trypanosomiasis rohit

8/6/2019 trypanosomiasis rohit

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AN ASSIGNMENTON

TRYPANOSOMIASIS, THEILERIOSIS

& ANAPLASMOSIS

(VPP-608)

Submitted to:

Dr. B.J.Patel

Professor,

Dept. Of Veterinary Pathology,

College of Veterinary Science & A. H.,

S.D.A.U., Sardarkrushinagar.

Submitted by:

PARMAR ROHIT. S.

Reg. No. : 04-00617-2010M.V.Sc (scholar),

Veterinary Pathology,*************************************************************************************


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1. Trypanosoma: INTRODUCTION:

Trypanosoma is a genus of kinetoplastids (class Kinetoplastida), a monophyletic[1]

group of unicellular parasitic flagellate protozoa. The name is derived from theGreek trypano (borer) and soma (body) because of their corkscrew-like motion.All trypanosomes are heteroxenous (requiring more than one obligatory host tocomplete life cycle) and are transmitted via a vector. The majority of species aretransmitted by blood-feeding invertebrates, but there are different mechanismsamong the varying species. Then in the invertebrate host they are generally foundin the intestine and normally occupy the bloodstream or an intracellular environment in the mammalian host. Trypanosomes infect a variety of hosts andcause various diseases, including the fatal human diseases sleeping sickness,caused by Trypanosoma brucei , and Chagas disease, caused by Trypanosomacruzi . The mitochondrial genome of the Trypanosoma , as well as of other kinetoplastids, known as the kinetoplast, is made up of a highly complex series of catenated circles and minicircles and requires a cohort of proteins for organisationduring cell division.

E TIOLOGY:

Trypanosomiasis is the most important and serious pathogenic protozoal disease of camel caused by Trypanosoma species. This parasite has a wide range of distribution throughout tropical and sub-tropical regions of the world. T. evansiwas reported originally from India, where the term 'surra' is used to describe thedisease. In South Africa, another form of Trypanosomiasis is prevalent which isknown as "nagana". T. evansi can also cause the disease in other species e.g. cattle,

buffaloes, sheep, goats and horses. T. evansi probably evolved from T. bruce, whencamels entered the tsetse fly belt and acquired infection. Later, the disease wasmaintained via mechanical transmission by biting flies, notably Tabanus species,Haematopota and Pangonia and spread to the Northern Africa, Middle East, Indiaand the Far East Asian countries (Lukins, 1992). The difference in species dependson size and shape of the body, position of nucleus, degree of development of theundulating membrane and flagellum (Smyth, 1996). The objective of the present


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study was to identify the trypanosomes species prevalent in camels of Sind area of Pakistan and to find the comparative infection rate in different age and sex groupsof camels.

Selected species

Species of Trypanosoma include the following:

y T. ambystomae in amphibiansy T. antiquus Extinct (Fossil in Eocene amber)y T. avium , which causes trypanosomiasis in birdsy T. boissoni , in elasmobranchy T. brucei , which causes sleeping sickness in humans and nagana in cattley T. cruzi , which causes Chagas disease in humansy T. congolense , which causes nagana in ruminant livestock, horses and a wide

range of wildlifey T. equinum , in South American horses, transmitted via Tabanidae,y T. equiperdum , which causes dourine or covering sickness in horses and

other Equidaey T. evansi , which causes one form of the disease surra in certain animals (a

single case report of human infection in 2005 in India was successfully

treated with suramin)y T. everetti , in birdsy T. hosei in amphibiansy T. levisi , in ratsy T. melophagium , in sheep, transmitted via Melophagus ovinus y T. paddae , in birdsy T. parroti , in amphibiansy T. percae , in the species Perca fluviatilis y T. rangeli , believed to be nonpathogenic to humansy T. rotatorium , in amphibiansy T. rugosae , in amphibiansy T. sergenti , in amphibiansy T. simiae , which causes nagana in pigs. Its main reservoirs are warthogs and

bush pigs


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y T. sinipercae , in fishesy T. suis , which causes a different form of surray T. theileri , a large trypanosome infecting ruminantsy T. triglae , in marine teleostsy T. vivax , which causes the disease nagana, mainly in West Africa, although

it has spread to South America

Transmission:

African trypanosomiasis is transmitted by the tsetse fly of the genus Glossina.

T.brucei protozoa are carried in tsetse fly saliva. Humans are the main reservoir for T. brucei gambiense and wild and domestic animals such as antelope and cattle arethe main reservoirs for T. brucei rhodesiense. Tsetse flies are grey-brown insectsthe size of a honey bee. They inhabit savannah areas, including game reserves andthrive in shade and humidity. American trypanosomiasis is transmitted throughcontact with the faeces of an infected reduviid (cone nose or kissing) bug(Triatoma infestans). The bugs inhabit walls and roofs of poorly constructedhousing such as that made of mud and thatch. T. cruzi are excreted in the faeces of the bug and inoculated into the blood stream through skin or mucous membranesduring feeding, or when the bite is scratched.Transmission of both species can also occur via blood transfusion, contaminatedneedles, or the congenital route.

Pathogenesis :

y The pathogenesis of trypanosomiasis of the CNS. Studies onparasitological and neurohistological findings in trypanosomarhodesiense infected vervet monkeys.


