Cattle experimentally infected by Anaplasma marginale: Inuence of splenectomy on disease pathogenesis, oxidative prole, and antioxidant status Rovaina L. Doyle a, c, * , Raqueli T. França a , Camila B. Oliveira b , Jo ~ ao F.P. Rezer b , Guilherme M. Klafke c , Jo ~ ao R. Martins c , Andrea P. Santos d , Naíla C. do Nascimento d , Joanne B. Mesick d , Sonia T.A. Lopes a , Daniela B.R. Leal b , Aleksandro S. Da Silva e , Cinthia M. Andrade a a Department of Small Animal, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil b Department of Microbiology and Parasitology, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil c Veterinary Research Institute Desiderio Finamor (FEPAGRO), Health Animal Sciences, Eldorado do Sul, RS, Brazil d Department of Comparative Pathobiology, College of Veterinary Medicine, Purdue University, West Lafayette, IN, USA e Department of Animal Science, Universidade do Estado de Santa Catarina, Chapeco, SC, Brazil article info Article history: Received 5 March 2016 Received in revised form 2 April 2016 Accepted 5 April 2016 Available online 7 April 2016 Keywords: Anaplasmosis Anemia Antioxidants Lipid peroxidation abstract Bovine anaplasmosis is caused by the obligate intraerythrocytic bacteria Anaplasma marginale. These bacteria are transmitted by tick species such as Rhipicephalus (Boophilus) microplus, blood-sucking in- sects, and fomites (needles, clippers, and other blood contaminated equipment). During the acute phase of infection, animals may develop fever, anemia, jaundice, and hepatosplenomegaly. The aims of this study are to quantify the bacteremia by quantitative PCR in eight naïve calves experimentally infected by A. marginale [splenectomized (n ¼ 4), and intact/non-splenectomized (n ¼ 4)], and to correlate these ndings with markers of oxidative stress on days 0, 8, 15, 21 and 23 post-infection. Complete blood counts (CBC) were performed in both groups. Lipid peroxidation was estimated by quantifying thio- barbituric acid reactive substances (TBARS); and non-enzymatic antioxidants were assessed by eryth- rocyte content of non-protein thiols (NPSH). There were no signicant differences in complete blood counts (CBC) between the two groups. However, both groups had a slight decrease on packet cell volume (PCV), erythrocytes and hemoglobin concentration, as well as an increase in total leukocyte counts due to elevated lymphocytes when comparing pre and post-infection with A. marginale. Progressive increase on TBARS levels and concomitant decrease on NPSH content were observed in all animals, without signif- icant differences between splenectomized and intact animals. A positive correlation between bacteremia and TBARS, and a negative correlation between bacteremia and NPSH were observed in both groups with higher correlation for NPSH in splenectomized animals. A negative correlation between TBARS and NPSH levels was observed in both groups indicating lipid peroxidation without a non-enzymatic antioxidant response. The results of experimental infection by A. marginale in cattle showed that bacteremia has an impact on lipid peroxidation regardless of the splenectomy. © 2016 Published by Elsevier Ltd. 1. Introduction Anaplasmosis is one of the most important tick-borne diseases in cattle. It causes signicant economic losses in dairy and beef herds in tropical and subtropical areas [1e4]. The etiologic agent is the obligate intraerythrocytic bacteria Anaplasma marginale [5]. In South America, its main vector is the tick Rhipicephalus (Boophilus) microplus, however, it also can be transmitted by blood sucking insects, which are less effective vectors than ticks [2,6,7]. In addi- tion, iatrogenic or transplacental transmissions have been reported [4]. In mammalian hosts, A. marginale infects red blood cells by forming a vacuole derived from the erythrocyte membrane itself, * Corresponding author. Department of Small Animal, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil. E-mail address: rovainadoyle@yahoo.com (R.L. Doyle). Contents lists available at ScienceDirect Microbial Pathogenesis journal homepage: www.elsevier.com/locate/micpath http://dx.doi.org/10.1016/j.micpath.2016.04.011 0882-4010/© 2016 Published by Elsevier Ltd. Microbial Pathogenesis 95 (2016) 193e199