Advances in Biological Research 9 (4): 210-224, 2015ISSN 1992-0067© IDOSI Publications, 2015DOI: 10.5829/idosi.abr.2015.9.4.9516

Corresponding Author: Samuel Derso, Department of Veterinary Clinical Medicine, Faculty of Veterinary Medicine,University of Gondar, P.O.Box:196, Gondar, Ethiopia.

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Tick Borne Hemoparasitic Diseases of Ruminants: A Review

Yitayew Demessie and Samuel Derso

Department of Veterinary Clinical Medicine, Faculty of Veterinary Medicine,University of Gondar, P.O.Box:196, Gondar, Ethiopia

Abstract: Tick borne diseases are caused by different microorganisms and transmitted by ticks. They are themost prevalent and devastating diseases in the developing countries all over the world. The objective of thispaper is to review tick borne hemoparasitic diseases of ruminants. Tick borne hemoparasitic diseases ofruminants such as Anaplasmosis, Babesiosis and Theileriosis remain most important in tropics areas.Anaplasmosis, a rickettsial disease of blood caused by Anaplasma marginale and characterized by progressiveanemia, jaundice and fever without hemoglobinuria. Babesiosis is the other tick- borne disease caused byprotozoan of the genus Babesia and characterized by haemolytic anemia and fever, with hemoglobinuria. It isa disease with a world-wide distribution affecting many species of mammals with a major impact oncattle.Theilerioses is also a tick borne protozoal disease in ruminants caused by hemoprotozoan parasitesbelonging to the genus Theileria. Theileria parva, is the most pathogenic species in Africa cause a diseasecalled East coast fever which is characterized by enlargement of superficial lymph nodes and a sustainablefever. Losses from tick borne hemoparasitic diseases of ruminants like reduction of milk and meat production,restricting the introduction of susceptible cattle breed with superior genetics, costs from death and abortionas well as costs for treatment and control purposes are taking away the benefits of livestock owner and nation.Effective diagnosis of tick borne hemoparasitic diseases of ruminants is helpful to implement appropriateprevention and control strategies. Tick control, chemoprophylaxis and immunoprophylaxis are the basicmethods to control tick borne hemoparasitic diseases of ruminants.

Key words: Anaplamoisis Babesiosis Ruminant Theileriosis Tick Borne

INTRODUCTION resulting in anemia, jaundice, anorexia, weight loss and

Hemoparasitic diseases have a global distribution, is a reflection of complex interaction involving thestretching from the polar circle to the equator. This is due causative organisms, vector, the vertebrate hosts and theto the fact that their vectors, ticks and blood sucking flies environment [4].have a global distribution. Tick borne hemoparasites Arthropod transmitted hemoparasitic diseases areincludes all tick-borne organisms which are visible economically important vector-borne diseases of tropicalwith light microscope and which occur in the circulating and subtropical parts of the world including Ethiopia.blood as part of their normal life-cycle [1]. The most Tick borne hemoparasitic diseases of ruminants areimportant hemoparasites are Babesia, Theileria and caused by the Babesia, Theileria and Anaplasma speciesAnaplasma. These hemoparasites are transmitted through and all are intracellular parasite species [5].ticks [2]. Anaplasmosis is a vector borne infectious blood

Hemoparasites are of great economic impact on disease in cattle caused by the rickettsial parasites,livestock affecting 80% of the world cattle population and Anaplasma (A) marginale and A. central in cattle andcauses economic loss due to morbidity and mortality. A. ovis in small ruminants. It occurs primarily in wormHemoparasite is a major threat to food security especially tropical and subtropical areas. The disease is notamong the livestock dependent communities within the contagious but transmitted most commonly by ticks.sub saharan Africa [3]. Haemoparasites have generally It can also be transmitted via contaminated surgicalbeen shown to cause destruction of red blood cells instruments, biting flies and mosquitoes. The intracellular

infertility. The occurrence and importance of hemoparasite

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parasites destroy the red blood cells. It causes anemia, significant vectors in field and it has been shown thatfever, weight loss, breathlessness, uncoordinated strains of A. marginale also co –evolve with particularmovements, abortion and death [6]. tick strain. After feeding on an infected animal, trans

Babesiosis is a haemolytic disease caused by intra stadial transmission may occur. Transovarial transmissionerythrocytic protozoan of the genus Babesia. The disease may occur although even in a single host Boophilusis characterized by fever (40-42°C) which may be sudden species [6]. Anaplasmosis may also be spreadin onset, anemia, icterus, hemoglobinuria, listless, mechanically by infected hypodermic needle, castrating,anorexic, jaundice and death. It is a disease of small and spaying and dehorning instruments, blood transfusionlarge ruminants. Bovine babesiosis is caused by multiple and embryo transplant. Additionally intra uterinespecies: Babesia (B) bigemina, Babesia divergens, infections also occur in cattle but much less frequently inBabesia bovis and Babesia major. Two species, B. field cases than in experimental once. Anaplasma canbigemina and B. bovis, have a considerable impact on transmit by biting flies of the family Tabanidae [9].cattle health and productivity in tropical and subtropical Geographic distribution: Anaplasma is found endemiccountries [7, 8]. in all six populated continents of the world; mostly in the