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Parasitological examinations of the cerebrospinal fluid of 20 vervet monkeys(Cercopithecus aethiops), that had been infected with Trypanosoma rhodesiense,revealed that the CSF was regularly infested with trypanosomes in the early phaseof the disease, at the earliest on the 13th day, in most of the animals in the 3rd or

4th week, after infection. Follow-up examinations of the CSF during the further course of the disease also regularly proved positive for trypanosomes. Histologicalstudies in the animals that died at a mean of 65 days after infection (range 35 to107 days) revealed encephalitis in the animal with the longest course of thedisease. In all the other animals, meningitis alone was found. This wasaccompanied by a modified early encephalitic reaction, characterized by lympho-

plasma-cellular infiltrates exclusively in the adventitial sheaths of those bloodvessels passing into the brain from the leptomeninges affected by inflammatory

infiltration. The early encephalitic reaction is interpreted as the morphologicalmanifestation of an infestation of the perivascular spaces (Virchow-Robin spaces)with parasites. It indicates that CSF parasitosis in the early phase represents the

point of departure for the encephalitis that develops in the late phase of thedisease, and that the encephalitis presumably develops as a result of the migrationof the trypanosomes out of the subarachnoid space into the perivascular spaces,and from there into the brain.

y Pathogenesis of Trypanosoma brucei infection in sheep : III.Hypophysial and other endocrine lesions.

Sheep experimentally infected with Trypanosoma brucei for 2 to 5 monthsdeveloped lesions in the pituitary body, thyroid and adrenal cortex, but not in theadrenal medulla, pancreas and parathyroid. Neurohypophysial lesions werecharacterized by gliosis and perivascular mononuclear infiltration extending to thesurrounding meninges. In the adenohypophysis, oedema, acute coagulativenecrosis and fibrosis were observed. Adrenal cortical hypertrophy and atrophy of the thyroid were the other endocrine lesions. There was massive localization of trypanosomes (so-called amastigote forms) in the interstitial tissue of the adeno-and neuro-hypophysis, but not in the other endocrine glands. It was suggested thattrypanosome-induced pituitary damage might explain some of the clinical signs inanimal trypanosomiasis, as is the case in human sleeping sickness.


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y Pathogenesis of African Trypanosomiasis

PRIMARY STAG E .

When metacyclic trypomastigotes are introduced subcutaneously and multiply.

In 2-3 days there is itching, swelling, pain and redness, and after 6 days atrypanosomal chancre may develop at the bite site. This is considered by most to

be an innocent boil and is disregarded.

BLOOD STAG E

The earliest sign of a generalized infection is fever; there may also be malaise,headache and pains in the joints. Five to12 days after infection trypanosomes are

found in the bloodstream. They are scanty in T. gambiense , and more abundanti.e.10 5/ml in T. rhodesiense. Trypanosomes also enter the lymphatics and there islymphadenopathy. Especially characteristic in T. gambiens e is the enlargedcervical lymph nodes, called Winterbottoms sign. The influx of B-cells results inlymph node enlargement and the lysis of trypanosomes release toxic materials thatstimulate macrophages to release tumor necrosis factor (TNF, also calledcachectin) and this produce cachexia. The release of trypanosome toxic factors andlymphokines gives rise to a cyclic (or relapsing) fever with an approximate cycleof 7-10 days.

LAT E STAG E

In the Rhodesian form there is a rapid illness with invasion of the CNS vialymphatics within a few weeks. Patients may die of myocarditis even before theCNS is invaded. In the Gambian form the disease progresses in a more insidiousfashion with personality changes, insomnia or irritability signaling invasion of theCNS. CNS involvement may not occur until one or more years after infection.Inflammatory changes lead to a demyelinating meningoencephalitis; there iscerebral edema, hemorrhages, pericarditis, and anemia. The encephalopathy leadsto apathy, somnolence and coma. Death is usually caused by intercurrent infectionssuch as pneumonia.


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The anemia seen in trypanosomiasis may be due to coating of host red blood cellswith trypanosome surface coat proteins and reaction with antibody to the variantantigens; demyelination may result from cross reactivity of anti-galactocerebrosideautoantibodies with a proteolipidic epitope of T. brucei . In experimental infections,

toxic metabolites of aromatic (ring) amino acids such as tryptophan, phenylalanineand tyrosine can produce anesthetic effects, damage blood vessels, inducetemperature changes, immunosuppression and somnolence.

Signs and Symptoms

African trypanosomiasisThere are two types of illness, east African trypanosomiasis caused by T. bruceirhodesiense, and west African trypanosomiasis caused by T.brucei gambiense. EastAfrican trypanosomiasis is a more acute illness with a rapidly progressive course.The first symptom to occur is a skin reaction at the site of the tsetse fly bite, knownas a trypanosomal chancre. This is commonly accompanied by regionallymphadenopathy and is more likely to occur in the east African disease.Following this local reaction the parasites disseminate and cause an irregular

pattern of fever persisting for several weeks. At this stage the symptoms of eastAfrican trypanosomiasis can be severe and if left untreated approximately 10% of infections are fatal.

During the next stage of the illness, trypanosomes cross the blood-brain barrier and cause encephalopathy with headache and mental status changes. Thisoccurs within weeks in the east African trypanosomiasis and within months withthe west African form. As the disease progresses to the terminal stage, patients

become comatose which gives the disease its name of sleeping sickness.

