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A retrospective study of the clinical hematology and biochemistry of canine ehrlichiosis in an animal hospital population in Bangkok, Thailand

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A retrospective study on 687 canine ehrlichiosis cases was carried out during January 2001–December 2003 at the Chulalongkorn Small Animal Teaching Hospital, Faculty of Veterinary Science, Chulalongkorn University. Data on rectal temperature,
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  Comp Clin Pathol (2006) 15: 107  –  109DOI 10.1007/s00580-006-0606-6 SHORT PAPER  Sukullaya Assarasakorn .Anuchai Niwetpathomwat .Somporn Techangamsuwan .Siram Suvarnavibhaja  A retrospective study of clinical hematology and biochemistry of canine hepatozoonosis on hospital populationsin Bangkok, Thailand Received: 13 December 2005 / Accepted: 26 February 2006 / Published online: 11 May 2006 # Springer-Verlag London Limited 2006 Abstract  Canine hepatozoonosis is an endemic tick-bornedisease of Thailand, but the clinical data for the disease arerarely reported. The objective of this study was intended tocharacterize the clinical hematology and biochemistry of admitted canine hepatozoonosis cases of the ChulalongkornSmall Animal Teaching Hospital, Bangkok from January2001 toDecember 2003.A total of342 dogs were examinedin this study. Most of the dogs presented with hypocytichypochromic anemia. Leukocyte and platelet counts werevariable and nonspecific in these cases. Additionally, serum biochemistry including blood urea nitrogen, creatinine, liver enzymes, total protein, albumin, and glucose of infecteddogs were within normal ranges. This study indicated that hypocytic hypochromicanemiawas a consistenthematolog-ical value feature of canine hepatozoonosis, but clinical biochemical findings were not consistent in this endemic-hospital population of canine hepatozoonosis. Keywords  Hepatozoonosis .Hematology .Biochemistry .Dogs Introduction Canine hepatozoonosis is a tick-borne disease caused by the protozoan  Hepatozoon  spp. It has been found widespread incountries including the United States, Africa, southernEurope, and Asia. Recently, the common outbreaks arecaused by  Hepatozoon canis  and  Hepatozoon americanum and have the main tick vector of   Rhipicephalus sanguineus and  Amblyomma maculatum , respectively (Baneth et al.2001; Cummings et al. 2005). The nature of transmission in dogs usually occurs after the ingestion of infected ticks that harbor sporulated oocysts of   Hepatozoon . The clinical presentations may range from asymptomatic stages to severesymptoms with life-threatening illness. Fever, lethargy,anemia, and emaciation are the main clinical signs (BanethandWeigler 1997).Other signs suchasdiarrhea,paraparesis,generalized muscle atrophy, hyperesthesia, purulent ocular and nasal discharges have been noted in some reports(Murata et al. 1991; Macintire et al. 1997). Moreover, the infection of   H. americanum  usually manifests by fever,lethargy, weight loss, stiffness, pain, paresis, and ocular discharge (Vincent-Johnson et al. 1997). The clinico-patho-logical changes of canine hepatozoonosis include elevatedleukocyte count, mild normocytic, normochromic regenera-tive anemia, thrombocytosis, or thrombocytopenia (JaurequiandLopez1995;Voyvodaetal.2004).Additionally,lowered glucose and albumin concentration, hyperglobulinemia, andincreased alkaline phosphatase (ALP) activity and inorganic phosphorus concentration have been found in some dogs(Alencar et al. 1997; Craig 1998; Voyvoda et al. 2004). In Thailand, although canine hepatozoonosis has beenidentified as an endemic tick-borne disease, there are fewreports describing the clinical manifestations and patholog-ical changes of dogs which are infected with  Hepatozoon .The purpose of this study was to analyze the clinicalhematology and biochemistry of canine hepatozoonosis indogs within hospital populations in Bangkok, Thailand. Materials and methods Study design and data collectionA retrospective study was carried out from January 2001 toDecember 2003 in out patient department (OPD) dogs