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The strategy of test, trace and isolate has been promoted and seen as a crucial tool in the fight against the COVID-19 pandemic. As simple as the slogan sounds, effectively implementing it turns into a complex endeavor with multiple moving parts and the need for multisector collaboration. In this study, we apply a systems thinking lens to analyse the design and implementation of the contact tracing strategy for COVID-19 in the district of Islamabad, Pakistan. The data collection included participatory observation, reflective exercises, key informant interviews and participatory workshops with district health managers and health providers. The information gathered was structured using process and stakeholder mapping to identify the lessons learned of the COVID-19 contact tracing strategy. The results showed that the elements crucial for implementation were, good coordination during a crisis, available resources mobilized effectively and establishment of early active surveillance for contact tracing. Furthermore, the main aspects to be improved were lack of preparedness and existing surveillance systems and task shifting leading to impact on regular health services. The results of this study highlight the importance of developing information systems that are coherent with existing processes and resources, even in times of crisis.

Staphylococcus aureus is a Gram-positive bacteria found on the skin of approximately 20-30% of healthy subjects, but on 30-100% of patients with atopic dermatitis (AD). 1 Recent reviews 2,3 have eloquently detailed a myriad of S. aureus-secreted toxins, enzymes, and cell-surfaceassociated antigens which contribute to AD pathogenesis (Figure 1). In brief, proteins, such as clumping factor B and fibronectin binding proteins, promote the adhesion of S. aureus to the stratum corneum. Staphylococcal Protein A can activate proinflammatory nuclear factor kappa B (NF-κB) signaling through direct engagement of tumor necrosis factor receptor 1 (TNFR1). 2,3 Lipoprotein and lipoteichoic acid induce TSLP in human keratinocytes via Toll-like receptors (TLR-) 2 and 6, 2 and phenol-soluble modulins also induce proinflammatory cytokines in human keratinocytes. 2,3 Additionally, secreted δ-toxin promotes mast cell degranulation via phosphoinositide 3-kinase (PI3K) and Ca 2+ influx-dependent mechanisms. 4 Staphylococcus aureus enterotoxins and toxic shock syndrome toxin can influence disease in many ways such as: acting as superantigens, promoting clonal T-expansion and inflammatory cytokine release; inducing IgE isotype switching in B-cells; directly activating mast cells and basophils; or stimulating secretion of itch-inducing interleukin 31 (IL-31). 2,3 Staphylococcal α-toxin not onlyThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.