Equine laminitis is a crippling disease affecting up to 1% of horses in USA. Treatments are typically unsuccessful, due to a lack of effective therapeutics, which reflects our lack of understanding of the pathophysiology of the disease. There are three prominent theories regarding the initial events leading to lamellar pathology: ischemia-reperfusion (I/R) injury, alterations in laminar metabolism and systemic inflammation. It is considered that matrix metalloproteinases (MMP) may contribute to tissue damage, irrespective of events governing the onset of laminitis. Two experimental models of laminitis were utilized, the black walnut extract (BWE) model, and the carbohydrate overload model (CHO). These model systems were used to examine the contributions of I/R, inflammation and MMPs to the development of laminitis. In the BWE model, we found no biochemical indicators of I/R injury, namely no conversion of xanthine dehydrogenase to xanthine oxidase. As early as 1.5 hours post-BWE administration, there was accumulation of proMMP-9, infiltration of neutrophils into the laminae and induction of genes encoding proinflammatory cytokines (e.g IL-1β, IL-8 and IL-6). Concentrations of proMMP-9 increased over time through to Obel grade 1 lameness (OG1), while proMMP-2 and MMP-2 did not change relative to controls. In CHO-induced laminitis, levels of proMMP-2 and MMP-2 remained similar to controls through OG1, but there was a significant accumulation of MMP-2 at later stages of the disease. ProMMP-9 was detectable as early as OG1, and was highly elevated at Obel grade 3 lameness (OG3). MMP-9 and MMP-2 were elevated to varying degrees in naturally acquired laminitis depending on the phase of the disease examined, being highest in animals with aggravated chronic laminitis. Lamellar ProMMP-9 correlated positively with myeloid cells, the majority of which are neutrophils during the stages of laminitis investigated. Despite the increases in gelatinase levels, all of which were shown by SDS-PAGE and zymography, there was no overall increase in native gelatinase activity relative to controls, suggesting association of MMP with tissue inhibitors of MMP (TIMPs). These results suggest that inflammation may play a role in the development of pathology in laminitis but raise questions regarding the contributions of MMP-9 and MMp-2 to tissue damage.

<p> Soap Lake, located in Washington State, was the subject of an NSF funded Microbial Observatory and is a naturally occurring saline and alkaline lake. Several organisms inhabiting this lake have been identified as producers of siderophores that are unique in structure. Two isolates SL01 &amp; SL28 were the focus of this study of siderophore production, structure elucidation and vesicle self-assembly. Bacterial isolates, enriched from Soap Lake sediment and water samples, were screened for siderophore production. Siderophore production was confirmed through the chrome azurol S (CAS) agar plate method. Isolates SL01 and SL28 were found to produce relatively high concentrations of siderophores in liquid medium. Extraction was performed by the methanol/water protocol in Varian cartridges and siderophore purification was done on HPLC with a 0-70% acetonitrile gradient. Lyophilization or <i> in vacuo</i> evaporation followed in order to store siderophores. Siderophore structure was determined using liquid chromatography and tandem mass spectrometry (LC/MS/MS) with fatty acid methyl ester (FAME) analysis. Vesicle self-assembly studies were performed using dynamic light scattering (DLS) and epifluorescence microscopy (employing cryoembedding and cryosectioning). Three new amphiphilic siderophore families (two from SL01 and one from SL28) were produced by the bacterial isolates, found to be most closely related to <i>Halomonas variablis</i> and <i>Halomonas pantelleriensis</i>, respectively. These siderophores resemble the amphiphilic aquachelin siderophores produced by <i>Halomonas aquamarina</i> strain DS40M3, a marine bacterium. Addition of ferric iron (Fe⁺³) at different equivalents demonstrated vesicle formation and this was confirmed by both DLS and epifluorescence microscopy. Bacteria thriving under saline and alkaline conditions are capable of producing unique siderophores resembling those produced by microbes inhabiting marine environments. Vesicle self-assembly was confirmed quantitatively and qualitatively. Amphiphilic siderophores may have different applications in medical and environmental fields.</p>

<p> Although swine diseases and parasites cause significant losses to producers in Hawai&lsquo;i, limited information is available on changing disease patterns and related farm practices. The objectives of this study were to identify practices used on Hawai&lsquo;i swine farms and to determine if there is a relationship between those practices and the absence or presence of a disease. A management and biosecurity practices survey was administered to farmers (n = 27). Survey questions were analyzed by region, sow population, and disease presence. Most common practices included cooking food waste (94% of farmers feeding food waste), feral pig exclusion (74%), and administering an anthelmintic (63%). Challenges faced by farmers include biosecurity concerns of on-farm sales, limited access to veterinary specialists, and excluding vermin from the production area. In addition, serological samples (n = 414) from swine farms (n = 57 out of 200 farms) were tested and found positive for antibodies against Porcine Circovirus Type 2b (PCV ELISA; 98% positive), Senecavirus (SVA IFA; 58%), Porcine Epidemic Diarrhea (PED IFA; 33%) and Porcine Reproductive and Respiratory Syndrome (PRRS ELISA; 16%). Fecal flotation detected coccidia oocysts (63%) on every island; Oesophagostomum dentatum (26%), Ascaris suum (18%), Strongyloides (11%), Metastrongylus spp. (8%), and Trichuris suis (8%) ova were on a subset of islands. Analysis indicates that disease prevalence is regionally distributed. Kaua&lsquo;i, which is protected by a quarantine order, has remained negative for PED, and Moloka&lsquo;i, which sees less interisland traffic, is negative for PRRS, PED, and SVA. Geographical patterns in disease distribution assist biosecurity and management practice recommendations, the design of vaccination protocols, and the judicious use of antibiotics.</p><p>