of  S. Assarasakorn .S. SuvarnavibhajaAcademic Affair, Faculty of Veterinary Science,Chulalongkorn University,Bangkok, 10330, ThailandA. Niwetpathomwat ( * )Department of Veterinary Medicine,Faculty of Veterinary Science, Chulalongkorn University,Bangkok, 10330, Thailande-mail: anuchai.n@chula.ac.thTel.: +662-218-9412Fax: +662-255-3910 S. TechangamsuwanDepartment of Veterinary Pathology,Faculty of Veterinary Science, Chulalongkorn University,Bangkok, 10330, Thailand  Chulalongkorn Small Animal Teaching Hospital, Faculty of Veterinary Science, Chulalongkorn University, Bangkok,Thailand. The dogs were diagnosed to have canine hepato-zoonosisbytheVeterinaryDiagnosticLaboratory,Facultyof VeterinaryScience,ChulalongkornUniversity.Dataofrectaltemperature, clinical hematology, and serum biochemistrywere collected once on the first day of admission. Mean andobservation data of patients were compared with thereference data. Results A total of 342 cases of canine hepatozoonosis werediagnosed at the Chulalongkorn Small Animal TeachingHospital from January 2001 to December 2003. Their mean rectal temperature was 103.15°F (range: 100  –  106.30°F) and 28% were more than 103°F. The meanhematological and serum biochemical values are shown inTable 1 and Table 2, respectively. The animal patients showed hypocytic hypochromic anemia and 8% of caseshad packed cell volume less than 20%. The white bloodcell (WBC) counts ranged from 2.06  –  45.78×10 3 cells/  μ  l,and 12 and 27% of the cases had WBC counts lower than6.0×10 3 cells/  μ  l and more than 17.0×10 3 cells/  μ  l,respectively. The mean platelets counts were within normalranges.The serum biochemistry of canine hepatozoonosis patients was varied but the mean of all serum biochemistrywas within normal ranges. Thirteen percent of all patientsshowed creatinine levels of more than 1.4 mg/dl, 19% of all patients had alanine phosphatase (ALP) levels of more than500 IU/l and 19% of all patients had alanine aminotrans-ferase (ALT) levels of more than 94 IU/l. Discussion Canine hepatozoonosis is an endemic tick-borne diseasedistributedthroughoutmanyareasofThailand,buttherearesome reportsdescribing theclinical pathologicalchanges indogs infected with  Hepatozoon . In this study, wedetermined hematological and serum biochemical valuesof 342 dogs which were confirmed with  Hepatozoon Table 1  Hematology of 342 cases of canine hepatozoonosis from Chulalongkorn Small Animal Teaching Hospital, Bangkok, ThailandParameters Units Patient data Reference data a  Mean Observation range Mean Reference rangeRBC ×10 6 /  μ  l 5.83 1.15  –  9.61 6.8 5.5  –  8.5Hemoglobin g/dl 12.05 2.60  –  20.0 15.0 12.0  –  18.0PCV % 37.14 7.8  –  60.1 45.0 37.0  –  55.0MCV Fl 59.10 41.0  –  69.0 70 60.0  –  77.0MCH Pg 18.67 11.0  –  24.0 22.8 19.5  –  24.5MCHC % 31.87 20.0  –  40.0 34.0 32.0  –  36.0WBC ×10 3 /  μ  l 14.41 2.06  –  45.78 11.5 6.0  –  17.0Segmenters ×10 3 /  μ  l 10.31 0.89  –  42.12 7.0 3.0  –  11.5Bands ×10 3 /  μ  l 0.28 0.0  –  7.46 0.07 0  –  0.30Lymphocytes ×10 3 /  μ  l 2.50 0.04  –  8.95 2.8 1.0  –  4.8Monocytes ×10 3 /  μ  l 0.45 0.0  –  3.48 0.75 0.15  –  1.35Eosinophils ×10 3 /  μ  l 0.74 0.0  –  3.94 0.55 0.10  –  1.25Basophils ×10 3 /  μ  l 0 0 0 RarePlatelets ×10 3 /  μ  l 229 37  –  765 300 200.0  –  500.0Parameters are listed in SI units for   RBC   Red blood cell,  PCV   packed cell volume,  MCV   mean cell volume,  MCH   mean corpuscular hemoglobin,  MCHC   mean corpuscular hemoglobin concentration,  WBC   white blood cells,  Segmenters  neutrophils,  Bands  pre-matureneutrophils a  Jain (1986) Table 2  Serum biochemistry of 342 cases of canine hepatozoo-nosis from Chulalongkorn SmallAnimal Teaching Hospital,Bangkok, ThailandParameters are listed in SI unitsfor   BUN   Blood urea nitrogen,  ALP   alkaline phosphatase,  ALT  alanine aminotransferase,  AST  aspartate aminotransferase a  Tvedten 2004Parameters Units Patient data Reference range a  Mean Observation rangeBUN mg/dl 29.96 5.0  –  270 7  –  32Creatinine mg/dl 1.19 0.40  –  9.50 0.5  –  1.4Total protein g/dl 6.70 4.20  –  8.40 5.3  –  7.6Albumin g/dl 3.90 2.90  –  5.30 3.2  –  4.2ALP IU/L 