficacy in camels. The recommended serological tests are Complement fixation(CF), Rose-Bengal test (RBT), Seroagglutination test (SAT) and Competitive enzyme-linked immunosorbent assay (c-ELISA). Treatment: Brucella organisms are Gram-negative coccobacilli which are sensitive to many broad-spectrum antibiotics, but the use of antibiotics is forbidden in many countries because of the uncertainty related to the infective status of the treated animals and because of the spread of antibiotic resistance. Treatment is unlikely to be cost efficient or therapeutically effective because of the intracellular sequestration of the organisms, mainly in the lymph nodes. However, cure rates between 65% and 100% have been reported in infected goats by daily intraperitoneal injection of 500 mg and 1,000 mg tetracyclines. It has also been found that treated seropositive dromedaries with a combination of oxytetracycline (25 mg/kg body weight) every two days for 30 days and streptomycin (25 mg/kg body weight) every two days for 16 days. In addition to this parenteral treatment,
milking camels received 10 ml of oxytetracycline as intramammary infusions in each teat every two days for eight days. This regimen of treatment was effective in eliminating the shedding of Brucella organisms through milk. All treated dromedaries also became serologically negative within 16 months of treatment. But the single untreated control camel remained positive over the same period of time. Using antibiotics may be a way to save valuable animals (e.g. racing camels) from being culled, but it is doubtful if antibiotic treatment on a herd-level basis can be successful. It is not clear from this investigation whether or not the shedding would have stopped anyway, without any antibiotic treatment, because the study did not include any untreated controlV+RZHYHUWKHDXWKRU¶VXQSXEOLVKHG treatment protocol clearly demonstrated that dromedary brucellosis is not treatable with antibiotics, although it is claimed otherwise. Control and prevention: Brucella has been eradicated in many regions of the world, but in others it is widespread and an economically important disease. Many cases of human brucellosis are found in regions where the disease has not been eliminated in livestock. Different strategic options can be adopted to first decrease the prevalence of brucellosis to an acceptable level (brucellosis control) and secondly to remove the foci of infection (brucellosis eradication). The choice of control strategy depends on a number of considerations, such as infection prevalence in different animal species, human clinical incidence and the capacity of Veterinary Services. It has been suggested that whole-herd vaccination in low-prevalence countries, and test-and-slaughter followed by vaccination in highprevalence countries.
In camel-racing countries, the culling method cannot be applied because racing dromedaries are often extremely valuable animals and play a very important role in Bedouin culture. Therefore, it is preferable to castrate all Brucella-positive bulls, not to breed positive females, and to vaccinate. No compromise should be made when it comes to camel dairy farms. They must be free of brucellosis. Dromedaries were successfully vaccinated with B. abortus strain S19 and with B. melitensis Rev 1but still Very little is known about the optimal vaccination age in camels and their serological response. 2. Tuberculosis: Tuberculosis is a chronic, contagious, granulomatous disease caused by mycobacterial species belonging to the Mycobacterium tuberculosis complex. Camelids were not considered highly susceptible to tuberculosis, but in recent years increased numbers of cases have been experienced in some countries. Clinical signs Tuberculosis is a chronic debilitating disease. The clinical signs in camelids include wasting, anorexia, respiratory distress, enlargement of superficial lymph nodes, recumbence and eventually death. Clinical signs are often associated with extensive respiratory pathology, and it is surprising that overt respiratory distress is sometimes not observed in animals with severe lung lesions. Animals are occasionally found dead with no previous clinical observations
Emaciated camel with suspicion T.B Pathology The pathology of Tb in camel was described nearly 100 years ago in cases detected in an Egyptian abattoir. Pathological reports on NWCs have also emerged in recent years. The organs most frequently affected in both groups of camelids are the lungs and associated thoracic lymph nodes, where typical caseo-necrotic lesions can be particularly extensive. Many authors mentioned that all cases in camel had lesions at these sites, 60% of cases exclusively involving these sites; other affected tissues included the liver, spleen, kidney, trachea and pericardium. Intestinal and cutaneous lesions have also been observed in llamas. The severity of pathological descriptions varies depending on how animals were selected for necropsy. Thus, animals selected following clinical disease often have severe pathology, whereas infected animals identified in ante-mortem immunological tests, and culled prior to development of clinical signs, are likely to have less severe gross lesions
Pulmonary tuberculosis in a dromedary bull with granulomatous pleuritis, consolidation and greyish discoloration of the lung
Cut surface of the same dromedary lung with grey appearance due to caseous granulomas of different shapes and sizes
Cut surface of a lung of a seropositive camel with central grey area due to tuberculous granulomas
Diagnosis A definitive diagnosis can be made only at post-mortem examination by demonstration of typical gross lesions, followed by histopathology and confirmatory bacterial culture. Mycobacteria are slow-growing organisms that may require incubation on selective media, such as Lowenstein-Jensen or Ogawa, for up to eight weeks. More rapid diagnosis can be made using polymerase chain reaction (PCR) assays. Initial identification of MTC bacteria can be made by targeting insertion sequences such as IS1081 or IS6110. Confirmation of mycobacterial species can then be made using primers for specific targets; for example, region of difference 4 (RD4) in M. bovis. In addition to providing a faster diagnosis than with traditional culture, PCR methods can also be used on formalin-fixed tissues when fresh samples are not available for culture; this approach was used to confirm Tb in an alpaca during investigation of a zoonotic incident. Nevertheless, there are currently some disadvantages associated with PCR. Firstly, it does not allow further discrimination of the isolate by molecular typing, which can be done using cultured isolates and is important for epidemiological studies. Secondly, poor sensitivity of PCR has been reported, possibly associated with low numbers and uneven distribution of the bacteria in tissues. Resilience of the mycobacterial cell wall inhibiting extraction of DNA may also affect the sensitivity of the assay, and, for fixed tissues, degradation of DNA associated with prolonged formalin fixation and the processing technique may be a factor In live animals, clinical diagnosis is often difficult because of the lack of specific signs. Ancillary ante-mortem tests would therefore be useful to confirm the diagnosis. None of the tests currently available, including the classic tuberculin skin test (TST) and various blood assays, can diagnose
Tb in camelids with certainty, and none has been properly validated in these animal species. Although estimates of sensitivity and specificity are provided in some reports, these calculations are usually of limited value because of the small number of animals studied. Bovine tuberculosis is a World Organisation for Animal Health (OIE) listed disease and testing of camelids should follow the OIE guidelines. The official Tb screening method for camelids traded internationally is the TST: the single intradermal comparative tuberculin test is used and the site of inoculation is the axilla (5). The axillary site was found to be superior to cervical and tail-fold sites in studies using small numbers of llamas and dromedaries. For statutory testing, purified protein derivatives of bovine and avian tuberculin (each 0.1 ml) are injected into a shaved area of the axilla, and the thickness of the skin is measured immediately before and 72 h after the injections. A positive result is indicated by an increase in skin thickness at the bovine site that is greater than the increase at the avian site. Some reports indicate that the TST has reasonable sensitivity and specificity, whereas others indicate a low predictive value. The reason for this variation between reports is not clear, but many causes of falsenegative and false-positive reactions have been proposed in cattle, and it is possible that these could also apply to camelids. The statutory 72 h interval between injection of tuberculin and measuring the response to injection is based on the protocol for cattle, which have a swelling of greatest intensity 48 h to 72 h post injection. In dromedaries, however, the most potent response to tuberculin was detected when skin thickness was recorded five days after tuberculin injection. It might therefore be the case in camelids that the optimal testing regime has yet to be identified. A negative impact of this lack of reliability in the interpretation of the TST results is that
testing for Tb in camelids has been discontinued in some zoological collections, resulting in reduced disease surveillance. From these observations it became obvious that any programme to control camelid Tb based only on the TST faces severe limitations. These findings have stimulated research into blood-based assays. Serological tests for the diagnosis of Tb have been developed since the 1980s and potentially offer a convenient and cost-effective means of Tb surveillance. Early attempts at developing enzyme- linked immunosorbent assays (ELISAs) did not convincingly discriminate between naturally infected and vaccinated animals and issues of cross-reactivity with other mycobacteria were not addressed. More recent serological tests include the multi-antigen print immunoassay (MAPIA) and the Vet TB Stat-3DNRUµUDSLG WHVW¶7KH MAPIA utilises a range of antigens printed onto nitrocellulose strips that are incubated with serum samples; the rapid test is a portable lateral-flow chromatographic assay that uses three MTC-specific antigens. These antigens have shown some promise for detecting MTC-infected camelids, but further validation is still required before they can be used reliably for field diagnosis. The discovery of immunodominant proteins will help to refine and improve the diagnostic accuracy of these assays in camelids: to date, MPB83 has been the most dominant antigen in sera from camelids infected with M. bovis and M. microti. The gamma interferon test (IFN-Ȗ DQGO\PSKRF\WH transformation assay are in vitro methods for measuring immune responses of circulating lymphocytes. The IFN-Ȗ test is acknowledged by the OIE as an alternative to the TST for internationally traded cattle but the currently used bovine IFN-Ȗ assay (Bovigam, Prionics, Switzerland) is unsuitable for camelids.
