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42Sangwan and Sangwanvaccinated against Foot and Mouth Disease. The initial mean value of 9.88 ± 0.14 (g%) and 30.71 ± 0.63animals were fed concentrate as per National Research (%) to 2.9 ± 0.5 (g%) and 9.0 ± 1.41(%), respectively,Council (1988). Wheat bhoosa (roughage) and green on day 25 post-infection. The clinical andfodder were provided ad libitum. After 15 days, haematological findings of bovine tropical theileriosisGroup-I animals were experimentally infected with T. reported here resembled those documented by otherannulata by attaching ten Theileria positive ticks (five authors (Preston et al., 1992; Sahu et al., 1996; Forsythpairs of females and males) on the ear of each calf, and et al., 1999).the other group was kept as a healthy uninfectedThe infected calves had significantly (p < 0.05) lowcontrol. Infection was monitored by daily clinicallevels of iron in whole blood and erythrocytes,examination (rectal temperature and lymph nodewhereas in plasma, the levels of iron did not changepalpation) and at 2-day intervals, Giemsa-stained thinmuch (Table II). The levels of iron in blood andblood and lymph node biopsy smears were examinederythrocytes reduced significantly (p < 0.05) fromafter the appearance of lymphadenopathy. The day of266.9 ± 7.38 to 67.9 ± 8.37 µg/ml and 384.3 ± 12.46 tothe death of infected calves was recorded. The blood72.7 ± 10.7 µg/ml, respectively, on day 25 postandplasma samples were collected in heparinised andinfection. Generally, the risk of iron inadequacy issterilized glass tubes on 0, 10, 15, 20 and 25 days postassessedby measuring blood hemoglobin and/or theinfection. The tissue samples of liver and spleen werehighly correlated PCV. However, in the study undercollected immediately after the death of infectedreport, the low levels of hemoglobin and PCV did notcalves (four animals). The iron concentrations incorrespond to the low levels of iron in the bodydifferent samples were estimated by using atomicreserves. The liver and spleen iron concentrationsabsorption spectrophotometery (Dunkan, 1976),were found to be 628.8 ± 78.23 [µg/g dry matter (DM)]following acid digestion of organic matter and byand 1647.7 ± 182.53 (µg/g DM), respectively. Theseusing calibration standards made in 0.1N HCl. Thevalues in infected group are much higher than thesamples of blood (1 ml) and plasma ( 2 ml) wererange reported by Georgievskii et al., 1982 i.e.digested separately with 10 ml of digest acid (4:1;180–376 µg/g DM for liver of adult cattle andnitric:perchloric acid ), dried, washed x 2 with 5 ml of200–400 µg/g on fresh basis for spleen, respectivelydeionised water, dried each time and reconstituted(Georgievskii, 1982). Therefore, it is important towith 10 ml and 5 ml of 0.1 N HCl, respectively. Thedistinguish anaemia associated with Theileriatissue samples of liver and spleen ( 0.25 g , dried andinfection from that caused by iron deficiency. Ironground ) were also digested as for plasma and thendeficiency is indicated by low levels of iron in thereconstituted in 10 ml of 0.1 N HCl. Simultaneously,liver, and a marginal band of 150–250 µg/g DM isblanks were also run. The iron concentrations intentatively proposed to separate deficient from normalerythrocytes were calculated by using the followingclaves (Green et al., 1993).formula: trace-element in erythrocytes/ml of blood =whole blood-plasma (1-packed cell volume/100). The high levels in liver and spleen could be attributedHaemoglobin and haematocrit were estimated by either to the increased haemolysis or animals' limitedusing cyanmethaemoglobin and microhaematocrit capacity to excrete iron (Kreutzer and Kirchgessner,methods, respectively (Schalm et al., 1975). The data 1991). If there would have been haemolysis that wouldwere subjected to standard error of means (SE) and have resulted in high plasma iron concentration. But inAnalysis of Variance (ANOVA) for statistical the present study, the plasma iron levels did notsignificance (Snedecor and Cochran, 1967).increase, which point towards the elimination ofRESULTS AND DISCUSSIONinfected erythrocytes by phagocytosis. Also, whilestudying the pathogenesis of anaemia in T. annulataDuring the course of Theileria infection, the calves infection, Hooshmand-Rad (1976) suggested that anshowed fever, anaemia, anorexia, cachexia, diarrhoea, autoimmune reaction was largely responsible for therespiratory distress and recumbancy. The clinical and development of anaemia and postulated that theparasitological findings are recorded in Table I. The production of antibodies was triggered by thedeath of infected calves occurred between 18–27 days development of schizonts; erythrocytic formspost-infection. The haematological responses of apparently were not involved. This contention hascalves are given in Table II. As the disease progressed, been supported by the finding that automarkedfall in hemoglobin and packed cell volume haemagglutinin antibodies were detected only in cases(PCV) were observed. The values for hemoglobin and of theileriosis due to a field or an agamogenous strainPCV were reduced significantly (p < 0.05) from the (lacking erythrocytic forms) but not in premune