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The selenium-deficient mouse-trypanosome system was used to study the effects of selenium deficiency in Swiss Webster mice infected with Trypanosoma musculi. In selenium-deficient mice, a low parasitemia was observed and infection was cleared by day 16 post-inoculation (PI), whereas control mice sustained the parasitemia until day 24 PI. There were no significant differences in size variability of the trypanosomes; however the range of variability in the length of parasites differed significantly between the three groups. In comparison to mice on complete or pair-fed diets, the selenium-deficient mice produced lower concentrations of IgG(1), IgG(2b), IgG(3), and IgM. The levels of IgG(2a) and IgA were lower than normal controls. The results of the present study indicated that there was a severe depression in primary and secondary antibody responses to sheep red blood cells in all inoculated mice. However, these responses were significantly less depressed in selenium-deficient mice.

The effects of zinc deficiency on hepatic cell mitotic and peritoneal macrophage phagocytic activities were examined in mice infected with Trypanosoma musculi or immunized with parasitic products. On a full-complement or pair-fed diet, infected and homogenate-inoculated mice showed mitotic activity gains of 7.9% to 80.3% and 6.5% to 99.0%, respectively. Infected and homogenate-inoculated mice on a zinc-deficient diet showed 21.8% to 95.7% and 17.2% to 65.2%, respectively, more dividing liver cells compared with controls. In comparison to controls, macrophages isolated from infected and homogenate-immunized mice on full-complement or pair-fed diets had phagocytized 13.4% to 31.4% more latex particles from day 50 to 80. In the zinc-deficient group, macrophages isolated from infected mice had significant numbers of phagocytized latex particles (1.8% to 38.5%) from day 20 to day 80 compared with controls. The homogenate-immunized mice also had increased numbers (18.6 to 30.8%) of phagocytized latex particles.

This study examined the effect of zinc deficiency on food consumption and the growth of mice infected with Trypanosoma musculi or immunized with parasite products. In addition, the effects of zinc deficiency on the growth and development of parasites in vivo was studied. Infected mice consumed more food than noninfected mice, and the level of food consumption in the zinc-deficient mice was much less and showed general decline during the observation period. Also, infected mice on both full-complement and zinc-deficient diets gained more body weight than control mice. Throughout the observational period, trypanosomes from zinc-deficient mice showed considerably higher variability in size as determined by coefficient of variation. In both dietary groups, the average length of trypanosomes was not significantly different.

A metabolic imbalance technique was used to study the effects of zinc deficiency on immunoglobulin levels in mice infected with Trypanosoma musculi or immunized with parasite products. Zinc-deficient mice developed higher numbers of parasitemia earlier and exhibited prolonged infection. Irrespective of the diet, higher IgG1, IgG2b, and IgM levels, lower IgG2a and IgA levels, and uniform IgG3 levels were exhibited primarily by mice infected with T musculi and to a lesser extent by mice immunized with parasite products. Zinc-deficient mice showed smaller increases in IgG1 and IgM, but larger gains in IgG2b compared with mice on full-complement and pair-fed diets. However, IgG2a decreased significantly in zinc-deficient mice.

Histochemical variations in tissues from rats inoculated with Trypanosoma lewisi and Trypanosoma rhodesiense were investigated. During peak parasitemia, the liver of rats inoculated with T lewisi showed increased glycogen distribution. However, glycogen depletion was noted in the liver and spleen of animals inoculated with living cells of T rhodesiense. Depletion was very apparent from day 4 to day 10. Throughout the period of observation, only a small amount of lipid infiltration occurred in tissues from animals inoculated with both organisms. Protein tests revealed a normal distribution of protein in tissues. Sections of the liver from rats inoculated with T lewisi showed strong alkaline phosphatase activity on days 7, 10, and 13. Alkaline phosphatase activity for T rhodesiense-infected animals was positive for days 4, 7, and 10. Strong positive reactions for acid phosphatase were observed on days 10 and 13 for some tissues (liver, spleen, and kidney) from rats inoculated with T lewisi. On days 4, 7, and 10, intense staining reactions also were observed for livers and spleens of animals inoculated with T rhodesiense. Regardless of tissues observed, histochemical variations were not observed in animals inoculated with the derivatives (ie, metabolic products and homogenates) of T lewisi and T rhodesiense.