The lymphocyte transformation assay is not used for routine diagnosis because it is time consuming and complicated to perform. Scientists in New Zealand have developed a blood test for the diagnosis of Tb in deer, which combines the lymphocyte transformation assay with ELISA and haptoglobin tests. This method has also been used in alpacas but its diagnostic benefit has not yet been demonstrated.
Intradermal tuberculin test at the axilla of a dromedary Treatment and control Tuberculosis is a reportable disease in many countries and, where this is the case, control is the subject of statutory regulation, with culling of infected animals. Treatment of infected animals is therefore not usually attempted, although there are some reports of anti-Tb drugs being used in captive wild animals. After the diagnosis of Tb in two Bactrian camels kept in a zoo, prophylactic treatment of the remaining 17 camels was attempted using isoniazid incorporated into pelleted feed at a dose of 2.4 mg/kg, fed ad libitum. However, possibly due to isoniazid toxicity, several camels died, exhibiting signs of bone marrow suppression.
Streptomycin and rifampicin also been recommended by some authors. National control programs are often based on intradermal tuberculin testing, but because of the limitations of this test in camelids, these programs are unlikely to be successful; however, a combination of antemortem assays could improve the sensitivity of herd testing. Control depends on the removal of infected animals and prevention of further introduction of infection into the herd, but the disease will not be eradicated until infection is controlled in reservoir hosts, such as in wildlife. Vaccines are not yet available for camelids. 3. Anthrax: Anthrax is a serious infectious bacterial disease affecting all wild and domestic hoofed animals caused by Bacillus anthracis and takes an acute or a peracute form leading to septicaemia and sudden death, with or without clinical manifestations. The disease is well-known to nomads and camel breeders, hence the many local names and synonyms given to it by nomads and camel breeders in many countries. Infection takes place in camels mostly through the alimentary tract, by ingesting contaminated food or drinking from stagnant water. It is a zoonotic disease and is most common in wild and domestic herbivores such as cattle, sheep, goats, camels, antelopes. Humans get the infection when exposed to tissue from infected animals, to contaminated animal products, or directly to B anthracis spores under certain conditions. Aetiology Bacillus anthracis is a large, gram-positive, non-motile, spore-forming bacterial rod. The three virulence factors of Bacillus anthracis are edema toxin, lethal toxin, and a capsular antigen. B anthracis spores can remain viable in soil for many years. During this time, they are a potential source
of infection for grazing livestock but generally do not represent a direct risk of infection for people. Grazing animals may become infected when they ingest sufficient quantities of these spores from the soil. In addition to direct transmission, biting flies may mechanically transmit B anthracis spores from one animal to another. It is transmitted directly by biting flies, e.g. Tabanus species or nasal bots (Cephalopina titillator). Feed contaminated with bone or other meal from infected animals can serve as a source of infection for livestock. Clinical signs: Typically, the incubation period is 3± GD\V UDQJH í GD\V 7KH clinical course ranges from peracute to chronic. The peracute form is characterized by sudden onset and a rapidly fatal course. High fever, staggering, dyspnea, trembling, collapse, a few convulsive movements, and death may occur with only a brief evidence of illness. Painful swellings sometimes develop at the throat, the base of the neck and groins. These are particularly large when the palate becomes involved due to a local puncture in the nasopharynx by bots or other means. There may be bloody discharges from the natural body openings. Some infections are characterized by localized, subcutaneous, edematous swelling that can be quite extensive. Areas most frequently involved are the ventral neck, thorax, and shoulders. Death usually occurs within 2±3 days of onset. Depending on the route of infection, host factors, and potentially strainspecific factors, anthrax can have several different clinical presentations. In herbivores, anthrax commonly presents as an acute septicemia with a high fatality rate, often accompanied by hemorrhagic lymphadenitis.
Post mortem Lesions: Rigor mortis is frequently absent or incomplete. Dark blood may ooze from the mouth, nostrils, and anus with marked bloating and rapid body decomposition. If the carcass is inadvertently opened, septicemic lesions are seen. The blood is dark and thickened and fails to clot readily. Hemorrhages of various sizes are common on the serosal surfaces of the abdomen and thorax as well as on the epicardium and endocardium. Edematous, red-tinged effusions commonly are present under the serosa of various organs, between skeletal muscle groups, and in the subcutis. Hemorrhages frequently occur along the GI tract mucosa, and ulcers, particularly over Peyer's patches, may be present. An enlarged, dark red or black, soft, semifluid spleen is common. The liver, kidneys, and lymph nodes usually are congested and enlarged. Meningitis may be found if the skull is opened. Diagnosis 1. Clinical diagnosis Diagnosis based on clinical signs alone is difficult. Typical signs like sudden death without premonitory signs, dark foamy blood oozing from the natural orifices, dyspnea, staggering etc. can be suggestive of Anthrax 2. Identification of the agent Demonstration of encapsulated B. anthracis in smears of blood or tissues from fresh anthrax-infected carcasses and growth of the organism on blood agar plates is relatively uncomplicated.Recovery of B. anthracis from old decomposed carcasses, processed specimens (bone meal, hides), or environmental samples (contaminated soil) is often difficult, requiring demanding and labour-intensive procedures. However live spores may be
recovered from the turbinate bones ofdead livestock and wildlife for an extended period after death Culture and identification of Bacillus anthracis Fresh specimens Bacillus anthracis grows readily on most types of nutrient agar, however, 5±7% horse or sheep blood agar is the diagnostic medium of choice. Blood is the primary clinical material to examine. Swabs of blood, other body fluids or swabs taken from incisions in tissues or organs can be spread over blood agar plates. After overnight incubation at 37°C, B. anthracis colonies are grey-white to white, 0.3±0.5 cm in diameter, nonhaemolytic, with a ground-glass surface, and very tacky when teased with an inoculating loop. Tailing and prominent wisps of growth trailing back toward the parent colony, all in the same direction, are sometimes seen. This characteristic has EHHQGHVFULEHGDVDµPHGXVDKHDG¶ RU µFXUOHG KDLU¶ DSSHDUDQFH &RQILUPDWLRQ RI B. anthracis should be accomplished by the demonstration of a capsulated, spore-forming, Grampositive rod in blood culture.
B. anthracis µPHGXVDKHDG¶
Capsule visualisation Virulent encapsulated B. anthracis is present in tissues and blood and other body fluids from animals that have died from anthrax. Thin smears may be prepared from blood from ear veins or other peripheral veins and exudate from orifices. However if the animal has been dead more than 24 hours, the capsule may be difficult to detect. The bacteria should be looked for in smears of these specimens that have been dried, fixed either using heat or by dipping the smear in 95± 100% alcohol for about 1 minute and air dried and then stained with polychrome methylene blue 0DF)DG\HDQ¶V reaction). The capsule stains pink, whereas the bacillus cells stain dark blue. The cells are found in pairs or short chains and are often square-ended (the chains are sometimes likened to a set of railway carriages ± so-FDOOHGµER[FDU¶RUµMRLQWHGEDPERR-URG¶DSSHDUDQFH Identification of B. anthracis from old, decomposed specimens, processed materials, and environmental samples, including soil, is possible but these
samples often have saprophytic contaminants that outgrow and obscure B. anthracis on non-selective agars. Ascoli test Ascoli (1911) published a procedure for the detection of thermostable anthrax antigen in animal tissue being used for by-products. This uses antiserum raised in rabbits to produce a precipitin reaction. The test lacks high specificity, in that the thermostable antigens of B. anthracis are shared by other Bacillus spp., and is dependent on the probability that only B. anthracis would proliferate throughout the animal and deposit sufficient antigen to give a positive reaction. To perform the Ascoli test, put approximately 2 g of sample in 5 ml of saline containing 1/100 final concentration of acetic acid and boil for 5 minutes. The resultant solution is cooled and filtered through filter paper. A few drops of rabbit antiserum are placed in a small test tube. The filtrate from the previous step is gently layered over the top of the antiserum. A positive test is the formation of a visible precipitin band in under 15 minutes. Positive and negative control specimen suspensions should be included. Confirmation the diagnosis Specific diagnostic tests include bacterial culture, PCR tests, and fluorescent antibody stains to demonstrate the agent in blood films or tissues. Western blot and ELISA tests for antibody detection are available in some reference laboratories. Differential diagnosis: In Camels, anthrax must be differentiated from other conditions that cause sudden death. Clostridial infections, bloat, and lightning strike (or any cause of sudden death) may be confused with anthrax. Also, acute
leptospirosis,
bacillary
hemoglobinuria,
anaplasmosis,
and
acute
poisonings by bracken fern, sweet clover, and lead must be considered. Treatment and control Early treatment and vigorous implementation of a preventive program are essential to reduce losses. Camels at risk should be immediately treated with a long-acting antibiotic to stop all potential incubating infections. This is followed by vaccination 7±10 days after antibiotic treatment. Simultaneous use of antibiotics and vaccine is inappropriate, because available commercial vaccines are live vaccines. Suspected contaminated feed should be immediately removed. Parenteral administration of penicillin (10000 IU per Kg) may be triedin the early stages of the disease. Oxytetracycline given daily in divided doses also
is
effective.
