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BOVINE TROPICAL
THEILERIOSIS(BTT)
Dr. Jibachha Sah
M.V.Sc,Lecturer, College of Veterinary Science,
NPI, Bhojad, Chitwan, Nepal
jibachhashah@gmail.com,00977-9845024121
INTRODUCTION
Bovine tropical theileriosis (Theileria annulata infection) is a protozoan disease
transmitted by several tick species, all belonging to the genus Hyalomma
Calf presented with bilateral pre scapular lymphnode enlargement,
petechiae on conjunctiva and bilateral exopthalmia with lacrymation
due to Tropical theileria
ETIOLOGY
●The two most virulent organisms in cattle are Theileria annulata, which causes
tropical theileriosis, and T. parva, which causes East Coast fever.
SPECIES AFFECTED
●T. annulata affects cattle, yaks and water buffalo.
●T. parva affects cattle and water buffalo (Bubalus bubalis). African buffalo (Syncerus caffer) and
cattle are important reservoir hosts for this organism.
●It can also infect sheep and goats, but does not cause significant illness in these animals.
GEOGRAPHICAL DISTRIBUTION
●T. annulata (tropical theileriosis) occurs in southern Europe, the Middle East and parts of
Asia.
●T. orientalis is widespread;
●T. parva (East Coast fever/ corridor disease) occurs in sub-Saharan
Africa
TRANSMISSION
●Theileria are transmitted by ticks acting as
biological vectors, and can be transmitted
transstadially. Transovarial transmission is not
thought to occur.
●Genera of ticks reported to act as vectors include
● Rhipicephalus (T. parva,), Hyalomma (T.
annulata,), Haemaphysalis (T. orientalis,) and
Amblyomma (T. mutans,).
●Transstadial transmission occurs when a
pathogen remains with the vector from one life
stage ("stadium") to the next.
● Transmitt especially by Hyalomma anatolicum
anatolicum
Transovarial and transstadial transmission
of the Ixodes tick
Ticks
●Susceptibility to infection of Hyalomma ticks for Theileria annulata and it was reported that
female ticks have higher infection than male ticks .
INCUBATION PERIOD
●The incubation period for tropical theileriosis is approximately 1-3 weeks.
●The incubation period for East Coast fever is 7-12 days in experimentally infected animals,
although some cases might appear as late as 3 weeks.
Theileria lifecycle
●Lymphocyte stage: - In lymphocytes, schizonts, also known as Koch’s blue bodies, are formed.
Then these schizonts multiply, replicating the parasites and allow disease to proliferates.
● Schizonts then disseminate through the lymphoid tissues before differentiating into merozoites.
● The merozoites enter the erythrocytes and form piroplasms which are infective to ticks and
capable of sexual reproduction.
● Sexual reproduction occurs within the nymph and larval stages of the tick and the final infective
stage is present within the salivary glands and is transmitted to mammalian hosts when blood
feeding.
● Transmission in the tick is then trans-stadial.
Infective sporozoitesTick feed and
transmit infectionInvade lymphocytes
(forms lymbhoblast)
Schixogony
Piroplasesses
in red blood cell
Tick feed and
become infected
Gametogcay in
Tick gut
Asexual multiplication
In salivary gland
Tick hostBovine host
Carrier Animals
●Indian native cows Sahiwal are resistant to Theileria because they are not affected by ticks and stand
by high temperature of 45°C. Cattle with subclinical infection are known as carrier animals as they have
low number of piroplasms in blood hence they act as a source of infection for the tick vectors.
● In carrier animals low numbers of piroplasms are present in erythrocytes and they become the source
for transmission of infection, the carrier animals were detected by Polymerase Chain Reaction test.
Pathogenesis
● After biting infected ticks the number of parasitized cells increases rapidly throughout the lymphoid
system, and from about day 14 onward, cells undergoing merogony are observed.
●This is associated with widespread lymphocytolysis, marked lymphoid depletion, and leukopenia.
●Piroplasms in RBCs infected by the resultant merozoites assume various forms, but typically they
are small and rod-shaped or oval.
●Typically, fever occurs 7–10 days after parasites are introduced by feeding ticks, continues
throughout the course of infection, and may be >106°F (41°C).
●Lymph node swelling becomes pronounced and generalized. Lymphoblasts in Giemsa-stained
smears of needle aspirates from lymph nodes contain multinuclear schizonts.
●Anorexia develops, and the animal rapidly loses condition; lacrimation and nasal discharge may
occur.
●Terminally, dyspnea is common. Just before death, a sharp decrease in body temperature is usual,
and pulmonary exudate pours from the nostrils.
●Death usually occurs 18–24 days after infection.
CLINICAL SIGNS
● A high temperature (41.2°C) is a common feature in acute cases.
