Table 1.

Key features of C. elegans infections

Source (type of infection)	Pathogen	Key feature(s)	Molecular and experimental aspects	Reference(s)
Natural	M. nematophilum	Swelling of tail region (Dar); nonlethal	Induces ERK MAPK response; infection limited to rectal area	26, 52, 54
	D. coniospora	Fungal infection: hyphae penetrate entire worm	Induces NLP and CNC response genes; difficult to grow or control infectious dose	13, 31, 59, 61, 83
	N. parisii	Intracellular parasite	Horizontal transfer of infection; unique immune response; cannot be cultured in vitro	78
	Nodavirus	Intestinal structure disrupted; life span unchanged	Induces natural RNAi response; horizontally transmitted	18
Human (bacterial)	P. aeruginosa	Medium-dependent fast and slow killing, which are toxin and infection based, respectively	Induces p38 MAPK response; killing mechanism is strain dependent	15, 36, 42, 71
	S. enterica	Persistent bacterial infection	Primarily an extracellular infection in C. elegans, unlike in mammals	3, 38
	S. marcescens	Grossly distended intestine; 6-day survival	Triggers inducible immune response; may be a natural host-pathogen interaction	37, 43, 65
	E. coli	Nonpathogenic food source; pathogenic strains exhibit fast and slow killing	Results in a behavioral conditioning response; type III secretion system not required (unlike mammalian host)	7, 8, 12, 47
	S. aureus	Intact bacteria overwhelm animal; not persistent until infection threshold reached	bar-1 and egl-5 response is key; conservation of virulence factors between C. elegans and mammals	22, 28, 29, 68
Human (fungal)	C. albicans	Persistent lethal infection	Coinfection model particularly informative	9, 55, 57, 70
	C. neoformans	Rapid infection, accumulation of yeast; not persistent	Mechanism of pathogenesis unclear; does not disseminate in C. elegans (unlike mammalian host)	51, 72, 79