The susceptibility of chickens to Trypanosoma brucei subspecies

Chickens were susceptible to infection with three different stocks of the subgenus Trypanozoon: two of presumptive Trypanosoma b. brucei and one of T. b. rhodesiense. Two groups of chickens were used: the first hatched following inoculation with either T. b. brucei or T. b. rhodesiense during embryonic development, and the second were infected as adult birds. In both experimental groups, parasitaemia persisted for prolonged periods, but was mostly subpatent and detectable only by subinoculation of blood into mice. In chickens infected as embryos, parasitaemias were patent for five weeks after hatching, but subpatent thereafter (to weeks 13 to 17). Quantitative estimations of the parasitaemias of seven of the birds hatched from embryos inoculated with T. b. brucei revealed fluctuations in the number of circulating trypanosomes, with an initial peak between days 2 to 9 after hatching. Between weeks 13 to 17 after hatching the chickens appeared to have recovered spontaneously from the trypanosome infections. Homologous challenge at week 20 failed to produce a recrudescence of parasitaemia, indicative of a possible acquired immunity. The infections of ten chickens inoculated with either T. b. brucei or T. b. rhodesiense as adult birds were microscopically subpatent throughout the observation period of six weeks, but subinoculation of blood into mice showed the chickens were parasitaemic from week one and thereafter. Different aspects of infection of avian hosts by the Trypanozoon subspecies are discussed.     

Immunoregulation in experimental murine Trypanosoma congolense infection: anti-IL-10 antibodies reverse trypanosome-mediated suppression of lymphocyte proliferation in vitro and moderately prolong the lifespan of genetically susceptible BALB/c mice

We infected highly susceptible BALB/c and relatively resistant C57BL/6 mice with cloned Trypanosoma congolense and followed the effects of these infections on the circulating parasite numbers, mouse mortality and cytokine expression. C57BL/6 mice controlled their parasitaemia and survived for up to 163 +/- 12 days, while BALB/c mice could not control their parasitaemia and succumbed to the infection within 8.4 +/- 0.5 days. Susceptible BALB/c mice had dramatically higher plasma levels of IL-10 than the resistant C57BL/6 mice from day 7 forward. This was preceded by an earlier and higher level induction of splenic IL-10 messenger RNA (mRNA) expression in the infected BALB/c mice. There was a strong negative correlation between the splenocyte proliferative responses to Concanavalin-A (Con-A) and their production of IL-10 in these infected BALB/c mice. Co-treatment of the Con-A-stimulated spleen cell cultures with monoclonal anti-IL-10 antibodies, but not isotype-matched control antibodies, could completely reverse this suppression of the splenocyte proliferative response. Finally, in three experiments, anti-IL-10 antibody treatment in vivo reduced the peak circulating parasitaemia of infected BALB/c mice by 43% and increased their median survival periods by 38% relative to isotype-matched control antibody-treated mice.     

Physical therapy and exercise therapy in the clinical rehabilitation after lung operations (author''s transl)

Using 90 albino rats, a comparison was made between the response to experimental infections of Trypanosoma brucei and T congolense of approximately three weeks duration by observation of parasitaemia, packed cell volume values, post mortem spleen and lymph weights, and histology of thymus, spleen, lymph nodes and bone marrow. In T congolense infection, phagocytosis of trypanosomes in the spleen appeared to be the main response of the host's haemopoietic tissues to the parasites, which were observed only intravascularly. In T brucei infection immunological responses occurred in the spleen and lymph nodes in addition to trypanosome phagocytosis. Trypanosomes were seen intercellularly in thymus, mediastinal tissue and lymph node sinuses and parasitaemia reached considerably higher values than in T congolense infection. Erythrophagocytosis in the spleen was the only histological feature which could account for the reduction in packed cell volume which occurred near death in both infections, medullary haemopoiesis being increased. Changes in the thymus, incorporating plasma cell production and depletion of cortical small lymphocytes, occurred in both infections.     