Theilerioses is a group of tick borne disease caused tropics and subtropics because of the broad range ofby Theilaria (T) species. The most important species are vectors and the difficulties of efficient vector control [10].T. parva and T. annulata which result death in cattle in The disease is an important economical factor even withtropical and subtropical areas of the world [6]. Bovine a developed veterinary service [13].Theileria species cause severe and mild infections in their Risk factor: Breeds; Bos taurus breeds are more likelyhosts. Two of them, T. annulata and T. parva, cause to develop acute Anaplasmosis than crossbred Zebu, butlymphoprolipherative disease with high mortality and Bos indicus are not commonly affected because of theirmorbidity in cattle, commonly known as Tropical resistance to heavy tick resistance [14]. AnaplasmaTheileriosis and East Coast fever, respectively [9]. East species can cause infections in bovine population of allcoast fever is an acute disease of cattle and characterized age categories where severity and mortality rate increasesby high fever, swelling of the lymph nodes, dyspnea and with augmentation of animal age. Anaplasmosis infectionhigh mortality which has greater effect on Africa [6]. is higher in female than male animals due to hormonal

Control of tick borne hemoparasitic diseases of disturbances, due to its use in milk production, draughtruminants using effective methods such as vector control, power and breeding system which pose it to weakenedchemoprophylaxis and immunization is crucial to control immune system [5]. In temperate regions seasonaltick borne hemoparasitic diseases and to increase the occurrence of the disease is associated with theproductivity of animals by improving their health occurrence of the vectors in which prevalence ofconditions in the tropics and other parts of the world Anaplasmosis is found higher in hot and humid weatherwhere tick borne diseases are prevalent [9]. Therefore, the associated with the abundance of vector ticks [10].objective ofthis seminar paper is:

To review tick borne hemoparasitic diseases of ticks is complex and coordinated with the tick feedingruminants cycle (Figure 1). Infected erythrocytes taken into ticks

Tick Borne Hemoparasitic Diseases of Ruminant infection for tick gut cells. After development of A.Anaplasmosis marginale in tick gut cells, many other tick tissuesEtiology: Anaplasmosis is caused by the members of become infected, including the salivary glands, fromgenus Anaplasma (Rickettsiales: Anaplasmataceae). where the rickettsiae are transmitted to vertebrates duringIn cattle, this disease is caused by A. marginale and A. feeding. At each site of infection in ticks, A. marginalecentrale; later less pathogenic than former [10] where as develops within membrane bound vacuoles or colonies.in sheep and goats A. ovis is the important causative The first form of A. marginale seen within the colony isagent [11]. the reticulated (Vegetative) form, which divides by binary

Epidemiology: Transmission: Anaplasmoiss is not of organisms. The reticulated form then changes into thecontagious; numerous species of tick vectors (Boophilus, dense form, which is the infective form and can surviveDermacenter, Rhipicephalus, Ixodes and Hyalomma) can outside the host cells. Cattle become infected with A.transmit Anaplasma species [12]. Not all of those are likely marginale when the dense form is transmitted during tick

Life Cycle: The developmental cycle of A. marginale in

with the blood meal provide the source of A. marginale

fission, forming large colonies that may contain hundreds

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Fig. 1: Life cycle of A. marginale Source: Kocan et al. [14]

feeding via the salivary glands [14]. Once Anaplasma abortion and mortality without hemoglobinemia andentered in to the blood; the organisms enters the redblood cells by invaginating the cell membrane so that avacuole is formed; thereafter it divides to form aninclusion body containing up to eight initial bodiespacked together [15].

Pathogenesis: The incubation period of infection varieswith the number of organisms in the infective dose andranges from seven to 60 days, with an average of 28 day[14]. A.marginale invades and multiplies in red bloodcells. As the disease progresses, infected and evenuninfected red blood cells are destroyed mainly in theliver and spleen, resulting in progressive hemolyticanemia and even death in severe cases, the number ofinfected erythrocytes increases drastically andphagocytosis by reticuloendothelial cells of parasitizederythrocytes lead to development of hemolytic anemiaand icterus [11].

Depending upon the strain and the susceptibility ofthe host, from 10-90% of erythrocytes may be parasitizedin the acute stage of the infection [9]. Cattle that surviveacute infection develop persistent infections characterizedby cyclic low-level rickettsemia. Persistently infectedcattle have lifelong immunity and are resistant to clinicaldisease on challenge exposure. However, persistentlyinfected cattle serve as reservoirs of A. marginalebecause they provide a source of infective blood for bothmechanical and biological transmission by ticks [14].

Clinical Sign: Anaplasmosis ischaracterized by fever,weight loss, decreased milk production, pale mucousmembranes, severe anaemia, jaundice, hyper-excitability,

hemoglobinuria during acute phase of the infection [16].The most marked clinical signs of Anaplasmosis areanemia and jaundice, the latter occurring late in thedisease [17]. Affected animals may die suddenly fromhypoxia if they are handled roughly [18].

Diagnosis: Clinical diagnosis of Anaplasmosis isperformed by observing anemia, icterus and constipation.The presence of tick vectors or numerous biting Dipteramay give an additional indication [19]. In endemic areas,Anaplasmosis in adult cattle showing chronic anemiawithout haemoglobinuria leading to cachexia [20].

