BOVINE BABESIOSIS
Dr. Jibachha Sah
M.V.Sc, Lecturer, College of Veterinary Science,
NPI, Bhojad, Chitwan, Nepal
jibachhashah@gmil.com,00977-9845024121
Introduction
SYNONYMS : Red fever,Tick fever,Texas fever,Piroplasmosis.
●Bovine babesiosis is a febrile, tick-borne disease of cattle and buffalo, caused by one
or more protozoan parasites of the genus Babesia.
● The term "Babesiosis" refers to the acute form. The acute form is generally
characterized by rapid growth and multiplication of the parasite in blood
with extensive erythrocytic lysis leading to anemia, icterus,
hemoglobinuria, enlargement of the spleen, and frequently, death.
● The term "Babesiosis“ also refers to the subclinical and chronic infections that usually
persist following recovery from initial attack by the parasite.
● The chronic form is poorly defined clinically and is associated with anemia and
variable weight loss.
HOST : Cattle, buffalo, horse, sheep, goat, dog, pig, wild animals, and humans.
ETIOLOGY : Bovine babesiosis is a febrile, haemolytic disease caused by intraerythrocytic
protozoan of the genus Babesia, including several species namely
Babesia bigemina,
B. divergens,
B. bovis, and
B. major.
INCUBATION PERIOD : 5-10 days.
Heavy tick infestation
Vector:
The chief vector of Babesia species is the
southern cattle fever tick Rhipicephalus
microplus (formerly Boophilus microplus).
●Sporozoites (Sz) injected into the bloodstream of a bovine during the blood meal of an infected
tick, invade erythrocytes and differentiate into trophozoites (T), which divide asexually into
usually two merozoites (M). Merozoites eventually exit erythrocytes and invade new ones,
continuing their replicative cycle.
Lifecycle
Pathogenesis
●Babesia species produces acute disease by two principle mechanism; hemolysis and circulatory
disturbance.
●During the tick bite, sporozoites are injected into the host and directly infect red blood cells. It
invades erythrocyte and cause intravascular and extra vascular hemolysis.
● The rapidly dividing parasites in the red cells produce rapid destruction of the erythrocytes with
accompanying haemoglobinaemia, haemoglobinuria and fever.
● This may be so acute as to cause death within a few days, during which the packed cell volume falls
below 20% which will lead to anemia.
(A)Cattle showed hemoglobinuria (B), poor body condition (C), pale mucous
membrane of eye and(D) pale mucous membrane of vagina due to babesiosis
Clinical sign
●Fever
● Anorexia
● Depression
● Increased respiratory rate particularly following exertion
● Muscle tremor
● Reluctance to move
● Haemoglobinuria
● Anaemia and jaundice
● Occasionally signs of cerebral derangement such as circling, head pressing, mania and convulsions.
This is associated with the sludging of parasitized R.B.C in brain capilaries(cerebral form of babesiosis)
● Abortions may occur when pregnant animals are severely affected.
●B. divergens causes spasm of the anal sphincter, causing the passage of "pipe stem" feces. The feces
are evacuated with great force in a long thin stream, even in the absence of diarrhea.
● Lactic acid generation from tissue hypoxia is considered the main reason for metabolic acidosis that
develops in animals with babesiosis.
●The fibrinogen-like proteins make erythrocytes more “sticky,” leading to additional erythrocyte
sludging in the capillaries.
●Vascular stasis from sludging of parasitized erythrocytes and their stroma within capillary beds is
thought to contribute to acute anemia and many of the other potential clinical signs.
●The most severe sludging appears to occur in the central nervous system (CNS) and muscles.
●Infected erythrocytes incorporate parasite antigens into
their surface and induce host opsonizing antibodies,
which leads to removal of infected erythrocytes by the
mononuclear-phagocyte system.
●The mononuclear phagocyte system has an
important role in defense against microorganisms,
including mycobacteria, fungi, bacteria, protozoa, and
viruses.
●Additionally soluble parasite antigens may adhere to
the surface of some non-infected erythrocytes and
platelets. This may lead to their opsonization by
antibodies, with or without complement, and account for
the hemolytic anemia and thrombocytopenia that is often
not correlated with the level of parasitemia.