● Diarrhoea with blood clots in a calf.
● Lymph node enlargement
● Theileria-annulata-piroplasms((pear shaped)- a stage that can infect or
transmit to other cattle.
● Pale, rather than healthy pink, vulva
● Increased respiratory and heart rate
●Less commonly seen clinical signs that can be seen include: excessive salivation, diarrhoea,
constipation, swelling of lymph nodes, and brown urine.
● Sick cows not responding as expected to treatment for conditions such as milk fever
● Cows are off their food and appear hollow sided
● A decrease in milk production
● Sudden death especially in late pregnancy or early lactation.
● Lacrimation, corneal opacity, nasal discharge
● Cows have no strength or energy to do anything.
● Pale or yellow whites of eyes (a sign of jaundice)
● Lethargy – exercise intolerance, cows lagging on the walk to the shed
A high temperature (41.2°C) is a common feature in acute cases.
●The alteration of protein picture in animals after infection could be referred to decrease in
protein synthesis as a consequence of anorexia and fever
●The increases of body temperature occur due to the liberation of endogenous progeny
because cellular lysis and high level of parasitemia lead to the stimulation of thermoregulatory
center in the hypothalamus
●Due to cellular lysis, endogenous pyrogen liberates in the blood stream causing raise of body
temperature which may leads inappetence (Glass et al. 2001)
Anorexia is a also common feature in tropical theileriosis acute cases.
●The cytokines (TNF-a, IL-1, and IL-6) produced by infected mononuclear cells are responsible for
the diverse clinical symptoms of tropical theileriosis, such as depression, pyrexia, anorexia,
cachexia, and disseminated haemorrhages,Forsyth et al. (1997) and Glass et al. (2003) .
● Diarrhoea with blood clots in a calf.
●As a result to inflammatory reaction and ulceration to abomasal and gastro intestinal tract
●In severe cases haemorrhagic diarrhoea is seen, this is due to ulcer formation in the gastrointestinal
tracts leading to blood mixed faeces.
●The decreased serum phosphorus and magnesium concentration in cattle with theileriosis is the
results of diarrhoea and renal wasting.
Lymph node enlargement
●The enlargement of superficial lymph node could be explained by lymphoid hyperplasia in early
stage of disease that occurs due to increases of proliferation of microschizonts inside the lymphocyte
caused inflammatory reaction in the infected lymph node(Jabbar et al. 2008).
Parotid Lymph node enlargementPrescapular Lymph node enlargement
Precrural lymph node enlargement Pronounce upward bulge temporal fossa
●The cells infected by schizonts induce massive and uncontrolled proliferation of both specific and
nonspecific T lymphocyte resulting in enlarged lymph nodes
Affected lymph nodes show reactive follicular hyperplasia, reticulo-
endothelial hyperplasia, enlarged germinal centers and slight increase
of interfollicular lymphoid tissue within the paracortical and cortical
regions
Prescapular lymph node enlargement
Recumbence
●The significant rises in the serum AST and ALT activities were due to muscle trauma caused by
prolonged recumbency in theileriosis.
Pale, rather than healthy pink, vulva
●One of the plausible reasons may be the oxidative damage to RBCs
● A significant feature of the disease is anemia owing to overproduction of cytokines and
reactive oxygen species.
●Immune-mediated mechanism such as erythrophagocytosis might be responsible RBCs count
reduction eventually
Haemolytic anaemia
●The other importing cause to make the anemia in bovine theileriosis infection was the hemolytic
anemia caused by an immune– mediated hemolytic which is indicated by the presence
haemagglutinin.
● The modern research explains the mechanism of anemia that occurs due to the activity of
antioxidant enzymes such as superoxide dismutase (SOD) was effective by parasites and results
increased fragility of RBCs and thus ,acceleration of erythrocytes clearance by Phyagocytic cells.
●This anemia could be due to both an autoimmune reaction (Hooshmand-Rad 1976) and the effect of
intra-erythrocytic piroplasms (Preston et al. 1992).
●In addition, pro-inflammatory cytokines, particularly TNF-α, have been implicated in mediating
anemia associated with tropical theileriosis.
●The decrease in RBC could be due to increased levels of activated complement products.
Additionally, since oxidized erythrocytes may be destroyed easily by erythropagocytosis,
oxygen radicals may also be involved in the pathogenesis of anemia
Jaundice
●It could be also a resultant of biliary obstruction which resulted in obstructive
jaundice with a reflux of cholesterol into the blood stream from the liver and
stimulate hepatic cell membrane for synthesis of cholesterol.
Increased respiratory and heart rate
Normal Infected
Heart rate (bpm)(65 to 80) 122
Respiratory rate (cpm) (15 to 35) 75
bpm: beats per minute
cpm: cycles per minute
●Anemia associated with theileriosis and secondary hypoxia and vasculitis, leading to
some degree of cardiovascular injury.