Study on the sequential tsetse-transmitted Trypanosoma congolense, T. brucei brucei and T. vivax infections to African buffalo, eland, waterbuck, N'Dama and Boran cattle

Susceptibility of African buffalo, eland, waterbuck, N'Dama and Boran cattle to sequential Glossina morsitans centralis-transmitted infections of Trypanosoma congolense, T. brucei brucei and T. vivax was compared, and their possible role as reservoirs of these parasites for G. moristans centralis, G. pallidipes, G. austeni, G. brevipalpis and G. longipennis determined. The buffalo, eland, waterbuck and N'Dama controlled T. congolense parasitaemias and were able to prevent anaemia. By contrast, one Boran became severely anaemic whilst the other controlled parasitaemia and anaemia. When the above five species of Bovidae were rechallenged with T. brucei brucei they showed persistent parasitaemias but did not develop anaemia. The buffalo died of other causes. When the remaining four bovids were rechallenged with T. vivax they became infected with mixed T. vivax/T. b. brucei parasites. Eland, waterbuck and N'Dama controlled parasitaemias and anaemia whereas the Boran became anaemic. Cyclical development of T. congolense occurred in G. moristans centralis when fed on the bovid hosts, with buffalo being infective for tsetse flies for a much longer period. There was no relationship between the levels of T. congolense parasitaemia in the bovid hosts and the resultant infection rates in tsetse flies. Glossina m. centralis was more susceptible than G. pallidipes to T. brucei brucei whilst G. austeni the least; G. brevipalpis and G. longipennis were refractory to the mature infection. Again there was no relationship between T. brucei brucei parasitaemia levels in the hosts and infection rates in the flies. Glossina m. centralis and G. pallidipes showed mixed T. brucei brucei/T. vivax infections whilst G. austeni, G. brevipalpis and G. longipennis became infected with T. vivax alone. Tsetse flies showed higher T. vivax infection rates when fed on the hosts with high parasitaemias than thosewith low parasitaemias. Thus trypanotolerant African buffalo, eland, waterbuck, N'Dama as well as some trypanosusceptible Boran cattle can serve as reservoirs of single or mixed trypanosome infections for tsetse flies. This study has also shown that the Ag-ELISA on the sera from the five bovid hosts had low sensitivity and species-specificity. Examinations of thin wet blood films and buffy coats with a phase-contrast microscope were not sensitive enough to detect the parasites on all occasions. Xenodiagnosis using mice for T. brucei brucei and T. congolense infections, and tsetse flies for all the three trypanosome species were most sensitive for the detection of trypanosome infections in the bovid hosts.     

Effects of Trypanosoma congolense infection and diet on puberty, age at first lambing and haematology changes in Djallonké ewe lambs

The interactions between T. congolense infection and nutritional supplements on onset of puberty and age at first lambing were observed in 24 young Djallonké ewes. As experimental design, a randomised complete block design was used with four treatment combinations, of which two were kept on a restricted diet (L), the remainder on an unrestricted diet (H) and half of each nutritional group being infected with T. congolense (LI and HI), the remainder serving as controls (LC and HC). Infection with T. congolense took place at an average age of 6 months and 15 days. Mortality due to trypanosome infection was zero and clinical symptoms were not obvious. Intensity of parasitaemia and packed cell volume (PCV) drop following trypanosome infection were similar in both infected groups (HI and LI). High dietary supplementation resulted temporarily in a better haematopoietic response following trypanosome infection, measured as a macrocytic anaemia. Dry matter intake (DMI) was significantly depressed in the HI group immediately following infection. Trypanosome infection had a negative effect on live weight gain during the chronic phase, with the difference being most obvious in the HI group (interaction diet x infection; p< or =0.05). Whereas trypanosome infection had no significant effect, high supplementary feeding significantly reduced the age at first cycling. Age at first lambing was similarly reduced by the diet. Trypanosome infection tended (p< or =0.09) to delay age at first lambing with a mean difference of 31.5+/-22.4 days between infected and controls. Interactions between diet and infection for age at first cycling/lambing were not significant, indicating these effects were just additive. Neither birth weights nor growth rates of offspring born to the experimental animals were significantly affected by previous trypanosome infection, nor by the diet of the dam. In contrast, lamb mortality up to 3 months of age was significantly increased by infection of the dam and most losses arose in group LI. In conclusion, the effects of trypanosome infection on puberty and age at first lambing were indirectly mediated through depression of growth rates. Nutritional supplementation enabled a better erythropoietic response to T. congolense infection and better offspring survival rates but resulted in more depressed weight gains. The results however clearly indicated the delaying effect of insufficient feeding on onset of puberty and reproductive performance in young Djallonké sheep.     