A metabolic imbalance technique was employed to study vitamin B(12) deficiency in rats infected with Trypanosoma lewisi. Throughout the observational period, animals on the deficient diet had lowered serum vitamin B(12) levels compared with complete and pair-fed animals. The decline in the level of the vitamin, ten days after the initiation of the experiment, continued progressively until the termination of the study. Body weight gains and food consumption in rats on complete, vitamin B(12)-deficient, or pair-fed diets and inoculated with T lewisi showed significant increase over inoculated controls. The rates of body weight and food consumption in vitamin B(12)-deficient animals were significantly less than that of the adequately fed animals.The indices of lowered resistance to infection in the vitamin B(12)-deficient rats were manifoid. Deficient rats suffered earlier and higher parasitemia followed by persistent infection. The delay in the synthesis of the reproductive inhibiting antibody (ablastin) resulted in prolonged variability in the length of the trypomastigotes. Severe depression in the primary and secondary antibody responses (IgG and IgM) to in vivo immunization of sheep erythrocytes was also observed in the deficient animals. In comparison, the level of IgG antibody decreased approximately one fifth the control values.

Progressive changes in iron levels, total iron binding capacity and hematocrit values in sera of rats infected with Trypanosoma lewisi are described. The host dietary group were: (1) complete or full complement; (2) iron-deficient, and (3) pair-fed or calorically restricted. The hematocrit values of T. lewisi-infected rats given the various diets were not significantly different from those of the controls. The decrease in total iron binding capacity (TIBC) of rats inoculated with T. lewisi and fed complete and pair-fed diets ranged up to 15% over uninfected controls. TIBC levels in rats fed an iron-deficient diet and inoculated with T. lewisi ranged up to 32% over uninfected controls. TIBC levels of deficient infected rats were significantly different from the controls from day 90 to infection to the end of the observation period. Serum iron (SI) values of non-infected rats regardless of dietary regimen showed significantly higher values than T. lewisi-infected animals between days 95 and 120. The average SI value, for this period, in adequately fed control rats was 204 +/- 7 microgram/100 ml as compared to 172 +/- 5 microgram/100 for trypanosome-infected rats. SI levels of rats on a pair-fed diet and infected with T. lewisi decreased to 17% over uninfected controls. SI levels of animals on an iron-deficient diet and infected with T. lewisi decreased up to 76% over uninfected controls.

Ten experiments were performed to compare mitotic activity in livers of rats infected with Trypanosoma rhodesiense and Trypanosoma lewisi. The host dietary groups were: (1) complete of full complement; (2) folic acid deficient, and (3) pair-fed or calorically restricted. Liver mitotic counts of T. lewisi-infected rats fed complete and pair-fed control diets showed a high degree of significance over that of control rats. From days 35 to 55, liver mitotic counts of T. lewisi-infected rats deficient in folic acid showed an average of 16 +/- 2 mitotic phases as compared to 9 +/- 2 for livers of uninfected animals. Liver mitotic counts of T. rhodesiense-infected and non-infected rats fed complete and pair-fed control diets showed that there were essentially no differences in the mitotic counts from that seen in liver from control, uninfected animals. On day 25 (day 5 of infection), folic acid-deficient infected rats showed a significantly higher number of dividing cells than the controls. Folate was measured in isolated, washed T. lewisi and T. rhodesiense cells. T. lewisi and T. rhodesiense contained 9.6 ng folate per 10(8) cells and 6.2 ng of folate per 10(8) cells respectively. Metabolic products of T. lewisi contained an average of 0.51 ng of folate per 10(8) trypanosomes. T. rhodesiense metabolic products contained 0.3 ng of folate per 10(8) trypanosomes.

The influence of trace metal contaminants (lead, cadmium, and mercury) on Sprague-Dawley rats was investigated to determine whether subclinical levels of these metals might have adverse effects on the host's ability to respond to an infective agent.In the present study, a trace metal contaminant-trypanosome system was employed to observe the hematological changes in rats infected with Trypanosoma lewisi. The animal groups were: (1) lead (Pb), (2) cadmium (Cd), (3) mercury (Hg), and (4) controls (animals not exposed to trace metals).Regardless of the trace metals, infected animals showed decreases in total erythrocyte counts and lower hematocrit values. Generally, infected animals also showed increases in total leucocyte counts, decreases in the percentages of lymphocytes and monocytes, increases in percentage of neutrophils, and no changes in percentages of eosinophils and basophils.

Vitamin A-deficiency was studied in mice infected with Trypanosoma musculi. Irrespective of diet, trypomastigotes (trypanosomes) appeared in peripheral tail blood of all inoculated mice after 6-day incubation periods. On the average, vitamin A-deficient mice had parasitemias about 10 times greater than animals fed a complete diet and 8 times pair-fed controls. Parasitemias lasted longer in vitamin-deficient hosts, and reached a maximum five days later than those from control hosts.

Glucose-6-phosphate dehydrogenase (G6PD) changes were studied in livers of rats inoculated with Trypanosoma lewisi, Trypanosoma rhodesiense, Trypanosoma congolense and Trypanosoma brucei. Marked increases in G6PD were directly related to the degree of parasitemia. No essential differences in G6PD levels were seen in animals inoculated with physiological saline when compared with uninoculated controls. Elevation of G6PD was observed only from day 10 to 20 in rats inoculated with T. lewisi. After day 20, the G6PD levels were not statistically significant from those of uninoculated controls. Liver G6PD levels were increased as early as day 3 post-inoculation and continued up to the time of death in rats inoculated with T. brucei, T. rhodesiense and T. congolense.

