Required for the use of ethanolamide (EA) as carbon, but not nitrogen, source (Probable). Involved in acetate metabolism during growth on EA, when expressed independently of the eut operon it can restore growth to a double pta-acs deletion mutant (PubMed:14996820). Required for acetate excretion during growth on EA (PubMed:16272400). Expression of the eut operon allows this bacteria to use ethanolamine (EA) as a carbon, nitrogen and energy source. It relies on cobalamin (vitamin B12) both as a cofactor for the ethanolamine ammonia-lyase (EAL) activity and to induce the operon (PubMed:3045078). EA enhances bacterial survival in macrophages in a concentration-dependent manner, suggesting it is an important nutrient during infection (PubMed:29531136). acetyl-CoA + phosphate = acetyl phosphate + CoA kcat is 1927 sec(-1). Optimum pH is 7.2. Amine and polyamine degradation; ethanolamine degradation. Homodimer. Part of the 17-gene eut operon transcribed from a single promoter, induced by ethanolamine and adenosylcobalamin (AdoCbl, vitamin B12). Can use ethanolamine (EA) as a nitrogen source but not as a carbon source (PubMed:2656649, PubMed:23585538). Not required for aerobic growth on EA supplemented with cobalamin (vitamin B12); deletions and mutations in this gene probably have polar effects on downstream gene expression. A double eutD-eutM and a quadruple eutP-eutQ-eutT-eutD deletion are not required for growth in the above conditions (PubMed:10464203). Somewhat reduced growth on EA, no excretion of acetate from cells. Reduced growth is due to residual nutrients from rich medium (PubMed:16272400, PubMed:23585538). A non-polar deletion mutant does not grow on EA between pH 5.5 and pH 8.5, releases slightly increased amounts of acetaldehyde on EA plus vitamin B12 (PubMed:16585748). Belongs to the phosphate acetyltransferase and butyryltransferase family.