El presente estudio se realizó en los mercados del cercado de Tacna. El objetivo de este trabajo de investigación fue evaluar la contaminación de hortalizas por Enteroparásitos; asimismo, identificar las especies de enteroparásitos de importancia en salud pública presentes en hortalizas aptas para el consumo humano. Se estudiaron 522 muestras correspondientes a cuatro especies de hortalizas obtenidas al azar; las muestras fueron procesadas por los métodos de sedimentación y observación directa, así como por la técnica de coloración de Ziehl-Neelsen modificado. El resultado del estudio es el siguiente: el 21,26% de las hortalizas que se expenden en los mercados del cercado de Tacna, están contaminados con enteroparásitos; los mercados de mayor contaminación fueron Grau (12,84%); Central (3,07%),Dos de Mayo (2,86%). Los enteroparásitos encontrados fueron Isospora sp. (17,06%), Cryptosporidium parvum(2,48%) y Giardia sp. (1,71%). Las hortalizas de mayor contaminación fueron la lechuga (6,13%), rabanito (5,55%), y repollo (5,59%). Las hortalizas comercializadas en los mercados del cercado de Tacna, constituyen un factor epidemiológico importante en la cadena de transmisión de enfermedades enteroparasitarias.

The human colon is an anaerobic environment densely populated with bacterial species, creating what is known as the human intestinal microbiome; an ecosystem imperative to physiological function with regards to metabolism of non-digestible residues, growth of cells and immune protection from invading organisms. As such, quantifying, and subsequently developing an understanding of the behaviour of this microbial population can be of great value. Unfortunately, because of the physical inaccessibility of many parts of the gastro-intestinal (GI) tract, routine experimentation with this environment is not practical. However, theoretical modelling techniques including in vitro and in silico simulation/experimental platforms provide a means by which further studying of intestinal microflora can be approached. Perfecting these theoretical models is an important step in further understanding colon microbiota. An existing in silico model of carbohydrate digestion in the colon, developed by Munoz-Tamayo et al. (2010) has been used as a platform for experimentation with the intention of of discovering features which may be removed and/or added to improve the performance and reliability of the design. The model is an adaptation of the waste-water engineering based mathematical model ADM1 (Anaerobic Digestion Model 1), developed to incorporate biochemical and environmental specifications as well as physical structures particular to the human colon. The model is then a system of 102-ordinary differential equation with 66 parameters.Simulations with the default model configuration as well as variations of input variables, namely dietary fiber consumption and system flow rate, were completed to study the effect on average biomass concentration, demonstrating significant sensitivity to input variables and an unexpected linearity based on the non-linearity of the original complex system. Simulations and further study suggest that advancements in in silico modelling of the colon rely on the development of a metric or scheme that can effectively compare mathematically generated data with that collected through traditional experimentation. Also, experimenting with various reactor configurations as a basis for mathematical modelling may prove simpler configurations capable of generating comparable data to more complicated designs which may then also be applicable to existing in vitro representations of the colon.