American trypanosomiasis

The initial acute phase of Chagas disease can often go undetected due to thenonspecific signs and symptoms of vomiting, diarrhoea and anorexia. A cutaneouslesion at the site of exposure to infected bug faeces can develop. If the organism


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enters via the eye, unilateral conjunctivitis and oedema may be present which isknown as Romaa sign. This acute phase is then followed by an indeterminate

phase with no clinical symptoms, and may last for the life of the patient. However,some patients will develop chagastic heart disease, with symptoms of palpitations,

chest pain, oedema,syncope and dyspnoea and occasionally sudden death. Cardiac embolism can alsooccur. In addition to cardiac disease a small number of patients developabnormalities of the alimentary tract, with regurgitation, dysphagia, loss of

peristalsis and constipation. This syndrome is termed mega disease.

Treatment

Travellers suspected of having trypanosomiasis should be referred to atropical disease specialist.

Parasites of both forms of illness can be detected in blood films, and inAfrican trypanosomiasis from the initial chancre.

There are several drugs available for the treatment of acute illness of bothAfrican trypanosomiasis and Chagas disease, but these have little effect onthe chronic stage of Chagas disease.

The cardiac and intestinal complications of Chagas are managed by

symptomatic therapy and occasionally with surgical intervention.

Prevention

There is no vaccine or chemoprophylaxis against trypanosomiasis. Awareness of risk and insect bite avoidance is therefore the only method of preventing infection.Tsetse flies are attracted by movement and the colour blue. They have been knownto follow moving vehicles; therefore windows should remain closed when drivingthrough endemic areas. Tsetse flies are also capable of biting through loose weave

fabrics and are unaffected by many insect repellents. Travellers are advised to wear insecticide treated close weave clothing. Reduviid bugs inhabit cracks in the wallsand roof of buildings constructed with mud or thatch. Travellers residing in suchaccommodation should sleep under a mosquito net and treat bedding with aninsecticide solution.


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Reference

J elinek T, Bisoffi Z, Bonazzi L et al. Cluster of African trypanosomiasis in

travellers to Tanzanian national parks. Emerging Infect. Dis. 2002; 8: 634-635


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2 . A naplasmosis

INTRODUCTION:E TIOLOGY:-

Anaplasmosis is an infectious disease of cattle caused by several species of the blood parasite Anaplasma . A. marginale is the most common pathogen of cattle .(Smith, B.P.) Sheep and goats are much less commonly affected. Anaplasmosis isalso called yellow bag or yellow fever as affected animals can develop a jaun-diced appearance. Anaplasmosis is seen worldwide and has been reported in atleast 40 states in the U.S. (Smith, B.P.) It is a common disease in the southern U.S.The highest incidence of anaplasmosis in Virginia seems to occur throughout thePiedmont area of Central Virginia. It is an important disease in Virginia as it tendsto cause outbreaks in a herd, which can lead to the death of adult cattle. Other economic losses include abortions, decreased weight gain, bull infertility, andtreatment costs. (Stokka and Faulkner. 2000).

The onset of the infection, after an incubation period of 4 to 6 weeks, ismarked by depression and fever and, in milking herds, a rapid drop in production.The infected animal becomes weak, separates from the herd, and may befrightened easily. The moist surfaces around the eyes and muzzle become yellow.As the disease progresses, the animal shows dehydration, constipation, markedanemia, extreme weakness, anorexia and a stiff unsteady gait. Animals that survivegradually recover but remain carriers.

Life cycle

The organism can go through a complete lifecycle in the gut of certain species of ticks but the flies appear to be only a mechanical vector, thus, not as important inmaintaining the disease in any given area. The disease causes severe anemia andwasting in infected adult cattle. Young cattle and most other ruminants will notshow clinical signs if infected but may serve as carriers. Since the organism"hides" from the body's immune system in red blood cells, it is difficult if not


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impossible for an infection to be totally cleared. As the immune response wanes,the organism again builds up and the host relapses.

Distribution

In the United States, anaplasmosis is notably present in the south and west wherethe tick hosts Dermacentor spp. are found. Although vaccines have beendeveloped, none is currently available in the United States. Early in the 20thcentury, this disease was considered one of major economic consequence in thewestern United States. In the 1980s and 1990s, control of ticks through newacaricides and practical treatment with prolonged-action antibiotics, notablytetracycline, has led to the point where the disease is no longer considered a major

problem.

Cases of coinfection with tick-born microorganisms are being increasinglyreported in the last decade perhaps explaining the variable manifestations andclinical responses noted in some patients with tick-transmitted diseases. In suchclinical settings, laboratory testing for coinfection is indicated to ensure that

appropriate antimicrobial treatment is given.

In 2005, Anaplasma ovis was found in reindeer populations in Mongolia.( Haigh J .et al .,2005) This pathogen and its associated syndrome (characterized by lethargy,fever and pale mucous membranes) was previously only observed in wild sheepand goats in the region, and is the first observed event of A. ovis in reindeer.

