"The general picture to have emerged over the years is that IgG and IgM antibodies to the spirochaete develop slowly and are directed against an increasingly diverse array of proteins as infection progresses (Craft et al, 1986; Dressler et al, 1993; Nowalk et al 2006). The earliest responses are to flagellin B (FlaB) and p66, followed by OspC (25kDa) with responses to a number of additional antigens, such as VlsE, fibronectin-binding protein (BBK32), FlaA (37kDa), BmpA (39kDa), and decorin-binding protein A (DbpA) developing as B. burgdorferi disseminates (Coleman and Benach, 1987; Engstron et al, 1995; Bacon et al 2003; Aguero-Rosenfeld et al 2005; Wilske et al, 2007). This temporal pattern is consistent with the notion that the bacterium draws upon an expanding repertoire of differentially expressed proteins once within its vertebrate host, including phased expression of paralogous surface-exposed lipoproteins.
The clinical ramifications of these observations are significant. Because approximately half of patients with EM do not mount detectable antibody responses to the pathogen, lack of seroreactivity cannot be used to rule out the diagnosis of EM (Steere, 2001; Dananche and Nadelman, 2008). Seroreactivity increases substantially following therapy for EM (Vaz et al, 2001; Dandache and Nadelman, 2008), indicating that killing of the bacterium enhances processing of spirochaetal antigens."
Prior to the 2006 IDSA Lyme disease guidelines, the first set of Lyme disease guidelines which were written contained this specific remark on laboratory criteria for diagnosis:
"Significant change in IgM or IgG antibody response to B. burgdorferi in paired acute and convalescent phase serum samples"
It seems to me that this would still be an important guideline to follow, yet I am aware of a number of stories where patients stated their family doctors gave them an ELISA blood test early after infection, were told it was negative, and because of this, were not given further testing.
This is an inappropriate response, especially given what is known about antibody response in Borrelia burgdorferi infection over time, and given the lack of adequate antibody response early in infection.
Retesting using the western blot several weeks after the initial test - even if negative - makes sense. And if someone is displaying unusually long and moderate-severe flulike symptoms even if there is no EM present, confirmation testing is sensible.
Given this is a serologically progressive infection, why isn't it possible to determine how far long the infection is to some degree (under delayed acute care, at the very least) if the antigens present in a specific order over time? In later infection, it is harder to detect - but doesn't ospA present itself again in neurological infection? Something I have to look into...
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