●Cardiac troponin I is released from myocytes in both reversible and irreversible
myocardial injury.
●Respiratory signs occur due to the accumulation of edematous fluid inside the lung
and thoracic cavity
Ocular oedema in a cow
Lacrimation with visible ocular odema Ocular odema
Ocular odema
●it is strongly believed that T. annulata in the foetal circulation might have got access into
cerebral circulation and caused increased vascular permeability.
●It is believed that the endothelial cells of the fine ocular blood vessels of the orbit were the
probable site of multiplication of the pathogen congenitally acquired from the dam during
gestation and consequential oedema of the orbits and eyelids(Vikrant Sudan et al 2012)
●The cornel opacity was explained by as a result of white blood cells infiltration.
Theileria opacity Corneal opacity
●The occurrence of parasites produces lesions in the endothelial lining of blood vessels, tissue
damage in organs, such as the liver, kidney, and lung, and multiple petechial haemorrhages
(Forsyth et al 1999), all of which play an important role in the development of coagulation defects
(Levi, et al.,1997)
Oedema of the jaw in a cow
●Oedematous jaw is due to decreased serum calcium concentration in infected cattle could be
attributed to the hypoalbuminaemia and kidney damage (Burtis and Ashwood, 1996).
●The reduction of serum protein level could be attributed to extra-vascular proteinaceous fluid in
body cavities due to infected lymph nodes, resulting in edema
●Hypoproteinaemia and hypoalboumineamia is possibly due to the harmful effect of toxic
metabolites of Theileria and also due to liver dysfunction.
Oedema
Theileria annulata induced brisket oedema in a bull
●Mediastinal lymph nodes around the base of cranial and caudal vena cava returning blood
to the heart may be affected by Theileria species.
●In this condition, jugular engorgement, oedema, inappetence are the clinical signs.
Beisket oedema
●Cutaneous nodules were perivascular infiltrate of lymphocytes,
macrophages and eosinophils
●Uilenberg and Zwart(1979) reported one case of cutaneous nodules in
which both T. parva schizonts and Demodex bovis were found.
Numerous skin nodules on the neck and shoulders
of a cow with bovine theileriosis
skin nodules
Innumerable skin nodules in calf
Nodules on medial thighs of a heifer Perivascular inflammatory infiltrate (lymphocytes,
macrophages and eosinophils) (haematoxylin)
Electrocardiography (ECG)
Electrocardiography (ECG) examination revealed high amplitude of QRS complex in bull infected
with Theileria annulata organisms
Improvement in the ECG findings (Lead-I)
CLINICOPATHOGY
●Reticulocyte count is an indicator of the
rate of erythrocyte production.
Reticulocytosis is caused by increased
RBC destruction.
● In theileriosis, the reason for this
imbalance is that anaemia causes a
greater stimulus for RBC production.
Singh et al. (2001).
●Activated partial thromboplastin time
(aPTT)) and PT were attributed to
impaired hepatic synthesis and the
consumption of several pro-coagulant
clotting factors in theileriosis.(Singh 2001)
●Marked decrease in both basophil and
monocyte counts in the infected group.
This variation could be due to
differences in stage and severity of
disease Omer et al. (2002),
●High levels of fibrinogen in cows infected with Theileria annulata infection, pro-inflammatory
cytokines, including TNF-a, IL-1, and IL-6, are released systemically from schizont-infected
macrophages and monocytes (Brown,1990; Forsyth,1999).
●According to Stockham et al. (2000) and Omer et al. (2002), the decrease in RBC could be due to
increased levels of activated complement products. Additionally, since oxidised erythrocytes may be
destroyed easily by erythropagocytosis, oxygen radicals may also be involved in the pathogenesis
of the anaemia.
●MCV increased and MCHC decreased called macrocytic hypochromic anaemia). In other forms
of anemia in which the average size and hemoglobin content of the red blood cells are within
normal limits are called normocytic normochromic anemias. Increase MCV and decrease PCV due to
toxic metabolite of Theileria sp.cause harmful effect on bone marrow for that interfere
erythropossis.
●Leukocytosis result from lymphocytes proliferation in lymphoid organs as a defensive reaction to
the invasion and multiplication of T. annulata (Modi et al. 2015) while, leukopenia may be the
consequence of the destruction of white blood cells by the parasites.
● The decline in the values of Hb, TEC, and PCV may be attributed to the destruction of piroplasm
infected erythrocytes by macrophages in the lymph nodes, spleen and other organs of the monocyte
macrophage system coupled with reduced erythropoietic activity.