Transmission A. marginale can be transmitted two different ways. First, it can be transmittedmechanically when red blood cells infected with A. marginale are inoculated intosusceptible cattle. This can occur through needles, dehorners, ear taggers,castrating knives or other surgical instruments, and tattoo instruments. Mechanical


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transmission can also occur through the mouthparts of biting insects, such as bitingflies. Face flies, houseflies, and other non-biting insects do not transmit thedisease. Horn flies, although they bite, typically do not go from animal to animalso they are not thought to spread Anaplasma . Mechanical transmission of infected

red blood cells must occur within a few minutes of the blood leaving the infectedanimal, as the blood parasite does not survive more than a few minutes outside theanimal.

Second, Anaplasma can be transmitted through its biological vector. The parasitereceives nourishment from, and may even multiply in, the biological vector. The

biological vector for anaplasmosis is the dermacentor , or wood, ticks. Once in thetick, the parasite can remain active throughout the lifecycle of the tick and can betransmitted several months later.

Once susceptible cattle are infected with Anaplasma , the organism multiplies inthe bloodstream and attaches to the animals red blood cells. The animals immunesystem destroys the infected red blood cells in an attempt to fight off the infection.Unfortunately, uninfected blood cells are also destroyed. When the number of

blood cells being destroyed exceeds the number of blood cells that the body can produce, the animal becomes anemic. It takes 3 to 6 weeks for clinical signs to

appear after the animal is infected. (Smith, B.P., 2002).The onset of the infection, after an incubation period of 4 to 6 weeks, is marked bydepression and fever and, in milking herds, a rapid drop in production. Theinfected animal becomes weak, separates from the herd, and may be frightenedeasily. The moist surfaces around the eyes and muzzle become yellow. As thedisease progresses, the animal shows dehydration, constipation, marked anemia,extreme weakness, anorexia and a stiff unsteady gait. Animals that survivegradually recover but remain carriers.

Outbreaks Although many outbreaks of anaplasmosis occur in the spring and summer, theycan occur at any time of the year. The many ways it can be transmitted and the

potential for carrier animals makes the source of an outbreak confusing. If anoutbreak occurs in spring or summer, it suggests that the source of the infection is


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from insect vectors. If the outbreak occurs 3 to 6 weeks after cattle are processed,that suggests Anaplasma was transferred from an infected animal to a susceptibleone during processing. If an outbreak occurs at other times, new arrivals or increased stress should be considered as the source of the disease. When any

outbreak occurs, it suggests that carrier animals are present either in your herd, or aneighboring herd, as carrier animals are an efficient source of infection. (Eriks et al., 1993 .) Carrier animals carry Anaplasma in their bodies, but do not showclinical signs and are able to infect other animals. Later, clinically ill animals cancontinue to spread the disease.

Pathogenesis I: E ntryo Host and bacterial adhesins

As A. phagocytophilum is an obligatory intracellular organism, it must invade hostcells to survive and replicate. To enter a host cell, a bacterium must bind to a cell-surface exposed receptor and set in motion a chain of signal transduction events. P-selectin glycoprotein ligand-1 (PSGL-1) and the sialic acid sialyl Lewis x (sLex)have been shown to be important receptors for A. phagocytophilum infection of neutrophils. Goodman et al first identified the importance of sLex in A.

phagocytophilum infection 51. This carbohydrate moiety was chosen because of its

rich expression on multiple cell types susceptible to invasion by A. phagocytophilum. Blocking of sLex with specific antibodies led to a significantreduction of A. phagocytophilum infection of both HL-60 cells and neutrophils(Box 1). Surprisingly, the antibodies did not prevent adhesion of the bacteria toHL-60 cells. Both adhesion and infection were however almost abolished bytreatment of HL-60 cells with neuraminidase. This enzyme, also known assialidase, cleaves terminal sialic acids. The importance of sLex as an A.

phagocytophilum receptor was also demonstrated by the fact that a HL-60variant cell line known to be resistant to A. phagocytophilum infection, showed avery low expression of sLex. In addition, the efficiency of A. phagocytophilumadhesion to HL-60 cells shows a correlation to the level of sLex expression. Asmany proteins and lipids can be modified by sLex, a subsequent study examinedmultiple sLex-decorated proteins and identified PSGL- 1 as the specific receptor for A. phagocytophilum 55. Antibodies against PSGL-1 blocked A.

phagocytophilum binding to and infection of HL-60 cells. To study the relative


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importance of both sLex and PSGL-1 in bacterial adhesion, the B lymphoblastoidcell line B J AB was used. This cell line does not express either PSGL-1 or Fuc-TVII, a fucosyltransferase important in the construction of sLex. When B J AB cellswere transfected with either PSGL-1 or Fuc-TVII alone, no efficient binding or

infection of the cells with A. phaghocytophilum took place. Only when the cellswere made to express both PSGL-1 and sLex, the cells were susceptible to A.

phagocytophilum, proving both protein and carbohydrate to be essential for infection of A. phagocytophilum.

o Mode of entryFollowing binding of a bacterium to a host cell, downstream signaling willcommence and lead to uptake of the organism. A. phagocytophilum binding toPSGL-1 leads to rapid phosphorylation of ROCK1 in both HL-60 cells and

neutrophils. The serine/threonine kinase ROCK1 is known to phosphorylate proteins which tether the receptor PSGL-1 to the cytoskeleton. Also reported to beinvolved in the early PSGL-1 signaling cascade is the protein Syk. Silencing thegenes encoding ROCK1 or Syk by siRNA leads to reduced A. phagocytophiluminfection of HL-60 cells, emphasizing the importance of this signaling pathway for

bacterial entry . Other signaling molecules believed to be important for A. phagocytophilum invasion are protein kinase A (PKA), phospholipase C (PLC),transglutaminase and protein tyrosine kinases (PTK). Chemical inhibition of these

proteins inhibited internalization of A. phagocytophilum in neutrophils. Thiscorresponds with microarray results in HL-60 cells where transglutaminase 3, PLCand Tec protein tyrosine kinase were found up-regulated three days after infectionwith A. phagocytophilum 30.

