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Non-human primates (NHP) are used to best understand and address pharmacology and toxicology obligations for human patients with highest and/or unmet need. In order to ensure the most appropriate care and use of NHP, it is important to understand the normal micro flora and fauna of NHP and ensure their utmost health to generate the most valuable and applicable data. There are many infections, including viral, bacterial, parasitic, and fungal that may perturb physiologic endpoints relevant to human health, and are essential to monitor and/or eradicate for NHP health. This publication captures a discussion involving the experience, knowledge and opinion from academic, industry and government experts regarding emerging and normal infections in NHP as they relate to immunotoxicity, and treatment and consequences of known infections. [ABSTRACT FROM AUTHOR]

Sodium methyldithiocarbamate (SMD) is an agricultural fumigant-type pesticide commonly used as a pre-plant biocide. SMD is currently listed by the US Environmental Protection Agency (EPA) as the third most commonly used conventional pesticide. Previously, SMD has been shown to be immunotoxic in mice. Initial immunotoxicological studies indicated that thymocytes are major targets of SMD or its breakdown products in mice. The purpose of the present study was to determine if this effect was mediated by an SMD-induced stress response. The decrease in thymus weight correlated to a decrease in all thymocyte subpopulations. However, as seen in earlier studies, the double positive (CD4 + CD8 + ) thymocyte subpopulation was more selectively decreased than the other subpopulations. The double negative (CD4 - CD8 - ) and single positive (CD4 + CD8 - or CD4 - CD8 + ) thymocyte subpopulations decreased in absolute numbers while increasing in percentage of the remaining cells in the thymus after SMD intoxication. In the current study, SMD caused an increase in serum corticosterone, a stress-related hormone. Blocking corticosterone either by 1) adrenalectomy or by 2) chemically blocking synthesis of nascent corticosterone in adrenal-competent animals abrogated the thymocyte atrophy caused by SMD. However, an additional stressor (restraint) did not act additively or synergistically to increase atrophy. Therefore, it is likely that SMD causes thymic atrophy by increasing serum corticosterone. [ABSTRACT FROM AUTHOR]

Metam sodium is the third most commonly used agricultural pesticide (by weight) in the U.S. A spill of 19,000 gallons of metam sodium into the Sacramento River in 1991 clearly demonstrated that a major uncontrolled release can have adverse ecological and human health effects. Furthermore, this incident revealed that estimates of Reference Exposure Levels for the major breakdown product of metam sodium (methylisothiocyanate, MITC) were reasonable with regard to the induction of discomfort. In fact, the irritant properties of MITC seem to account for many of the most commonly reported symptoms in this incident. However, neurotoxicity may also account for some of these symptoms. There is evidence that metam sodium can act as a contact sensitizer in humans, inducing allergic dermatitis. It also may exacerbate or induce respiratory allergy (asthma). The ecological impact of routine use of metam sodium is not clear, but adverse effects on non-target plants have been inferred from modeling studies, and adverse effects on soil microbes have been observed. These issues deserve further study. Human health effects of occupational or routine environmental exposure to metam sodium are not known, but there is limited evidence for immunological (hypersensitivity) and developmental effects as well as irritation and associated symptoms. Animal studies suggest a potential for immunological, developmental, carcinogenic, and atherogenic effects. Metam sodium and some of its breakdown products have a wide variety of molecular and cellular actions that could explain the health effects noted here. However, further studies are needed to relate specific molecular or cellular actions to specific health effects. [ABSTRACT FROM AUTHOR]