Another important difference may manifest itself if we were to consider a disease with long-lasting immunity, obeying SIR dynamics, or other compartmental structure, including complex intervention strategies and comparable tracing and recovery timescales. Our preliminary work in this direction suggests that our novel result about clustering reducing contact tracing efficacy can be extremely significant in other contexts, however a full consideration of this would take us significantly beyond the aims of the present work.  Serological Profiling of a Candida albicans Protein Microarray Reveals Permanent Host-Pathogen Interplay and Stage-Specific Responses during Candidemia Candida albicans in the immunocompetent host is a benign member of the human microbiota. Though, when host physiology is disrupted, this commensal-host interaction can degenerate and lead to an opportunistic infection. Relatively little is known regarding the dynamics of C. albicans colonization and pathogenesis. We developed a C. albicans cell surface protein microarray to profile the immunoglobulin G response during commensal colonization and candidemia. The antibody response from the sera of patients with candidemia and our negative control groups indicate that the immunocompetent host exists in permanent host-pathogen interplay with commensal C. albicans. This report also identifies cell surface antigens that are specific to different phases (i.e. acute, early and mid convalescence) of candidemia. We identified a set of thirteen cell surface antigens capable of distinguishing acute candidemia from healthy individuals and uninfected hospital patients with commensal colonization. Interestingly, a large proportion of these cell surface antigens are involved in either oxidative stress or drug resistance. In addition, we identified 33 antigenic proteins that are enriched in convalescent sera of the candidemia patients. Intriguingly, we found within this subset an increase in antigens associated with heme-associated iron acquisition. These findings have important implications for the mechanisms of C. albicans colonization as well as the development of systemic infection. The yeast Candida albicans exists in a dichotomist relationship with the human host. C. albicans is frequently found as a commensal organism on the human skin, gastrointestinal (GI) tract and the vulvovaginal tract [1] . Close to 60% of healthy individuals carry C. albicans as a commensal in the oral cavity. Colonic and rectal colonization is even higher, ranging from 45% to 75% among patient groups. Alterations in the host immunity, physiology, or normal microflora rather than the acquisition of novel or hypervirulent factors associated with C. albicans, are suggested to lead to the development of candidiasis [2] . Both neutrophils and mucosal integrity of the GI tract, are critical in preventing hematogenously disseminated candidiasis [3] . The development of candidemia can begin with the translocation of C. albicans into the bloodstream from initial commensal GI colonization or the shedding from developing biofilms on indwelling catheters [4, 5] . Fungal cells that evade the host immune system can spread to deep organ systems leading to hematogenously disseminated candidiasis, which has an estimated mortality rate of 40%, even with the use of antifungal drugs [2] .