366.22 45  –  2,351 0  –  90ALT IU/L 69.53 6  –  849 10  –  94AST IU/L 49.47 10  –  174 10  –  62Glucose mg/dl 71.50 50  –  92 53  –  117108  infection from January 2001 to December 2003. The patients showed clinical signs of fever. The hematologicalfindings demonstrated hypocytic hypochromic anemia,variable leukocyte count, and normal platelet count.These findings were different from other studies in whicha mild normocytic, normochromic, regenerative anemiaand an elevated leukocyte count had been consistent findings with cases of canine hepatozoonosis (Jaurequiand Lopez 1995; Paludo et al. 2003). These common abnormalities are usually found in animals with high parasitemia (Baneth and Weigler  1997). Moreover, changein platelet count could be found in some dogs, andthrombocytopenia would be expected with concurrent   Ehrlichia  infection (Macintire et al. 1997).In the present study, serum biochemical values, includ-ing BUN, creatinine, liver enzymes, total protein, albumin,and glucose were within normal ranges. Abnormality of serum chemistry in canine hepatozoonosis such as glucose,albumin, globulin, and ALP could be found in some dogs(Alencar et al. 1997; Voyvoda et al. 2004). For example, low glucose concentration is responsible for the extremeneutrophilia. However, increased ALP (19%), ALT (19%),and azotemia (13%) were found in some patients in thisstudy. Dogs which had elevated BUN and creatinine mayhave had renal disease because glomerulonephritis caused by amyloid deposit had occasionally developed in somesevere cases (Craig 1998).In conclusion, the most consistent clinical pathologicalchange associated with  Hepatozoon -infected dogs in thisstudy was hypocytic hypochromic anemia. Leukocyte andthrombocyte counts and serum biochemical values werevariable and nonspecific in canine hepatozoonosis. Acknowledgements  We would like to thank Veterinary DiagnosticLaboratory and Chulalongkorn Small Animal teaching Hospital,Faculty of Veterinary Science, Chulalongkorn University for thehospitality and the great collaboration in this study. Also, thanks toDr. Terry Heard for correcting the manuscript. References Alencar NX, Kohayagawa A, Santarem VA (1997)  Hepatozooncanis  infection of wild carnivores in Brazil. Vet Parasitol70:279  –  282Baneth G, Weigler B (1997) Retrospective case-control study of hepatozoonosis in dogs in Israel. J Vet Intern Med 11:365  –  370Baneth G, Samish M, Alekseev E, Aroch I, Shkap V (2001)Transmission of   Hepatozoon canis  to dogs by naturally-fed or  percutaneously-injected  Rhipicephalussanguineus ticks.JParasitol87:606  –  611Craig TM (1998) Canine hepatozoonosis. In Greene CE (ed)Infectious diseases of the dog and cat, 2nd edn. Saunders,Pennsylvania, pp 458  –  465Cummings CA, Panciera RJ, Kocan KM, Mathew JS, Ewing SA(2005) Characterization of stages of   Hepatozoon americanum and of parasitized canine host cells. Vet Pathol 42:788  –  796Jain MC (1986) The dog: normal hematology with comments onresponse to disease. In Jain MC (ed) Veterinary hematology, 4thedn. Lea&Febiger, Philadelphia, USA, pp 103  –  125Jaurequi LE, Lopez GM (1995) Canine hepatozoonosis. Vet Int 7:30  –  38MacintireDK,Vincent-JohnsonN,DillonAR,BlagburnB,LindsayD,Whitley EM, Banfield C (1997) Canine hepatozoonosis: in dogsof 22 cases (1989-1994). J Am Vet Med Assoc 210:916  –  922Murata T, Shiramizu K, Hara Y, Inoue M, Shimoda K, Nakama S(1991) First case of   Hepatozoon canis  infection of a dog inJapan. J Vet Med Sci 53:1097  –  1099Paludo GR, Dell ’ Porto A, de Castro e Trindade AR, McManus C,Friedman H (2003)  Hepatozoon spp .: report of some cases indogs in Brasilia, Brazil. Vet Parasitol 118:243  –  248Tvedten H (2004) Reference values. In Willard MD, Tvedten H(eds) Small animal clinical diagnosis by laboratory methods,4th edn. Elsevier, Missouri, USA, pp 417  –  419Vincent-Johnson N, Macintire DKE, Baneth G (1997) Caninehepatozoonosis: pathophysiology, diagnosis, and treatment.Small Anim 19:51  –  62Voyvoda H, Pasa S, Uner A (2004) Clinical  Hepatozoon canis infection in a dog in Turkey. J Small Anim Pract 45:613  –  617109
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