●Hosts may develop anti–erythrocyte membrane
antibodies against self antigens and have increased
erythrophagocytic activity of macrophages, which can
contribute to the immune mediated anemia.
●In addition to immune-mediated destruction, multiple mechanisms appear to account for the hemolysis
seen with babesiosis. Parasitemia results in osmotically fragile erythrocytes, hemolysis, and subsequent
anemia.
● Direct parasitic injury during penetration and occupation of the cell contributes to the hemolytic
process.
●Oxidative stress is another possible cause of damage to erythrocytes that also results in increased
susceptibility to phagocytosis. Oxidative stress is an imbalance between free radicals and antioxidants
in animal body.
● Increased urinary methemoglobinemia levels, as a result of hemoglobin oxidation followed by
hemolysis, have been found in dogs with naturally occurring B. canis infections.
●A syndrome similar to septic shock has been described in a low percentage of dogs infected with a
large Babesia species presumed to be B. canis canis.
● Resultant tissue damage from the infection probably causes the release of cytokines, which support
widespread inflammation and additional damage to multiple organs.
●Other possible complications include membranoproliferative glomerulonephritis, which may have an
immune-mediated pathogenesis.
●Azotemia and proteinuria are common in dogs infected with B. microti–like parasites, and their
presence has been associated with increased mortality.
Complete blood cell count test of Babesia infected cow
Source:Mohamad et al.,2018
Infected cow
●The affected cattle showed significant reduction in total RBC count, HGB concentration, MCV, HCT,
and MCHC. These results indicated that the infected cattle might suffer from a microcytic
hypochromic type of anaemia. Such a reduction in MCHC could be attributed to haemolysis resulting
from the replication of Babesia within the RBCs( Hillman RS.1998).
.
●The reason for neutropenia, lymphopenia and subsequently leukopenia may be attributed to
sequestration of leucocytes in the spleen.
● While the significant increase in eosinophils due to infected cows mostly with parasitic tick
infestation on skin cause allergic reactions
Coffee colour urinate
Jaundice
Biochemical test of Babesia infected cow
Source:Mohamad et al.,2018
Infected cow
●Increase in the AST and ALT may be due to indirect damage of liver, kidney tissue and
myocardium(Y fruham 1998)
●The increase in total bilirubin due to damage of liver and increase in the indirect bilirubin was due
to erythrocyte haemolysis(Jain NC,1986)
●the presence of Babesia piroplasms inside the
erythrocytes and destruction of large number of
these erythrocytes by the parasite resulting in
hemoglobinemia and consequently hemoglobinuria
Coffee colour urine
●The neurological signs could be attributed to cerebral thrombosis and hypotension by activation of
plasma kallikrein and disseminated intravascular coagulation leading to high mortality rates in cerebral
babesiosis (Radostits et al., 2000)
Cerebral babesiosis in calf with neurological sign
●Cerebral babesiosis, characterized by hyperexcitability, convulsions opisthotonos, coma, and
death, may be observed in cattle, particularly those infected with Babesia bovis.
Diagnosis
●Peripheral blood smear
Babesia is usually diagnosed by blood smear using Giemsa stained
●Antibody testing
The Indirect Flourescent Antibody Test (IFAT) and enzyme-linked immunosorbent
assay (ELISA) are the most commonly available tests.
Giemsa-stained blood smear of naturally infected cow showing intra-erythrocytic Pyriform
(Pear-shape) of Babesia bigemina in pairs
Lane M, molecular size marker 100 bp plus,Lane P
positive control and N negative controls,Lane A–D
showing amplified B. bigeminagenomic DNA from the
blood of animalspositive for infection, Lane E showing
noamplification of B. bigemina genomic DNAfrom the
blood of animal negative for infection.
Source, A Sharma et al.2016.,J Arthropod-Borne Dis,
●PCR testing
Agarose gel (1.5%) electrophoresis showing amplified DNA
(689bp) from Babesia bigemina targeting SSU rRNA gene using
primer Bg3/Bg4
Cadaver, calf. |
There is moderate subcutaneous icterus. (Source:
Laboratory of Anatomic Pathology, Universidade,
Brazil)
Postmortem and
histopathology lesion
Cerebellum, calf.
Capillaries are diffusely expanded and as a result are more visually prominent
(Source: Laboratory of Anatomic Pathology, Universidade, Brazil)
Spleen, calf.
