Different C. parvum strains do not respond equally to clofazimine.
That difference gave us a way to genetically map resistance.
The most surprising part: this resistance-associated ΔAA ndh2 allele is already widespread in C. parvum and C. hominis populations.
So Cryptosporidium may carry pre-existing genetic heterogeneity that lets it rapidly adjust under drug pressure.
Registration & abstract submission are open for the 37th Molecular Parasitology Meeting (MPM XXXVII) 🧫
@MJGubbels @Deepali_Ravel @omartheharb
Sept 13–17, 2026 | Woods Hole, MA + virtual
Abstract deadline: June 19
@rmc9z.bsky.social @mjgubbels.bsky.social @omarharb.org
parasitesrule.com/mpm-xxxvii
So… what does it clofazimean?
NDH2 heterogeneity may act as a metabolic rheostat, enhancing parasite adaptability.
Host diet, metabolism, microbiome, and immune pressure likely reshape parasite redox balance and drive allele dynamics.
Bulk segregant analysis pointed to one sharp locus on chromosome 7.
At that locus we found ndh2, encoding type II NAD(P)H dehydrogenase. A small 2-bp deletion near the start of the gene became enriched under drug pressure.
Excited to share our new paper, co-led by Gracyn Buenconsejo and me.
Why did a promising anti-#Cryptosporidium drug fail?
We asked whether the parasite itself might already be genetically prepared to escape treatment.
doi.org/10.1038/s415...
#Clofazimine #forwardgenetics