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Trypanosomiasis cruzi in mice with trichinosis
CORRESPONDENCE
individuals and the duration of the disease. The more longstanding the parasitosis, the more diminished is the parasitic intensity, while the clinical manifestations are more systematized and more abundant, the extradigestive ones predominating. This phenomenon is known in general parasitology, but I have the impression that it has not been pointed out in connexion with strongyloidiasis previously, perhaps because most of the studies of this disease have been made in warm countries, where the abundance of heterogenetic generations and the consequent multiplication of the parasites, prevents the evaluation of parasitic intensity. I am, etc., PAULDANCESCU
Faculty of Medicine, Bd. Dr. P. Gvoxa 8, Bucharest 35, Romania 25th April, 1975 References Dancescu, P. (1968). Investigations on the intensity of the infection in a strongyloidiasis focus: the coal culture method. Transactions of the Royal Society of Tropical Medicine and Hygiene, 62, 490495. Tanaka, H. (1966). Genus Strongyloides. Progressive Medicine and Ptirasitology, Japan, 3, 592-
Trypanosomiasis cruzi in mice with trichinosis St&-In a previous letter in this journal it was reported that trichinosis in rats suppressed the parasitaemia of superimposed Trypanosoma equiperdum or T. lewisi infections (MEEROVITCH and ACKERMAN, 1974). We have attempted to extend this finding by determining whether Tvichinella infections would enhance the survival of mice infected with the human pathogen T. cruzi. In one experiment, trichinous mice (inoculated 31 days earlier with 200 T. spiralis larvae each) and non-trichinous mice were inoculated subcutaneously with a Brazilian strain of T. cruzi. The mice used were CFl females weighing approximately 20 g. They had been randomly assigned to groups of five mice each at the beginning of the experiment, and were held under comparable conditions throughout. Among mice given 1,000 T. cruzi each, the mortality rate over a 60-day observation period was 35 ‘A for 20 trichinous mice and 60 % for 20 nontrichinous mice. Among the same numbers of mice given 10,000 T. cruzi each, the mortality rate was 70% for trichinous mice and 90% for non-tricbinous. Although the mortality rate was lower in trichinous mice, the difference is not statistically significant (Mann-Whitney U test) and those trichinous mice that died had a mean survival time (26.1 days and 22.6 days for 1,000 and 10,000 T. cuuzi, respectively) that was not different from the survival time of non-trichinous mice (26.3 days and 22.3 days). Examination of wet mounts of tail blood of each mouse on day 11 or 14 of infection, revealed at least as many trypanosomes per microscope field in the case of trichinous mice as in non-trichinous. In a second experiment, trichinous mice (inoculated 28 days earlier with 250 Trichinella larvae each) and nontrichinous mice were inoculated subcutaneously with 50,000 organisms of the same strain of T. cruzi. All of the mice died within three weeks. The mean survival time of the trichinous mice (15.2k2.5 days) was not signifi-
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cantly different from that of the non-trichinous mice (16,2i-2.3 days). Both of the above experiments included mice infected with Trichinella alone and no deaths were recorded in those groups. In the first experiment the Trichinellainfected mice weighed 15 ‘A less than the non-trichinous mice at the time of T. cvuzi inoculation, and in the second experiment they weighed 27 % less than the non-trichinous mice (an expected result of the Trichinella infection). At the termination of the first experiment, digestion of each surviving Trichinella-inoculated mouse confirmed the infection in all cases,and yielded a mean of 43,600*4,600 larvae per mouse in the Trichinella-only group. It is possible that the relatively lower weight of the trichinous mice made them significantly more susceptible to the lethal effect of T. cruzi infection and thereby masked a protective effect that would otherwise have been evident. Further, the small groups of mice used in the expectation of a strong degree of protection do not permit us to rule out the occurrence of a modest degree of protection. Nevertheless, it is clear that within the limitations of the experimental circumstances, trichinosis failed to provide significant protection against the lethal effect of T. cruzi in mice. We are, etc., WILLIAM C. CAMPBELL CHRISTINE M. MALANGA JOYCE A. CONROY Merck Institute for Therapeutic Research, Rahway, New Jersey 07065 23rd May 1975 Reference Meerovitch, E. & Ackerman, S. J. (1974). Trypanosomiasis in rats with trichinosis. Transactions of the Royal Society of Tropical Medicine and Hygiene, 68, 417.