o Residing vacuoleAfter entry into neutrophils, A. phagocytophilum resides and replicates within amembrane-bound cytoplasmic vacuole. As these vacuoles incorporatedendocytosed colloidal gold particles, it was suggested they were part of theendocytic pathway. However, the bacterial inclusions do not co-localize withmarkers of either early endosomes (rab5, annexins) or late endosomes (LAMP-1,CD36) 80. A recent study by Niu et al postulated the A. phagocytophiluminclusions to be autophagosomes.Autophagy mediates the degradation of cytosolic components and organelles bysequestering cytoplasm in vesicles named autophagosomes and delivering these tothe lysosome. Several hallmarks of autophagosomes, such as a double membrane


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and the marker Beclin 1, can also be found in A. phagocytophilum inclusions.Though the exact nature of the bacterial inclusions may not yet be elucidated, it isclear these vacuoles do not fuse with lysosomes. The vesicles could not be labeledwith the low pH indicators DAMP or acridine orange. Vesicles containing

myeloperoxidase were seen surrounding, but never fusing with the bacterialinclusions.Pathogenesis II: Neutrophil functional changesIn living and replicating within neutrophils, A. phagocytophilum has chosen adangerous residence. Neutrophils constitute the bodys first line of defense againstinvading pathogens. These abundant leukocytes are equipped with a large array of microbicidal functions, including the respiratory burst, phagocytosis and granulerelease. To survive in this hostile environment, A. phagocytophilum has found

numerous unique mechanisms to effect its host cells behavior.o Reduction of the respiratory burst

A. phagocytophilum inhibits superoxide generation (Box 2). This inhibition has been shown in vitro in HL-60 cells, human and ovine neutrophils and in vivo in amurine model of infection and neutrophils of HGA patients.

Clinical SignsAfter an animal is inoculated with A. marginale infected blood, the

organisms invade mature red blood cells (RBCs). The RBCs are then consumed

(phagocytized), which results in the development of anemia. The incubation periodis variable (7-60 days), but averages one month. Clinical signs develop when one

percent of the animals RBCs have been infected with Anaplasma organisms.However, up to 70% of an animals red blood cells can become infected during theacute phase of anaplasmosis. The individual clinical signs that are seen aredependant on many factors, including age, possibly breed, and geographic region.In general, the severity of disease increases with the age of the animal. Youngcalves are typically asymptomatic. Calves up to two years of age generally have

mild to moderate disease while adult cattle are often severely affected.Anaplasmosis is unusual because the clinical signs are most severe in adultanimals. Calves less than a year old that are infected with A. marginale usually donot show clinical signs of the disease, but will become carriers. Carrier animalshave immunity against anaplasmosis, so even if they are infected later in life, theywill generally not get sick. Cattle 1 to 3 years old will showincreasingly more


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severe clinical signs. Recovered animals will also become carriers. Newly infectedadult cattle over 3 years will show the most severe clinical signs, and 30 percent to50 percent will die if they are not treated early.

Unless cattle are being watched carefully, dead cows are frequently the first thingnoticed with an anaplasmosis outbreak. If cattle are carefully observed, weaknessmay be the first clinical sign that is noticed with anaplasmosis. Infected cattle willfall behind the rest of the herd and will not eat or drink. Cows with light skin willinitially look pale around the eyes and muzzle, but later this can change to ayellowish color (jaundice). This jaundice is due to the destruction of the blood cellsand their contents being released into the blood stream. Weight loss is rapid. Cattlecan become extremely aggressive if they are oxygen deprived due to the severeanemia. Oxygen deprivation can also result in abortions in pregnant cows.Constipation, high fever, and labored breathing can also be seen. The most critical

period is the first 4 to 9 days after clinical signs appear. (Richey and Palmer;Richey, 1992) Cows that survive this period have an increased chance of survival.

Diagnosis:-

An accurate history along with the previously mentioned clinical signs shouldarouse suspicion of anaplasmosis. However, differential diagnoses would includeleptospirosis, babesiosis, bacillary hemoglobinuria, hepatotoxic plant poisonings,and other causes of anemia or icterus. Anemia can be established by assessing the

packed cell volume. In the acute phase of disease, A. marginale organisms can bedetected within red blood cells by microscopic examination of stained (Wrights,new methylene blue, Giemsa) blood smears. The organisms are basophilic stainingand are found at the margin, within the erythrocytes, in small clumps of two toeight organisms referred to as a morula.