Other
antibacterials,
including
amoxicillin,
chloramphenicol, ciprofloxacin, doxycycline, erythromycin, gentamicin, streptomycin, and sulfonamides also can be used, but their effectiveness in comparison with penicillin and the tetracyclines has not been evaluated under field conditions. Control measures are aimed at breaking the cycle of infection. Each of the following actions must be rigorously implemented: xCut off infection source and dispose of anthrax carcasses correctly xCorrectly disinfect, decontaminate and dispose of contaminated materials xVaccinate exposed susceptible animals and, where possible, humans in at-risk occupations xObservation of general sanitary procedures by people who handle diseased animals, both for their own safety and to prevent spread of the disease. Contaminated soils are very difficult to completely decontaminate,
but formaldehyde will be successful if the level is not excessive. The process generally requires removal of soil. Vaccination Camels can be immunised passively or actively by using hyperimmune serum, vaccine or both. A suspension of viable Bacillus anthracis Sterne Strain 34F2 spores in saponinis currently available. In areas where anthrax is known to be a problem, it is advisable to revaccinate annually approximately 4 weeks prior to the time the disease usually appears. For control of outbreaks, vaccination of all animals not showing symptoms is recommended. Not all animals will be protected by this procedure but taking action as suggested may stop further spread of the disease. It is also recommended that animals showing symptoms be isolated and treated with antibiotics as permitted. Animals being vaccinated or recently vaccinated should not receive antibiotics, as antibiotics will interfere with effective vaccination. Inject 1 ml subcutaneously into each animal. Revaccinate in 2-3 weeks in heavily contaminated areas In addition to therapy and immunization, specific control procedures are necessary to contain the disease and prevent its spread. Human infection is controlled through reducing infection in livestock, veterinary supervision of animal production and slaughter to reduce human contact with potentially infected livestock or animal products, and in some settings either pre-or post exposure prophylaxis. In countries where anthrax is common and vaccination coverage in livestock is low, people should avoid contact with livestock and animal products that were not inspected before and after slaughter. In general, consumption of meat from animals that have exhibited sudden death, meat obtained via emergency slaughter,
and meat of uncertain origin should be avoided. Routine vaccination against anthrax is indicated for individuals engaged in work involving large quantities or concentrations of B. anthracis cultures or activities with a high potential for aerosol production. 4. Pasteurellosis (Hemorrhagic septicemia) Hemorrhagic septicemia is an acute fatal disease of camels caused by Pasteurella multocida type A or several serotypes of Mannheimia haemolytica is characterized by fever ˬedema of the throat region, dyspnea, and sudden death P. multocida type A is considered to be a common inhabitant of the upper respiratory tract and it may cause disorders, in association with other microorganisms
such
as
parainfluenzatype 3 virus, in animals weakened by exposure to coldˬ malnutrition or gastrointestinal parasitism. Morbidity depends on immunity and environmental conditions, including both weather and husbandry; morbidity is higher when animals are herded closely, in poor condition, or exposed to wet conditions. Mortality is nearly 100% unless the animal is treated very early in the disease; few animals survive once they develop clinical signs. Predisposing factors: The worst epidemics occur during the rainy season, animals in poor physical condition. The disease is primarily found when the resistance of the body is lowered by harmful environmental influences such as transportation over long distances, deficiencies of dietary vitamins and minerals, concomitant infections, virulence factors, heavy parasitic infestation, and sudden changes in weather. It has also been observed that pasteurellosis is commonly observed in camels when there is a history of trypanosomiasis.
Transmission: P. multocida is transmitted by direct contact with infected animals and on fomites. Camel become infected when they ingest or inhale the causative organism, which probably originates in the nasopharynx of infected animals. Clinical Signs: Disease develops within 10 to 14 days (cough, dyspnea, mucopurulent nasal and occular discharges).Animals may die as a result of toxemia (young animals (2-3 days) before development of pulmonary lesions.
Mucopurulent nasal discharge There are three different clinical forms in camels with Pasteurella infection: peracute, acute, and abdominal forms. It has been suggested that the acute form is identical to hemorrhagic septicemia. Clinical signs of pasteurellosis include increased rectal temperature (40°C), pulse, and respiration rate, dyspnea, dullness, depression, and abdominal pain associated with hemorrhagic enteritis. There is subcutaneous swelling of the neck and between the mandibles.
Mandibular and cervical lymph nodes also become enlarged and painful. Affected camels also show signs of dilated nostrils and open-mouthed breathing. In some cases, there is a tar colored feces (melena), abdominal pain, and coffee colored urine. Prognosis is guarded in these cases. Both recovered and sick animals will discharge the organism through excretions and secretions of the body. Laboratory diagnosis. P. multocida is not always found in blood samples before the terminal stage of the disease, and is not consistently present in nasal secretions or body fluids of sick animals. Blood from tips of ears (from live animal only).In freshly dead animals, a heparinized blood sample or swab should be collected from the heart within a few hours of death, and a nasal swab. A long bone should be taken from animal that have been dead for a long time. Other visceral organs may also be sampled if a necropsy is not feasible, blood samples can be taken from the jugular vein by aspiration or incision; blood samples should be placed in a standard transport medium and transported on ice packs. Spleen and bone marrow provide excellent samples for the laboratory, as these are contaminated relatively late in the post-mortem process by other bacteria. The diagnosis of HS depends on the isolation of the causative organism, P. multocida, from the blood or bone marrow of a dead animal by cultural and biological methods, and the identification of the organism by biochemical, serological and molecular methods. Blood smears from affected animals can be stained with GraP /HLVKPDQ¶V RU PHWK\OHQH EOXH VWDLQV 7KH organisms appear as Gram-negative, bipolar-staining short bacilli. No conclusive diagnosis can be made on direct microscopic examinations alone.
Samples may be cultured on casein/sucrose/yeast agar containing 5% blood. Conventional blood agar may also be used. Details, including biochemical methods for identification of the organisms.Serotyping methods
include
the
rapid
slide
agglutination
test,
indirect
haemagglutination test, somatic antigen agglutination tests, agar gel immunodiffusion and counter immunoelectrophoresis. PCR technology can be applied for rapid, sensitive and specific detection of P. Multocida; the rapidity and high specificity of two of the P. multocida- specific assays provide optimal efficiency without the need for additional hybridisation Treatment: Antimicrobial susceptibility testing (AST) is particularly necessary for P. multocida for which resistance to commonly used antimicrobial agents has occurred. The following agents have proven their clinical efficacy: penicillin, amoxicillin (or ampicillin), cephalothin, ceftiofur, cefquinome, streptomycin,
gentamicin,
spectinomycin,
florfenicol,
tetracycline,
sulfonamides, trimethoprim/sulfamethoxazole, erythromycin, tilmicosin, enrofloxacin (or other loroquinolones), Amikacin and norfloxacin. Prevention: -Vaccination is routinely practiced in endemic Areas Three preparations are used ±dense bacterins combined with either alum adjuvant or oil adjuvant, and formalin- Inactivated bacterins; the oil adjuvant bacterin is thought to provide protection for up to one year and the alum bacterin for 4±6 months. Maternal antibody interferes with vaccine efficacy in calves.
