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Clinico-Pathological Investigation and Management of Babesiosis in Kankrej cattle.

Introduction

Babesiosis is an important tick borne protozoan infection caused by the genus Babesia which is clinically characterized by high fever, inappetence, emaciation, anemia, jaundice and hemoglobinuria, occasionally diarrhea and abortion may occur in pregnant cattle (Salem et al., 2016). The infection leads to huge loss of production and occasional mortality (Banerjee et al., 2005). Bovine babesiosis is very well known to cause anemia of various type viz. hemolytic, hypochromic as well as normochromic, this change is associated with reduction in erythrogram parameters as well as alterations in serum biochemical parameters (Sharma et al., 2016).The study describes the clinical, hematological and biochemical observations in Babesia infected Kankrej cattle with successful therapeutic management.

History and Clinical Observations

The present study includes total eight Kankrej cattle (5 cows and 3 bullock) aged eight to twelve years with history of hemoglobinuria, inappetence and high fever. Clinical examination revealed high rectal temperature (103.2[degrees]F-104.3[degrees]F), ruminal atony, swollen lymph nodes, pale pink to pale conjunctival mucous membrane, tachycardia, tachypnea and mild to moderate tick infestations.

Thin blood smears were prepared from ear vein of all animals and stained with Giemsa stain to observe under light microscope for presence of intraerythrocytic stages of hemoparasite. Blood samples were collected from jugular vein into [K.sub.3]EDTA-vacutainers for determination of hematological parameters using automatic blood analyzer and Clot activator-vacutainers to determine serum biochemical parameters using semi-automatic clinical chemistry serum analyzer. The blood glucose was estimated by automatic glucometer.

Diagnosis and Treatment

The pyriform bodies of Babesia organism was observed in thin blood smear (Fig. 1). The hemato-biochemical alteration were also recorded in Table-1. All animals were treated with Inj. Nilbery (a) (Diminazine diaceturate) @ 3.5 mg/kg b.wt. intramuscularly at two different site in neck muscles along with supportive therapy including Inj. Melonex (a) (Meloxicam) @ 0.5 mg/kg, Inj. Tribivet (a) (Vit [B.sub.1], [B.sub.6] and [B.sub.12]) @ 10 ml, Inj. Anistamin (a) (Chlorpheni-ramine maleate) @ 10 ml and Inj. Feritas (a) (Iron Sorbitol citric acid complex, Folic acid and Hydroxycobalmin) @ 10 ml intramuscularly on day one. After 12 hours of treatment and by the end of 24 hours, the color of urine was almost normal in color and appetite was partially restored so supportive treatment with Inj. Intalyte (a) (20 percent Dextrose and Electrolytes) @ 2 lit I/V, Inj. Tribivet (a) @ 10 ml I/V as well as Inj. Anistamin (a) @ 10 ml and Inj. Melonex (a) @ 0.5 mg/kg intramuscularly was continued for three days while Bolus Feritas (a) @ 2 boli BID and Liq. Amblycure D.S. (b) (Liver tonic) @ 50 ml BID were given till complete recovery.

Discussion

The tick-borne infection leads to negative impact on livestock health as well as great economic losses. The light microscopy examination for detection of Babesia piroplasms is relatively cheap, quick and gold standard method even though for chronic infection. The clinical signs including high fever, loss of appetite, anemia, hemoglobinuria, pale mucus membranes and suspended rumination which are in support with Constable et al. (2017).

The lower level of hemoglobin, TEC, PCV, MCHC and platelets along with increase in MCV value in infected animals advocates presence of macrocytic hypochromic anemia. Anemia is an important feature of Babesia because the presence of protozoa lead to destruction of RBCs and creating hemolysis (Kakoma and Ristic, 1984). The low values of platelets count is due to lower production or high destruction which is usually correlated with immune-mediated process and hemolysis (Riond et al., 2008). However, leukocytosis, monocytosis and lymphocytosis in clinically infected animals which is close to Salem and El-Sherif (2015). This is because of RBC destruction by Babesia spp. stimulates phagocytic activity of lymphocytes and monocytes to clean up the body from toxic remnants of ruptured red blood cells which is explained by Guglielmone et al. (1996) that Babesia infection stimulates the body defense mechanism for production of antibodies.