Source: Osama H Omer et al.,2003Biochemical analyze carried out in sera from 23 young
and 20 adult Friesian cattle infected from Theileria
annulata
●Low serum total protein(hypoproteinaemia) concentration in cattle infected naturally from Theileria
annulata possible due to hypoalbuminaemia and hypoglobulinaemia arising from harmful effect of
toxic metabolite, liver failure and and sever lymphocytopaenia(Singh et al.,2001)
●The cardiac infracts and sever liver damage seen in rise in Aspartate aminotransferase (AST) and
Alkaline phosphate (AP) activity(Laiblin et al 1978).
●AST and ALT are involved in amino acid and carbohydrate metabolism. These enzymes are present in
high concentrations in the muscles and liver. Elevation of these enzymes in the blood is indicator of
organ necrosis (Murray et al., 1996).
●Significant increase in bilurubin due to hepatic dysfunction and haemolytic anaemia (Singh et al 2001).
The increase in bilirubin levels is due to the destruction of parasitized erythrocytes by
erythrophagocytosis in the spleen, lymph nodes, and other organs of the reticuloendothelial system.
● Creatinine concentration decrease has no clinically significant. How ever muscle wasting and
rapidly emaciated associated with reduce the level of creatinine (Mehlhorn et al1994).
●Increase in BUN and uric acid due to the kidney damage, (Sandhu et al. (1998)
●The significant decrease in cholesterol and triglycerides may be attributed to anorexia associated
with the high rise of temperature and diarrhoea (Sharma et al. (1987)
Source: Osama H Omer et al.,2003Biochemical analyze carried out in sera from 23 young
and 20 adult Friesian cattle infected from Theileria
annulata
●Decrease the serum copper and iron concentration is usually no clinical significance
●Decrease the serum phosphorus and magnesium associated with diarrhoea and renal wasting(Agus
et al,1982)
●Decrease the potassium concentration associated with inappetance,diarrhoea and
hypomaganesaemia(Yadave and Sharma,1986).
POSTMORTEM EXAMINATION
Bovine, lung.
The lung tissue is diffusely tan-brown, and
lobules are non-collapsed and rubbery
(interstitial pneumonia)
Bovine, popliteal lymph node.
The node is enlarged and diffusely pale, and
contains numerous petechiae.
Bovine, kidney.
There are multiple petechiae on the surface
of the cortex. The lymph node near the hilus
is markedly enlarged.
Bovine lymphoblasts contain intracytoplasmic Theileria
parva.
Punched-out ulceration in abomasum a pathognomic lesion
DIAGNOSTIC TEST
●PCR is often used in diagnosis as “gold standard test”, and can identify Theileria in the blood of
both carriers and clinical cases.
●Antibodies to T. parva and T. annulata can be detected with ELISAs, indirect fluorescent
antibody test (IFA) or other serological assays.
Theileria-annulata-piroplasms-cattle
Differential diagnosis
• Heartwater
• Trypanosomosis
• Babesiosis
• Anaplasmosis
• Malignant catarrhal fever
• Contagious bovine pleuropneumonia
MORBIDITY AND MORTALITY
●The mortality rate for tropical theileriosis is reported to be 40-90% in newly introduced cattle but <
5% in some indigenous animals.
●The morbidity rate in small ruminants infected with T. lestoquardi can approach 100%, with
reported mortality rates of 46-100%
●In theileriosis, parasites invade to lymphoid cells and at a later stage of infection invade to
the erythrocytes and causes fever, anemia and leads to death (Soulsby 1982).
Death
●A leucocyte count below 1,000/mm3 is considered critical and fatal in a majority of the
cases (Mehlhorn and Armstrong 2001)
TREATMENT
●Parvaquone and buparvaquone are 2 effective drugs against tropical theileriosis.
●The recovery rate of animals treated with parvaquone was 60.7% and with buparvaquone it was
88.7% (Hashemi-Fesharki, 1991).
●Buparvaquone (Butalex) at a dose rate of 1 ml/20 kg (2.5 mg/kg) body weight intramuscularly along
with supportive therapy like inj. meloxicam,B-complex and fluid therapy. In severe and advanced
cases, a second treatment may be required at 48-72 hrs after the initial injection at the same dose
rate.
●Ascorbic acid was found better in treating clinical cases of bovine tropical theileriosis indicated
by decreased levels of oxidative stress such as plasma malondialdehyde (MDA), return to normal
activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD) enzymes post
treatment( Ashwani Kumar,2014).
Note: Butalex should never be given by intravenous or subcutaneous injection
CONTROL
●Topical application of flumethrin 1 % pour-on preparation (Bayticol pour-on) over the vertebral
column is also advised.