5. Camel Plague: Plague, a deadly zoonosis caused by the Gram-negative bacterium Yersinia pestis. Y. pestis is mainly transmitted by fleas from tolerant rodents. Ticks of the genus Hyalomrna and Ornithodoros are also able to transmit the disease mechanically Plague has been reported to occur in camel and both Bactrians and dromedaries play an important role in the transmission to humans. Clinical Signs: The incubation tim'e in camels is 1 to 6 days followed by death within 20 days. There are two forms of plague. In bubonic plague, the bacteria reach the regional lymph nodes, which become inflamed, soft and may suppurate (buboes). Dissemination via the blood stream may lead to pneumonia and meningitis. The pneumonic plague is an airborne infection and droplets may allow aerosol infection between humans. This form of plague is fatal. Bubonic plague in camel, Mild fever developed and subsided in two to three weeks of infection. Small, rapidly healing abscesses developed at the site of inoculation. Subcutaneous lymph nodes all over the body were affected by acute or subacute purulent or non-purulent inflammation. In addition to a cutaneous manifestation, septicemic and pulmonary forms also occur in the camel. Treatment and prevention: Prevention involves eliminating contact with infected rodents, cats and rabbits and their fleas. Before necropsy of a plague-suspected camel is carried out, the entire carcass should be sprayed with insecticides to destroy any ectoparasites. Streptomycin and tetracyclines in combination are effective and, based on human cases, should be administered for at least 5
days. Many authors used a freeze-dried anti-plague vaccine for the immunization of camels; their immunity lasted for 6 months. A genetically modified vaccine against bubonic plaque has recently been developed in Britain, mainly to protect armed forces operating in countries where plaque occurs naturally and where Y. pestis may be used in biological warfare. 6. Enterotoxemia: All types of C. perfringens as well as C. soydellii and C. spiroforme can cause the enterotoxemia complex. C. perfringens, most frequently type A, is also found in the intestines of healthy animals so that cultural evidence of C. perfringens has little disease-predictive value. Enterotoxemia caused by C. perfringens is found all over the world and is also found in all types of domestic animals. The factors that predisposing to disease include dietary errors, climatic influences, change of pasture, transportation, and weighing of animals. Acute and subacute enterotoxemia as well as hemorrhagic enteritis due to C. perfringens, types A, C and D have been described in camels. Peracute and acute enterotoxemia in breeding and racing dromedaries as well as severe P\RFDUGLDOGHJHQHUDWLRQDQG³SXOS\ NLGQH\´LQGURPHGDU\ calves are known to occur. Clinical signs: The camels affected exhibited the following clinical signs: - Perspiration, muscle tremor, ataxia, aggression, hyperexcitability, seizures. Affected animals died within one hour after the onset of clinical signs.
Post mortem changes: The pathological changes found in autopsied animals were mild. They included - petechiae in the thoracic musculature, petechiae in the cerebellum and brain, petechiae in the pharyngeal mucosa, subpleural and subepicardial petechiae, petechiae in the mucosa of the third compartment and the stomach, hydropericardium with fibrinous exudate, dark kidneys, with adherence of the capsule to the parenchyma, hemorrhagic colitis.
C. perfringens enterotoxemia: subpleural hemorrhages
C. perfringens enterotoxemia: petechial hemorrhages in Compartment 3
The target organs for C. perfringens type A toxins in young dromedaries are the heart and kidneys. ´SXOS\ NLGQH\´ PD\ RFFXU LQ -6-week-old dromedary calves. Degeneration, calcification and necrosis of the myocardium in 3 to 5-week-old camel calves.
C. perfringens enterotoxemia: kidney capsule adherent to parenchyma
C. perfringens enterotoxemia in a young dromedary: severe myocardial degeneration Diagnosis: Depending on history of vaccination, history of mortality rate and post mortem changes.
Treatment and prevention: Treatment of sick dromedaries with a bovine C. perfringens hyperimmune serum is very rewarding. Many valuable racing camels were saved by the intravenous application of 100 mL of antiserum. This procedure can be repeated without any side effects. For the prevention of this important disease, sanitation, feeding and general husbandry
practices
should
be
optimal.
In
endangered
herds,
chlortetracyclines at a rate of 25 mg/kg feed should be added to the feed. Toxoid vaccines are commonly used to prevent enterotoxemia outbreaks in cattle, sheep and llamas.
References: Abbas, B., Agab, H., 2002. A review of camel brucellosis. Preventive Veterinary Medicine 55, 47±56. Abbas, B., El Zubeir, A.E.A., Yassin, T.T.M., 1987. Survey for certain zoonotic diseases in cDPHOV LQ 6XGDQ 5HYXH GHµ (OHYDJH HW 0HGLFLQH Veterinaire des Pays Tropicaux 40, 231±233. Abbas, B., Saint-Martin, G., Planchenauct, D., 1993. Constraints to camel production in eastern Sudan: a survey of pastoralists conception. Sudan Journal of Veterinary Science and Animal Husbandry 32 (1), 31±41. Abbas, B., Tilley, P., 1990. Pastoral management for protecting ecological balance in Halaib District, Red Sea Province, Sudan. Nomadic Peoples 29, 77±86. Abdel Moghney, F.R.A., 2004. A preliminary study on brucellosis on camels at Behira province. Assuit University Bulletin Environmental Researche 7, 39±43. Abdurahman O.S. & Bornstein S. (1991). ± Diseases of camels (Camelus dromedarius) in Somalia and prospects for better health. Nomadic Peoples, 29, 104±112. Abou-Eisha, M.J., 2000. Brucellosis in camels and its relation to public health. Assiut Veterinary Medicine Journal 44, 54±64. Abu Damir, H., Kenyon, S.J., khalfalla, E.A., Idris, F.O., 1984. Brucella antibodies in Sudanese camels. Tropical Animal Health and Production 16, 209±212. Abu Damir, H., Tag Eldin, M.H., Kenyon, S.J., Idris, O.F., 1989. Isolation of B. abortus from experimentally infected dromedary camels in Sudan: a preliminary report. Veterinary Research Communications 13, 403±406. Afzal, H., Sakkir, M., 1994. Survey of antibodies against various infectious disease agents in racing camels in Abu Dhabi, United Arab Emirates. Revue Scientifique HW7HFKQLTXHGHOµ2IILFH,QWHUQDWLRQDOGHV(SL]RRWLHV 13, 787±792. Agab, H., 1993. Epidemiology of Camel Diseases in Eastern Sudan with Emphasis on Brucellosis. M.V.Sc. Thesis. University of Khartoum. pp. 172.
Agab, H., Abbas, B., Ahmed, H.J., Mamoun, I.E., 1996. First report on the isolation of B. abortus biovar 3 from camels (Camelus dromedarius) in Sudan. Camel Newsletters 12, 52±55. Agab, H., Abbas, B., El Jack Ahmed, H., Maoun, I.E., 1994. First report on the isolation of Brucella abortus biovar 3 from camel (Camelus dromedarius) in the Sudan. Revue delevage et de medicine veterinarie des pays tropicaux 47, 361±363. Agrawal, R.P., Beniwal, R., Sharma, S., Kochar, D.K., Tuteja, F.C., Ghori, S.K., Sahani, M.S., 2005. Effect of raw camel milk in type 1 diabetic patients: 1 year randomised study. Journal of Camel Practice Research 12 (1), 27±31. Ahmad, R., Nemat, Z., 2007. Brucellosis of camels in Iran, Shahid Bahonar University of Kerman. Iran, Copyright 2007 Priory Lodge Education, priory.com. Ajmal, M., Ahmed, D.M., Arshad, M., 1989. Sero surveillance of brucellosis. Pakistan Veterinary Journal 9, 115±117. Al-Khalaf, S., El-Khaldi, A., 1989. Brucellosis of camels in Kuwait. Comparative Immunology, Microbiology and Infectious Diseases 12, 1±4. Alsaad KM (2009). Clinical, haematological and biochemical studies of anaplasmosis in Arabian one-humped camels (Camelus dromedarius). Journal of Animal and Veterinary Advances 8:1794-1797. Angesom Hadush1, 2*, Mahendra Pal1 , Tesfu Kassa3 and Fikre Zeru Journal of Veterinary Medicine and Animal Health -Vol. 5(9), pp. 269275, September, 2013: Sero-epidemiology of camel brucellosis in the Afar region of Northeast Ethiopia Anthrax (4thEdition) WHO 2008.3. Ayoub M, El-Khouly A and Mohamed T (2003). Some haematological and biochemical parameters and steroid hormone level in the one humped camel during different physiological conditions. Emirates Journal of Food and Agriculture 15:44-55. Bacterial diseases of dromedaries and bactrian camels, I.E.MUSTAFA Executive Vice-Chancellor, University of the Sudan in Kordofan. Barlow A.M., Mitchell K.A. & Visram K.H. (1999). ± Bovine tuberculosis in llama (Lama glama) in the UK. Vet. Rec., 145(22), 639±640.