Transketolase and pyruvate changes were studied in rats infected with Trypanosoma lewisi and fed complete, thiamine-deficient and pair-fed control diets. Regardless of the dietary group, marked increases in pyruvate levels were observed in the infected animals. There were no significant differences in erythrocyte transketolase activity of rats given a full complement diet. Significant decreases, however, were observed in the transketolase activity of pair-fed and thiamine deficient rats. The greater decreases occurred in the infected animals.

Oxygen consumption of Trypanosoma lewisi grown in albino and black rats was measured by the direct method of Warburg. Respiration rates in buffered Ringer's solution, with and without glucose and in normal serum from the respective hosts, were determined for T lewisi grown in albino and black rats. Significantly higher respiratory rates were obtained for trypanosomes grown in albino hosts: 31 percent higher in buffered Ringer's solution with glucose and 26 percent higher in homologous serum.In this study, in which the development of the parasitemia was observed for 27 days, T lewisi populations were higher in albino rats than in black rats.

An experimental model composed of the folic acid deficient Sprague-Dawley rat and Trypanosoma rhodesiense was used to study folate levels in sera and tissues. Serum folate levels in well fed rats inoculated on day 21 averaged 21 plus or minus ng/ml; well fed normal rats averaged 18 plus or minus 4 ng/ml. In rats given the pair-fed control diet, serum folate levels averaged 17.2 plus or minus 4 ng/ml for trypanosome-free animals and 20.2 plus or minus 3 ng/ml for infected ones. In rats given the folic acid-deficient diet, serum folate levels averaged 8.6 plus or minus 2 ng/ml for noninfected control animals and 9.3 plus or minus 2 ng/ml for trypanosome-infected ones. Regardless of diet, the infected animals inoculated on day 56 had higher serum folate levels over the controls on the last day of observation (day 5 of infection). Livers from rats fed complete and pair-fed diets and inoculated on day 21 showed no significant differences in folate content when compared to control animals. However, livers of rats on a deficient diet showed significantly more folate when compared with uninfected controls, reaching a maximum of 362% of day 25. Liver folate levels of rats (regardless of the dietary regimen) inoculated on day 56 showed significantly higher values than the controls on day 60. Irrespective of the time of inoculation or diet, brain and spinal cord of T. rhodesiense-infected rats had significantly higher folate values than their controls on day 5 of infection. The folate level of the brain and spinal cord, at this time, ranged up to 58 and 107% respectively.

MACROPHAGE ACTIVITY WAS STUDIED IN RATS INFECTED WITH TRYPANOSOMA LEWISI IN THREE PROTOCOL GROUPS: one group was fed complete diet, a second group was given a vitamin B(12)-deficient diet, and a third group was fed a pair-fed control (calorically restricted) diet. Throughout the observational period, in animals fed complete and pairfed diets, marked increases in acid phosphatase levels in peritoneal macrophages were directly related to the degree of parasitemia. Acid phosphatase levels in rats deprived of vitamin B(12) were approximately one third that of animals with an adequate supply of the vitamin. Irrespective of the diets, the infection with T lewisi also elicited increased macrophage phagocytosis of polystyrene latex particles and macrophage spreading. Both of these activities occurred at a much slower rate in the vitamin B(12)-deficient animals.

Accumulative evidence in the scientific literature relating malnutrition and susceptibility to infection in human beings and animals has contributed significantly to the understanding of the maladies among the malnourished of the world. In the dispensation of health care systems around the world, little or no emphasis has been placed on trace-element nutrition. This paper adds to the available evidence by using a metabolic imbalance technique to investigate the effects zinc deficiency exert on the course of a parasitic infection. A model composed of zinc-deficient mice and Trypanosoma musculi was used to study changes in serum immunoglobulins.

The effects of trace metal contaminants (lead, cadmium, and mercury) on the immunologic responses of rats infected with Trypanosoma lewisi were investigated to determine whether chronic exposures to subclinical levels of these metals have adverse effects on the host's ability to respond to an infective agent.Earlier and higher levels of parasitemia were detected in animals exposed to cadmium, lead, and mercury. The variability in length of trypanosome cells in metal-exposed animals became constant at a later time and persisted for a longer time, indicating a delay in antibody synthesis. Serum levels of IgG and IgM were increased in infected animals exposed to trace metals; however, lower levels were observed when compared with infected control animals. Animals exposed only to trace metals showed decreases in serum levels of IgG and IgM. In contact sensitivity to dinitrofluorobenzene (DNFB), animals exposed to trace metals demonstrated no significant difference in sensitization when compared with those infected and exposed to trace metals.