Microscopic examination of Giemsa stained bloodfilms Anaplasma inclusion in the red cells are usuallysufficient for diagnosis. Under microscope A. marginaleare seen as small, round, dark red ‘inclusion bodies’located near the periphery of red blood cells as indicatedin Figure. 2 [15].

Serological methods such as Enzyme-LinkedImmunosorbent Assay (ELISA), complement fixations test(CFT), or card agglutination test have been used to detectantibodies in animals which have recovered from infection[21]. CFT has been used extensively in the past, but, itlacks sensitivity and doesn’t detect some carrier. Cardagglutination test is sensitive, simple, rapid and can beused in the field. ELISA using a positive and negativeantigen can eliminate non-specific reaction [19]. For thedetermination of the persistently infected cattle moleculardiagnosis is mostly applicable [22].

At necropsy, pale and icteric carcass and organs,splenomegally, constipation, congestion of the liver andhardening of the omasum are indicative of Anaplasmosis[19].

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Fig. 2: Blood smear was analyzed by Giemsa staining antibiotics bears the risk of causing selection of resistantAnaplasma like structure is to detect in one of the strains [14].erythrocyte (Arrow). Source: Noaman et al. [22] The introduction of the disease into herds by carrier

Differential diagnosis: Anaplasmosis has to Attention should also be given to preventing iatrogenicdistinguish from other infections that cause fever, anemia, transmission with instruments used for injections oricterus in the absence of haemoglobinuria. Thus, the surgical operations by disinfection after use on eachfollowing diseases can be considered as differential animal. The eradication of Anaplasmosis is not adiagnosis: Babesiosis often associated with practicable procedure in most countries at the presenthaemoglobinuria and specific vector ticks are always time because of the wide range of insects which arepresent. Trypanosmosis occurs in regions infested by capable of carrying the disease,the long period oftsetse flies, tabanids and other biting flies. Theileriosis infectivity of carrier animals and, in some areas, theoften characterized by swollen lymph nodes and specific presence of carriers in the wild animal population [9].Invector ticks in the region.Certain intoxication by copper or endemic areas, control measures are aimed at minimizingplant [19]. stress in indigenous reared cattle [18].

Treatment: Tetracycline compounds are effective in Economic Importance: Bovine Anaplasmosis causestreatment if given early in the course of the disease and important economic loss in most countries, mainly due toespecially before the parasitaemia has reached its peak. the high morbidity and mortality in susceptible cattleTetracycline is effective when injected at five to ten herds. The losses due to Anaplasmosis are measuredmg/kg, provided the treatment is repeated two times at 24 through several parameters: low weight gain, reduction inhour interval. The treated animal is not free from milk production, abortion, the cost of AnaplasmosisAnaplasma after treatment, but can be eliminated treatments and mortality [14].completely by a longer treatment [19]. More recentlyimidocarb has been shown to be effective and may also Babesiosis: The disease also called piroplasmosis, Cattleused to sterilize carrier animals [15] tick fever, Red water fever or Taxes fever [8].

Symptomatic treatment such as blood transfusion,drugs that stimulates erythropiosis, drugs which protects Etiology: The causative agents of Babesiosis are specificliver cells may help recovery [19]. for particular species of animals. In cattle: B. bovis, B.

Prevention and Control: Methods for the control of motasi are known to be pathogenic agents in sheep andAnaplasmosis have consists of tick control with goats [23].acaricides, chemotherapy for prevention and vaccination.Weekly dipping in an acaricide is used in tropical areas to Epidemiology: Transmission: Babesia species iscontrol this disease. Animals that are to be introduced transmitted by hard ticks in which Babesia passesinto an enzootic area should be vaccinated. Vaccination transovarially, via the egg, from one tick generation to thehas been an economical and effective way to control next [24, 25].

bovine Anaplasmosis worldwide. Vaccines for the controlof Anaplasmosis can be divided into two major types: liveand killed vaccines. Both types of vaccines rely on theuse of A. marginale from infected bovine erythrocytes.Both types induce protective immunity that reduces orprevents clinical disease, but these vaccines do notprevent cattle from becoming persistently infected with A.marginale [9].

Chemotherapy, probably used more often forprevention of Anaplasmosis in the United States than inother areas of the world, is expensive and often notapplicable to range cattle and the intensive use of

animals should be prevented by prior serological testing.

bigemina, B. divergens and B. major [9].B. ovis and B.

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Geographic occurrence: Babesiosis occurs Life Cycle: Babesia multiplies in erythrocytes bythroughout the world [23]. However,the distribution of thecausative protozoa is governed by the geographical andseasonal distribution of the insect vectors [9]. The vectorof Babesia, Boophilus (B) microplus is wide spread intropics and subtropics [26].

Host occurrence: Bovine Babesiosis associated withB. bigemina and B. bovis is an important disease oftropical and sub tropical regions of the world. Bothspecies are transmitted transovarially by Boophilus ticks,but only tick larvae transmit B, bovis, where as nymphsand adults transmit B. bigemina and B. divergens. BovineBabesiosis transmitted by Ixodes ricinus is widespread.Small ruminants Babesiosis is caused by B. ovis [27].