Bekele T, Lundeheim N and Dahlbornemail K (2011). Milk production and feeding behaviour in the camel (Camelus dromedarius) during 4 watering regimens. Journal of Dairy Science 94:1310-1317. Bush M., Montali R.J., Phillips L.G. & Holobaugh P.A. (1990).± Bovine tuberculosis in a Bactrian camel herd: clinical,therapeutic, and pathologic findings. J. Zoo Wildl. Med., 21(2), 171±179. Coles EH (1986). Veterinary Clinical Pathology, 4th Ed. Saunders Comp. Philadelphia, London, Toronto, Schmidt. Connolly D.J., Dwyer P.J., Fagan J., Hayes M., Ryan E.G.,Costello E., Kilroy A. & More S.J. (2008). ± Tuberculosis in alpaca (Lama pacos) on a farm in Ireland. 2. Results of anepidemiological investigation. De la Rua-Domenech R., Goodchild A.T., Vordermeier H.M., Hewinson R.G., Christiansen K.H. & Clifton-Hadley R.S.(2006). ± Ante mortem diagnosis of tuberculosis in cattle: a UHYLHZ RI WKH WXEHUFXOLQ WHVWV Ȗinterferon assay and other ancillary diagnostic techniques. Res. vet. Sci., 81, 190±210. Dean G.S., Crawshaw T.R., de la Rua-Domenech R., Farrant L., Greenwald R., Higgins R.J., Lyashchenko K.,Vordermeier H.M. & Twomey D.F. (2009). ± Use of serological techniques for diagnosis of Dekker N.D.M. & van der Schaaf A. (1962). ± Open tuberculosis in a camel [in Dutch]. Tijdschr. Diergeneeskd., 87(17), 1133±1140. Dinkla E.T.B., Haagsma J., Kuyvenhoven J.V., Veen J. & Nieuwenhuijs J.H.M. (1991). ± Tuberculosis in imported alpacas in the Netherlands: a zoonosis ± now what? [inDutch]. Tijdschr. Diergeneeskd., 116(9), 454± 460. Donchenko A.S., Fatkeeva E.A., Kibasov M. & Zernova L.A.(1975). ± 'HVWUXFWLRQRIWXEHUFOHEDFLOOLLQFDPHOV¶ milk and µVKXEDW¶DODFWLFDFLG product [in Russian]. Veterinariya (Moscow), 2, 24±26. Elmossalami E., Siam M.A. & El Sergany M. (1971). ± Studies on tuberculous-like lesions in slaughtered camels. Zentralbl. Veterinärmed . B, 18(4), 253±261. Feldman, J* =LQNO DQG -DLQ 1& 6HKDOP¶V 9HWHULQDU\ Haematology, 5th Ed, Williams and Wilkins, Phildalphia and Baltimore.
Fowler M.E. (2010). ± Infectious diseases. In Medicine and surgery of camelids (M.E. Fowler, ed.), 3rd Ed. Wiley-Blackwell, Ames, Iowa, 173± 230. García-Bocanegra I., Barranco I., Rodríguez-Gómez I.M., Pérez B., Gómez-Laguna J., Rodríguez S., Ruiz-Villamayor E. & Perea A. (2010). ± Tuberculosis in alpacas (Lama pacos)caused by Mycobacterium bovis. J. clin. Microbiol., 48 (5), 1960±1964. Hawari Azmi Dawood American Journal of Agricultural and Biological Sciences 3 (3): 623-626, 2008: Brucellosis in Camels (Camelus dromedorius) in the south province of Jordan. Hesketh J.B., Mackintosh C.G. & Griffin J.F.T. (1994). ±Development of a diagnostic blood test for tuberculosis in alpacas (Lama pacos). NZ. vet. J ., 42(3), 104±109. Johnson C.T., Winkler C.E., Boughton E. & Penfold J.W.F. (1993). ± Mycobacterium kansasii infection in a llama. Vet. Rec., 133(10), 243±244. Johnson L.W., Thoen C.O. & Schultheiss P.C. (1989). ±Diagnostic procedures for detecting llamas exposed to mycobacteria. In Proc. 93rd Annual Meeting of the United States Animal Health Association (USAHA), 241±244. Kagramanov A.I., Blagodarnyi I.A., Makarevich N.M., Blekhman I.M. & Iakunin M.P. (1977). ± Ticks: a possible carrier of tubercular infection [in Russian]. Probl. Tuberk.,45(9), 60±64. Kinne J., Johnson B., Jahans K.L., Smith N.H., Ul-Haq A. & Wernery U. (2006). ± Camel tuberculosis: a case report. Trop. anim. Hlth Prod Littlewood W. (1888). ± Camel tuberculosis. Egyptian Official Lyashchenko K.P., Greenwald R., Esfandiari J., Meylan M., Burri I.H. & Zanolari P. (2007). ± Antibody responses in New World camelids with tuberculosis caused by Mycobacterium microti Vet. Microbiol., Lyashchenko K.P., Singh M., Colangeli R. & Gennaro M.L.(2000). ± A multi-antigen print immunoassay for thedevelopment of serological diagnosis of infectious diseases. J. immunol. Meth., 242(1±2), 91±100. Maymona A Mohammed, 2 Mohamed T Shigidy and 3 Abdulwahab Y Al juboori: International Journal of Animal and Veterinary Advances 5(2): 82
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Yaqoob, M., Nawaz, H., 2007. Potential of Pakistani camel for dairy and other uses. Animal Science Journal 78, 467±475. Zaki, R., 1948. Brucella infection among ewes, camels and pigs in Egypt. Journal of Comparative Pathology 58, 145±151.
&KDSWHU7ZR 9LUDOGLVHDVHV
9LUDOGLVHDVHV 1. Camel pox: +LJKO\FRQWDJLRXVYLUDOGLVHDVHRIFDPHOVUHODWHGWR3R[YLULGDHIDPLO\JHQXV 2UWKRSR[YLUXVFKDUDFWHUL]HGE\IHYHUDQGSR[OHVLRQRQVNLQDQGOHVLRQRQ PXFRXVPHPEUDQHRIUHVSLUDWRU\DQG*,7 (WLRORJ\ &DPHOSR[LVDZLGHVSUHDGLQIHFWLRXVYLUDOGLVHDVHRI2OG:RUOGFDPHOLGV 1HZ:RUOGFDPHOLGVDUHDOVRVXVFHSWLEOH7KHFDPHOSR[YLUXVEHORQJVWRWKH IDPLO\3R[YLULGDHVXEIDPLO\&KRUGRSR[YLULQDHJHQXV2UWKRSR[YLUXV
Method of transmission: By direct contact or indirect by contaminated environment (virus excreted in milk, nasal, eye and mouth discharge). Dried scabs shed from the pox lesions may contain live virus for at least 4 months and contaminate the environment. The virus has been isolated from camel ticks (Hyalomma dromedarii) removed from infected animals. It is believed that the ticks can transmit the disease from camel to camel. This theory is supported by increases in Camelpox infections immediately following heavy rains, during which the camel tick population increases greatly. Pathogenesis: Incubation period about (3 ±15 days) the onset of skin lesion after fever by 3 days average, the lesion begin as erythematous macules then to papules and vesicles which rupture and make pustules (due to secondary infection) or dry to form crusts, lesion may take up to 4 -6 weeks to heel, lesion begin in head then to neck and may be generalized to whole body , and may be extend to mucous membrane of GIT and respiratory tract.
Clinical signs: -The incubation period of Camelpox is between 3 and 15 days. The clinical manifestations range from inapparent infection to mild, moderate and, less commonly, severe systemic infection and death. The disease is characterized by fever, local or generalized pox lesions on the skin and in the mucous membranes of the mouth and respiratory tract. The lesions begin as papules and vesicles, and later turning into pustules. Crusts develop on the ruptured pustules. These external symptoms usually begin on the head, neck, eyelids, nostrils and the margins of the ears but eventually spread throughout the body, being especially concentrated on the limbs and genitalia.
Pox lesion in different area of the body
The disease occurs more frequently and more severely in young animals and pregnant females. Pregnant females may abort. Death is usually caused by secondary infections and septicaemia. Diagnosis: -Camelpox diagnosis can be based on symptoms. However, both Camel Contagious
Ecthyma
(Orf)
and
Camel
Papillomatosis
cause
indistinguishable symptoms under similar conditions. Several diagnostic methods are available and more than one should be used to make a confirmatory diagnosis of disease. Transmission electron microscopy (TEM):-The fastest method of confirmation the camelpox by the demonstration of the characteristic, brick-shaped orthopoxvirions in skin lesions, scabs or tissue samples. Immunohistochemistry:- Camelpox can be confirmed by demonstration of the camelpox antigen in scabs and pock lesions in tissues Virus isolation in cell cultures:- Camelpox virus shows typical cytopathic effect on a wide variety of cell cultures. Virus isolation on chorioallantoic membrane (CAM) of embryonated chicken eggs:- After 5 days, characteristic lesions can be observed on the CAM Polymerase chain reaction:- The presence of viral nucleic acid may be confirmed by polymerase chain reaction, and different strains of camelpox virus may be identified using DNA restriction enzyme analysis. Virus Neutralization test (VN):- In this method the test sera are titrated against a constant titter of camelpox virus. ELISA:-Detection of antibodies against camelpox virus.