Control of spontaneous activity during development

The African trypanosome Trypanosoma brucei expresses the active variant surface glycoprotein (VSG) gene in a telomeric VSG gene expression site. We have generated trypanosomes with a neomycin resistance gene inserted behind an active VSG gene expression site promoter, and a hygromycin resistance gene behind a silent one. By alternating drug selection, we could select for trypanosomes that had switched between the two marked VSG gene expression sites. Surprisingly, trypanosomes that had activated a new VSG gene expression site had often lost the old one. Using polymerase chain reaction (PCR), we screened large numbers of switched trypanosomes and found that sequences lost invariably included the drug marker near the promoter, as well as the telomeric VSG gene many tens of kilobases away. We postulate that stable activation of a new expression site requires silencing of the old one. If silencing does not occur at a sufficient rate by normal switch-off, stable activation of the new site can only occur if the old site is lost in random deletion events. The fact that we pick up these normally infrequent deletions, indicates that inactivation of the old VSG expression site could be rate limiting during switching in our strain of T. brucei.     

Long-term lipid-based total parenteral nutrition activates mononuclear cells and modulates membrane lipid composition in pigs

This study aims to assess the possible strain-dependent variations in detection of Toxoplasma antigens and antibodies. The virulent RH strain or avirulent Beverley strain of T. gondii were injected into mice, intraperitoneally, and their antigens, antibodies and parasites were identified from the blood or tissues; liver, brain and spleen by ELISA, Western blot and PCR. In mice infected with RH strain, circulating antigens and parasitemia were first detected from 2 days after infection, and Toxoplasma DNA were found in the blood, liver, brain and spleen from 3 days after infection. It was impossible to detect specific IgM and IgG antibodies to T. gondii, and any specific band was not found by Western blot. In mice infected with Beverley strain, circulating antigens were detected between day 10 and day 35. The Toxoplasma DNA was found in the blood and liver from day 15 until day 60, and in the brain from day 20. But Toxoplasma DNA in the spleen were mainly detected between day 10 and day 30. The IgM antibodies were first appeared on day 10 post-infection, and were noted obviously increased between day 15 and 25. The IgG antibodies were first detected on day 15, and showed progressively increased titers. The antibody binding bands were specific according to infection period. Sera from mice infected with Beverley strain reacted mainly with the antigen of 27.5-kDa and 32.5-kDa. In conclusion, mice infected with RH strain revealed Toxoplasma antigens strongly, but not antibodies. However, mice infected with Beverley strain revealed both the Toxoplasma antigens and antibodies. The present results showed that immune responses are different between avirulent and virulent T. gondii.     