After cattle recover from acute anaplasmosis, up to 0.1% of theerythrocytes remain infected, which makes identification of inclusion bodies very

difficult. Therefore, the best way to diagnose persistently infected cattle is byserology, which is not as useful for acutely affected animals. Serological methodshave historically included complement fixation and card agglutination tests.However, in recent years a competitive inhibition ELISA kit has been developedand studied. The new ELISA kit has a reported sensitivity of 96% and specificityof 95%, making it a very useful tool in screening to identify carrier cattle. Lesions


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that might be noted at necropsy include paleness or icterus, thin and watery blood,splenomegaly, hepatomegaly with yellow-orange discoloration, and pericardial

petechiae.

Treatment Treatment of anaplasmosis is most effective if given in the early stage of thedisease. A single dose of long-acting oxytetracycline (ex. LA-200) isadministered subcutaneously at 9 mg per pound of body weight. Bloodtransfusions are occasionally used. Animals in later stages of the disease may be soanemic that the stress of handling them will kill them. There is also evidence thatantibiotics at this stage are not effective. (Richey, 1999) Therefore, for veryweakened or belligerent cattle, antibiotic treatment is not recommended. Contactyour veterinarian if you suspect anaplasmosis on your farm. This will allow a

positive diagnosis of anaplasmosis to be made and the best course of treatmentimplemented.

All affected animals should be provided with easy access to food and water and alow-stress environment. It may take surviving animals up to 3 months to com-

pletely recover from the disease. Animals treated with a single dose of antibioticsand those not treated at all will both become carrier animals. Carrier animals can

be cleared of anaplasmosis with repeated injections of long-acting oxytetracyclineor prolonged feeding of chlortetracycline.

General Control ProgramsControl programs for anaplasmosis will be different depending on the prevalenceof the disease in the area. The prevalence can be categorized as follows:

Heavily infected area Moderately infected area Non-infected area


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References:

1. Aiello, Susan E. 1998. Anaplasmosis. The Merck Veterinary Manual. 8:21-23

2. Eriks, I.S., Stiller, D., and Palmer, G.H. Impact of persistent Anaplasmamarginale rickettsemia on tick infection and transmission, Journal of Clinical Microbiology 31:2091-2096, 1993.

3. Haigh J , Gerwing V, Erdenebaatar J , Hill J . 2008. A novel clinical syndromeand detection of Anaplasma ovis in Mongolian reindeer (Rangifer tarandus).J Wildlife Dis 44(3): 569-577.

4. Richey, E. J . Bovine Anaplasmosis, American A ssociation of Bovine Practitioners, Proceedings No. 24 , 1992.

5. Richey E. J . Bovine Anaplasmosis , College of Veterinary Medicine,University of Florida, 1999.

6. Smith, B.P. Diseases of the hematopoietic and hemolymphatic systems: Large Animal Internal Medicine , 3rd ed. St. Louis, Mosby 2002, pp.1049-1051.

7. Stokka, G., and Faulkner, R., Van Boening, J . Anaplasmosis , Kansas StateUniversity, J anuary 2000.


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3 . The il e riosis

SYNONYMS:-

East Coast Fever, Corridor Disease, Theileriasis, January Disease, ZimbabweTick Fever, African Coast Fever; Tropical Theileriosis, Mediterranean Coast Fever,Mediterranean Theileriosis.

Importance

Infection by Theileria parasites limits the movement of cattle betweencountries and can result in production losses and high mortality in susceptibleanimals. Because these diseases are most severe in recently introduced animals,they are a constraint on the importation of new breeds or improved stock. The twodiseases with the greatest economic impact in cattle are East Coast fever (infectionwith Theileria parva ) and tropical theileriosis (infection with Theileria annulata ).Theileria lestoquardi, which causes a severe disease with a high morbidity andmortality rate, is the most important species in sheep and goats.

E tiology

Theileriosis results from infection with protozoa in the genus Theileria of thesuborder Piroplasmorina. Theileria spp. are obligate intracellular parasites. Thetwo most important species in cattle and water buffalo are T. parva , which causesEast Coast fever, and T. annulata , which causes tropical theileriosis.A number of other Theileria species including T mutans, T buffeli, T. velifera, T.taurotragi and T. sergenti can also infect domesticated and wild ruminants. Many

of these organisms are carried asymptomatically, but some can cause anemia, andconcurrent infections may increase the severity of East Coast fever or tropicaltheileriosis.

T lestoquardi (formerly T hirci ) is the most virulent species in sheep andgoats. T. separata and the nonpathogenic species T. ovis also occur in smallruminants.


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Species Affected

T. parva can infect cattle, African buffalo ( Syncerus caffer ), water buffalo( Bubalus bubalis ), and waterbucks ( Kobus spp.). Symptomatic infections arecommon only in cattle and water buffalo. T. annulata occurs in cattle, yaks, water

buffalo and camels. Mildly pathogenic and nonpathogenic species found in cattleinclude T. mutans, T. buffeli, T. velifera, T. taurotragi and T. sergenti . T. taurotragihas also been recognized in eland. Theileria spp. have been found in most wildBovidae in Africa. They have also been reported in wild animals on other continents.T. lestoquardi, T. separata , T. ovis and other species occur in sheep and goats.

Geographic Distribution

T. parva (East Coast fever) is found in sub-Saharan Africa. T. annulata (tropicaltheileriosis) occurs from southern Europe and the Mediterranean coast through theMiddle East and North Africa, and into parts of Asia. T. parva and T. annulata arenot usually found in the same region; these two parasites seem to occur together only in southern Sudan.