Risk Factors: Host factor: Bos indicus breeds of cattleare more resistance to Babesiosis than Bos Taurus [28].This is a result of evolutionary relationship between Bosindicus cattle, Boophilus species and Babesia [9].Because of natural selection pressure, indigenouspopulations, having lived for a long time with local ticksand tick-borne diseases, have developed either an innateresistance or an innate ability to develop a good immuneresponse to the tick or tick-borne hemoparasitic diseasein question. Sheep were highly susceptible to B. ovis thangoats [29]. It is frequently stated that there is an inverseage resistance to Babesia infection in that young animalsare less susceptible to Babesiosis than older animals; thepossible reason is passive transfer of maternal antibodyvia colostrum. The severity of the clinical Babesiosisincreases with age [15, 30].

Pathogen Factor: Many Intra-erythrocyte hemoparasitessurvive the host immune system through rapid antigenicvariation which has been demonstrated for B. bovis andB. bigemina [9]. B. bovis is the most pathogenic organism,resulting in high mortality rates among susceptible cattle[31]. The effects of B. ovis are usually less severe than B.motasi [24].

Environmental Factor: There is a seasonal variation in theprevalence of clinical Babesiosis, the greatest incidenceoccurring soon after the peak of the tick population. Ofthe climatic factors, air temperature is the most importantbecause of its effect on tick activity; higher temperaturesincrease its occurrence.Heaviest losses occur in marginalareas where the tick population is highly variabledepending on the environmental conditions [9].Babesiosis infection in cattle mostly reaches peak insummer [7].

asynchronous binary fission, resulting in considerablepleomorphism (Figure. 3). This replication eventuallygives rise to gametocytes that are ingested by the vectortick. Conjugation of gametocytes occurs in the tick gutfollowed by multiplication by multiple fission andmigration to various tissues including the salivary glands.Further development occurs in the salivary glands beforetransmission. The ovaries are also invaded, which leadsto transovarial transmission [32]. The host gets theinfection when the larva sucks blood. After one moultingthe larva transforms into nymph which also infect as larva.Nymph transforms into adult after moulting and theytransmit infection in similar way [30]. The infective stageof Babesia, sporoziote, enters in to the host when the ticksucks blood [19].

Pathogenesis: Babesia produces acute disease by twoprinciple mechanism; hemolysis and circulatorydisturbance [33]. During the tick bite, sporozoites areinjected into the host and directly infect red blood cells.In the host, Babesia sporozoites develop into piroplasmsinside the infected erythrocyte resulting in two orsometimes four daughter cells that leave the host cell toinfect other erythrocytes [34]. It invades erythrocyte andcause intravascular and extravascular hemolysis [33].The rapidly dividing parasites in the red cells producerapid destruction of the erythrocytes with accompanyinghaemoglobinaemia, haemoglobinuria and fever. This maybe so acute as to cause death within a few days, duringwhich the packed cell volume falls below 20% which willlead to anemia. The parasitaemia, which is usuallydetectable once the clinical signs appear, may involvebetween 0.2% up to 45% of the red cells, depending onthe species of Babesia [25].

Clinical Sign: Affected animals suffered frommarked risein body temperature, loss of appetite, cessation ofrumination, labored breathing, emaciation, progressivehemolytic anemia, various degrees of jaundice (Icterus)from paleness in mild cases to severe yellow discolorationof conjunctival and vaginal mucous membranes in moreprogressive cases; haemoglobinuria, accelerated heartand respiratory rates, ocular problems and drop in milkproduction.The fever during infections in some casescause abortion to pregnant cattle [7]. Coffee colored urineis the characteristics clinical feature of Babesiosis [30].Babesia parasites cause both acute and persistentsubclinical disease in cattle [35].

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Fig. 3: Life-cycle diagram of Babesia speciesSource: Gray [32]

Ovine Babesiosis is a progressive hemolytic anemia Thin and Thick Blood Smears: Blood smeardisease of sheep [36]. High rise of body temperature, examination has been considered to be the standardanorexia, dyspnea, haemoglobinurea, emaciation, pale technique for routine diagnosis, particularly in acutemucous membrane, jaundice, constipation and cases, but not in sub-clinical infections where therecumbency were the main clinical signs in both sheep parasitemia is usually much lower [35, 39]. Thin bloodand goats. Chronically infected sheep are usually smears were the first method to detect Babesia parasitessymptomless, except for parasitemia and unthriftiness in clinical samples, a method still used today very[24]. Animals that recover from the acute disease remain effectively in most diagnostic laboratories.Blood isinfected for a number of years with B. bovis and a few usually collected, combined with an anticoagulant andmonths in the case of B. bigemina. No clinical signs smeared on a glass slide, air-dried, fixed with methanolappear during this carrier state [6]. and stained with Giemsa or a similar stain for several

Neurological signs are exhibited due to B. bovis minutes. The slide is then washed thoroughly and dried.infectionas erythrocytes get adhered to the capilliaries of Intra-erythrocytic parasites are observed under athe brain like nystagmus, circling movement, head microscope using a 100X objective and a drop ofpressing, hyperesthesia, convulsion, ataxia, teeth grinding immersion oil. The observation of paired Intra-and muscle tremor [30]. erythrocytic merozoites is indicative of infection but there

