Extracellular bacteria (pink) can induce autophagy by stimulating TLRs (i) or NODs (ii) upon shedding of PAMPs or during phagocytosis (iii). The latter induces a hybrid process termed LAP. Intracellular bacteria can be eliminated through canonical autophagy sponsored by SLRs. Some SLRs can recognize galectins (Gal) bound to β-galactoside glycans on pathogen-associated damaged vacuolar membranes (iv), whereas all SLRs identified thus far recognize ubiquitin (Ubq) on cytosolic bacteria or associated host molecules (v). A viral core can be recognized by TRIMs, which act as receptors and inducers of autophagy, thus helping to eliminate retroviral material en route to the nucleus (vi). Fusion with lysosomes leads to formation of autolysosomes (from canonical autophagy acting on cytosolic targets) or autophagolysosomes (from LAP phagosomes or from damaged conventional phagosomes). Elimination of many pathogens involves not one but a spectrum of autophagic processes (processes i–vi correspond to the above descriptions): AP, autophagy; X1, xenophagy mixed with autophagy of host membranes; X2, xenophagy of microbes only; HSX, highly selective xenophagy.