Praziquantel is an anthelmintic used in most schistosome and many cestode infestations. Praziquantel effects the permeability of the cell membrane resulting in the contraction of schistosomes. The drug further causes vacuolization and disintegration of the schistosome tegument. The effect is more marked on adult worms compared to young worms. An increased calcium influx may play an important role. Secondary effects are inhibition of glucose uptake, lowering of glycogen levels and stimulation of lactate release. The action of praziquantel is limited very specifically to trematodes and cestodes; nematodes (including filariae) are not affected.
Praziquantel works by causing severe spasms and paralysis of the worms' muscles. This paralysis is accompanied - and probably caused - by a rapid Ca 2+ influx inside the schistosome. Morphological alterations are another early effect of praziquantel. These morphological alterations are accompanied by an increased exposure of schistosome antigens at the parasite surface. The worms are then either completely destroyed in the intestine or passed in the stool. An interesting quirk of praziquantel is that it is relatively ineffective against juvenile schistosomes. While initially effective, effectiveness against schistosomes decreases until it reaches a minimum at 3-4 weeks. Effectiveness then increases again until it is once again fully effective at 6-7 weeks. Glutathione S-transferase (GST), an essential detoxification enzyme in parasitic helminths, is a major vaccine target and a drug target against schistosomiasis. Schistosome calcium ion channels are currently the only known target of praziquantel.
TargetActionsOrganismA
Schistosome calcium ion (Ca2+) channelsother/unknown
SchistosomaAbstract
Purpose : We present a case of severe biltaral visual loss caused by taking overdose of Praziquantel and Triclabendazole.
Methods : We observed the development and recovery of toxic retinopathy by swept-source optical coherence tomography (SS-OCT).
Results : This patient presented to our clinics with acute onset of severe bilateral visual loss for one month after ingesting 1g praziquantel and 2g triclabendazole daily for 4 days. His visual acuity was light perception bilateral. Anterior chamber examination was unremarkable. Cancer-associated retinopathy and melanoma-associated retinopathy were already excluded. SS-OCT showed outer plexiform layer thinning, outer nuclear layer disrupted, external limiting membrane, myoid zone, ellipsoid zone and interdigitation zone disappeared, and increased reflex of the RPE/Bruch’s complex in macular region. It also showed increased diameter of choroidal vessels (Figure 1). Ganglion cell layer-inner plexiform layer (GCL-IPL) in the macular region revealed significant loss. He was diagnosed bilateral toxic retinopathy and prescribed mecobalamin 0.5mg three times daily. One month later, the visual acuity increased to 0.1 bilateral. On SS-OCT, retinal thinning progressed, in which outer nuclear layer most significant. Diameter of choroidal vessels decreased. GCL-IPL in the macular region presented progressive loss. It was interesting that ellipsoid zone reappearance was observed in foveal, which could explain the improvement of patient’s central visual acuity (Figure 2).
Conclusions : Praziquantel (PZQ) and triclabendazole (TCBZ) are common anthelmintics applied worldwide. The known adverse effects of PZQ and TCBZ include abdominal discomfort or pain, vomiting, diarrhea and headache. The recommended total dosage of PZQ is 40-60mg/kg, and TCBZ 10-30mg/kg. To the best of our knowledge, this is the first case of toxic retinopathy related to overdosage of praziquantel and triclabendazole. Further animal toxicity research would be necessary for approving this phenomenon.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.