Phylogenetic reconstruction using an unsupervised growing neural network that adopts the topology of a phylogenetic tree

Mice infected with African trypanosomes produce exceptionally large amounts of serum IgM, a major part of which binds to non-trypanosome antigens such as trinitrophenol and single-strand DNA. In this paper, we describe that in cattle infected with Trypanosoma congolense and T. vivax, similar antibodies are found, although they bind mainly to protein antigens, such as beta-galactosidase, ovalbumin and ferritin. The parasite non-specific IgM antibodies appear around the same time as the parasite-specific antibodies, but their origin and function are not clear. We tested the hypothesis that CD5+ B cells (or B-1 cells), which increase during trypanosome infections in cattle, are responsible for production of antibodies to non-trypanosome antigens. Splenic CD5+ and CD5- B cells from infected cattle were sorted and tested in a single cell blot assay. The numbers of immunoglobulin-secreting cells were similar in both B-cell populations. However, antibodies with reactivity for non-trypanosome antigens were significantly more prevalent in the CD5+ B-cell fraction and were exclusively IgM. The preference for production of these antibodies by CD5+ B cells and the expansion of this subpopulation during infections in cattle, strongly suggest that CD5+ B cells are the main source of trypanosome non-specific antibodies. We propose that these antibodies are natural, polyreactive antibodies that are predominantly secreted by CD5+ B cells. Since B-1 cells are up-regulated in many states of immune insufficiency, the immunosuppression associated with trypanosome infections may be responsible for the increase of this subset and the concomitant increase in trypanosome non-specific antibodies.     

A silicone centrifugation technique for the detection of low parasitaemias of salivarian trypanosomes

A method using silicone fluid of specific gravity 1.075 was employed to detect low numbers of salivarian trypanosomes in rats infected with T. brucei, T. gambiense, T. congolense or mouse-adapted T. vivax. This method compared favourably with other microsensitive techniques such as the miniature anion-exchange centrifugation and microhaematocrit buffy-coat microscopy methods. The silicone centrifugation technique is based on the density differences between the host's erythrocytes and the parasites. Under the conditions used, the red cells are pelleted by centrifugation through a layer of silicone fluid whereas the trypanosomes remain in the plasma supernatant.     

B-cell activation in the mesenteric lymph nodes of resistant BALB/c mice infected with the murine nematode parasite Trichuris muris

Immune responses in resistant BALB/c mice infected with the murine nematode parasite Trichuris muris were examined. Following the establishment of infection, worm burdens of T. muris were expelled by BALB/c mice by day 21 postinfection (p.i.). Specific immunoglobulin G1 (IgG1) antibodies to T. muris excretory/secretory (E/S) antigens were detected in sera from infected mice, though specific IgG2a antibodies were not observed during infection. Ig-producing cells increased in the mesenteric lymph nodes (MLN) of infected mice on days 7, 14, and 21 p.i., with the greatest increase in numbers of IgG- and IgA-producing cells occurring on day 14. Marked increases in the relative percentages of B220+ and surface Ig+ (sIg+) cells were observed in the MLN of infected mice on days 14 and 21 p.i. Furthermore, cellular expansion of the MLN in infected mice resulted in an increase in the absolute numbers of B220+ and sIg+ cells. The levels of interleukin 2 (IL-2), IL-4, and interferon-gamma (IFN-gamma) detected in the supernatants from concanavalin A-stimulated MLN cells of infected mice were higher than those found in normal mice. Consequently, the expulsion of T. muris in resistant BALB/c mice was concomitant with cytokine production and B-cell activation in the MLN of infected mice. These results suggest the involvement of B-cell responses in protective immunity to T. muris infection.     

Adherence phenomena in Trypanosoma congolense (author''s transl)]

Two adherence phenomena in Trypanosoma congolense as a possible cause of trypanosome aggregation in the capillaries of certain organs are described: 1. Adherence of trypanosomes to blood cells of nonimmune mice, 2. dovetailing of trypanosome membranes into one another and into the vessel wall.     

Persistence of Ehrlichia phagocytophila infection in lambs in relation to clinical parameters and antibody responses

Five lambs were infected experimentally with Ehrlichia phagocytophila and examined regularly during the next six months. The lambs all had recurrences of parasitaemia at various times but had a fever on only 21 per cent of these occasions. A reduced number of leucocytes was observed in all the lambs for at least eight weeks. All the lambs were still infected four months after inoculation with E phagocytophila. After six months, blood from four of the five lambs was infective when inoculated into susceptible lambs.     