Prevention and control: -Animal can be vaccinated by either live attenuated or inactivated vaccine. The live attenuated vaccine gives long-term protection against camelpox. However, a booster vaccination is recommended for young animals at the age of 8±12 months, 2±3 months after the initial vaccination to avoid interference by maternal antibodies. When inactivated vaccine is used, the animals must be vaccinated annually. The disease can be treated with antiviral medications. The most common medication used to treat Camelpox is Cidofovir, a broad spectrum antiviral that acts by inhibiting the viral DNA polymerase. Cidofovir has proven to be 100% effective at preventing death in infected camels. 2. Contagious ecthyma (ORF) orContagious pustular dermatitis: Highly contagious viral disease related to family (poxviridae) genus (parapox) affecting camel, sheep, goat, lama and some wild animals on the skin primarily around mouth. Methods of transmission: By direct contact or indirect by contaminated environment, unhealthy skin play a role in transmission. Morbidity from 10 ±80% of 2 -3 months old camel reach up to 100% in one year old camel, while, Mortality is less than 1% but may reach to 38% in young 1-3 months camel. Clinical signs: Fever reach 39 C , panting, show pain sometimes. Begin with pustules around lips of mouth transform to papules ending with scab formation may be cover all mouth lead to large and hard scabby lips. Head may be show swelling rather than normal. Lesion may be appear around lips of vagina , prepuce or around teat of udder.
Diagnosis: 1-Clinical signs. 2-Electron microscope. 3-Serology (ELISA). Differential diagnosis: 1-Pox. 2-Papilloma virus. 3-Reaction of insect pits. Treatment: The virus is mainly self-laminated with no specific successful treatment but some emollient medications contain antibiotic will be helpful (e.g: R/Scavon cream). Also antibiotic spray (e.g: terramycin spray).Antipyretic NSAIDs for fever and antibiotic injection for secondary bacterial infection. Supportive treatment like vitamin C injection or powder in water. The disease can be prevented by vaccination. 3. Rabies: Rabies is an acute, progressive viral encephalomyelitis that principally affects carnivores andbats, although any mammalincluding Camelcan be affected. The disease is fatal once clinicalsigns appear. Rabies is found throughout the world, but a few countries claim to be free of thedisease because of either successful elimination programs or their island status and Enforcement of rigorous quarantine regulations. Globally, the dog is the most importantreservoir, particularly in developing countries. Etiology Rabies is caused by lyssa viruses in the Rhabdovirus family. Lyssaviruses are usually confined to one major reservoir species in a given geographic area, although spillover to other species is common.
Clinical signs Transmission almost always occurs via introduction of virus-laden saliva into tissues, usually by the bite of a rabid animal. Most rabies cases in dogs develop within 21±80 days after exposure, but the incubation period may be shorter or considerably longer. The male camel was especially dangerous when showing the furious form of the disease, attacking and biting nearby objects and mutilating its own body. The clinical signs of the disease were restlessness, salivation and rotation of head and neck in all directions. These signs were soon followed by paralysis, recumbent and death. Results also showed that camels did not transmit rabies to humans. A rabid camel is usually segregated from the herd and left to die in the desert, or destroyed when aggressive. The clinical course may be divided into three general phases prodromal, acute excitative, and paralytic/end stage. During the prodromal period, which lasts ~1±3 days, animals show only vague nonspecific signs, which intensify rapidly. The disease progresses rapidly after the onset of paralysis, and death is virtually certain a few days thereafter. Some animals die rapidly without marked clinical signs. 7KHWHUP³IXULRXVUDELHV´UHIHUVWRDQLPDOVLQZKLFKDJJUHVVLRQ WKHDFXWH QHXUDOH[FLWDWLYHSKDVH LVSURQRXQFHG³'XPERUSDUDO\WLFUDELHV´UHIHUV to animals in which the behavioral changes are minimal, and the disease is manifest principally by paralysis. Some authors summarized the clinical signs symptoms of rabies in dromedary camels as hyper excitability, attacking inanimate objects, self -biting of forelimbs, salivation sternal recumbency, paralysis of hind legs, and death within 3-7 days.
Diagnosis Clinical diagnosis is difficult, especially in areas where rabies is uncommon, and should not be relied on when making public health decisions. In the early stages, rabies can easily be confused with other diseases or with normal aggressive tendencies. Therefore, when rabies is suspected and definitive diagnosis is required, laboratory confirmation is indicated. Suspect animals should be euthanized, and the head removed for laboratory shipment. Antigen detection 1. Fluorescent antibody (FA) test: A quick and easy procedure for the diagnosis of rabies is the use of a suitable dye for the detection of Negri bodies. Histopathological techniques have, however, been replaced in most laboratories by the fluorescent antibody (FA) test. The FA technique is a highly sensitive method for detecting rabies antigen in fresh specimens. It is recommended that fresh tissue be examined where possible. When specimens are received in 50% glycerol-saline, it is imperative that the tissue be washed several times in saline before staining. 2. Cell-culture isolation techniques: Fixed rabies viruses can grow in a wide variety of cells. Successful in vitro cultivation of rabies virus was first reported in 1936. Tests for the isolation of street rabies in cell culture were first carried out in the mid 1970s using baby hamster kidney cells, line 21 (BHK-21), and chick embryo-related (CER) and neuroblastoma cells. These studies demonstrated that rabies infection could be detected by immunofluorescence from as early as 4-5 hours up to 5 days following inoculation. 3.Enzyme-linked immunosorbent assay (ELISA): ELISA called rapid rabies enzyme immunodiagnosis (RREID), is based upon the detection of rabies virus nucleocapsid antigen in brain tissue. In this test, microplates
are coated with purified IgG and an IgG-peroxidase conjugate is used to react with immunocaptured antigen. RREID is a simple and relatively cheap technique, which can be especially useful for epidemiological surveys. It may be used to examine partially decomposed tissue specimens for evidence of rabies infection, but it cannot be used with specimens that have been fixed in formalin. Since the antigen can be visualized with the naked eye, the test can be carried out in laboratories that do not have the necessary equipment for FA tests. 4.Virus identification using monoclonal antibodies: Monoclonal antibodies are produced by hybridomas of fused mouse myeloma cells and splenocytes from mice immunized with either the rabies virus or rabiesrelated viruses. These hybridomas secreted monoclonal antibodies directed against the glycoprotein (G protein) or nucleocapsid of rabies virus. Although monoclonal antibodies are mainly used for epidemiological investigations, they were found to be very useful for rabies diagnosis in certain circumstances, such as imported cases of human rabies and rabies associated with uncertain exposure, and also routinely in countries where large-scale programs for oral vaccination of foxes are under way to establish that no infections are caused by the vaccine strain. 5. Intra vitam diagnosis: In addition to the brain and spinal cord, rabies virus antigen can be detected by FA in the peripheral nerves, salivary glands, saliva, and also in the cornea and skin during the final stages of the disease. Prevention and Control Comprehensive guidelines for control in dogs have been prepared internationally by the World Health Organization. They include the following: 1) Notification of suspected cases, and euthanasia of dogs with clinical signs and dogs bitten by a suspected rabid animal.
2) Reduction of contact rates between susceptible dogs by leash laws, dog movement control, and quarantine. 3) Mass immunization of dogs by campaigns and by continuing vaccination of young dogs. 4) Stray dog control and euthanasia of unvaccinated dogs with low levels of dependency on, or restriction by, people. 5) Dog registration. Many effective vaccines, such as modified-live virus, recombinant, and inactivated types, are available for use throughout the world. Recommended vaccination frequency is every 3 years after an initial series of two vaccines 1 year apart. Vaccines available for use in cattle and sheep can be used in Camels also. 4. Rift Valley Fever: Rift Valley fever (RVF) is a zoonotic viral disease that can affect a variety of species, including ruminants and camels, causing high mortality in young animals and/or abortions in adults. RVF virus (RVFV), a spherical enveloped RNA virus of the family Bunyaviridae and genus Phlebovirus is an arthropod- borne viral zoonotic disease that affects a wide range of animals including sheep, goats, cattle, camels and humans. The current theory is that RVFV is maintained in aedine mosquito eggs and epidemics occur following an increase in the mosquito population after abnormally heavy rains. Clinical signs: In camels, it presents as a sub-acute, acute or peracute disease, with sudden death in 100,000 oocysts/g of feces in severe outbreaks), but because diarrhea may precede the heavy output of oocysts by 1±2 days and may continue after the oocyst discharge has returned to low levels, it is not always possible to find oocysts in a single fecal sample; multiple fecal examinations of one animal or single fecal examinations of animals housed in the same environment may be required.