Diagnosis: Accurate and correct diagnosis of Babesial which present different forms and sizes depending on theinfections plays an important role in monitoring, species and these make their detection difficult and timemanagement and control of infection [35]. Clinical consuming [39]. B. bigemina is larger in size and havingsymptoms, because of their unspecificity, cannot be used paired structure at an acute angel to each other in theto make a correct diagnosis [37]. erythrocyte while B. bovis is smaller in size and having

Microscopy Detection Methods: Microscopic examination Merozoites of B. bovis are usually found in the center ofstill cheapest and fastest methods used to identify erythrocyte where as merozoites of B. bigeminaare pear-Babesia parasites [38]. Identification of the different shaped [20].B. motasi is pyriform in shape; B. ovis hasstages of the parasite in mammalian or arthropod host rounded shape and marginally located inside thetissues can be used for direct diagnosis purpose [39]. erythrocytes [40].

are other stages of the parasite like the trophozoites,

paired forming an obtuse angel to each other [7].

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Fig. 4: Giemsa stained Babesia species inside the bovine erythrocytes (Thin arrow) where as thick arrow shows anuninfected bovine erythrocyte. Source: Chaudhry et al. [26]

Another technique developed to detect low levels of IFAT is based on the recognition of parasite antigens byparasitemia, especially in cases where B. bovis is serum antibodies in the blood of the tested animal.It isinvolved, is based on thick smears of infected blood easy to do but requires a good quality antigen, which isstained with Giemsa (Figure. 4). The advantage of the difficult to obtain [39].thick smear is that a large amount of erythrocytes isanalyzed in a reduced amount of space; therefore the Molecular Diagnosis: Molecular methods aimed toprobability of finding infected cells is ten times higher detect nucleic acids have been very useful whenthan in the thin smear [39]. immunological methods do not work. Detecting nucleic

Brain Smears: When a bovine has died and it is are still considered indirect methods. However, thepresumed to be from Babesiosis caused by B. bovis due sensitivity and specificity of these methods are veryto presence of nervous clinical signs, identification of the high [39].parasite can be done by brain smears [26]. In this case, asmall sample of grey matter of the cerebral cortex is placed Polymerase Chain Reaction: PCR is more sensitive andon a slide and the tissue is smeared using another slide. specific technique and offers an alternative approach forThe brain tissue is fixed and stained. The diagnosis is the detection of Babesiosis [39]. An advantage of thisbased upon observation of brain capillaries filled with method is that it allows identification of the parasite in theinfected erythrocytes. Almost one hundred percent of early stage of disease which enables early diagnosis,erythrocytes present in the brain capillaries are infected. implementation of therapy and avoidance ofSmears of other organs as the kidney or liver can also be complications [37].carried out with good results [39].

Immunological Methods: Serological tests, including early diagnosis and the prompt administration of effectiveindirect fluorescent antibody test (IFAT) and ELISA are drug. The first specific drug used against bovinecapable of detecting antibodies of Babesia in sub-clinical Babesiosis was Trypan blue, which is a very effectiveinfections. Drawbacks of these tests are the occurrence of compound against B. bigemina infections, however, it didfalse-positive and false-negative results, involving cross- not have any effect on B. bovis and it had thereactive antibodies and/or atypical specific immune disadvantage of producing discoloration of animal’s flesh,responses [27]. Another drawback is that antibodies can so it is rarely used. Diminazene aceturate, which is widelybe detected even months after recovery of infection used currently in the tropics as a Babesiacide, wasthough no active infection is prevalent,so these methods withdrawn from Europe for marketing reasons [41].cannot help in revealing the exact picture of prevalence of Imidocarb is the principal Babesiacide used in animals, theinfection at that particular point [35]. only one that consistently clears the host of parasites and

IFAT is the most widely used test for the detection of for over 20 years, it has been used in the treatment andantibodies to B. bovis and B. bigemina but serological prophylaxis of Babesiosis and Anaplasmosi. Imidocarbcross reactions make species diagnosis difficult [26]. retained in edible tissues of ruminants for long periods

acids is an indirect way of detecting the parasite so they

Treatment: The success of the treatment depends on

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after treatment [39]. The combination of imidocarb the tick before the infective sporozoite develop in thedipropionate and oxytetracycline is the most effective salivary gland [25]. Significant factors currently affectingtreatment of Babesiosis in sheep and goats [24]. the control of Babesiosis and Anaplasmosis include

In addition, supportive therapy such as blood increased resistance to acaricides by ticks and thetransfusions, anti-inflammatory drugs, tick removal, iron numerous drawbacks of the current live vaccines [45].preparations, dextrose, vitamin B complex, purgatives andfluid replacements, may be necessary in severe cases of Economic Importance: Recently Babesia becomes theBabesiosis [39]. Vitamin E also acts as supportive therapy most widespread parasite due to exposure of 400 millionas vitamin E ameliorates the oxidative effect of Babesia by Cattle to infection through the world, with consequentincrease antioxidant effect [42]. heavy economic losses such as mortality, reduction in