Local immunity in lung-associated lymph nodes in a murine model of pulmonary histoplasmosis

Local immunity against acute pulmonary histoplasmosis was studied in the lung-associated lymph nodes of normal nonimmune mice infected intratracheally with live Histoplasma capsulatum yeasts. The phenotypes and distribution of cells in lung-associated lymph nodes and spleens were determined by flow cytometry. In addition, the immune responsiveness of these cells was evaluated by in vitro blastogenesis. Anti-H. capsulatum antibodies in serum and H. capsulatum antigen in tissue were measured by immunoassays. Cellular immune responses were greater in the lymph nodes than in the spleens. In lymph nodes 7 days after infection, a marked increase in the number of B lymphocytes caused the percentage to rise to 43%, compared with 26% in controls, and it remained elevated throughout the course of infection. A CD3+ cell that did not express CD4 or CD8 increased in number until it constituted 21% of lymph node cells, compared with 5% in controls, by day 14. The numbers of CD4+ and CD8+ T lymphocytes were modestly increased from days 7 to 35, but their percentages dropped because of the greater numbers of B lymphocytes and CD3+4-8- cells. Macrophages consistently constituted 2 to 3% of lymph node cells during the study. In spleens 7 days after infection, the percentage of macrophages in infected mice rose to 21%, compared with 9% in controls, but the total spleen cell number did not increase until day 14, when all cell subsets were nearly double in number. The in vitro blastogenic response of lymph node cells to H. capsulatum peaked at day 7, but spleen cell response was minimal during the course of infection. Histoplasma-specific serum immunoglobulin G antibodies reached peak levels by day 21 and remained high to the end of the study. In contrast, levels of antigen-specific immunoglobulin M antibodies were very low. These data suggest that antigen-specific immune responses occur in lung-associated lymph nodes and that this draining lymph node response may be an important component in host defense against Histoplasma lung infection.     

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The present study investigated the influence of dietary protein on the intensity of parasitaemia, degree of anaemia and erythropoietic responses, in sheep experimentally infected with Trypanosoma congolense and given either a high protein diet (116 g digestible crude protein [DCP] per day) or a low protein diet (51.5 g DCP per day). It was observed that infected and control animals on the high protein diet grew at similar rates while infected animals on the low protein diet experienced marked retardation of growth compared with their uninfected controls. Dietary protein had no influence on the degree of anaemia that followed infection. Measurement of blood volumes revealed that low protein infected group had significantly lower mean circulating red cell volume than their controls. Ferrokinetic measurements indicated that plasma iron turnover rates (PITR) and 59Fe incorporation rates were higher in the high protein infected group than in the low protein infected group, although these differences were not significant. These observations indicate that infected animals on a high protein tended to show greater enhancement of erythropoietic activity that infected animals on low protein diet.     

CNS regulation of blood lactate concentration in anesthetized rats

This study evaluated the effect of stimulating the central nervous system (CNS) with neostigmine, an inhibitor of acetylcholinesterase, on the blood lactate concentration in fed rats and in rats fasted for 48 hours. After the rat was anesthetized with pentobarbital, neostigmine was stereotaxically injected into the third cerebral ventricle. In fed rats, the central injection of neostigmine significantly increased the blood lactate level, while concomitantly increasing plasma glucagon, epinephrine and norepinephrine concentrations. Constant infusion of somatostatin throughout the experiments, to inhibit glucagon secretion from the pancreas, did not affect alterations in blood lactate by central injection of neostigmine. In adreno-medullated rats, CNS-stimulation by neostigmine still increased plasma norepinephrine significantly, however, the alteration in blood lactate was only one-third of that in intact rats. Intraperitoneal propranolol, but not phentolamine, prevented the rise in lactate. Neostigmine increased lactate in fasted rats as well as in fed rats. We conclude that in anesthetized rats, stimulation of the CNS by neostigmine increases blood lactate mainly through circulating epinephrine and partially through circulating norepinephrine or direct sympathetic nervous stimulation; glucagon does not appear to be involved in the increase in blood lactate.     