Bioactive food components containing n-3 polyunsaturated fatty acids (PUFA) and curcumin modulate multiple determinants that link inflammation to cancer initiation and progression. In this dissertation, both transgenic and dietary mouse models were used to elucidate the effect of n-3 PUFA and curcumin treatment on murine intestinal inflammation. Specifically, fat-1 transgenic mice, which convert endogenous n-6 PUFA to n-3 PUFA in multiple tissues, exhibited a reduced number of colonic adenocarcinomas per mouse (1.05 plus/minus 0.29 versus 2.12 plus/minus 0.51, P = 0.033), elevated apoptosis (P = 0.03), and a decrease in n-6 PUFA–derived eicosanoids compared with wild-type (wt) mice in an azoxymethane (AOM) - dextran sodium sulfate (DSS) model. Following a 2-week recovery period after 5 days of DSS exposure, colonic inflammation and ulceration scores returned to pretreatment levels only in fat-1 mice. In addition, fat-1 vs wt mice exhibited decreased (P < 0.05) levels of CD3 , CD4 T helper, and macrophage cell numbers in the colon. The ability of n-3 PUFA to favorably modulate the resolution of intestinal inflammation in fat-1 mice was linked to an enhancement (P < 0.05) in the percentage of colonic lamina propria (cLP) CD4 FoxP3 cells and a decrease in both splenic and cLP Th17 cells (0.8 vs 1.2 percent in spleen, 1.4 vs 1.7 percent in colon) (P < 0.05) in fat-1 mice compared to wt. These results suggest that the antitumorigenic effect of n-3 PUFA may be mediated via its anti-inflammatory properties. The combined effect of n-3 PUFA and curcumin on DSS induced colitis was assessed in C57BL/6 mice. Addition of fish oil (FO) and/or curcumin to a corn oil (CO) based diet increased animal mortality compared to CO alone (P < 0.05). Consistently, following 1 or 2 cycles of DSS treatment, both dietary FO and curcumin promoted mucosal injury/ulceration compared to CO. However, compared to other diets, FO and curcumin combined feeding enhanced the resolution of chronic inflammation and suppressed (p < 0.05) a key inflammatory mediator, NF-kB, in colon mucosa. Mucosal microarray analysis revealed that dietary FO and curcumin differentially modulated the expression of genes induced by DSS treatment. These results suggest that dietary lipids and curcumin interact to regulate mucosal homeostasis and the resolution of chronic inflammation in the colon.

The pathogenesis of the enteric protozoan parasite Entamoeba histolytica remains poorly understood. Moreover, the host responses during the early periods of interaction in the gut remain to be clarified. In this study I investigated the cell specific responses to the parasite and the importance of cross talk between epithelial-immune cells that could potentially influence the outcome of infection, with a central focus on Nuclear factor (NF)-kappaB. NF-kappaB is a ubiquitous transcription factor that plays a critical role in mucosal inflammation and its regulation by E. histolytica has not been studied so far. Gal-lectin is a well characterized parasite virulence factor and vaccine candidate. I first characterized the interactions between Gal-lectin and macrophages and found that several proinflammatory genes are upregulated as early as 2h. The Gal-lectin activated NF-kappaB and up-regulated Toll like receptor-2 expression in an NF-kappaB- and p38 Mitogen Activated Protein (MAP) kinase-dependent manner. As intestinal epithelial cells (IEC) form the first line of active host defense against mucosal pathogens, I determined the interaction between ameba soluble proteins and naive IEC. I observed that the parasite could elicit a chemokine response via activation of PI3 kinase and phosphorylation of p65 subunit to induce monocyte chemoattractant protein-1. The consequent recruitment of immune cells could be responsible for colonic inflammation. Finally, I made the novel observation that in macrophage-primed IEC, ameba proteins elicited a cytoprotective stress response. Using a combination of siRNA and over expression studies, I demonstrated that amebic proteins increased the expression and phosphorylation of Heat shock protein (Hsp) 27 thereby enhancing its association with and subsequent inhibition of Inhibitory kappaB kinase (IKK). The resulting inhibition of NF-kappaB could be a potential mechanism that explains the absence of inflammation in the majority of infected individuals. Taken together, the findings of this study open up a new facet in the pathogenesis of amebiasis and unravel a novel paradigm to study host-parasite interactions in the gut.

Non-alcoholic fatty liver disease (NAFLD) includes simple hepatic steatosis (SS) and non-alcoholic steatohepatitis (NASH). NAFLD is tightly linked to obesity and is thought to be secondary to various noxious signals, some of which may originate from the intestinal microbiota (IM). Despite a growing body of evidence supporting a link between obesity and altered IM, there are no studies assessing the IM of patients with NAFLD. In this cross-sectional study we aimed at comparing fecal levels of total bacteria, Bacteroidetes, C. coccoides, C. leptum, Bifidobacteria, E. coli, and Archaea between healthy controls (HC) and patients with SS or NASH. We found higher C. coccoides levels in NASH compared to SS and lower percentage Bacteroidetes in NASH compared to SS and HC. Controlling for body mass index and fat intake we found an association between presence of NASH and percentage Bacteroidetes. The latter inversely correlated with insulin resistance.