Prevention and Control: Epidemiological surveillance is measures of ticks. Babesiosis, especially in cattle hasthe important aspect to control Babesiosis [43]. Active great economic importance, because unlike many otherprevention and control of Babesiosis is achieved by three parasitic diseases, it affects adults more severely thanmain methods: immunization, chemoprophylaxis and young cattle, leading to direct losses through death andvector control. Ideally, the three methods should be the restriction of movement of animals by quarantine lawsintegrated to make the most cost-effective use of each and [8, 46]. The disease is also a barrier to improvingalso to exploit breed resistance and the development and productivity of local cattle by cross-breeding due to themaintenance of enzootic stability [44]. high mortality of genetically superior but highly

Chemotherapy/chemoprophylaxis: Several groups of Babesia-free areas [47]. The consequence is that thecompounds have been used in the chemical control of quality of cattle in endemic areas remains low, thereforeBabesiosis. Of these, only imidocarb dipropionate, impeding the development of the cattle industry and thediminazene aceturate and tetracycline antibiotics remain wellbeing of producers and their families [39].freely available in most endemic countries.Chemoprophylaxis is not a viable long-term alternative to Theileriosiseffective immunization, but imidocarb and diminazene Etiology: Theileria species, tick transmitted, intracellularhave been used to protect cattle for several months protozoan parasites infecting leukocytes and erythrocytesagainst Babesiosis [44]. At dosage of three mg/kg, of wild and domestic large and small ruminants. In cattle:imidocarb provides protection for Babesiosis for around T. parva,T. annulata, T. mutans, T. velifera, T.four weeks and will eliminate B. bovis and B. bigemina tarurotragi and T. buffeli [19]. In small ruminants: T.from carrier animals [6]. lestoquardi, T. ovis and T. separate [30]. T. annulata and

Immunization: Using blood from carrier animals has been species of Theileria affecting cattle [48]. T. lestoquardipracticed for many years in tropical areas and more (formerly T hirci) is the most virulent species in sheep andrecently in Australia [15] Vaccination has been done with goats [6].varying degree of success with live and dead wholeparasite and isolated parasite antigen.Several findings Epidemiology: Transmission: Economically importantsupport the development of vaccines against Babesiosis. Theileria species that infect cattle and small ruminants areFirst, cattle which recover from a primary Babesia transmitted by ixodid ticks of the genera Rhipicephalus,infection or that have been immunized with attenuated Amblyomma, Hyalomma and Haemaphysali [49]. Theileriaparasites are resistant to challenge infection. Second, sporozoites are transmitted to animals in the saliva of theimmunization of cattle with native Babesia antigen extracts feeding tick [30].or culture-derived supernatants containing secreted The most economically important species in Africa isBabesia antigens elicit protective immunity against both T. parva [50]. Three subspecies are recognized in T.homologous and heterologous challenge [9]. parva, namely T. parva parva causing classical East

Vector Control: it is done by repeated treatment of cattle Corridor disease transmitted from buffalo to cattle and T.with acaricides in areas of high challenge; such treatment parva bovis, the causing agent of Zimbabwe Theileriosis,may require to be carried out twice weekly in order to kill a more benign form also known as “January disease“[50].

meat and milk yield and indirectly through control

susceptible cattle, especially dairy cattle, imported from

T. parva are considered to be the most pathogenic

Coast Fever (ECF). T. parva lawrencei responsible for

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Fig. 5: A generalized life cycle for the Theileria using T. parva as an example.Source: Mans et al. [57].

Table 1: A comparison of three species of Theileria of veterinary importanceSpecies Host Vector Disease DistributionT. parva Cattle Rhipicephalus East Coast Fever East and Central AfricaT. annulata Cattle Hyalomma Mediterranean or Tropical Theileriosis North Africa, South Europe, Middle East, AsiaT. hrici Sheep and goats Hyalomma Malignant ovine (caprine) Theileriosis North Africa, South Europe, Middle East. AsiaSource: Kaufaman [20]

It is important to emphasize that endemic region of T. hosts are their ability to exist free in the host cellannulata and T. parva do not overlap [51] however, there cytoplasm and their ability to transform the host cellwere reports of coexistence in southern Sudan [52]. reversibly, leading to uncontrolled proliferation of the

Host Sensitivity: T. parva is highly virulent for Europeandairy cattle, however, the indigenous cattle breeds and Environmental Factor: Theileriosis occurs when there isAfrican buffaloes in endemic areas have a natural much tick activity, mainly during summer but a single tickresistance to this Theileria species [9]. The introduction can cause fatal infection [55]. The pattern of seasonalof T. parva infection into a previously unexposed cattle occurrence of Rhipicephalus (R) appendiculatus (Vectorpopulation results in an epidemic situation with mortality of T. parva) is determined by climate [50]. R.up to 95% in all age categories of cattle. When the disease appendiculatus is most active following onset of rain,is established, the older animals that have survived outbreak of ECF may be seasonal or, where rainfall isprimary infection become immune. In these situations, relatively constant, may occur at any time [15]only calves and newly introduced stocks are at risk ofprimary infection and mortality is estimated high. T. Host Factor: Increasing age is associated with increasedannulata highly virulent for European dairy cattle but T. parva sero prevalence [56]. The frequency ofinfection in local breed cattle is mild [19]. T. hirci causes occurrence of ECF is higher in female than in male cattleclinical illness and mortalities in sheep than in goats [53]. [55].