The present investigation exhibited hypoglycemia, higher level of AST, hypoproteinemia, hypoalbuminemia, hyperglobulinemia and increased values of creatinine and BUN in Babesia infected animals. The harmful effect of toxic metabolites of Babesia spp. on liver cells leading to higher level of AST, hypoproteinemia and hypoalbuminemia (Yeruham et al., 2003) while on renal tissue causing impairment and alterations of the kidney enzymes viz. creatinine and BUN and hemoglobinuric nephrosis (Sharma et al., 2016). The significant increase in serum globulins in present study could be attributed to immune response against Babesia and hypoglycemia is associated with anorexia as suggested by Fujinaga (1981). Diminazine diaceturate acts by blocking the replication of DNA of the parasite which has been reported to be highly effective drug against babesiosis (Kumar et al., 2008). The present study suggested that early detection as well as specific chemotherapy and intensive supportive therapy are essential for successful management of babesiosis in Kankrej cattle.

Acknowledgements

The authors are grateful to Department of Veterinary Pathology for providing the facilities to carry out this work.

References

Banerjee, P.S., Suresh, D., Stuti, V., Bhatt, P and Yadav, C.L. (2005). Babesiosis in a cross bred-cow with clumping of parasitized red blood cells. J Vet Parasitol. 19: 153-54.

Constable, P.D., Hinchcliff, K.W., Done, S.H. and Grunberg, W. (2017). Veterinary Medicine - A Textbook of Diseases of Cattle, Horses, Sheep, Pigs and Goats. 11th Edn. Saunders.

Fujinaga, T. (1981). Bovine Babesiosis in Japan clinical and clinic pathological studies on cattle experimentally infected with Babesia ovata. Japan J. Vet. Sci. 43: 803-13.

Guglielmone, A.A., Gaido, A.B. and Mangold, A.J. (1996). Light microscopy diagnosis of Babesia and Theileria in haemolymph of artificially infected Boophilus microplus engorged female ticks. Vet. Parasitology. 61: 15-20.

Kakoma, I. and Ristic, M. (1984). Malaria and Babesiosis - Research findings and control measures. Springer, p. 85-93.

Kumar, B., Verma, S.P., Sinha, B. and Shekar, S. (2008). Therapeutic efficacy of alum-boric acid in bovine babesiosis. Indian Vet. J. 85: 1107.

Riond, B.M.M., Braun, U., Deplazes, P., Joerger, K., Thoma, R. and Lutz, H. (2008). Concurrent infections with vector-borne pathogens associated with fatal anaemia in cattle: hematology and blood chemistry. Comparat. Clin. Pathol. 17: 171-17.

Salem, N.Y. and El-sherif, M.A. (2015). Malondialdehyde status, trace minerals and hematologic results of anemic - T. equi infected Egyptian horses. Int J Vet Sci. 4: 118-22.

Salem, N.Y., Yehia, S.G., Farag, H.S. and Elkhiat, M.A. (2016). Clinical, hemato-biochemical alterations and oxidant-antioxidant biomarkers in Babesia infected calves. Int. J Vet. Sci and Med. 4: 17-22

Sharma, A., Singla, L.D., Batth, A. and Kaur, P. (2016). Clinicopath-biochemical alterations associated with sub-clinical babesiosis in dairy animals. J Arthropod. Borne Dis. 10: 259-67.

Yeruham, I., Avidar, Y., Aroch, I. and Hadani, A. (2003). Intra-uterine infection with Babesia bovis in a 2-day- old calf. J. Vet. Med. B. Infect. Dis. Vet. Public Health. 50: 60-62.

