Trypanosoma brucei infections in mice: studies on the anaemia

Trypanosoma brucei infections in mice: studies on the anaemia

342 T W E L F T H S E M I N A R ON T R Y P A N O S O M I A S I S the choroid plexus so that it blocked the passage of cerebrospinal fluid (CSF) thro...

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T W E L F T H S E M I N A R ON T R Y P A N O S O M I A S I S

the choroid plexus so that it blocked the passage of cerebrospinal fluid (CSF) through the foramina of the brain in man. ORMEROD and VENKATESAN (1970) demonstrated visible swelling of the choroid plexus of rats infected with T. brucei. We have carried out preliminary experiments (5) to investigate changes which might occur in the drainage of cerebrospinal fluid through the ventricles and foramina of the brains of rabbits infected with T. brucei. T h e technique was that of DAWSON, HOLLINGSWORTH and SEGAL (1970). Although we found evidence of diminished drainage of C S F , the experiments did not suggest that any significant degree of blockage of the foramina occurred in rabbits suffering from trypanosomiasis. In 3 of the experiments the secretion of C S F was also measured by injecting "blue dcxtran" into the ventricle and its dilution estimated by spectrophotometry. These experiments indicated some degree of inhibition of C S E secretion in rabbits with trypanosomiasis. We propose to repeat these experiments with other species in which the pathological physiology of the C S F in trypanosomiasis may resemble more closely the conditions of the disease as they appear to occur in man.

Trypanosoma brucei i n f e c t i o n s i n m i c e : s t u d i e s o n t h e a n a e m i a F. W. J E N N I N G S , G. M. U R Q U H A R T AND M. M U R R A Y

University of Glasgow Veterinary School Work currently in progress has shown that mice infected with a derivative of T. brucei T R E U 667 developed anaemia within 7 days. T h i s was normochromic with a moderate degree of reticulocytosis. Examination of bone marrow showed normoblastic hyperplasia. T h e r e was marked erythroblastic activity in the spleen. Experiments utilizing c h r o m i u m 51 labelled red cells indicated that there was a more rapid turnover of red cells in the infected mice. Red cell "half-life" was 31 days in normal mice (intact or splenectomized) and 24 days in infected mice (intact or splenectomized). I r o n - 5 9 was removed more rapidly from the plasma of infected mice and incorporated into the circulating red cells. All these factors could be consistent with a haemorrhagic type anaemia. However, the loss of injected iron-59, based on whole-body counting, was not significantly different in infected and control mice and this finding would be more consistent with an anaemia of haemolytic origin.

T h e i m m u n e r e s p o n s e to h e l m i n t h i n f e c t i o n i n t r y p a n o s o m e - i n f e c t e d G. M. U R Q U H A R T , M. M U R R A Y AND F. W. J E N N I N G S

animals

University of Glasgow Veterinary School T h e immunosuppressive effects of trypanosomiasis recently reported by GOODWIN (1970) p r o m p t e d us to study the i m m u n e response of trypanosome-infected rats to a primary infection with the nematode Nippostrongylus brasih'ensis. 60 hooded Lister rats were infected intraperitoneally with a derivative of T R E U 667; blood films were positive 7 days later and remained so throughout the course of the experiment. 18 days after infection these rats, together with controls, received 1,000 larvae subcutaneously. Subsequently groups of rats were killed 10, 14 and 21 days after the helminth infection when worm burdens and intestinal mast cell counts were established; on day 21 serum was obtained to determine the level of protective and of reaginic antibodies; the former was assessed by passive immunization of rats on days 1 and 3 of a primary infection, the latter by P C A tests. T h e results showed that rats with chronic trypanosomiasis were not able to m o u n t a proper i m m u n e response to a primary infection with the helminth N. brasiliensis. Instead the expulsion of adult worms and the development of the normal mast cell response were delayed and the production of protective antibody and to a lesser degree reaginic antibody was suppressed. It is possible that this immunosuppression may have been even more marked had the rats had the trypanosome infections for a period longer than 18 days before their nematode infection. At this stage it is only possible to speculate on the mechanism underlying the i m m u n o suppressive effect. It would appear that this was not due to lymphoid depletion nor inability