Acanthamoeba keratitis (AK) is a dangerous infectious disease, which is associated with
a high risk of blindness for the infected patient, and for which no standard therapy exists thus far.
Patients suffering from AK are thus treated, out of necessity, with an off-label therapy, using drugs
designed and indicated for other diseases/purposes. Here, we tested the capability of the off-label
anti-amoebic drugs chlorhexidine (CH; 0.1%), dibromopropamidine diisethionate (DD; 0.1%), hexamidine diisethionate (HD; 0.1%), miltefosine (MF; 0.0065%), natamycin (NM; 5%), polyhexamethylene
biguanide (PHMB; 0.02%), povidone iodine (PVPI; 1%), and propamidine isethionate (PD; 0.1%)
to suppress trophozoite formation of Acantamoeba castellanii and Acanthamoeba hatchetti cysts on
non-nutrient agar Escherichia coli plates. Of the eight off-label anti-amoebic drugs tested, only PVPI
allowed for a complete suppression of trophozoite formation by drug-challenged cysts for all four
Acanthamoeba isolates in all five biological replicates. Drugs such as NM, PD, and PHMB repeatedly
suppressed trophozoite formation with some, but not all, tested Acanthamoeba isolates, while other
drugs such as CH, DD, and MF failed to exert a relevant effect on the excystation capacities of
the tested Acanthamoeba isolates in most, if not all, of our repetitions. Our findings suggest that
pre-testing of the AK isolate with the non-nutrient agar E. coli plate assay against the anti-amoebic
drug intended for treatment should be performed to confirm that the selected drug is cysticidal for
the Acanthamoeba isolate