Bovine tropical theileriosis-Dr.Jibachha Sah,M.V.SC

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Bovine tropical theileriosis-Dr.Jibachha Sah,M.V.SC

  • 1. BOVINE TROPICAL THEILERIOSIS(BTT) Dr. Jibachha Sah M.V.Sc,Lecturer, College of Veterinary Science, NPI, Bhojad, Chitwan, Nepal jibachhashah@gmail.com,00977-9845024121
  • 2. INTRODUCTION Bovine tropical theileriosis (Theileria annulata infection) is a protozoan disease transmitted by several tick species, all belonging to the genus Hyalomma Calf presented with bilateral pre scapular lymphnode enlargement, petechiae on conjunctiva and bilateral exopthalmia with lacrymation due to Tropical theileria
  • 3. ETIOLOGY ●The two most virulent organisms in cattle are Theileria annulata, which causes tropical theileriosis, and T. parva, which causes East Coast fever.
  • 4. SPECIES AFFECTED ●T. annulata affects cattle, yaks and water buffalo. ●T. parva affects cattle and water buffalo (Bubalus bubalis). African buffalo (Syncerus caffer) and cattle are important reservoir hosts for this organism. ●It can also infect sheep and goats, but does not cause significant illness in these animals.
  • 5. GEOGRAPHICAL DISTRIBUTION ●T. annulata (tropical theileriosis) occurs in southern Europe, the Middle East and parts of Asia. ●T. orientalis is widespread; ●T. parva (East Coast fever/ corridor disease) occurs in sub-Saharan Africa
  • 6. TRANSMISSION ●Theileria are transmitted by ticks acting as biological vectors, and can be transmitted transstadially. Transovarial transmission is not thought to occur. ●Genera of ticks reported to act as vectors include ● Rhipicephalus (T. parva,), Hyalomma (T. annulata,), Haemaphysalis (T. orientalis,) and Amblyomma (T. mutans,). ●Transstadial transmission occurs when a pathogen remains with the vector from one life stage ("stadium") to the next. ● Transmitt especially by Hyalomma anatolicum anatolicum Transovarial and transstadial transmission of the Ixodes tick
  • 7. Ticks ●Susceptibility to infection of Hyalomma ticks for Theileria annulata and it was reported that female ticks have higher infection than male ticks .
  • 8. INCUBATION PERIOD ●The incubation period for tropical theileriosis is approximately 1-3 weeks. ●The incubation period for East Coast fever is 7-12 days in experimentally infected animals, although some cases might appear as late as 3 weeks.
  • 9. Theileria lifecycle ●Lymphocyte stage: - In lymphocytes, schizonts, also known as Koch’s blue bodies, are formed. Then these schizonts multiply, replicating the parasites and allow disease to proliferates. ● Schizonts then disseminate through the lymphoid tissues before differentiating into merozoites. ● The merozoites enter the erythrocytes and form piroplasms which are infective to ticks and capable of sexual reproduction. ● Sexual reproduction occurs within the nymph and larval stages of the tick and the final infective stage is present within the salivary glands and is transmitted to mammalian hosts when blood feeding. ● Transmission in the tick is then trans-stadial.
  • 10.
  • 11. Infective sporozoitesTick feed and transmit infectionInvade lymphocytes (forms lymbhoblast) Schixogony Piroplasesses in red blood cell Tick feed and become infected Gametogcay in Tick gut Asexual multiplication In salivary gland Tick hostBovine host
  • 12. Carrier Animals ●Indian native cows Sahiwal are resistant to Theileria because they are not affected by ticks and stand by high temperature of 45°C. Cattle with subclinical infection are known as carrier animals as they have low number of piroplasms in blood hence they act as a source of infection for the tick vectors. ● In carrier animals low numbers of piroplasms are present in erythrocytes and they become the source for transmission of infection, the carrier animals were detected by Polymerase Chain Reaction test.
  • 13. Pathogenesis ● After biting infected ticks the number of parasitized cells increases rapidly throughout the lymphoid system, and from about day 14 onward, cells undergoing merogony are observed. ●This is associated with widespread lymphocytolysis, marked lymphoid depletion, and leukopenia. ●Piroplasms in RBCs infected by the resultant merozoites assume various forms, but typically they are small and rod-shaped or oval. ●Typically, fever occurs 7–10 days after parasites are introduced by feeding ticks, continues throughout the course of infection, and may be >106°F (41°C). ●Lymph node swelling becomes pronounced and generalized. Lymphoblasts in Giemsa-stained smears of needle aspirates from lymph nodes contain multinuclear schizonts. ●Anorexia develops, and the animal rapidly loses condition; lacrimation and nasal discharge may occur. ●Terminally, dyspnea is common. Just before death, a sharp decrease in body temperature is usual, and pulmonary exudate pours from the nostrils. ●Death usually occurs 18–24 days after infection.
