Those of who have active EBV, HHV-6 following your ADRs from antibiotics, see the article below. There is strong evidence that antibiotics can reactivate the mentioned infectious pathogens. Its likely it activates other infectious pathogens, since antibiotics are immune suppressants. It seems that antibiotics dysregulate the immune system. Many complained of lyme disease symptoms, subsequently found to carry active Borrellia Burg, which were previously dormant.

Adverse antibiotic-induced eruptions associated with epstein barr virus infection and showing Kikuchi-Fujimoto disease-like histology.
Carlson JA, Perlmutter A, Tobin E, Richardson D, Rohwedder A.

Division of Dermatology, Department of Pathology, Albany Medical College, Albany, New York 12208, USA. carlsoa@mail.amc.edu

The antibiotic-induced eruption of infectious mononucleosis is a well-known clinical phenomenon. Latent viral infection with herpesviridae (eg, human herpes virus 6 (HHV-6) and Epstein-Barr virus (EBV)) is suspected to play a role in the drug hypersensitivity syndrome. The cutaneous pathologic findings have not been reported in the former, and are infrequently reported in the latter entity. Herein, we describe the biopsy findings of a cefprozil-induced rash in infectious mononucleosis and a minocycline-associated drug hypersensitivity syndrome. Biopsy of these exanthematous eruptions revealed an acute vacuolar interface superficial and deep perivascular and interstitial lymphocytic dermatitis. CD8(+) lymphocytes predominated and were associated with non-neutrophilic nuclear (karyorrhectic) debris and numerous small CD68(+) and CD123(+) monocytes. These aforementioned features have been described in cutaneous lesions of Kikuchi-Fujimoto disease, an entity whose clinicopathologic findings overlap with both infectious mononucleosis and lupus erythematosus. Serologic evidence of active and chronic active EBV infection was found in both patients, respectively. No evidence of EBV or HHV6 was found in the cutaneous lesions. Plasmacytoid monocytes (CD68(+)/CD123(+) cells), which produce type I interferon, are believed to play a role in viral immunity by protecting other cells from viral infections and promoting survival of antigen-activated T cells. Their presence in these two putative examples of viral-drug immune dysregulation could be a clue to pathogenesis and represent a common cellular component of some adverse cutaneous drug eruptions.

http://www.ncbi.nlm.nih.gov/pubmed/16456....Pubmed_RVDocSum