There is moderate splenomegaly. (Source: Laboratory of
Anatomic Pathology, Universidade, Brazil)
Kidney, calf.
The renal cortex is discolored as a result of
hemoglobinuria; the pelvis shows profound icterus.
(Source: Laboratory of Anatomic Pathology,
Universidade, Brazil)
Cerebrum,calf.
There is a diffuse pink discoloration of the brain as
a result of marked cerebral congestion and
sequestration of parasitized erythrocytes (Source: Laboratory
of Anatomic Pathology, Universidade, Brazil)
●Diminazine aceturate @3.5 mg/kg body weight intramuscularly,Mechanism o action of Diaminazine
aceturate is acts by blocking the replication of DNA of the parasite (Bhatt et al., 2005 and Bipin Kumar et
al., 2008).
●For treatment, imidocarb(imidocarb dipropionate) is given SC at 1.2 mg/kg(Imizol 12 % - 1 ml /100 kg by
s/c injection.Mechanism of action of imidocrab is interference with the production and/or utilization of
polyamines, or prevention of entry of inositol into the erythrocyte containing the parasite. The
mechanism of Imidocarb includes nucleic acid damage and inhibition of cellular repair and replication
●Supportive treatment is advisable, particularly in valuable animals, and may include the use of anti-
inflammatory drugs, corticosteroids, and fluid therapy. Blood transfusions may be life-saving in very
anemic animals.
Treatment
●Use of Flumethrin or deltametrin for control of tick infestation. Flumethrin is a type II synthetic
pyrethroid and causes a long-lasting prolongation of the normally transient increase in sodium
permeability of the nerve membrane during excitation, resulting in long- lasting trains of repetitive
firing.
●At a dosage of 3 mg/kg, imidocarb provides protection from babesiosis for ~4 wk and will also
eliminate B bovis and B bigemina from carrier animals
Control:
Bovine babesiosis-Dr.Jibachha Sah.M.V.Sc,Lecturer,NPI

Bovine babesiosis-Dr.Jibachha Sah.M.V.Sc,Lecturer,NPI

  • 1.
    BOVINE BABESIOSIS Dr. JibachhaSah M.V.Sc, Lecturer, College of Veterinary Science, NPI, Bhojad, Chitwan, Nepal [email protected],00977-9845024121
  • 2.
    Introduction SYNONYMS : Redfever,Tick fever,Texas fever,Piroplasmosis. ●Bovine babesiosis is a febrile, tick-borne disease of cattle and buffalo, caused by one or more protozoan parasites of the genus Babesia. ● The term "Babesiosis" refers to the acute form. The acute form is generally characterized by rapid growth and multiplication of the parasite in blood with extensive erythrocytic lysis leading to anemia, icterus, hemoglobinuria, enlargement of the spleen, and frequently, death. ● The term "Babesiosis“ also refers to the subclinical and chronic infections that usually persist following recovery from initial attack by the parasite. ● The chronic form is poorly defined clinically and is associated with anemia and variable weight loss.
  • 3.
    HOST : Cattle,buffalo, horse, sheep, goat, dog, pig, wild animals, and humans. ETIOLOGY : Bovine babesiosis is a febrile, haemolytic disease caused by intraerythrocytic protozoan of the genus Babesia, including several species namely Babesia bigemina, B. divergens, B. bovis, and B. major. INCUBATION PERIOD : 5-10 days. Heavy tick infestation Vector: The chief vector of Babesia species is the southern cattle fever tick Rhipicephalus microplus (formerly Boophilus microplus).
  • 4.
    ●Sporozoites (Sz) injectedinto the bloodstream of a bovine during the blood meal of an infected tick, invade erythrocytes and differentiate into trophozoites (T), which divide asexually into usually two merozoites (M). Merozoites eventually exit erythrocytes and invade new ones, continuing their replicative cycle. Lifecycle
  • 6.
    Pathogenesis ●Babesia species producesacute disease by two principle mechanism; hemolysis and circulatory disturbance. ●During the tick bite, sporozoites are injected into the host and directly infect red blood cells. It invades erythrocyte and cause intravascular and extra vascular hemolysis. ● The rapidly dividing parasites in the red cells produce rapid destruction of the erythrocytes with accompanying haemoglobinaemia, haemoglobinuria and fever. ● This may be so acute as to cause death within a few days, during which the packed cell volume falls below 20% which will lead to anemia.