  • 14. CLINICAL SIGNS ● A high temperature (41.2°C) is a common feature in acute cases. ● Diarrhoea with blood clots in a calf. ● Lymph node enlargement ● Theileria-annulata-piroplasms((pear shaped)- a stage that can infect or transmit to other cattle. ● Pale, rather than healthy pink, vulva ● Increased respiratory and heart rate
  • 15. ●Less commonly seen clinical signs that can be seen include: excessive salivation, diarrhoea, constipation, swelling of lymph nodes, and brown urine. ● Sick cows not responding as expected to treatment for conditions such as milk fever ● Cows are off their food and appear hollow sided ● A decrease in milk production ● Sudden death especially in late pregnancy or early lactation. ● Lacrimation, corneal opacity, nasal discharge ● Cows have no strength or energy to do anything. ● Pale or yellow whites of eyes (a sign of jaundice) ● Lethargy – exercise intolerance, cows lagging on the walk to the shed
  • 16. A high temperature (41.2°C) is a common feature in acute cases. ●The alteration of protein picture in animals after infection could be referred to decrease in protein synthesis as a consequence of anorexia and fever ●The increases of body temperature occur due to the liberation of endogenous progeny because cellular lysis and high level of parasitemia lead to the stimulation of thermoregulatory center in the hypothalamus
  • 17. ●Due to cellular lysis, endogenous pyrogen liberates in the blood stream causing raise of body temperature which may leads inappetence (Glass et al. 2001) Anorexia is a also common feature in tropical theileriosis acute cases. ●The cytokines (TNF-a, IL-1, and IL-6) produced by infected mononuclear cells are responsible for the diverse clinical symptoms of tropical theileriosis, such as depression, pyrexia, anorexia, cachexia, and disseminated haemorrhages,Forsyth et al. (1997) and Glass et al. (2003) .
  • 18. ● Diarrhoea with blood clots in a calf. ●As a result to inflammatory reaction and ulceration to abomasal and gastro intestinal tract ●In severe cases haemorrhagic diarrhoea is seen, this is due to ulcer formation in the gastrointestinal tracts leading to blood mixed faeces. ●The decreased serum phosphorus and magnesium concentration in cattle with theileriosis is the results of diarrhoea and renal wasting.
  • 19. Lymph node enlargement ●The enlargement of superficial lymph node could be explained by lymphoid hyperplasia in early stage of disease that occurs due to increases of proliferation of microschizonts inside the lymphocyte caused inflammatory reaction in the infected lymph node(Jabbar et al. 2008). Parotid Lymph node enlargementPrescapular Lymph node enlargement
  • 20. Precrural lymph node enlargement Pronounce upward bulge temporal fossa
  • 21. ●The cells infected by schizonts induce massive and uncontrolled proliferation of both specific and nonspecific T lymphocyte resulting in enlarged lymph nodes Affected lymph nodes show reactive follicular hyperplasia, reticulo- endothelial hyperplasia, enlarged germinal centers and slight increase of interfollicular lymphoid tissue within the paracortical and cortical regions Prescapular lymph node enlargement
  • 22. Recumbence ●The significant rises in the serum AST and ALT activities were due to muscle trauma caused by prolonged recumbency in theileriosis.
  • 23. Pale, rather than healthy pink, vulva ●One of the plausible reasons may be the oxidative damage to RBCs ● A significant feature of the disease is anemia owing to overproduction of cytokines and reactive oxygen species. ●Immune-mediated mechanism such as erythrophagocytosis might be responsible RBCs count reduction eventually Haemolytic anaemia
  • 24. ●The other importing cause to make the anemia in bovine theileriosis infection was the hemolytic anemia caused by an immune– mediated hemolytic which is indicated by the presence haemagglutinin. ● The modern research explains the mechanism of anemia that occurs due to the activity of antioxidant enzymes such as superoxide dismutase (SOD) was effective by parasites and results increased fragility of RBCs and thus ,acceleration of erythrocytes clearance by Phyagocytic cells. ●This anemia could be due to both an autoimmune reaction (Hooshmand-Rad 1976) and the effect of intra-erythrocytic piroplasms (Preston et al. 1992). ●In addition, pro-inflammatory cytokines, particularly TNF-α, have been implicated in mediating anemia associated with tropical theileriosis. ●The decrease in RBC could be due to increased levels of activated complement products. Additionally, since oxidized erythrocytes may be destroyed easily by erythropagocytosis, oxygen radicals may also be involved in the pathogenesis of anemia
  • 25. Jaundice ●It could be also a resultant of biliary obstruction which resulted in obstructive jaundice with a reflux of cholesterol into the blood stream from the liver and stimulate hepatic cell membrane for synthesis of cholesterol.