Oocysts of Old World Camelids: Eimeria dromedarii
Eimeria cameli
Treatment: Coccidiosis is a self-limiting disease. Following the multiplication stages in the intestine, recovery is often spontaneous and occurs without any specific treatment. Anticoccidials are used to control coccidiosis outbreaks in livestock. However, very little is known about the doses and efficacy of anticoccidial drugs in camelids. sulfadimethoxin (Theracanzan@ 5, 0 mg/kg i.m. for 3 to 5 days. In young animals, the authors recommend formosulfathiazol (SocatyP), 100-200 mg/ kg given orally for 3 to 5 days, and in severe cases in combination with Theracanzan@ Another drug is toltrazuril (Baycox@) which is given orally: 15-20 mg/kg for 3 to 5 days. Camels seem to be very susceptible to poisoning by ionophorous antibiotics, and overdosing with Salinomycin and Monensin has recently been reported in dromedaries. Poisoning is characterized by skeletal and heart muscle degeneration and splayed legs in conjunction with extremely elevated muscle enzymes. C. Ectoparasites: 1. Mange: Sarcoptic mange occurs in more than 100 species of mammals including humans. The disease in humans is generally referred to as scabies. The causative mite is Sarcoptes scabiei. The mite is thought to have a number of subspecies or variants, each designated according to which host it has been isolated from S. scabiei var. hominis, S. scabiei var cameli, S. scabiei var. aucheniae etc. Sarcoptic mange is regarded as one of the most prevalent and serious camel diseases. It is often ranked second in importance to all the disorders in dromedary camels, and second only to
trypanosomosis. It can generally be regarded as a chronic debilitating condition with high morbidity and low mortality. Life Cycle The developmental cycle of S. scabiei consists of egg, larval, protonymphal and tritonymphal stages. The sarcoptic mites differ from most other mange mites; they inhabit the epidermis of the skin excavating tunnels in the outer cell layers. The mites burrow in the stratum corneum through the dead cell layers until they reach living cells in the stratum granulosum and stratum spinosum. Due to the continual outgrowth of the epidermis the burrows containing the mites and eggs are mostly found in the comeum. The mites are rarely found beneath the stratum germinativum. The fertilized female lays her eggs in tunnels. Her lifespan is about four weeks and the development time from egg to adult is about 12 to 16 days. The eggs are produced at a rate of three to four daily. The eggs hatch in 35 days and larvae with three pairs of legs emerge. Clinical signs: The first signs of infection are small hyperemic papules often appearing on the medial aspect of the thighs or inguinal region, the head and neck, medial areas of the flanks, udder, and shoulder. In severe cases any part of the body may be affected. Most authors report that the humps and dorsal aspects of the neck are usually free of any signs of mange. However, it has been found that mangy lesions on the dorsum (including the hump) both in naturally and experimentally infected camels. These lesions are often accompanied by intense pruritus with excoriation and secondary infections. The itching and rubbing causes alopecia.
Hairless areas with serous exudation forming scabs follow the first acute signs and itching may increase, seriously disturbing the animals. Grazing and even milk production may show a rapid decrease. The camels desperately rub, bite and scratch trying to alleviate the extreme pruritus. The lesions spread and aggravate excoriation, alopecia, and crusting, resulting in more scabs. The latter may be rubbed away revealing a "red raw surface", erosions and wounds. Localized or generalized acute exudative dermatitis develops. If untreated, camels with severe acute sarcoptic mange decondition. Within a few weeks, the acute disease may develop to the chronic stage, which is the stage most often encountered in the field. Hyperkeratosis and proliferation of the dermis leads to the skin becoming thicker, fissured, and corrugated-appearing like a dried cracked field of clay. Camels with generalized mange may eventually die from extreme wasting caused by the reduction in normal feed intake due to intense irritation and pruritus.
Camel with extensive mange
Camel with mange
Diagnosis: Demonstration of mites in skin scrapings taken from the edge of the lesions.
Sarcoptic Mange
Differential Diagnosis Several skin diseases may mimic sarcoptic mange. These are: 1. Ringworm 2. Demzatopkilus congolensis (contagious 3. Infestations with other ectoparasites 4. Staphylococcus aureus dermatitis; 5. Endocrinal dermatopathy; 6. Inhalant or food allergies 7. Irritant dermatitis associated with contact with abrasive surfaces 8. Camel pox, particularly the papule and scab formation stages; 9. Idiopathic hyperkeratosis Treatment: These mites are superficial and are therefore not very sensitive to Ivermectin (200 µg/kg, sc.) but it may be an aid in controlling the foot mange. Dips and sprays may be used (Psaraptes avis). Ivermectin applied topically (500 µg/kg) is effective against chorioptic mange. Crotoxyphos (0.25%) applied as a spray can also be used against the leg mite. Chorioptic mange Today, chorioptic mange is a very common condition in many herds worldwide, particularly among alpacas. Clinical signs of chorioptic mange may mimic sarcoptic mange, but animals affected usually exhibit a milder pruritus and sometimes none at all (subclinical). Individuals with a heavy infestation may be free of any clinical signs of mange although others in the same herd with lower infestations may show severe extensive skin lesions. Often alopecia and scaling are seen on the feet. Often, as in sarcoptic mange, it is found between the toes and the base of the tail. Lesions may spread to the ventral abdomen, medial limbs and often the ears.
Lichenification and hyperpigmentation (greying of the skin) develop in chronic cases. The acute phase of the infestation might be due to a hypersensitivity reaction to the mites as is thought to be the case in the hosts' reaction to Psoroptes sp. infestations as well as against S. scabiei infections Psoroptic mange Psoroptic mange is often seen at predilection sites; pinnae and external ear canals, as erythema, crusting, papules, serum exudates and alopecia. Pruritus is evident emanating from these lesions. Typical lesions seen in the external ear canals are big flakes. Exudate occasionally appears, which is most likely due to secondary infections. Ears and parotid regions may sometimes become grossly swollen. However, lesions as well as pruritus may be generalized with or without involvement of the external ear canal. Other sites with lesions reported include nares, axillae, groin, neck, legs, abdomen, perineum, shoulders, back and its sides and the base of the tail. Intermittent bilateral ear twitching and head shaking may indicate otitis due to Psoroptes sp. infestations. The Psoroptes sp. of alpacas and llamas has previously been referred to as P. auchenia or P. communis auchinae, but adequate identifications of the different isolates of the mites have not yet been done.
Psoroptes spp. 2. Ticks: Ticks are obligate blood-feeding parasites of terrestrial vertebrates. They have worldwide distribution and cause tick worry, anemia, skin injury and sometimes tick paralysis during feeding on their host.In addition, ticks can act as vectors for some pathogenic agents including bacteria, virus and protozoa. This role of ticks is very important in public health and veterinary medicine. Hard ticks are very important type that infest the camel. Hard ticks are the most important external parasites of camel in the world and can easily constitute a limiting factor to successful stock farming unless appropriate measures are taken to control them. The geographic distributions of many original ticks are, however, not related with gross climatic conditions of the world, but rather with factors within the microclimate of the vegetation within their distribution variety. The most endemic tick species in Somalia are Rhipicephaluspulchelus, Hyalomma Dromedarii, Amblyomma Gamma and Amblyomma Variegatum.
The most important side effect of ticks is by damaging hide and skin of livestock including camels.
Hyalomma dromedarii male
Hyalomma dromedarii ± Female
Amblyomma spp.
Rhipicephalus pulchellus Clinical signs: Camels can be attacked by many different ticks. Ticks usually be found attached to the legs, head and the underbelly. If wounds are left untreated they will become infected with the maggots of different flies which feed on the blood and meat. Tick infestation are common in camel, They result in Swellings and small wounds in the skin from the bites, The tick feeds on blood and infections result in loss of blood, weight loss and weakening of the animal, Ticks can spread other diseases, Poisons from some ticks affect the nervous system and muscles and the animal cannot move (paralysis) which can lead to death. The camel suddenly shows signs of paralysis and its body temperature will drop.
Nostril of camel infested with tick
Udder region of camel infested with tick Diagnosis: Diagnosis is based on presence of ticks on the camel body. Treatment: Acaricides
to
the
predilection
sites
(chlorinated
hydrocarbons,
organophosphates, carbamates, synthetic pyrethroids or the macrocyclic lactones), can be used for treatment. A 1% flumethrin (BayticoP Bayer) pour-on formulation was successfully usedin controlling H. dromedarii infestations on camels. The drug (1 to 2mL/10kg) was poured from the shoulder along the middle of the back over the hump to the tail. Subcutaneous injections of ivermectin (10mg/50 kg) are effective in controlling both larvae and nymphs of the spinose ear tick There is no effective treatment that can neutralize the tick paralysis toxin. However, Ixodes hoZocyclus canine hyperimmune serum is used in affected small animals and calves (cattle) at a dose rate of 0.5 mL/kg curing about 75% of cases. This hyperimmune serum was used without success in tick paralysis of a llama caused by I. holocyclus.