T. mutans has been found in African and on some Caribbean islands, and wasreported from the U.S. in 1950 and 1975. T. velifera and T. taurotragi occur inAfrica, while T. sergenti has been reported from parts of Asia. T. buffeli iswidespread, and has been reported from Europe, Asia, Australia, North Americaand parts of Africa.

T. lestoquardi has been documented in Asia, the Middle East and parts of Africa and Europe. T. ovis and T. separata occur in Asia.

TransmissionTheileria spp. are transmitted by ticks acting as biological vectors.

Rhipicephalus appendiculatus is the most important vector for T. parva, but R. zembeziensis and R. duttoni carry this organism in parts of Africa. T. annulata is

transmitted by ticks in the genus Hyalomma . Hyalomma spp. are also the vectorsfor T lestoquardi, T. ovis and T. separata , while T. buffeli and T. sergenti aretransmitted by Haemaphysalis spp,. and T mutans and T. velifera are transmitted

by Amblyomma spp. Ticks in the genus Rhipicephalus spread T. taurotragi .Theileria sporozoites are transmitted to animals in the saliva of the feeding tick.

Ordinarily, T. parva and T. annulata only mature and enter the saliva after the tick attaches to a host; a tick must usually be attached for a few days before it becomes


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infective. However, if environmental temperatures are high, infective sporozoitesof T. parva can develop in ticks on the ground, and may enter the host withinhours of attachment. Transovarial transmission does not occur with Theileria spp.

Inside the mammalian host, Theileria sporozoites undergo a complex life cycle

involving the replication of schizonts in leukocytes and piroplasms in erythrocytes.Cattle that recover from Theileria infections usually become carriers for months or years. Iatrogenic transmission can also occur via blood (e.g., on re-used needles).

Incubation PeriodThe incubation period for East Coast fever is 8 to 12 days in experimentally

infected animals. It might be as long as three weeks in naturally infected animals.The incubation period for tropical theileriosis is thought to be approximately 1 to 3weeks.

Clinical SignsIn East Coast fever, the clinical signs include generalized lymphadenopathy,

fever, anorexia and loss of condition with decreased milk yield. Petechiae andecchymoses may be found on the conjunctiva and oral mucous membranes.Lacrimation, nasal discharge, corneal opacity and diarrhea can also be seen.Terminally ill animals often develop pulmonary edema, severe dyspnea and afrothy nasal discharge. Some cattle have a fatal condition called turning sickness.In this form of the disease, infected cells block capillaries in the central nervous

system and cause neurological signs. Animals that recover from East Coast fever often become asymptomatic carriers, but some animals have poor productivity andtheir growth is stunted.

Tropical theileriosis generally resembles East Coast fever, but these parasitesalso destroy red blood cells, causing jaundice, anemia, and in some cases,hemoglobinuria. Hemorrhagic diarrhea may be seen in the late stages. Petechiaeare often found on the mucous membranes. Neurological signs have beendocumented in some terminally ill water buffalo, but turning sickness does notseem to be a feature of tropical theileriosis in cattle. Abortions can be seen.

Other species of Theileria including T. mutans , T. sergenti and T. buffeli cancause anemia in cattle or increase the severity of clinical signs in animalscoinfected with T. parva or T. annulata . On their own, these organisms usuallycause mild disease compared to East Coast fever or tropical theileriosis. Somespecies such as T. velifera appear to be non-pathogenic.T. lestoquardi is the most virulent species in small ruminants, and often causesfatal disease. The clinical signs may include fever, anorexia and weight loss,


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listlessness, lymphadenopathy, edema of the throat, difficulty breathing, anemiaand icterus. Subacute, chronic or mild cases can also be seen.

Post Mortem LesionsPetechial and ecchymotic hemorrhages are often found on the serosal surfaces

of internal organs, and the body cavities may contain serous fluid. In acutelyinfected animals, the lymph nodes are usually enlarged and may be edematous andhemorrhagic. In chronic cases, they may be shrunken. The spleen is typicallyenlarged. The liver may also be larger than normal, and white foci of lymphoidinfiltration (pseudoinfarcts) may be present in the liver and kidney. Thegastrointestinal tract can have signs of hemorrhagic enteritis, particularly in thesmall intestine and abomasum.Interlobular emphysema and severe pulmonary edema are common in animals that

die of East Coast fever. A frothy exudate may be found around the nostrils and inthe trachea and bronchi. The lungs are hyperemic and full of fluid. Pulmonaryedema also occurs in goats infected with T. lestoquardi .

Morbidity and MortalityMorbidity and mortality vary with the hosts susceptibility, and the strain and

dose of the parasite. The case fatality rate for untreated East Coast fever can be ashigh as 100% in taurine, zebu or sanga cattle from nonendemic areas. In contrast,the morbidity rate approaches 100% among indigenous cattle, but the mortalityrate is usually low. Similarly, tropical theileriosis is more severe in introduced

breeds, with a mortality rate of 40-90%, while the mortality rate in indigenouscattle can be as low as 3%. Breeds of cattle that are relatively resistant toexperimental infection with T. annulata include the Sahiwal breed of Bos indicusand the Kenana breed of B. taurus . Infections with Theileri a spp. other than T.

parva and T. annulata are rarely fatal in cattle.In sheep and goats, the morbidity rate from T. lestoquard i can approach 100%,

with a mortality rate of 46-100%. Diagnosis

Cl inica l East Coast fever should be suspected in tickinfested animals with a fever and

enlarged lymph nodes. Terminal pulmonary edema and a high mortality rate inintroduced breeds are also suggestive. Indigenous animals with tropical theileriosismay be in poor condition, with wasting and signs of anemia.


