Perceptions and experiences with eating disorder treatment in the first year of COVID-19: A longitudinal qualitative analysis

Objective: The COVID-19 pandemic created significant challenges in accessing and receiving treatment for individuals with eating disorders (EDs). The purpose of this study is to explore perceptions of and experiences with ED treatment during the first year of the pandemic among individuals with past and self-reported EDs in the United States. Methods: Online surveys were administered to adults (N = 510) with a past or current self-reported ED at 13 timepoints between April 2020 and May 2021. Using longitudinal qualitative analysis, 5651 free-text responses were examined to capture experiences with ED treatment and generate inferences of change over time. Results: We categorized results into four sequential, temporal quarters and identified patterns that explained participants' perceptions of facilitators, barriers, and experiences with ED treatment over time: Quarter 1. Treatment Disruption and Reorienting Recovery; Quarter 2. Accumulating COVID-19 Stress and Virtual Treatment Woes; Quarter 3. A Continuation of Inadequate Care; and Quarter 4. Ongoing Adaptation and Adjustment to Uncertainty. Participant experiences were marked by numerous barriers to accessing care, challenges adjusting to virtual treatment, unmet treatment needs, and beginning acceptance of telehealth. Discussion: Our findings present a timeline to help evaluate challenges related to navigating the switch to virtual care which created significant disruption to ED recovery. Participants spent much of the first year trying to adjust to unemployment, loss of insurance, and lack of access to in-person treatment. Future research should identify additional strategies to improve the receipt and experience of care for EDs. Public Significance: Our findings suggest that individuals with eating disorders were significantly challenged by accumulating COVID-19 stress, worsening symptomatology, and limited access to effective treatment during the first year of the pandemic. This knowledge can guide clinicians, treatment centers, and policy makers in addressing the behavioral health needs of individuals impacted by disordered eating amidst emergent public health crises

Numbers of symptomatic and asymptomatic children at the six sampling time points.

<p>At each sampling time point (from July 2004 to May 2005), the 126 children were grouped into three categories; children with clinical malaria (blood film parasitaemia, fever and at least one other symptom of malaria and no other obvious cause for the fever, described as Symp), children with blood film parasitaemia but no clinical symptoms (Asymp) and children with no blood film parasites (Uninfected).</p

Variations in the quality of malaria-specific antibodies with transmission intensity in a seasonal malaria transmission area of Northern Ghana

<div><p>Introduction</p><p><i>Plasmodium falciparum</i> induced antibodies are key components of anti-malarial immunity in malaria endemic areas, but their antigen targets can be polymorphic. Induction of a high proportion of strain-specific antibodies will limit the recognition of a broad diversity of parasite strains by these responses. There are indications that circulating parasite diversity varies with malaria transmission intensity, and this may affect the specificity of elicited anti-malarial antibodies. This study therefore assessed the effect of varying malaria transmission patterns on the specificity of elicited antibody responses and to identify possible antibody correlates of naturally acquired immunity to malaria in children in an area of Ghana with seasonal malaria transmission.</p><p>Methods</p><p>This retrospective study utilized plasma samples collected longitudinally at six time points from children aged one to five years. Multiplex assays were used to measure antibody levels against four <i>P</i>. <i>falciparum</i> AMA 1 variants (from the 3D7, FVO, HB3 and CAMP parasite strains) and the 3D7 variant of the EBA 175 region II antigen and the levels compared between symptomatic and asymptomatic children. The relative proportions of cross-reactive and strain-specific antibodies against the four AMA 1 variants per sampling time point were assessed by Bland-Altman plots. The levels of antibodies against allelic AMA1 variants, measured by singleplex and multiplex luminex assays, were also compared.</p><p>Results</p><p>The data show that increased transmission intensity is associated with higher levels of cross-reactive antibody responses, most likely a result of a greater proportion of multiple parasite clone infections during the high transmission period. Anti-AMA1 antibodies were however associated with a history of infection rather than protection in this age group.</p><p>Conclusion</p><p>The data contribute to understanding the underlying mechanism of the acquisition of strain-transcending antibody immunity following repeated exposure to diverse parasite strains.</p></div

Antigen-specific antibody level and parasite density variations over the study period.

<p>Levels of either the antigen specific antibodies (A-E) or parasite density (F) at the six sampling time points were compared by the Kruskal-Wallis test, followed by the Bonferroni post-hoc test to assess pair-wise differences. Results (p values) after post-hoc tests are presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0185303#pone.0185303.s002" target="_blank">S2 Table</a>.</p

Relation between antibody levels and clinical malaria outcome^#.

<p>Relation between antibody levels and clinical malaria outcome<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0185303#t003fn002" target="_blank">^#</a>.</p

Numbers of symptomatic and asymptomatic children at the six sampling time points.

<p>At each sampling time point (from July 2004 to May 2005), the 126 children were grouped into three categories; children with clinical malaria (blood film parasitaemia, fever and at least one other symptom of malaria and no other obvious cause for the fever, described as Symp), children with blood film parasitaemia but no clinical symptoms (Asymp) and children with no blood film parasites (Uninfected).</p

Comparison of protein sequences (aa25–545) of the for AMA1 antigen variants.

<p>All antigens were produced in <i>Pichia pastoris</i> and devoid of N-glycosylation sites. These have been replaced with amino acid residues (indicated in red) that occur in AMA1 sequences from other <i>Plasmodium</i> parasites (N162K, T288V, S373D, N422D, S423K, N499Q). Each protein consists of a portion of the prodomain (aa25–96), domain I (aa97–315), domain II (aa316–425) and domain III (aa426–545). All antigens reacted with the reduction-sensitive rat monoclonal antibody 4G2 on western blots (Faber et al 2008), which was taken as a surrogate measure of conformational integrity.</p