3. Lice: Anoplurida (Sucking Lice) the only blood-sucking lice reported to occur both on Bactrians and dromedaries in Asia as well as in Africa is Microthoracius cameli. Lice infestation is characterized by licking, scratching and rubbing. Anemia may follow heavy infestations, particularly in young animals. The coat becomes rough and secondary bacterial infections may follow the pruritus. Infestation may result in damaged hides. Camel lice are generally only a problem in temperate regions where the animals have long winter hair. The llama and the alpaca may be infested with M. praelongiceps, M. mazzai and M. minor. Sucking lice are usually found around the head, neck and withers. They may be quite difficult to see with the naked eye, being smaller than the biting lice (two-thirds their size) and often hidden in the fiber, taking a blood meal.
Microthoracius cameli
Bovicola (syn Damalinia) (Lepikentron) breviceps The biting or the chewing louse, is more common in llamas than in alpacas. It has a blunt broad head that is distinctly different from the elongated mouthparts of sucking lice. Bovicola (Damalinia) breviceps is distinguished from other species of the genera by the morphology of their ventral terminalia and the configuration of their sclerites. Llamas and alpacas may be infested with three species of sucking lice, Microthoracius spp. (M. mazzai, M. praelongiceps and M. minor). The lice have a simple life cycle. Eggs (nits) are deposited by the female, are glued singly onto fibers close to the skin and give rise to three nymphal stages. The life cycle, egg to adult takes about 30-35 days, but some other authors reported that life cycle can be completed within 2-5 weeks. The adult female lays about 30 eggs during her lifetime of 15-40 days. Clinical signs of infestations of B. breviceps are often a lack of lustre and a ragged looking coat. Infested animals exhibit pruritus. Heavy infestations result in matting and loss of fibres, but do not seem to have negative effects on the quality of the fibres or pose any health risk to alpacas. Nevertheless severe infestations may result in a reduction of the price of the infested fleece. Clinical signs of Microthoracius spp are pruritus, restlessness, hair loss and poor growth. Severe infestations can cause anaemia.
Microthoracius mazzai (a sucking louse) Diagnosis is made on the bases of clinical signs and identifications of the lice in coat brushings. Searching for lice need bright light, parting of the fibres down to the skin, meticulous observation for movement of small `specks` and perhaps a magnification glass. The Microthoracius spp are seen partly imbedded in the skin taking a blood meal or clinging to a fibre. The characteristic eggs (nits) of the lice may be found attached to the fibres. However, few of the commonly used acaricidal substances and insecticides have been experimentally evaluated. $QXPEHURIDXWKRUVKDYHXVHGLYHUPHFWLQDWȝJNJE\VXEFXWDQHRXV injection with variable results against mange mite infestations. Some have employed higher doses, HJȝJNJDQGZLWKPRUHIUHTXHQW applications (even weekly) than the recommended standard dosages used for other livestock. Also topical use of products containing ivermectin, eprinomectin, doramectin and moxidectin have proved efficacious in some treatments, but not in others.
Perhaps an earlier recommendation to employ hand-dressing of the thick hyperkeratotic areas of the skin with water, soap and keratolytic agents, would shorten the recovery time and reduce the amount of acaricides used.
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Fungal diseases 1. Ring Worm (Dermatophytosis): Ringworm occurs commonly in young camels while camels above four years of age are apparently immune. The most commonly isolated dermatophytes are Trichophyton spp. and Microsporum sp. Fungal infections are more common during the cooler months, and three clinical forms have been described: superficial, follicular and generalized. The latter form is associated with loss of body condition and rather severe skin lesions, which are sometimes purulent. Clinical signs: Although camel owners are familiar with ringworm and are able to differentiate this dermatitis from other skin infections, dermatophytoses are extremely variable in their clinical appearances. There are two clinical types of ringworm in camels. The first shows typical lesions that are graywhite in color. These lesions are characterized by small, round alopecic areas, which may coalesce and mainly occur on the legs, neck and head of young animals.
Small, round alopecic areas with ring worm
Ring worm lesions in legs The second is a more generalized infection on head, neck, limbs and flanks whereby these lesions may initially be confused with mange. The disease is zoonotic and handlers often become infected, exhibiting typical ringworm lesions on their arms.
Typical circular ring worm lesions Diagnosis: Direct microscopic examination of hairs or skin scrapings might reveal
characteristic hyphae and/or arthrospores. However, fungal culture is the most effective and specific means of diagnosis, although growth usually requires 10 to 14 days of incubation. Hairs or scrapings from the periphery ofsuspicious areas are examined for fungal elements in a wet preparation (20% potassium hydroxide, KOH in water) that has been warmed and squashed out under a coverslip. A 10 to 20 min. incubation of the slide at room temperature should facilitate the microscopic examination. A fluorescent staining with Acridin Orange can make the identification of fungal spores and septate hyphae easier. Microsporum spp. and Trichophyton spp. as well as other fungi should be cultured on Sabouraud dextrose agar and on Mycoline agar slide (bioMerieux) and incubated for 10 to 14 days at 27°C. Definite diagnosis and species identification requires removal of hyphae and macroconidiae from the surface of the colony with acetate tape and microscopic examination with Lactophenol Cotton Blue (LPCB) stain. Culture on Mycoline agar slide is especially helpful when saprophytic contamination is expected. A number of keratin-proliferative dermatoses have been seen in camelids, and not all are caused by dermatophytes . It is therefore essential that any skin lesions should be carefully investigated and multiple deep skin scrapings (containing blood) should be dispatched for laboratory diagnosis.
Microsporum spp.
Trichophyton spp. Treatment and Prevention Lesions should firstly be scrubbed clean with warm soapy water and all scabs removed. A variety of common fungicidal and fungistatic agents such as iodine, 5% sulfur in sesame oil (w/v), 5% salicylic acid, coal tar phenols (3.25%) with copper acetate (0.58%) and hydroxyquinolines may be applied topically as ringworm ointments onto the affected areas. Captan@ is a fungicide for ornamental plants. The use of Captan@ has been advocated. Treatment of dermatophytoses with griseofulvin is very effective in cattle, but it causes side effects in camels such as nausea and diarrhea and is therefore not recommended. Successful vaccination programs against Trichophyton spp. and Microsporum spp. in camels have been reported from Kazakhstan. Camelvac Tricho@ (IDT Dessau-Tornau, Germany) has been used in the Republic of Kazakhstan, This vaccine is used with very good success not only for prophylactic but also for therapeutic purposes. Camels suffering from dermatophytoses were healed after one or two injections with Camelvac Tricho@.
2. Aspergillosis: Aspergillus spp., particularly A. furnigutus, are associated with infections of the respiratory system and of the placenta in livestock, but may also cause mastitis and rumenitis. Moldy litter and feed are often suspected as sources of infection in outbreaks of aspergillosis. Aspergillosis is an opportunistic fungal infection and has been reported in alpacas and dromedaries. Clinical signs Aspergillosis causing respiratory and enteric syndrome. The diseased camels had a diminished appetite and were lethargic. Some animals developed a mild, dry cough. In many cases there was a swelling of the throat with enlargement of the submandibular lymph nodes. In terminal cases, some camels also developed bloody diarrhea. Affected camels showed a slight increase in body temperature. Death occurred 5 to 7 days after the onset of the first clinical signs. Diagnosis: Tissue scrapings or any other material can be examined directly with KOH microscopically, and histopathological sections should be stained by the PAS stain. For the isolation of Aspergillus spp., Sabouraud, dextrose agar is used. Pieces of tissue are gently pushed into the agar and the culture is incubated at 37°C for up to 5 days. The colonies usually appear within 2 to 5 days of incubation. The identification is done by colonial morphology and microscopic appearance of the fruiting heads. Immunofluorescent procedures can be used to identify hyphae in tissue sections. The agar gel immunodiffusion test (AGID) for serum fungal antibodies is a reliable technique for diagnosis and an improved sensitivity may be possible with techniques such as ELISA.
Treatment: Treatment of aspergillosis has been unsatisfactory. Drugs used have included thiabendazole, flucytosine, and amphotericin B, but very little is known about their effect on camelids. The application of thiabendazole as an antifungal agent had no effect on the outcome of the disease in racing camels.
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