Risk Factor Life Cycle: Generalized life cycles for the Theileria genusAgent Factor: The two unique features of the include secretion of infective sporozoites during tickleukoproliferative Theileria parasites in their vertebrate feeding into the feeding site (Figure 5). Sporozoites then

parasite and the host cell [54].

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infect leukocytes and multiply by merogony, after Clinical signs of ECF characterized, unlike Tropicalwhich merozoites are released, which invade redblood cells thereby establishing the piroplasm stage.During a next feeding cycle, larval or nymphal vectorticks ingest piroplasms and the released parasitesundergo syngamy in the tick gut, forming a zygote,the only diploid stage. The zygote divides into motilekinetes that infect the tick gut epithelial cells andmigrate to the haemolymph and subsequently infect thesalivary glands. After moulting and commencement offeeding by the tick, sporogony results in themultiplication of sporozoites in the salivary gland acinibefore injection into the feeding site by nymphs or adultticks [57].

Pathogenesis: Sporozoites of T. parva are injected intothe bovine host by the tick in its saliva. The sporozoitesthen enter lymphocytes and develop into schizonts in thelymph node draining the area of attachment of the tick,usually the parotid node. Infected lymphocytes aretransformed to lymphoblasts which continue to dividesynchronously with the schizonts so that each daughtercell is also infected [15]. Eventually, infectedlymphoblasts are disseminated throughout the lymphoidsystem and in non lymphoid organs where they continueto proliferate. Later, some schizonts differentiate intomerozoites, are released from the lymphoblasts and invadeerythrocytes which lead to development of anemia. Thedominating pathological lesion is generalized lymphoidproliferation resulting from uncontrolled proliferation of T-lymphocytes containing schizonts. This is followed laterby necrosis of infected lymphoblasts induced bycytotoxic T-Iymphocytes. The severe lymphocytolysisoften leads to immunosuppression. Terminally, the animaldevelops severe pulmonary edema, probably due torelease of vasoactive substances from lymphocytesdisintegrating in the lungs. Erythrocytic indices areusually unchanged, but there may be terminal anemia inJanuary disease [9].

Clinical Findings: Tropical Theileriosis of cattlecharacterized by lymphproliferative disordersassociated with lymph nodes enlargement in its earlyphases. The first lymph nodes involved are the prescapular lymph node as a result of the predilection sitesof the vector ticks and by lymph destructive disordersassociated with fever, pronounced leukopenia, diarrhea,lateral recumbency and marked anemia in its latephases[15] Weight loss, weakness, anorexia, conjunctivalpetechia and cough are the most common symptoms [58].

Theileriosis, by the absence or limited intensity of anemiaand high frequency of respiratory sign. Other symptomsinclude; diarrhea, corneal opacity leading to blindnessand subcutaneous edema [19]. In susceptible cattle, ECFis characterized by enlargement of superficial lymphnodes starting with the parotid lymph node, a sustainablefever and diverse clinical signs associated with invasionof non lymphoid tissues with parasitized lymphoblast.ECF causes high mortality with death occurringapproximately three weeks after infection, mainly as aresult of severe pulmonary oedema [59].

Malignant Theileriosis of sheep and goats is usuallyacute and highly fatal disease of adult animals manifestedby high fever associated with conjunctival and nasaldischarge, jaundice, enlargement of superficial lymphnodes,emaciation, reduced appetite, labored breathingand sometimes hemoglobinurea [60, 61].

Diagnosis: Tentative diagnosis of Theileriosis in the fieldis mainly based on clinical signs and tick infestation onthe infected animals. However, confirmation of thediagnosis depends on microscopic examination of bloodand lymph node smears stained with Giemsa in acutecases [58, 62].

Microscopic Examination: The presence of multinucleateintracytoplasmic and free schizonts, in lymph node biopsysmears, is a characteristic diagnostic feature of acuteinfections with T. parva and T. annulata [59]. Piroplasmof T. hirci appeared as a small oval, round or dotes- likeinside erythrocytes and machroschizont in largelymphocyte [60]. Microscopic examination alone is not afully reliable method of diagnosis unless coupled withother serological and molecular diagnostic assay [63].

Serological Diagnosis: The main weaknesses ofserological tick-borne disease diagnosis have beenreported as cross reactivity, low specificity and sensitivityand being poor at detecting low piroplasm levels in carrieranimals [64].

Molecular Diagnosis: PCR technique: PCR technique canbe used as a gold standard method and also can be usedfor screening of T annulata carrier cattle. PCR is highlysensitive and specific method, which used to detect therate of native carrier cattle harboring T. annulata [65].