  • 26. Increased respiratory and heart rate Normal Infected Heart rate (bpm)(65 to 80) 122 Respiratory rate (cpm) (15 to 35) 75 bpm: beats per minute cpm: cycles per minute ●Anemia associated with theileriosis and secondary hypoxia and vasculitis, leading to some degree of cardiovascular injury. ●Cardiac troponin I is released from myocytes in both reversible and irreversible myocardial injury. ●Respiratory signs occur due to the accumulation of edematous fluid inside the lung and thoracic cavity
  • 27. Ocular oedema in a cow Lacrimation with visible ocular odema Ocular odema Ocular odema ●it is strongly believed that T. annulata in the foetal circulation might have got access into cerebral circulation and caused increased vascular permeability. ●It is believed that the endothelial cells of the fine ocular blood vessels of the orbit were the probable site of multiplication of the pathogen congenitally acquired from the dam during gestation and consequential oedema of the orbits and eyelids(Vikrant Sudan et al 2012)
  • 28. ●The cornel opacity was explained by as a result of white blood cells infiltration. Theileria opacity Corneal opacity
  • 29. ●The occurrence of parasites produces lesions in the endothelial lining of blood vessels, tissue damage in organs, such as the liver, kidney, and lung, and multiple petechial haemorrhages (Forsyth et al 1999), all of which play an important role in the development of coagulation defects (Levi, et al.,1997)
  • 30. Oedema of the jaw in a cow ●Oedematous jaw is due to decreased serum calcium concentration in infected cattle could be attributed to the hypoalbuminaemia and kidney damage (Burtis and Ashwood, 1996). ●The reduction of serum protein level could be attributed to extra-vascular proteinaceous fluid in body cavities due to infected lymph nodes, resulting in edema ●Hypoproteinaemia and hypoalboumineamia is possibly due to the harmful effect of toxic metabolites of Theileria and also due to liver dysfunction. Oedema Theileria annulata induced brisket oedema in a bull
  • 31. ●Mediastinal lymph nodes around the base of cranial and caudal vena cava returning blood to the heart may be affected by Theileria species. ●In this condition, jugular engorgement, oedema, inappetence are the clinical signs. Beisket oedema
  • 32. ●Cutaneous nodules were perivascular infiltrate of lymphocytes, macrophages and eosinophils ●Uilenberg and Zwart(1979) reported one case of cutaneous nodules in which both T. parva schizonts and Demodex bovis were found. Numerous skin nodules on the neck and shoulders of a cow with bovine theileriosis skin nodules Innumerable skin nodules in calf
  • 33. Nodules on medial thighs of a heifer Perivascular inflammatory infiltrate (lymphocytes, macrophages and eosinophils) (haematoxylin)
  • 34. Electrocardiography (ECG) Electrocardiography (ECG) examination revealed high amplitude of QRS complex in bull infected with Theileria annulata organisms Improvement in the ECG findings (Lead-I)
  • 35. CLINICOPATHOGY ●Reticulocyte count is an indicator of the rate of erythrocyte production. Reticulocytosis is caused by increased RBC destruction. ● In theileriosis, the reason for this imbalance is that anaemia causes a greater stimulus for RBC production. Singh et al. (2001). ●Activated partial thromboplastin time (aPTT)) and PT were attributed to impaired hepatic synthesis and the consumption of several pro-coagulant clotting factors in theileriosis.(Singh 2001) ●Marked decrease in both basophil and monocyte counts in the infected group. This variation could be due to differences in stage and severity of disease Omer et al. (2002),
  • 36. ●High levels of fibrinogen in cows infected with Theileria annulata infection, pro-inflammatory cytokines, including TNF-a, IL-1, and IL-6, are released systemically from schizont-infected macrophages and monocytes (Brown,1990; Forsyth,1999). ●According to Stockham et al. (2000) and Omer et al. (2002), the decrease in RBC could be due to increased levels of activated complement products. Additionally, since oxidised erythrocytes may be destroyed easily by erythropagocytosis, oxygen radicals may also be involved in the pathogenesis of the anaemia. ●MCV increased and MCHC decreased called macrocytic hypochromic anaemia). In other forms of anemia in which the average size and hemoglobin content of the red blood cells are within normal limits are called normocytic normochromic anemias. Increase MCV and decrease PCV due to toxic metabolite of Theileria sp.cause harmful effect on bone marrow for that interfere erythropossis. ●Leukocytosis result from lymphocytes proliferation in lymphoid organs as a defensive reaction to the invasion and multiplication of T. annulata (Modi et al. 2015) while, leukopenia may be the consequence of the destruction of white blood cells by the parasites. ● The decline in the values of Hb, TEC, and PCV may be attributed to the destruction of piroplasm infected erythrocytes by macrophages in the lymph nodes, spleen and other organs of the monocyte macrophage system coupled with reduced erythropoietic activity.