Influence of acute-phase parasite load on pathology, parasitism, and activation of the immune system at the late chronic phase of Chagas' disease

To obtain low and high parasite loads in the acute phase of Chagas' disease, A/J mice were infected with 10(3) or 10(5) Trypanosoma cruzi trypomastigotes of the Y strain and treated on day 6 with benznidazol. One year later, chronically infected mice were screened for subpatent parasitemias, tissue pathology, and immune response. Mice infected with the high parasite inoculum showed higher levels of chronic parasitemias, heart and striated muscle inflammation, and activation of the immune system than did mice infected with the low inoculum. Concerning the activation of the immune system, the main findings for high-dose-infected mice were (i) increased numbers of splenocytes, with preferential expansion of CD8(+) and B220(-) CD5(-) cells, many of them bearing a macrophage phenotype; (ii) higher frequencies of B (B220(+)), CD4(+), and CD8(+) large lymphocytes; (iii) a shift of CD4(+) cells towards a CD45RBLow phenotype; (iv) increased frequencies of both CD45RBLow and CD45RBHigh large CD4(+) cells; (v) augmented numbers of total immunoglobulin (Ig)-secreting cells, with predominance of IgG2a-producing cells; and (vi) increased production of gamma interferon and interleukin 4. In addition, these mice presented lower IgM and higher IgG2a and IgG1 parasite-specific serum antibody levels. Our results indicate that the parasite load at the acute phase of T. cruzi infection influences the activation of the immune system and development of Chagas' disease pathology at the late chronic phase of the disease.     

Consequences of retirement activities for distress and the sense of personal control

Mink were infected with Aleutian Mink Disease Parvovirus (AMDV) and sacrificed at monthly intervals after infection. During this time humoral immune responses and leucocyte numbers in blood, mesenteric lymph node, spleen and thymus were monitored. Serum hypergammaglobulinaemia was observed together with elevated antibody responses to AMDV NS1 and VP1/2 proteins. In blood, a highly significant increase in CD8+ lymphocytes was observed. However, (presumed)CD4+ cells defined as CD3+CD8- cells, and B lymphocytes remained relatively constant throughout the study. The (presumed)CD4+/CD8+ ratio decreased significantly from greater than 2 to less than 0.5 and MHC-II+ blood leucocytes increased significantly during infection, a large proportion of these being CD8+. Similar changes were observed in the mesenteric lymph node and spleen. Immunohistology of lymph nodes showed a massive expansion of the paracortical area due to increased numbers of CD8+ cells. The staining intensity of B lymphocytes in lymph nodes with a CD79a reactive monoclonal antibody was decreased in the late infection, indicating a possible greater number of plasma cells. Thymic involution was observed during the AMDV infection, although relative increases in CD3high (presumed)CD4+ and CD3highCD8+ single positive cells were observed. These increases were countered by a corresponding reduction in the CD3low(presumed)CD4+CD8+ double positive cell population. Immunohistology of the thymus in normal mink showed that most of the matured CD3+ T cells were present in the inner medulla, while only few CD3+ cells could be found in the outer cortex. In severely infected mink the thymic structural organisation vanished, and CD3+ cells were found throughout the organ.     

