Exposure to Poaceae airborne pollen (PAP) has been shown to induce allergic reactions in individuals sensitive to PAP. Patient care for individuals sensitive to PAP can be aided by knowledge of PAP profiles. Air samples were collected using a Rotorod M40 rotation impact sampler from February 2005 to September 2017. Air samples were collected daily, excluding weekends and winter months, and are expressed in grains per cubic meter (g/m3). Light microscopy at 400x magnification was used to analyze samples. Pollen was classified according to the classifications provided by the American Academy of Allergy Asthma and Immunology and the National Allergy Bureau. Detection of PAP onset averaged on day 84 (March 25th); end day averaged on day 285 (October 12th); average duration was 202 days; average peak level onset was on day 146 (May 26th) and the average peak level was 135 g/m3. Average number of days during Poaceae season with 1 to 19 g/m^3 detected was 95; with 20 to 39 g/m^3 was 7; with 40 to 59 g/m^3 was 4; and with 60 g/m^3 or more was 2. Day of onset of PAP trended to be 1.6 days earlier in the year over the course of our data collection, with R2= 0.3476. Poaceae airborne pollen in Johnson City, Tennessee was noticeable for almost 7 months out of the year. We can assume the riskiest months of the year are from March to October with the highest risk period being the end of May.

This study demonstrates the first case report in which an NK Cell deficiency initially presented as an asymptomatic disseminated herpes simplex viremia (HSV). A pre-term 13- day- old patient presented with disseminated HSV after investigation because his twin brother was found to have HSV vesicular lesions. The patient remained asymptomatic throughout the entire hospital course. While 40% of neonates never exhibit vesicular lesions, most of the infants will be symptomatic with DIC and/or respiratory and/or hepatic failure. The HSV development in his twin brother prompted immediate multiple HSV PCR testing even though he was asymptomatic. The results were positive for HSV in both plasma & nasopharynx. He received intravenous acyclovir treatment for 21 days. Both CSF & brain MRI studies demonstrated no CNS involvement. He was discharged home with oral acyclovir for one year. Two months after being off acyclovir he developed herpetic vesicles which resolved with acyclovir treatment. Currently, he is on chronic acyclovir treatment. Lymphocyte enumeration tests demonstrated NK cell deficiency. Typically, HSV is a virulent symptomatic infection especially when it presents with viremia. Here we have a case of asymptomatic HSV viremia. Likewise, HSV infection does not usually recur after 1 year of acyclovir treatment. Here, we have a child presenting with what seems to be recurrent congenital HSV infection even with adequate treatment. These atypical HSV presentations may have been due to NK cell deficiency. We, therefore, propose that clinicians should consider NK cell deficiency as possible etiology when HSV presents in an atypical manner as described in our case.

Fungi represent one of the most diverse and abundant eukaryotes on earth. The interplay between mold exposure and the host immune system is still not fully elucidated. Literature research focusing on up-to-date publications is providing a heterogenous picture of evidence and opinions regarding the role of mold and mycotoxins in the development of immune diseases. While the induction of allergic immune responses by molds is generally acknowledged, other direct health effects like the toxic mold syndrome are controversially discussed. However, recent observations indicate a particular importance of mold/mycotoxin exposure in individuals with pre-existing dysregulation of the immune system, due to exacerbation of underlying pathophysiology including allergic and non-allergic chronic inflammatory diseases, autoimmune disorders, and even human immunodeficiency virus (HIV) disease progression. In this review, we focus on the impact of mycotoxins regarding their impact on disease progression in pre-existing immune dysregulation. This is complemented by experimental in vivo and in vitro findings to present cellular and molecular modes of action. Furthermore, we discuss hypothetical mechanisms of action, where evidence is missing since much remains to be discovered.