  • 7.
    (A)Cattle showed hemoglobinuria(B), poor body condition (C), pale mucous membrane of eye and(D) pale mucous membrane of vagina due to babesiosis
  • 8.
    Clinical sign ●Fever ● Anorexia ●Depression ● Increased respiratory rate particularly following exertion ● Muscle tremor ● Reluctance to move ● Haemoglobinuria ● Anaemia and jaundice ● Occasionally signs of cerebral derangement such as circling, head pressing, mania and convulsions. This is associated with the sludging of parasitized R.B.C in brain capilaries(cerebral form of babesiosis) ● Abortions may occur when pregnant animals are severely affected.
  • 9.
    ●B. divergens causesspasm of the anal sphincter, causing the passage of "pipe stem" feces. The feces are evacuated with great force in a long thin stream, even in the absence of diarrhea.
  • 10.
    ● Lactic acidgeneration from tissue hypoxia is considered the main reason for metabolic acidosis that develops in animals with babesiosis.
  • 11.
    ●The fibrinogen-like proteinsmake erythrocytes more “sticky,” leading to additional erythrocyte sludging in the capillaries. ●Vascular stasis from sludging of parasitized erythrocytes and their stroma within capillary beds is thought to contribute to acute anemia and many of the other potential clinical signs. ●The most severe sludging appears to occur in the central nervous system (CNS) and muscles.
  • 12.
    ●Infected erythrocytes incorporateparasite antigens into their surface and induce host opsonizing antibodies, which leads to removal of infected erythrocytes by the mononuclear-phagocyte system. ●The mononuclear phagocyte system has an important role in defense against microorganisms, including mycobacteria, fungi, bacteria, protozoa, and viruses. ●Additionally soluble parasite antigens may adhere to the surface of some non-infected erythrocytes and platelets. This may lead to their opsonization by antibodies, with or without complement, and account for the hemolytic anemia and thrombocytopenia that is often not correlated with the level of parasitemia. ●Hosts may develop anti–erythrocyte membrane antibodies against self antigens and have increased erythrophagocytic activity of macrophages, which can contribute to the immune mediated anemia.
  • 13.
    ●In addition toimmune-mediated destruction, multiple mechanisms appear to account for the hemolysis seen with babesiosis. Parasitemia results in osmotically fragile erythrocytes, hemolysis, and subsequent anemia. ● Direct parasitic injury during penetration and occupation of the cell contributes to the hemolytic process. ●Oxidative stress is another possible cause of damage to erythrocytes that also results in increased susceptibility to phagocytosis. Oxidative stress is an imbalance between free radicals and antioxidants in animal body. ● Increased urinary methemoglobinemia levels, as a result of hemoglobin oxidation followed by hemolysis, have been found in dogs with naturally occurring B. canis infections.
  • 14.
    ●A syndrome similarto septic shock has been described in a low percentage of dogs infected with a large Babesia species presumed to be B. canis canis. ● Resultant tissue damage from the infection probably causes the release of cytokines, which support widespread inflammation and additional damage to multiple organs. ●Other possible complications include membranoproliferative glomerulonephritis, which may have an immune-mediated pathogenesis. ●Azotemia and proteinuria are common in dogs infected with B. microti–like parasites, and their presence has been associated with increased mortality.
  • 16.
    Complete blood cellcount test of Babesia infected cow Source:Mohamad et al.,2018 Infected cow
  • 17.
    ●The affected cattleshowed significant reduction in total RBC count, HGB concentration, MCV, HCT, and MCHC. These results indicated that the infected cattle might suffer from a microcytic hypochromic type of anaemia. Such a reduction in MCHC could be attributed to haemolysis resulting from the replication of Babesia within the RBCs( Hillman RS.1998). . ●The reason for neutropenia, lymphopenia and subsequently leukopenia may be attributed to sequestration of leucocytes in the spleen. ● While the significant increase in eosinophils due to infected cows mostly with parasitic tick infestation on skin cause allergic reactions
  • 18.
  • 20.
