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Obesity is an enormous public health problem, arising as a consequence of alterations in eating behavior and how the body regulates energy intake, expenditure, and storage. Although an increased intake of energy-dense foods, especially when combined with reduced physical activity, contributes to the high prevalence of obesity, the existence of complex systems that regulate energy balance requires that this paradigm be considered in a larger context. In particular, recent evidence suggests that the gut microbiota may play a role in obesity by increasing the host’s energy-harvesting efficiency.

The treatment of obesity is challenging. Various surgical procedures designed to interfere with the ingestion and/or absorption of foods have been developed over the last 60 years. The Roux-en-Y gastric bypass (RYGB), currently the most commonly performed operation, involves creating a small gastric pouch from the stomach. This surgery leads to changes in acid exposure to the gastric remnant and proximal small bowel, restricts the amount and types of food that can be comfortably ingested, promotes a modest degree of nutrient malabsorption by shortening the length of the small bowel, and may result in intestinal dysmotility, all of which might be expected to alter the gut microbiota. Presently, very little is known about the changes in the gut microbiota that occur after RYGB, and no information has been published on changes in microbial diversity after RYGB in humans.

A recent study used the traditional Sanger and high-throughput 454 pyrosequencing methods to analyze the human gut microbiota in 9 individuals, 3 in each of the categories of normal weight, morbidly obese, and post-gastric bypass surgery. The goals were to identify specific microbial lineages that may play important roles in the development of obesity and also to determine whether the presence or abundance of these microorganisms changes after RYGB.

Human gut microbiota in obesity and after gastric bypass. PNAS USA January 21, 2009
Recent evidence suggests that the microbial community in the human intestine may play an important role in the pathogenesis of obesity. We examined 184,094 sequences of microbial 16S rRNA genes from PCR amplicons by using the 454 pyrosequencing technology to compare the microbial community structures of 9 individuals, 3 in each of the categories of normal weight, morbidly obese, and post-gastric-bypass surgery. Phylogenetic analysis demonstrated that although the Bacteria in the human intestinal community were highly diverse, they fell mainly into 6 bacterial divisions that had distinct differences in the 3 study groups. Specifically, Firmicutes were dominant in normal-weight and obese individuals but significantly decreased in post-gastric-bypass individuals, who had a proportional increase of Gammaproteobacteria. Numbers of the H2-producing Prevotellaceae were highly enriched in the obese individuals. Unlike the highly diverse Bacteria, the Archaea comprised mainly members of the order Methanobacteriales, which are H2-oxidizing methanogens. Using real-time PCR, we detected significantly higher numbers of H2-utilizing methanogenic Archaea in obese individuals than in normal-weight or post-gastric-bypass individuals. The coexistence of H2-producing bacteria with relatively high numbers of H2-utilizing methanogenic Archaea in the gastrointestinal tract of obese individuals leads to the hypothesis that interspecies H2 transfer between bacterial and archaeal species is an important mechanism for increasing energy uptake by the human large intestine in obese persons. The large bacterial population shift seen in the post-gastric-bypass individuals may reflect the double impact of the gut alteration caused by the surgical procedure and the consequent changes in food ingestion and digestion.

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• Gut Feeling
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What is genomics? How will it affect our lives? In this primer on the genomics revolution, entrepreneur Barry Schuler says we can at least expect healthier, tastier food. He suggests we start with the pinot noir grape, to build better wines.

Bees are important contributors to the economies of many countries, but as Travis Glare and Maureen O’Callaghan discuss in this article in Microbiology Today, they are many threats to the survival on the humble bee, including the risk of disease from micro-organisms:

There are many threats to bee survival, including the risk of disease caused by micro-organisms. The vast majority of our knowledge of bee diseases focuses on the honey bee, Apis mellifera, although there are actually over 20,000 species, both stingless and stinging, from those with solitary lifestyles to complex societies such as honey bee hives. Viruses, fungi, protozoa and bacteria are all known to cause infections in bees, sometimes leading to collapse of colonies, and causing serious threats to the bee-keeping industry. Bees have two distinct life forms, brood (egg, larva and pupal stages which develop within the hive) and adult. Most diseases are specific to just one of these life stages. While the list of diseases is quite long, only a few are of serious concern to apiculturists.

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Nice microbiology video from the Royal Sussex County Hospital NHS Trust.

A decade ago, a new variant form of Creutzfeldt-Jakob disease was identified. The emergence of this prion disease in humans was the consequence of the zoonotic transmission of bovine spongiform encephalopathy through dietary exposure. Since then, the control of human exposure to prions has become a priority, and a policy based on the exclusion of known infectious materials from the food chain has been implemented. Because all investigations carried out failed to reveal evidence of infectivity in milk from affected ruminants, this product has continuously been considered as safe. In this study, researchers demonstrate the presence of prions in colostrum and milk from sheep incubating natural scrapie and displaying apparently healthy mammary glands. This finding indicates that milk from small ruminants could contribute to the transmission of prion disease between animals. It also raises some concern with regard to the risk to humans associated with milk products from ovine and other dairy species.