Experimental infection of Glossina morsitans morsitans (Mall) with Trypanosoma congolense (ZRE/G143/90). Parasite cycle and vector competence in the tsetse fly

This report presents an experimental study of the life cycle of Trypanosoma congolense (ZRE/G 143/90) in relation to the vectorial competence of Glossina morsitans (Mall). The rate of engorgement at the time of an infectious meal and the mortality before day 15 of the life cycle were not significantly different between male and female flies. The mesocyclic forms of trypanosomes were regularly observed in the proventriculus, crop duct, oesophagus, cibarium and proboscis, except in the crop. On day 12 of the cycle, epimastigote forms were predominant in the proboscis. On day 13 of metacyclogenesis, four out of six rats (67%) used for feeding the flies were positive for trypanosomes upon buffy coat examination. These results demonstrate the short incubation period of trypanosomes in the vertebrate host and precociousness of the vectorial competence of some individuals of G m morsitans (Mall). Among the three cyclic stages, only the procyclic forms in the intestine showed a significant difference between the sexes, the male flies being more infected than the females. Metacyclogenesis undergoes three cleavages leading to the successive and permanent establishment of the procyclic, mesocyclic and metacyclic forms in the midgut, proventriculus and proboscis respectively.     

Twenty-four-hour rhythms of plasma catecholamines and their relation to cardiovascular parameters in healthy young men

Diurnal and ultradian rhythms of plasma norepinephrine and epinephrine and their role in the regulation of cardiovascular parameters were investigated over 24 h of recumbency in a group of five men. Catecholamines were measured at 10 min intervals, and blood pressure and heart rate were recorded continuously. Norepinephrine and epinephrine rapidly fluctuated in each subject, with no obvious diurnal rhythm. Spectral analysis suggested two ultradian rhythms with periods of around 12 h and 50-100 min for both catecholamines. The pulse detection programs PULSAR and CLUSTER revealed 20-30 pulses/24 h for norepinephrine and epinephrine, with a significant correlation between the two rhythms (r = 0.63-0.80, P < 0.001). Neither the frequency nor the amplitude of these rapid fluctuations differed between day and night. Arousal in the morning caused a small increase in plasma catecholamines and getting out of bed a large increase. Thus changes in posture and activity are the main influences on the diurnal variations of plasma catecholamines reported previously, while the ultradian rhythms of sympathoadrenomedullary activity appear to be of intrinsic origin. Blood pressure and heart rate exhibited a diurnal rhythm with a nightly decrease. Arousal and rising from bed increased blood pressure and heart rate significantly. Although the amplitude of the rapid fluctuations of plasma catecholamines at times exceeded those caused by postural changes in the morning, when both plasma norepinephrine and epinephrine levels correlated highly with all cardiovascular parameters, correlations were not significant during recumbency. Thus the intrinsic ultradian fluctuations of plasma catecholamines appear not to be involved in the control of cardiovascular parameters during recumbency, and the increase in blood pressure and heart rate in the morning appears to be controlled by direct sympathetic neural input to the heart and vasculature in response to changes in activity and posture rather than by an endogenous surge of plasma catecholamines.     

Exacerbation of toxoplasmosis in neutrophil-depleted mice

Studies were performed to determine whether resistance to Toxoplasma gondii infection in mice depends on a mechanism involving neutrophils. Immunocompetent C57BL/6 and C.B-17 mice infected with T. gondii by gavage had an increased percentage of neutrophils in their peripheral blood. C57BL/6 mice selectively depleted of neutrophils by injections of RB6-8C5 monoclonal antibody died during the acute phase of the disease. Depletion of neutrophils had no effect on interferon gamma production, but had a profound effect on the total numbers of peripheral blood CD4+ and CD8+ T cells. Neutrophil-depleted C.B-17 mice survived longer than neutrophil-depleted C57BL/6 mice when infected with T. gondii, however they became much sicker, and were less able to survive long-term than infected, control mAb-treated mice as indicated by severe sustained weight loss. This study shows that neutrophils play an important role in resistance to acute primary T. gondii infection and that depletion of neutrophils reduces the numbers of CD4+ and CD8+ lymphocytes recoverable from peripheral blood of infected but not uninfected mice. This effect on lymphocytes may contribute to the reduced long-term survival of neutrophil-depleted mice.