Abstract:
BACKGROUND: Trypanosomosis caused by Trypanosoma congolense is a major constraint to animal health in sub-Saharan
Africa. Unfortunately, the treatment of the disease is impaired by the spread of drug resistance. Resistance to diminazene
aceturate (DA) in T. congolense is linked to a mutation modifying the functioning of a P2-type purine-transporter responsible
for the uptake of the drug. Our objective was to verify if the mutation was linked or not to drug pressure.
METHODOLOGY/PRINCIPAL FINDINGS: Thirty-four T. congolense isolates sampled from tsetse or wildlife were screened for the
DA-resistance linked mutation using DpnII-PCR-RFLP. The results showed 1 sensitive, 12 resistant and 21 mixed DpnII-PCRRFLP
profiles. This suggests that the mutation is present on at least one allele of each of the 33 isolates. For twelve of the
isolates, a standard screening method in mice was used by (i) microscopic examination, (ii) trypanosome-specific 18S-PCR
after 2 months of observation and (iii) weekly trypanosome-specific 18S-PCR for 8 weeks. The results showed that all mice
remained microscopically trypanosome-positive after treatment with 5 mg/kg DA. With 10 and 20 mg/kg, 8.3% (n = 72) and
0% (n = 72) of the mice became parasitologically positive after treatment. However, in these latter groups the trypanosomespecific
18S-PCR indicated a higher degree of trypanosome-positivity, i.e., with a unique test, 51.4% (n = 72) and 38.9%
(n = 72) and with the weekly tests 79.2% (n = 24) and 66.7% (n = 24) for 10 and 20 mg/kg respectively.
CONCLUSION/SIGNIFICANCE: The widespread presence of the DA-resistance linked mutation in T. congolense isolated from
wildlife suggests that this mutation is favourable to parasite survival and/or its dissemination in the host population
independent from the presence of drug. After treatment with DA, those T. congolense isolates cause persisting low
parasitaemias even after complete elimination of the drug and with little impact on the host’s health.
