Barriers to Timely Diagnosis and Treatment of Vector-Borne Diseases in a Changing Climate: A Case Report.

This case study examined current trends in the prevalence of vector-borne diseases and the impact of climate change on disease distribution. Our findings indicate that the dynamics of the Anopheles mosquito population in particular has changed dramatically in the past decade and now poses an increasing threat to human populations previously at low risk for malaria transmission. Given their geographic location and propensity for sustaining vector-borne disease outbreaks, southeastern states are particularly vulnerable to climate-induced changes in vector populations. We demonstrate the need to strengthen our hospital and laboratory infrastructure prior to further increases in the incidence of vector-borne diseases by discussing a case of uncomplicated malaria in a patient who arrived in one of our hospitals in Louisiana. This case exemplifies a delay in diagnosis and obtaining appropriate treatment in a timely manner, which suggests that our current health care infrastructure, especially in areas heavily affected by climate change, may not be adequately prepared to protect patients from vector-borne diseases. We conclude our discussion by examining current laboratory protocols in place with suggestions for future actions to combat this increasing threat to public health in the United States.

A pro-inflammatory and fibrous cap thinning transcriptome profile accompanies carotid plaque rupture leading to stroke.

Atherosclerotic plaque rupture is the etiology of ischemic stroke and myocardial infarction. The molecular mechanisms responsible for rupture remain unclear, in part, due to the lack of data from plaques at the time of rupture. Ribosome-depleted total RNA was sequenced from carotid plaques obtained from patients undergoing carotid endarterectomy with high-grade stenosis and either (1) a carotid-related ischemic cerebrovascular event within the previous 5 days ('recently ruptured,' n = 6) or (2) an absence of a cerebrovascular event ('asymptomatic,' n = 5). Principal component analysis confirmed plaque rupture was responsible for the greatest percentage of the variability between samples (23.2%), and recently ruptured plaques were enriched for transcripts associated with inflammation and extracellular matrix degradation. Hierarchical clustering achieved differentiation of the asymptomatic from the recently ruptured plaques. This analysis also found co-expression of transcripts for immunoglobulins and B lymphocyte function, matrix metalloproteinases, and interferon response genes. Examination of the differentially expressed genes supported the importance of inflammation and inhibition of proliferation and migration coupled with an increase in apoptosis. Thus, the transcriptome of recently ruptured plaques is enriched with transcripts associated with inflammation and fibrous cap thinning and support further examination of the role of B lymphocytes and interferons in atherosclerotic plaque rupture.