Treatment: Chemotherapeutic agents such asparvaquone, buparvaquone which is givenintramuscularly and halofuginone, coccidostat given per

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Fig. 6: Giemsa stained blood smears of infected cattle reveal the presence of intra-erythrocytic forms (Arrows)morphologically compatible with theilerial piroplasms. Some of the infected erythrocytes showed morphologicaldisorders represented by round-shaped appearance and irregular thorn-like Protrusions. Source: Hassan [55]

orally are available to treat clinical T. parva and T. Quarantine measures, particularly with respect toannulata infections. Treatments with these agents do not importation of livestock from endemic areas into regionscompletely eradicate Theilerial infections leading to the where suitable tick vectors exist, are of great importancedevelopment of carrier states in their hosts [20]. [9].Oxytetracycline has a therapeutic effect if given at the Another method of Theileriosis control is cattletime of infection; they are no value in the treatment of movement restriction from Theileriosis-specified areas.clinical cases [25]. Movements within endemic areas are allowed. However,

Prevention and Control: The main methods in the allowed on the following conditions: the animals to beprevention control of ECF include tick control, cattle moved must test negative serologically by IFAT, they aremovement control, host immunization and chemotherapy treated with acaricide before they are moved to insure thatand integrated control that combines any of the methods they are tick-free, they are subjected to compulsoryGachohi et al. [56]. quarantine under close veterinary supervision [50].

Tick Control Methods: Includes direct application of Economic Importance: Tropical Theileriosis threatens anacaricides to cattle through dipping, spray races, hand estimated 250 million cattle and acts as a major constraintspray, pour-ons and hand dressing. However, acaricides on livestock production and improvement in manyhave their own disadvantages; they are expensive, ticks developing countries [67, 68]. Total economic lossescan easily develop resistance to them and they can be because of Tropical Theileriosis include three maindetrimental to the environment [56]. parameters: production losses, control costs and other

The most cost effective and sustainable control indirect economic losses [69].method is immunization. Vaccines against Theileriosis are T. parva infection poses a significant threat to theof two types; the sporozoite vaccine and the schizont livestock sector in two ways: through the economicvaccine but the latter is preferred [30]. Vaccination against impact of the disease from cattle morbidity and mortalityT. parva is based on a method of infection and treatment and production losses in all production systems, as wellin which cattle are given a subcutaneous dose of tick- as from the costs of the measures taken to control ticksderived sporozoites and a simultaneous treatment with a and the disease. The costs of acaricide application, whichlong-acting tetracycline formulation. This treatment is the primary means of tick control, is estimated to rangeresults in a mild or in apparent ECF reaction followed by between US$6 and US$36 per adult animal in Kenya,recovery [66]. Efforts have been made to produce anti tick Tanzania and Uganda. The disease further prevents thevaccination to immunize animal by using whole somatic introduction of the ECF susceptible but more productiveantigen of tick and protein of salivary gland [30]. exotic breeds of cattle, hampering the development of the

Chemotherapy: Oxytetracyclines are effective in incurred, directly and indirectly, by ECF are extremelycontrolling Theileriosis if given at the same time as high. With more than 38% of the African total bovineinfection as applied to block both parasite and disease population affected and an estimated mortality of 1.1development [50]. million cattle per year. ECF remains probably the most

movements from endemic areas to non-endemic areas are

livestock sector considerably [56]. The financial losses

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important cattle disease in terms of economic losses and immune response of cattle to ticks and parasites.restriction of livestock development in affected countries Therefore, based on this conclusion the followingof eastern, central and southern Africa [19]. ECF was recommendations are forwarded:estimated to have been responsible for 170 million USdollars worth of economic loss in 1989 alone and limits Economic losses from tick borne hemoparasticintroduction of more productive exotic (Bos taurus) cattle diseases ruminants are very high so that concernedin much of eastern, central and southern Africa [49]. organization should give attention to control and

Epidemiology of Tick Borne Hemoparasite of Ruminants Since chemical control can result in resistance andin Ethiopia: Tick borne hemoparasitic diseases environmental contamination, environmentally friendtransmitted by the major tick species in Ethiopia are control mechanisms like vaccination and biologicalAnaplasmosis, Babesiosis and benign Theileriosis. The methods should be further developed. principal biological vector of A. marginale namely B. Awareness should be created on mode ofdecoloratus, Hyalomma marginatumrufipes, transmission, control and prevention methods of tickRhipicephalus evertsi evertsi are prevalent in Ethiopia. borne hemoparasitic diseases to livestock owners.The vectors of B. bigemina in Ethiopia are B. decoloratus, Proper identification and characterization of ticksB. annulatus and Rhipicephalus evertsi evertsi. The involved in the transmission of disease should bevectors of T. mutans; Rhipicephalus evertsi evertsi and done to implement particular control strategy.Ambylomma variegatum are also commonly found in New vaccines and drugs should be designed thatdifferent regions of Ethiopia [70]. eliminates carrier states of hemoparasites in

In Cattle: T. velifera, T. mutans, T. orientalis complex andT. annulata were found in northern Ethiopia(Addis ACKNOWLDGEMENTSZemen, Humera andSheraro) in which T. annulata, thecause of Tropical Theileriosis, was the first report in In the first place, I would like to thank God for hisEthiopia, Humera. In small ruminants: T. ovis and T. invaluable gift and innumerable favor upon meseparata found also in these areas [71]. throughout all works of my life.

Indigenous cattle breeds such as Horro and Borna are Secondly, I would like to express my gratitude andmore resistance to tick infestation than others [70]. heartfelt thanks to my advisor Dr. Samuel Derso for his

CONCLUSION this paper. I also thank Dr Samson Leta the course

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