Prions in Milk from Ewes Incubating Natural Scrapie. 2008 PLoS Pathog 4(12): e1000238
Since prion infectivity had never been reported in milk, dairy products originating from transmissible spongiform encephalopathy (TSE)-affected ruminant flocks currently enter unrestricted into the animal and human food chain. However, a recently published study brought the first evidence of the presence of prions in mammary secretions from scrapie-affected ewes. Here we report the detection of consistent levels of infectivity in colostrum and milk from sheep incubating natural scrapie, several months prior to clinical onset. Additionally, abnormal PrP was detected, by immunohistochemistry and PET blot, in lacteal ducts and mammary acini. This PrPSc accumulation was detected only in ewes harbouring mammary ectopic lymphoid follicles that developed consequent to Maedi lentivirus infection. However, bioassay revealed that prion infectivity was present in milk and colostrum, not only from ewes with such lympho-proliferative chronic mastitis, but also from those displaying lesion-free mammary glands. In milk and colostrum, infectivity could be recovered in the cellular, cream, and casein-whey fractions. In our samples, using a Tg 338 mouse model, the highest per ml infectious titre measured was found to be equivalent to that contained in 6 µg of a posterior brain stem from a terminally scrapie-affected ewe. These findings indicate that both colostrum and milk from small ruminants incubating TSE could contribute to the animal TSE transmission process, either directly or through the presence of milk-derived material in animal feedstuffs. It also raises some concern with regard to the risk to humans of TSE exposure associated with milk products from ovine and other TSE-susceptible dairy species.

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Cholera is an infectious form of gastroenteritis caused by the enterotoxin-producing strains of the curved Gram-negative bacillus Vibrio cholerae. Transmission to humans occurs through ingesting food or water that is contaminated with faecal matter from infected people. Classically the disease occurs where there is a lack or failure of sanitation, e.g. in crowded urban conditions in developing countries or following natural disasters. In its most severe forms, cholera is one of the most rapidly fatal illnesses known – in some circumstances infected patients may die within hours if medical treatment is not provided. Usually the disease progresses from the first liquid stool to shock (due to dehydration) in 4 to 12 hours, with death following in 18 hours to several days, unless oral rehydration therapy is provided.

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How does a tiny bacterium cause such rapid deaths? Cholera is a toxin-mediated disease. Vibrio cholerae produces cholera toxin, an enterotoxin which acts on the mucosal epithelium lining the small intestine, causing cell death and massive loss of body fluids into the gut, resulting in the the characteristic massive diarrhoea associated with the disease. Death is caused by hypovolemic shock due to the loss of body fluids, so first aid for cholera involves oral rehydration with isotonic liquids to combat these symptoms. Antibiotics are then given to speed up resolution of the infection.

Cholera seems to have originated in the Indian subcontinent and the disease spread by trade routes to Russia, then to Western Europe, and from Europe to North America during the nineteenth century. The history of cholera has been marked by a series of pandemics:

• 1816-1826 – First cholera pandemic
• 1829-1851 – Second cholera pandemic
• 1852-1860 – Third cholera pandemic. During this pandemic in 1854 John Snow identified contaminated water as the source of the disease by removal of the handle of the Broad Street pump in London.
• 1863-1875 – Fourth cholera pandemic
• 1881-1896 – Fifth cholera pandemic
• 1899-1923 – Sixth cholera pandemic
• 1961-1970s – Seventh cholera pandemic

Currently the disease is following a more endemic pattern, cropping up in poor countries and after natural disasters.

Vaccines against cholera are available but are not currently recommended for routine use. New oral vaccines against cholera are being developed, including a live-attenuated vaccine containing genetically manipulated V. cholerae, and an alternative vaccine containing killed whole-cell V. cholerae in combination with purified recombinant B subunit of the cholera toxin. Although the ultimate answer to cholera lies in public health and sanitation, at present the only feasible answer to cholera in poor countries is in vaccine development.

Cholera: Latest News

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• Cracking the cholera code
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Researchers have found novel prion infectivity in white and brown fat tissues of mice. Prion diseases, also known as transmissible spongiform encephalopathies, are infectious progressive fatal neurodegenerative diseases which affect humans as well as wild and domestic animals. Distribution of prion infectivity in organs and tissues is important in understanding prion disease pathogenesis and designing strategies to prevent prion infection in animals and humans. Previous studies in animals including sheep, goats, cattle, deer, mink, hamsters and mice, have found prion infectivity mostly in nervous system tissues such as the brain and spinal cord. The tissues studied in a mouse model demonstrate a proof of principle that white and brown fat tissues are sites of prion agent deposition and therefore may play a previously unrecognized role in prion infectivity and transmission of prion disease. The authors state clearly that it will be important to extend their studies to prion-infected large animals, such as cattle, sheep, deer, and elk where they may be potential sources of contamination of human and domestic animal food chains. Results of the current and future studies may merit additional consideration of steps to eliminate from the food chain any fat from ruminants suspected of exposure to or infection with prions.

Detection of Prion Infectivity in Fat Tissues of Scrapie-Infected Mice. 2008 PLoS Pathog 4 (12): e1000232
Distribution of prion infectivity in organs and tissues is important in understanding prion disease pathogenesis and designing strategies to prevent prion infection in animals and humans. Transmission of prion disease from cattle to humans resulted in banning human consumption of ruminant nervous system and certain other tissues. In the present study, we surveyed tissue distribution of prion infectivity in mice with prion disease. We show for the first time detection of infectivity in white and brown fat. Since high amounts of ruminant fat are consumed by humans and also incorporated into animal feed, fat-containing tissues may pose a previously unappreciated hazard for spread of prion infection.

Related:

• MicrobiologyBytes: Prions
• Prion Diseases
• How Now Mad Cow

BBC News reports that Britain is running out of mycologists. There were 32 in the 1990s, but just eight now. Scientists say we should be worried as, without a British research base, other countries could stand to make lucrative fungi-based discoveries in everything from medicine to engineering.

10 things fungi have done for us

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• MicrobiologyBytes: Mycology