The persistence of symptoms in some Lyme disease patients treated with antibiotics has never been conclusively explained. This is known as post-treatment Lyme disease syndrome (PTLDS). It is possible that in common with animal models like mice and monkeys, human Borrelia burgdorferi infection results in residual, persistent infection even after treatment. Continued bacterial presence and/or an ongoing immune response could cause PTLDS. In an effort to identify antibiotics that might completely eradicate bacterial replication, the GLA-funded research team of Dr. Kim Lewis followed up earlier observations that beta-lactam antibiotics might be effective. The team found that vancomycin was effective against in vitro cultures of growing B. burgdorferi. However, this class of drugs is not expected to work on stationary cells, in which growth is very slow, and cell wall synthesis is expected to be minimal. Unexpectedly, when tested on stationary B. burgdorferi, they found that cell wall synthesis still occurred, and could be blocked by vancomycin. To extend their studies to an in vivo model, the group treated B. burgdorferi-infected, immunodeficient mice for five days. They found that vancomycin and ceftriaxone each completely blocked bacterial growth, compared with partial eradication by doxycycline. These studies suggest that more effective antimicrobial drugs, used early in infection, may prevent or reduce the occurrence of persisting infection. However, ceftriaxone and vancomycin are intravenously administered, and are not justifiable when most Lyme patients recover with oral doxycycline. Better identification of the subset of patients for whom doxycycline is inadequate would pave the way to studying whether vancomycin might reduce the incidence of PTLDS.