The work described in this thesis was concerned with identifying the prevalence and risk factors associated with colonisation by the intestinal spirochaete Brachyspira pilosicoli in: humans: long term residents of Perth, Western Australia (WA) and Indonesians either living temporarily in Perth or as long term residents in urban and rural areas of Bali, Indonesia, animals: domestic animals including alpacas, birds, cattle, cats, chickens, dogs, doves, ducks, goats, horses, pigs, and sheep (housed at a wide variety of places around Perth), and a range of wild animals housed in various Zoos and wildlife centres in WA. This study shows that for humans: • Brachyspira pilosicoli was significantly more prevalent in Indonesians of all sub groups, be they temporary residents of Perth (9.4% - 216 faecal samples from 180 individuals), or long term residents of Indonesia (12.6% - 992 faecal samples from 617 individuals) compared with long term residents of Australia living mainly in Perth (0.2% of 766 sampled), even in those with gastrointestinal complaints. This suggests a relationship between a high prevalence of B. pilosicoli and living in Indonesia; • In Bali, B. pilosicoli was significantly more prevalent in the impoverished urban area of Sesetan (20.3-23.4%) where the husbandry of pigs is poor and effluent treatment is non-existent compared to four traditional farming villages (Badung, Karang Suwung, Melinggih, Payangan Desa) (3.3-22.6%). In the latter villages effluent and drainage is better and there is less likely to be contamination of drinking water • There was no significant association between the presence of B. pilosicoli and the presence of clinical symptoms including headaches, abdominal pains, diarrhoea, joint/muscular pain and constipation. • Amongst Indonesians living in Indonesia, there was no significant difference in the prevalence of B. pilosicoli between people with and without contact with animals and between farmers and other occupational groups. • Indonesians visiting Perth who were positive for B. pilosicoli originated from nine cities and five main islands in Indonesia. This suggests that B. pilosicoli is endemic throughout Indonesia. • Strain typing of isolates of B. pilosicoli showed that they were genetically heterogenous and did not show any consistent pattern with respect to geographical location, family of origin or disease status. Isolates from the same individual were sometimes unrelated, suggesting the probability of re-infection with another strain between the samplings. • Some households (~7%) had more than one member positive for B. pilosicoli. Strain analysis suggested transmission between family members, and this could be due to either faecal-oral transmission, or from a common external source, such as contaminated water. • B. pilosicoli was cultured from only 0.2% of Australians. This low prevalence may be a result of little or no exposure to B. pilosicoli due to good personal hygiene and environmental sanitation. • B. pilosicoli strain H1b and H171 that were isolated from healthy Indonesians were able to colonise mice and day-old chickens, and induced clinical signs of pasty faeces in the latter. Histological sections showed mild typhlitis and typical end-on attachment of B. pilosicoli to the caecal epithelial mucosa of the chickens. This finding suggests that the human isolates had pathogenic potential. This study showed that for animals investigated: • Intestinal spirochaetes were cultured from 46.4% (13/28) of bilbies with 14.3% (4/28) positive for B. pilosicoli. Spirochaetes were also cultured from the faeces of two Western Barred bandicoots and one (1.2%) kangaroo. • Intestinal spirochaetes were not isolated from any alpacas, cattle, goats, horses, pigs, and sheep but were detected in 40.5% of ducks, 14.3% of chickens, 14.9% of ostriches and 1.5% of cats. • Few pets that are commonly kept in households (dogs, cats and aviary birds) were colonised, suggesting that they are not an important focus of B. pilosicoli infection in Australia.

Thesis (Ph. D.)--University of Washington, 1988. / Vita. Bibliography: leaves [141]-155.

Diss. (sammanfattning) Uppsala : Univ., 2004. / Härtill 5 uppsatser.

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 1993. / Vita. Abstract. Includes bibliographical references (leaves 105-119). Also available via the Internet.

Thesis (Ph. D.)--University of Washington, 2007. / Vita. Includes bibliographical references (leaves 92-105).