Effect of Anaplasma marginale Infection upon Blood Gases and Electrolytes in Splenectomized Calves

Abstract

The principal pathologic manifestation of Anaplasma marginale infection in bovines is anemia, which in acute cases may cause packed cell volumes (PCV) to fall below 10% within 4 to 5 days after the onset of parasitemia. Mortality seen in acute cases appears directly related to the anemic process. However, the underlying mechanisms connecting anemia and mortality have not been well documented. Furthermore, the death or survival of an infected animal is difficult to predict from its PCV, parasite count, and outward appearance. The rapid destruction of 02and CO2-carrying red blood cells (RBC's) and the concomitant rapid release of RBC contents within the host in acute anaplasmosis could conceivably lead to imbalances in blood pH and salts. Thus we examined blood gases, pH, and electrolytes to determine whether any of these parameters change during A. marginale infection in a manner incompatible with life. The 6to 10-month-old splenectomized calves studied were animals involved in other continuing experiments at this station. The use of splenectomized calves was justified by the findings of Roby et al. (1961, Am. J. Vet. Res. 22: 982-985) who found that splenectomized, mature cows were similar to nonsplenectomized animals in susceptibility to inoculation with anaplasma-infected blood. Ten calves were infected with A. marginale (1.4 x 108 infected particles), four calves received no inoculum. In addition, observations were made on three calves that spontaneously revealed Eperythrozoon wenyoni infections after splenectomy and survived. Blood samples for gas and pH analyses were collected anaerobically in heparinized syringes by jugular venipuncture, iced immediately, and analyzed at 37 C within an hour on a Corning blood gas analyzer. Blood samples for other analyses were collected in evacuated tubes with lithium-heparin as an anticoagulant. Plasma K+ and Na+ were assayed by flame photometry; chloride, by titration (Schales, 1953. In Standard methods of clinical chemistry, Vol. 1, M. Reiner, [ed.], Academic Press, New York, New York, pp. 37-42); and blood urea nitrogen (BUN), colorimetrically (Mattenheimer, 1970. Micromethods for the Clinical and Biochemical Laboratory, Ann Arbor Science Pub., Ann Arbor, Michigan, pp. 126-127). Hemoglobin (Hb) was assayed as methemoglobin (Mattenheimer, 1970, loc. cit. p. 88). Percent reticulocytosis was estimated from counts of at least 3,000 Giemsa-stained RBC's. Until the time of anemic crisis, the only noticeable changes in all infected calves were decreases in Hb and in oxygen content (OC, sum of free, dissolved 02 and 02 bound to Hb), which roughly paralleled decreases in Hb. However, at anemic crisis, dramatic reductions in pH and HCO3concentration were observed in the calves that died. Thus, we compared all measured or calculated values of all the infected calves at anemic crisis (the time of lowest Hb concentration, usually the last observations on the calves in the AMF group), and contrasted them with values from the control group. The infected calves were divided into three groups: A. marginale fatalities (AMF), A. marginale survivors (AMS), and E. wenyoni survivors (EWS); data were subjected to analyses of variance, and the significance of differences among infected groups and between infected and control groups was determined by Duncan's multiple range test at the 5% level. No significant difference in the mean plasma levels of Na+ or Clwas found among the four groups (data not shown). The mean OC's of all infected groups were lower than the mean of the control, but they did not differ significantly from one another (Table I). The mean BUN's of all infected groups were higher than the controls but were not high enough to indicate glomerular dysfunction