    Biochemical test ofBabesia infected cow Source:Mohamad et al.,2018 Infected cow
  • 21.
    ●Increase in theAST and ALT may be due to indirect damage of liver, kidney tissue and myocardium(Y fruham 1998) ●The increase in total bilirubin due to damage of liver and increase in the indirect bilirubin was due to erythrocyte haemolysis(Jain NC,1986)
  • 22.
    ●the presence ofBabesia piroplasms inside the erythrocytes and destruction of large number of these erythrocytes by the parasite resulting in hemoglobinemia and consequently hemoglobinuria Coffee colour urine
  • 23.
    ●The neurological signscould be attributed to cerebral thrombosis and hypotension by activation of plasma kallikrein and disseminated intravascular coagulation leading to high mortality rates in cerebral babesiosis (Radostits et al., 2000) Cerebral babesiosis in calf with neurological sign ●Cerebral babesiosis, characterized by hyperexcitability, convulsions opisthotonos, coma, and death, may be observed in cattle, particularly those infected with Babesia bovis.
  • 24.
    Diagnosis ●Peripheral blood smear Babesiais usually diagnosed by blood smear using Giemsa stained ●Antibody testing The Indirect Flourescent Antibody Test (IFAT) and enzyme-linked immunosorbent assay (ELISA) are the most commonly available tests. Giemsa-stained blood smear of naturally infected cow showing intra-erythrocytic Pyriform (Pear-shape) of Babesia bigemina in pairs
  • 25.
    Lane M, molecularsize marker 100 bp plus,Lane P positive control and N negative controls,Lane A–D showing amplified B. bigeminagenomic DNA from the blood of animalspositive for infection, Lane E showing noamplification of B. bigemina genomic DNAfrom the blood of animal negative for infection. Source, A Sharma et al.2016.,J Arthropod-Borne Dis, ●PCR testing Agarose gel (1.5%) electrophoresis showing amplified DNA (689bp) from Babesia bigemina targeting SSU rRNA gene using primer Bg3/Bg4
  • 26.
    Cadaver, calf. | Thereis moderate subcutaneous icterus. (Source: Laboratory of Anatomic Pathology, Universidade, Brazil) Postmortem and histopathology lesion
  • 27.
    Cerebellum, calf. Capillaries arediffusely expanded and as a result are more visually prominent (Source: Laboratory of Anatomic Pathology, Universidade, Brazil)
  • 28.
    Spleen, calf. There ismoderate splenomegaly. (Source: Laboratory of Anatomic Pathology, Universidade, Brazil)
  • 29.
    Kidney, calf. The renalcortex is discolored as a result of hemoglobinuria; the pelvis shows profound icterus. (Source: Laboratory of Anatomic Pathology, Universidade, Brazil)
  • 30.
    Cerebrum,calf. There is adiffuse pink discoloration of the brain as a result of marked cerebral congestion and sequestration of parasitized erythrocytes (Source: Laboratory of Anatomic Pathology, Universidade, Brazil)
  • 31.
    ●Diminazine aceturate @3.5mg/kg body weight intramuscularly,Mechanism o action of Diaminazine aceturate is acts by blocking the replication of DNA of the parasite (Bhatt et al., 2005 and Bipin Kumar et al., 2008). ●For treatment, imidocarb(imidocarb dipropionate) is given SC at 1.2 mg/kg(Imizol 12 % - 1 ml /100 kg by s/c injection.Mechanism of action of imidocrab is interference with the production and/or utilization of polyamines, or prevention of entry of inositol into the erythrocyte containing the parasite. The mechanism of Imidocarb includes nucleic acid damage and inhibition of cellular repair and replication ●Supportive treatment is advisable, particularly in valuable animals, and may include the use of anti- inflammatory drugs, corticosteroids, and fluid therapy. Blood transfusions may be life-saving in very anemic animals. Treatment
  • 32.
    ●Use of Flumethrinor deltametrin for control of tick infestation. Flumethrin is a type II synthetic pyrethroid and causes a long-lasting prolongation of the normally transient increase in sodium permeability of the nerve membrane during excitation, resulting in long- lasting trains of repetitive firing. ●At a dosage of 3 mg/kg, imidocarb provides protection from babesiosis for ~4 wk and will also eliminate B bovis and B bigemina from carrier animals Control: