Common medications that may trigger G6PD-related hemolytic anemia include:

Acetaminophen: an analgesic (pain-relieving) drug

Acetylsalicylic acid (aspirin): an anti-inflammatory drug

Chloramphenicol: an antibiotic drug

Chloroquine: an immunosuppressant and antimalarial drug

Colchicine: a gout medication

Diaminodiphenyl sulfone (Dapsone): an antibiotic and antimalarial drug

Diclofenac sodium: an anti-inflammatory drug

Diphenhydramine: an antihistamine drug

Glyburide: a diabetes drug

Ibuprofen: an anti-inflammatory drug

Izoniazid: an antibiotic drug
L-dopa: a Parkinson’s disease treatment

Methylene blue: a dye and blood disorder treatment

Nitrofurantoin: an antimicrobial drug

Phenazopyridine: an analgesic drug

Primaquine: an antimalarial drug

Rasburicase: a gout medication

Streptomycin: an antibiotic drug

Sulfa drugs: a group of antibiotics that includes co-trimoxazole, sulfacetamide, and trimethoprim

Tripelennamine: an antihistamine drug

Vitamin K: a dietary supplement

Caution if using herbal supplements or extracts containing Rhizoma coptidis (also called Huang Lian) or Coptis chinensis. These herbs can be used to produce a supplement called berberine.

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Human Genetic Resistance to Malaria

Innate Resistance to HIV

Hemoglobin Subunit Beta
Hemolytic Anemia
G6PD

CCR5 (HIV)
G6PD (Malaria)

https://en.m.wikipedia.org/wiki/Hemolytic_anemia

https://en.m.wikipedia.org/wiki/Glucose-6-phosphate_dehydrogenase

https://en.m.wikipedia.org/wiki/Human_genetic_resistance_to_malaria

https://en.m.wikipedia.org/wiki/Innate_resistance_to_HIV

https://en.m.wikipedia.org/wiki/CCR5

https://en.m.wikipedia.org/wiki/Sickle_cell_disease

https://en.m.wikipedia.org/wiki/Hemoglobin_subunit_beta

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G6PD
Glucose-6-Phosphate Dehydrogenase
Hemolytic Anemia
Human Genetic Resistance to Malaria

Chromosome
Enzyme Catalyst

Cytosolic, Cytosol cytoplasmic matrix or groundplasm.

Genetic variation in human G6PD resulted from generations of adaptation to malarial infection.

Human genetic resistance to malaria refers to inherited changes in the DNA of humans which increase resistance to malaria.

X-linked genetic deficiency of G6PD makes a human prone to non-immune hemolytic anemia.

Modified F420-dependent G6PD is found in Mycoplasma Tuberculosis.

Common medications that may trigger G6PD-related Hemolytic Anemia.

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Highly Reduced Genomes of Protist Endosymbionts Show Evolutionary Convergence

https://www.sciencedirect.com/science/article/pii/S0960982219317038

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the usefulness of carboxylic ionophores is based on selective toxicity to protozoan parasites and bacteria and margins of safety in the approved target species. Desirable effects occur when animals are provided feed containing approved dosage ranges, but higher levels may result in adverse effects.

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Ionophore
Protonophore
EDTA Chelation
Nonactin
Nitrogen

Human genetic resistance to malaria
Innate resistance to HIV
Vertically transmitted infection
Parasitic chromosome
Selfish genetic element

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i suspect the reason is because something is already in that position, called genetic disease, autoimmune, making it difficult for other kind of similar disease to take root.

one of my suspensions is we can live with those kind of symbionts, but they need to somehow be reset or rebooted to be neuroprotective, not parasitic.