As a host-pathogenic mechanism, we found that MyD88 signaling blocks autophagy flux (i.e., autophagosome-lysosomal fusion) in macrophages following lethal IOE infection, which leads to inhibition of mitochondrial autophagy (i.e., mitophagy) as well as blockage of ehrlichial degradation via lysosome due to lack of colocalization of autophagosomes with lysosomes. The gene discussed is MYD88; the disease is infection.