  • 37. Source: Osama H Omer et al.,2003Biochemical analyze carried out in sera from 23 young and 20 adult Friesian cattle infected from Theileria annulata
  • 38. ●Low serum total protein(hypoproteinaemia) concentration in cattle infected naturally from Theileria annulata possible due to hypoalbuminaemia and hypoglobulinaemia arising from harmful effect of toxic metabolite, liver failure and and sever lymphocytopaenia(Singh et al.,2001) ●The cardiac infracts and sever liver damage seen in rise in Aspartate aminotransferase (AST) and Alkaline phosphate (AP) activity(Laiblin et al 1978). ●AST and ALT are involved in amino acid and carbohydrate metabolism. These enzymes are present in high concentrations in the muscles and liver. Elevation of these enzymes in the blood is indicator of organ necrosis (Murray et al., 1996). ●Significant increase in bilurubin due to hepatic dysfunction and haemolytic anaemia (Singh et al 2001). The increase in bilirubin levels is due to the destruction of parasitized erythrocytes by erythrophagocytosis in the spleen, lymph nodes, and other organs of the reticuloendothelial system. ● Creatinine concentration decrease has no clinically significant. How ever muscle wasting and rapidly emaciated associated with reduce the level of creatinine (Mehlhorn et al1994). ●Increase in BUN and uric acid due to the kidney damage, (Sandhu et al. (1998) ●The significant decrease in cholesterol and triglycerides may be attributed to anorexia associated with the high rise of temperature and diarrhoea (Sharma et al. (1987)
  • 39. Source: Osama H Omer et al.,2003Biochemical analyze carried out in sera from 23 young and 20 adult Friesian cattle infected from Theileria annulata
  • 40. ●Decrease the serum copper and iron concentration is usually no clinical significance ●Decrease the serum phosphorus and magnesium associated with diarrhoea and renal wasting(Agus et al,1982) ●Decrease the potassium concentration associated with inappetance,diarrhoea and hypomaganesaemia(Yadave and Sharma,1986).
  • 41. POSTMORTEM EXAMINATION Bovine, lung. The lung tissue is diffusely tan-brown, and lobules are non-collapsed and rubbery (interstitial pneumonia) Bovine, popliteal lymph node. The node is enlarged and diffusely pale, and contains numerous petechiae.
  • 42. Bovine, kidney. There are multiple petechiae on the surface of the cortex. The lymph node near the hilus is markedly enlarged. Bovine lymphoblasts contain intracytoplasmic Theileria parva.
  • 43. Punched-out ulceration in abomasum a pathognomic lesion
  • 44. DIAGNOSTIC TEST ●PCR is often used in diagnosis as “gold standard test”, and can identify Theileria in the blood of both carriers and clinical cases. ●Antibodies to T. parva and T. annulata can be detected with ELISAs, indirect fluorescent antibody test (IFA) or other serological assays. Theileria-annulata-piroplasms-cattle
  • 45. Differential diagnosis • Heartwater • Trypanosomosis • Babesiosis • Anaplasmosis • Malignant catarrhal fever • Contagious bovine pleuropneumonia
  • 46. MORBIDITY AND MORTALITY ●The mortality rate for tropical theileriosis is reported to be 40-90% in newly introduced cattle but < 5% in some indigenous animals. ●The morbidity rate in small ruminants infected with T. lestoquardi can approach 100%, with reported mortality rates of 46-100%
  • 47. ●In theileriosis, parasites invade to lymphoid cells and at a later stage of infection invade to the erythrocytes and causes fever, anemia and leads to death (Soulsby 1982). Death ●A leucocyte count below 1,000/mm3 is considered critical and fatal in a majority of the cases (Mehlhorn and Armstrong 2001)
  • 48. TREATMENT ●Parvaquone and buparvaquone are 2 effective drugs against tropical theileriosis. ●The recovery rate of animals treated with parvaquone was 60.7% and with buparvaquone it was 88.7% (Hashemi-Fesharki, 1991). ●Buparvaquone (Butalex) at a dose rate of 1 ml/20 kg (2.5 mg/kg) body weight intramuscularly along with supportive therapy like inj. meloxicam,B-complex and fluid therapy. In severe and advanced cases, a second treatment may be required at 48-72 hrs after the initial injection at the same dose rate. ●Ascorbic acid was found better in treating clinical cases of bovine tropical theileriosis indicated by decreased levels of oxidative stress such as plasma malondialdehyde (MDA), return to normal activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD) enzymes post treatment( Ashwani Kumar,2014). Note: Butalex should never be given by intravenous or subcutaneous injection
  • 49. CONTROL ●Topical application of flumethrin 1 % pour-on preparation (Bayticol pour-on) over the vertebral column is also advised.