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Differential diagnosisIn cattle, the differential diagnosis for theileriosis includes heartwater,

hemorrhagic septicemia, trypanosomiasis, babesiosis, Rift Valley fever andmalignant catarrhal fever. In sheep and goats, T. lestoquardi infections must be

distinguished from babesiosis, Rift Valley Fever and malignant catarrhal fever.

ControlTheileriosis is not transmitted by casual contact. If the infection is newly

introduced to an area, it might be eradicated with movement controls, by cullinginfected animals and by preventing ticks from becoming infected.In endemic areas, the tick burden can be decreased with acaricides and other methods of tick control such as rotational grazing. The transfer of blood betweenanimals must also be avoided. Antiparasitic drugs are effective in animals with

clinical signs, but animals may remain carriers. Treatment is most effective in theearly stages of the disease.Animals can be protected from both East Coast fever and tropical theileriosis

by vaccination. Attenuated vaccines are used to control tropical theileriosis insome countries. Vaccination against East Coast fever is done by simultaneouslyinjecting virulent T. parva and an antibiotic (usually a long-acting tetracycline).This process generally results in a mild or inapparent infection, and the animal

becomes a carrier. T. parva stocks that infect cattle asymptomatically have beenidentified, and might be used without simultaneous antibiotic therapy.Considerations in T. parva vaccination include the possibility of introducing liveorganisms into areas where they are not currently endemic.

Recent developments in research and control of Thei l eria annu l ata in IndiaDuring the first two decades of this century, theilerial organisms were

regularly recorded in the blood of cattle maintained at Muktheswa, Uttar Pradesh.Since then, several reports describing the detection of theilerial piroplasms in the

blood of cattle have appeared in the literature. Acute clinical cases of theileriosiswere first recorded on 12 J une, 1922, in hill bulls. From 1923 to 1924, the presenceof theilerial piroplasms was reported in the blood smears of 1,368 out of 5,158cattle examined. In 1930, outbreaks of clinical theileriosis were recorded inimported herdsmaintained at Lahore, Bangalore, Allahabad and Kirkee. Since then,occasional outbreaks of theileriosis have been recorded, mainly in cross-bred andexotic cattle. The disease signs recorded in these animals were high fever, lymphnode enlargement, anaemia, petechiae of the mucous membranes and variousdegrees of jaundice. Indigenous cattle and buffaloes ( Bubalus bubalis) have an


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inherent resistance to disease and harbour theilerial piroplasms in their erythrocytes as symptomless carriers. Until the mid-1960s, theileriosis wasenzootically stable. This stability was upset with the large-scale introduction of exotic (taurine) cattle and with the advent of extensive cross-breeding programs for the improvement of milk production. Today,India has approximately 200 million cattle, of which 10 million are either pure-

bred or taurine crosses. With the establishment of many Bull Mother Farms of exotic breeds, there has been a rapid increase in the taurine blood in dairy cattle,which show a high degree of susceptibility to theileriosis. India has approximately26,000 artificial insemination stations and several embryo transfer centres activelyengaged in upgrading the existing 82% nondescript cattle.With the rapid increasein the number of cross-bred cattle, the previous enzootic stability of theileriosis has

been upset and outbreaks of acute disease with 30 to 60% mortality have beenrecorded.

Drugs such as tetracyclines, halofuginone (Terit, Hoechst), parvaquone(Clexon, Coopers Animal Health) and buparvaquone (Butalex, Coopers Pitman-More) have been used for the treatment of clinical theileriosis. Buparvaquone isreported to be the most effective and safe drug when used at 2.5 mg/kg bodyweight on day 3 after detection of theilerial schizonts in biopsy smears. However,the drug is reported to be expensive and is presently not available commercially.

Many research centres established under an All India Coordinated ResearchProject are engaged in developing diagnostic, chemotherapeutic and prophylacticmeasures for control of theileriosis. A dot enzyme-linked immunosorbent assay(DOT-EIA) using piroplasm antigen has been developed by the PunjabAgricultural University, which awaits evaluation under field conditions. It isexpected that the test will facilitate large-scale epidemiological studies.

The Animal Disease Research Laboratory of the National DairyDevelopment Board, Anand, has developed a tissue-culture vaccine using the ODE(Anand) isolate of T. annulata at 150 passages. The vaccine has been extensivelystudied for safety and potency under laboratory and field conditions. Thegovernment of India has cleared the vaccine for large-scale production and IndianImmunologicals, a unit of the National Development Dairy Board, begancommercial production and marketing in February 1989 under the trade name

`Rakshavac-T. More than 100,000 pure-bred and cross-bred cattle over twomonths of age and at different stages of pregnancy and lactation have beenvaccinated. In tropical countries, cattle and buffalo are frequently heavily infestedwith many genera of ticks, which, apart from transmitting diseases such astheileriosis, babesiosis and anaplasmosis, also cause extensive damage to thehealth of these livestock. Research should be directed towards developing vaccines


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trypanosomiasis rohit

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