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<p> Over the last several decades declines in pollinator populations, especially those of wild bees and other insects, have raised awareness of the economic impact pollination services have for crop production. This awareness and concern was heightened by an ongoing loss of millions of managed honey bee colonies since the early 1950s. Colonies are used predominantly for pollination services in fruit and vegetable crops. During 2007, an unusually large overwintering loss in colonies that was not characterized by the presence of dead bees was termed colony collapse disorder (CCD), a syndrome in which hives lacked sufficient worker caste bees to maintain the queen and brood. Potential factors hypothesized to be associated with CCD include parasite infestations (e.g., <i>Varroa </i> mite) and pathogen infections (<i>Nosema</i> spp. fungus and viruses), insecticide exposure (especially to the neonicotinoid class), and poor nutrition owing to a reduction in landscape areas containing high quality floral resources. Although no one stressor has been definitively associated with CCD, possible interactions among them have only recently been studied. Of particular interest are possible interactions of <i>Nosema </i> spp. with neonicotinoid insecticide exposure. The main objective of this dissertation was an examination of these potential interactions using a combination of literature analysis, empirical study of <i>Nosema</i> infection prevalence in adult bees, and simulation modeling of the combined effects of several stressors on worker population abundance. After the introduction, the dissertation is divided into four chapters addressing the following objectives: (1) Comparison of regulatory procedures for risk assessment of insecticides potentially impacting honey bees in the United States and in the European Union; (2) Analysis of published literature that document potential interactions between bee pathogens, parasites, and neonicotinoid insecticide residues; (3) Analysis of field-collected apiary bees for prevalence of <i>Nosema </i> spores in association with land uses and the presence of neonicotinoid residues; (4) Use of the honey bee colony model BEEHAVE to predict colony collapse in the presence of pathogens and insecticide-induced mortality. Results of the various analyses suggest a need for modifying risk assessment procedures to include the interaction of pesticide residues with parasite/pathogen stressors. </p><p>

African trypanosomiasis occurs in 36 African countries following the geographic distribution of the tsetse fly. About 55 million people are at risk of acquiring infection and over 300,000 are already infected (WHO news, August 1996). Domestic animals excluded from about 70% of the land encompassing the tsetse habitat. However, many wild animals co-exist with the tsetse fly and are resistant to trypanosomiasis. Our Lab chooses Cape buffalo as a wild animal model to study the trypanoresistant mechanism. Cape buffaloes survive with low parasitemia and no sip of disease in the tsetse habitat. The superior ability of Cape buffaloes to limit the density of the trypanosome population in their bloodstream is related to the presence in their plasma or serum of material that kills all species of African trypanosome (123). The previous results from our lab had shown that the trypanocidal component in Cape buffalo serum was correlated with the presence of a 146 kDa polypeptide revealed by reducing SDS-PAGE. The amino acid sequence of the 146 polypeptide was 84–100% homologous with the sequence of human, mouse and rat xanthine:oxygen oxidoreductase (XO/XDH) suggesting that the trypanocidal protein might be XO (123). The main objective of this thesis was to explore the mechanism of Cape buffalo to control African trypanosomiasis. My work has shown that Cape buffalo serum XO generates trypanocidal H2O2 during catabolism of hypoxanthine and xanthine to uric acid. Furthermore, Cape buffalo serum contains adenosine deaminase, purine nucleoside phosphorylase, and guanine deammase, which together with xanthine oxidase catabolize adenosine, inosine, guanosine, guanine, hypoxanthine, and xanthine to uric acid yielding H 2O2. Paradoxically, Cape buffalo serum also contains catalase that catabolizes H2O2 to H2O and prevents expression of trypanocidal activity under physiological condition. However, I have shown that an infection-induced decline of blood catalase activity results in the accumulation of H2O2 in Cape buffalo blood and allows the Cape buffalo serum to express trypanocidal activity. A high xanthine oxidase activity is also found in sera from Eland, Giraffe and Greater Kudu, which might be responsible for their resistance for trypanosomiasis. Trypanosusceptible animals, which support high parasitemia and die after the infection, are unable to accumulate a trypanocidal concentration of H 2O2 in their bloodstream because of their low serum xanthine oxidase activity, sustained catalase activity and/or the presence of additional serum component(s) that protect trypanosomes from H2O2. The studies contribute to the data base of host anti-trypanosomiasis mechanisms, which may ultimately provide information to develop new measures to control African trypanosomiasis.

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