Vijay L. Parmar (1), Binod Kumar (2), B.J. Thakre (2), A.K. Bilwal (3) and J.S. Patel (4)

Department of Veterinary Medicine College of Veterinary Science and Animal Husbandry Junagadh Agricultural University (JAU) Junagadh - 362001 (Gujarat)

(1.) Assistant Professor and Corresponding author.

E-mail: dr.vijayvets@yahoo.com

(2.) Assistant Professor, Department of Veterinary Parasitology

(3.) Assistant Professor

(4.) Professor and Head

(a) - Brand of Intas Animal Health, Ahmedabad

(b)- Brand of Aimil Pharmaceuticals India Ltd., Delhi
Table 1: Hemato-biochemical parameters of Babesia infected Kankrej
cattle

Parameter                     Cattle   Cattle   Cattle   Cattle   Cattle
                                1        2        3        4        5

Hematological
Hemoglobin (g/dl)               6.7      7.2      6.9      7.5      7.1
TEC (x [10.sup.6]/[micro]l)     3.9      4.3      4.1      4.0      4.2
PCV (%)                        20.4     21.8     20.9     20.2     21.6
MCV (fl)                       52.3     50.8     51.2     50.4     51.5
MCHC (g/dl)                    32.8     33.0     33.0     35.6     32.8
Platelets                     173      181      178      163      172
([10.sup.3]/[micro]l)
TLC (x[10.sup.3]/[micro]l)     16.3     16.7     15.6     17.1     16.9
Neutrophils (%)                58       55       51       60       48
Lymphocytes (%)                67       63       68       71       66
Monocytes (%)                  11       14       10       15       11
Eosinophils (%)                 2        1        3        1        1

Biochemical
Glucose (mg/dl)                38       36       39       41       39
AST (U/l)                     163      167      161      159      160
Total Protein (g/dl)            5.4      5.3      5.0      5.6      5.1
Albumin (g/dl)                  0.5      0.6      0.4      0.5      0.5
Globulin (g/dl)                 4.9      4.7      4.6      5.1      4.6
BUN (mg/dl)                    32       34       31       29       30
Creatinine (mg/dl)              4.1      4.3      3.9      3.7      4.1

Parameter                     Cattle   Cattle   Cattle   Reference
                                 6        7        8      Range (*)

Hematological
Hemoglobin (g/dl)               6.5      7.4      6.8      8.5-12.2
TEC (x [10.sup.6]/[micro]l)     3.7      4.1      3.9      5.1-7.6
PCV (%)                        20.3     21.4     21.1     22-33
MCV (fl)                       54.8     52.1     54.2     38-50
MCHC (g/dl)                    32.0     34.6     32.2     36-39
Platelets                     182      169      175      200-650
([10.sup.3]/[micro]l)
TLC (x[10.sup.3]/[micro]l)     15.2     17.4     16.4      4.9-12
Neutrophils (%)                53       59       45       18-63
Lymphocytes (%)                64       73       75       16-56
Monocytes (%)                  13       17       12        0-8
Eosinophils (%)                 2        1        2        0-9
Biochemical
Glucose (mg/dl)                42       40       37       45-75
AST (U/l)                     172      157      163       78-132
Total Protein (g/dl)            4.9      5.2      5.6      5.7-8.1
Albumin (g/dl)                  0.3      0.3      0.6      2.1-3.6
Globulin (g/dl)                 4.6      4.9      5.0      3.6-4.5
BUN (mg/dl)                    31       33       34        6.0-27
Creatinine (mg/dl)              4.3      4.2      4.3      1-2

(*) Constable et al. (2017)
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Article Details
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Title Annotation:Clinical Article
Author:Parmar, Vijay L.; Kumar, Binod; Thakre, B.J.; Bilwal, A.K.; Patel, J.S.
Publication:Intas Polivet
Geographic Code:9JAPA
Date:Jul 1, 2018
Words:1614
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