The treatment of congenital trypanosomiasis SIR-In a recent paper a case of congenital trypanosomiasis was reported from Nigeria. The case ended fatally, although suramin therapy was attempted. The author (OLOWE, 1975) commented on an apparent lack of information concerning the treatment of this condition. In Zambia, a transplacentally infected premature baby, weighing I.7 kg, was successfully treated (BUYST, 1973). The child was born in an endemo-epidemic area of Trypanosoma rhodesiensesleeping sickness on the northern edge of the Luangwa flybelt (BUYST, 1974), and was collected at the village when he was only two days old. During the 72 km journey to hospital the general condition of the child was very poor and death seemed imminent. A blood smear taken on admission was positive for trypanosomes and the next day (day four) the cerebrospinal fluid revealed trypanosomes and 44 leucocytes per mm3 (92 % lymphocytes, 8 % neutrophils). The child was lethargic, slightly jaundiced and anaemic (Hb: 7.3 g %), and showed signs of prematurity and eye infection. The mother also had a positive blood smear and her cerebrospinal fluid contained trypanosomes and 67 leucocytes per mm3 (88 % lymphocytes, 12 % neutrophils). Her blood group was A Rhesus positive. The child received penicillin, chloroquine, parenteral
individuals and the duration of the disease. The more longstanding the parasitosis, the more diminished is the parasitic intensity, while the clinical manifestations are more systematized and more abundant, the extradigestive ones predominating. This phenomenon is known in general parasitology, but I have the impression that it has not been pointed out in connexion with strongyloidiasis previously, perhaps because most of the studies of this disease have been made in warm countries, where the abundance of heterogenetic generations and the consequent multiplication of the parasites, prevents the evaluation of parasitic intensity. I am, etc., PAULDANCESCU
Faculty of Medicine, Bd. Dr. P. Gvoxa 8, Bucharest 35, Romania 25th April, 1975 References Dancescu, P. (1968). Investigations on the intensity of the infection in a strongyloidiasis focus: the coal culture method. Transactions of the Royal Society of Tropical Medicine and Hygiene, 62, 490495. Tanaka, H. (1966). Genus Strongyloides. Progressive Medicine and Ptirasitology, Japan, 3, 592-
Trypanosomiasis cruzi in mice with trichinosis St&-In a previous letter in this journal it was reported that trichinosis in rats suppressed the parasitaemia of superimposed Trypanosoma equiperdum or T. lewisi infections (MEEROVITCH and ACKERMAN, 1974). We have attempted to extend this finding by determining whether Tvichinella infections would enhance the survival of mice infected with the human pathogen T. cruzi. In one experiment, trichinous mice (inoculated 31 days earlier with 200 T. spiralis larvae each) and non-trichinous mice were inoculated subcutaneously with a Brazilian strain of T. cruzi. The mice used were CFl females weighing approximately 20 g. They had been randomly assigned to groups of five mice each at the beginning of the experiment, and were held under comparable conditions throughout. Among mice given 1,000 T. cruzi each, the mortality rate over a 60-day observation period was 35 ‘A for 20 trichinous mice and 60 % for 20 nontrichinous mice. Among the same numbers of mice given 10,000 T. cruzi each, the mortality rate was 70% for trichinous mice and 90% for non-tricbinous. Although the mortality rate was lower in trichinous mice, the difference is not statistically significant (Mann-Whitney U test) and those trichinous mice that died had a mean survival time (26.1 days and 22.6 days for 1,000 and 10,000 T. cuuzi, respectively) that was not different from the survival time of non-trichinous mice (26.3 days and 22.3 days). Examination of wet mounts of tail blood of each mouse on day 11 or 14 of infection, revealed at least as many trypanosomes per microscope field in the case of trichinous mice as in non-trichinous. In a second experiment, trichinous mice (inoculated 28 days earlier with 250 Trichinella larvae each) and nontrichinous mice were inoculated subcutaneously with 50,000 organisms of the same strain of T. cruzi. All of the mice died within three weeks. The mean survival time of the trichinous mice (15.2k2.5 days) was not signifi-
163
cantly different from that of the non-trichinous mice (16,2i-2.3 days). Both of the above experiments included mice infected with Trichinella alone and no deaths were recorded in those groups. In the first experiment the Trichinellainfected mice weighed 15 ‘A less than the non-trichinous mice at the time of T. cvuzi inoculation, and in the second experiment they weighed 27 % less than the non-trichinous mice (an expected result of the Trichinella infection). At the termination of the first experiment, digestion of each surviving Trichinella-inoculated mouse confirmed the infection in all cases,and yielded a mean of 43,600*4,600 larvae per mouse in the Trichinella-only group. It is possible that the relatively lower weight of the trichinous mice made them significantly more susceptible to the lethal effect of T. cruzi infection and thereby masked a protective effect that would otherwise have been evident. Further, the small groups of mice used in the expectation of a strong degree of protection do not permit us to rule out the occurrence of a modest degree of protection. Nevertheless, it is clear that within the limitations of the experimental circumstances, trichinosis failed to provide significant protection against the lethal effect of T. cruzi in mice. We are, etc., WILLIAM C. CAMPBELL CHRISTINE M. MALANGA JOYCE A. CONROY Merck Institute for Therapeutic Research, Rahway, New Jersey 07065 23rd May 1975 Reference Meerovitch, E. & Ackerman, S. J. (1974). Trypanosomiasis in rats with trichinosis. Transactions of the Royal Society of Tropical Medicine and Hygiene, 68, 417.
The treatment of congenital trypanosomiasis SIR-In a recent paper a case of congenital trypanosomiasis was reported from Nigeria. The case ended fatally, although suramin therapy was attempted. The author (OLOWE, 1975) commented on an apparent lack of information concerning the treatment of this condition. In Zambia, a transplacentally infected premature baby, weighing I.7 kg, was successfully treated (BUYST, 1973). The child was born in an endemo-epidemic area of Trypanosoma rhodesiensesleeping sickness on the northern edge of the Luangwa flybelt (BUYST, 1974), and was collected at the village when he was only two days old. During the 72 km journey to hospital the general condition of the child was very poor and death seemed imminent. A blood smear taken on admission was positive for trypanosomes and the next day (day four) the cerebrospinal fluid revealed trypanosomes and 44 leucocytes per mm3 (92 % lymphocytes, 8 % neutrophils). The child was lethargic, slightly jaundiced and anaemic (Hb: 7.3 g %), and showed signs of prematurity and eye infection. The mother also had a positive blood smear and her cerebrospinal fluid contained trypanosomes and 67 leucocytes per mm3 (88 % lymphocytes, 12 % neutrophils). Her blood group was A Rhesus positive. The child received penicillin, chloroquine, parenteral