February 2011 - OurFood-news

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24.02.2011: Detection of prion infection in vCJD disease associated with the ingestion of BSE food [1]
Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disorder originating from exposure to bovine-spongiform-encephalopathy-like prions. This disease has a long and clinically silent incubationsposing and is a risk to others via blood transfusion, blood products, organ or tissue grafts, and contaminated medical instruments. The authors report the development of an assay for detection dormant infections. It is based on a solid-state binding matrix to capture and concentrate disease-associated prion proteins coupled with direct immunodetection of this surface-bound material. The authors stress that it is a prototype blood test for diagnosis and can be further developed to allow large-scale screening tests for asymptomatic vCJD prion infection.

People become infected by BSE prions by eating food containing material from BSE‐infected cattle, although other sources of exposure are possible. Much of the UK population born before 1996 (when rigorous measures to limit exposure were enforced) have potentially been exposed to BSE‐contaminated food and the number of people who may carry the infection but remain healthy is unknown. [2]

[1] Edgeworth JA, Farmer M, Sicilia A, Tavares P, Beck J, Campbell T, Lowe J, Mead S, Rudge P, Collinge J, Jackson GS: Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay. Lancet. 2011 Feb 5;377(9764):487-93. Doi:10.1016/S0140-6736(10)62308-2
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2810%2962308-2/abstract

[2] Blood test for variant CJD. National Prion Clinic at the National Hospital for Neurology and Neurosurgery. 02/02/2011
http://www.prion.ucl.ac.uk/clinic-services/investigations-tests/#BloodTest


21.02.2011: Gut microbiota symbiotic interaction with humans
Khoruts and Sadowsky 2011 report an example of the importance of gut microbiota and interaction with its host. The authors report treatment of Clostridium difficile gut infections with foecal transferes after collapse of the microbial community caused by antibiotic therapy or infection with pathogen. A better understanding of the interactions of humans with bacteria and synergistic are expected to result of these studies. [1]

According to Laparra and Sanz 2010 the beneficial effects of prebiotics mainly relay on their influence on the gut microbiota composition and their ability to generate fermentation products which may improve the status of immunity and metabolism of the host. The gut microbiota enhance the antioxidant effects of polyphenols transforming them in bioavailable compounds. Prebiotics may stimulate beneficial bacteria inhibiting pathogenic strains. The modulation of the intestinal microbiota can be used to treat intertinal disfunctions and may enhance the biological activity of micronutrients.based on the interactions of gut bacteria on human health. [2]

Roberfroidet al 2010 define as 'normobiosis' the composition of the gut 'ecosystem' in which micro-organisms with potential health benefits predominate in number over potentially harmful ones, in contrast to 'dysbiosis', in which one or a few potentially harmful micro-organisms are dominant, thus creating a disease-prone situation. The authors concluded that prebiotics may cause a selective modification in the composition of the gut microbiota leading to normobiosis could either induce beneficial physiological effects or reducing the risk of dysbiosis and associated intestinal and systemic pathologies.[3]

[1] Khoruts A, Sadowsky MJ: Therapeutic transplantation of the distal gut microbiota. Mucosal Immunol. 2011 Jan;4(1):4-7
http://www.ncbi.nlm.nih.gov/pubmed/21150894

[2] Laparra JM, Sanz Y: Interactions of gut microbiota with functional food components and nutraceuticals. Pharmacol Res. 2010 Mar;61(3):219-25.
http://www.ncbi.nlm.nih.gov/pubmed/19914380

[3] Roberfroid M et al: Prebiotic effects: metabolic and health benefits. Br J Nutr. 2010 Aug;104 Suppl 2:S1-63.
http://www.ncbi.nlm.nih.gov/pubmed/20920376


21.02.2011: The World Community Grid [1]
The aim of the community ist to provide computing power to studies in scientific field such as:
- New and existing infectious disease research - development of treatments for HIV/AIDS, Malaria, Severe Acute Respiratory Syndrome (SARS), etc.
- and disease - functions of proteins that are coded by human genes and how they might relate to cures for common diseases
- Environmental research - meteorology and severe weather warning, pollution, remediation, climate modelling, and others
- Natural disasters and hunger - earthquake warning, information on improving crop yields and livestock production, and evaluation of the supply of critical natural resources such as water. Ongoing studies are:

The mission of Discovering Dengue Drugs – Togehther- [2]
The mission of Discovering Dengue Drugs - Together - is to identify promising drug candidates to combat the Dengue, Hepatitis C, West Nile, Yellow Fever, and other related viruses. These drugs target the viral NS3 protease, an enzyme critical for virus replication, and its amino acid sequence and atomic structure are very similar among the different disease-causing flaviviruses. In this study advanced structure-based computational drug discovery methods are used to identify small molecule protease inhibitors.

Malaria research and Plamodium Yoelii Yoelii [3]
The Bonneau Lab is working on microbiome projects such as analysing the malaria parasite Plasmodium Yoelii Yoelii. The team stresses that this rodent malaria parasite is important for understanding the function of human malaria.

The Human Microbiome Project [4]
A microbiome is the totality of microbes, their genetic elements (genomes), and environmental interactions in a defined environment. The microbiome usually includes microbiota and their complete genetic elements. Researchers in the Human Microbiome Project are sampling and analyzing the genome of microbes from five sites on the human body: nasal passages, oral cavities, skin, gastrointestinal tract, and urogenital tract. Microbiome studies the microorganisms included as part of the human genome, because of their influence on human physiology.

The Human Microbiome Project (HMP) is a United States National Institutes of Health initiative with the goal of identifying and characterizing the microorganisms which are found in association with both healthy and diseased humans (their microbial flora). This microbiome project is to test if changes in the human microbiome are associated with human health or disease. [5]

Nanotechnology to improve filtration and desalination of water [6]
Scientists of the National Centre for Nano Science and Technology of the Chinese Academy hope optimize the process which will allow water to flow even more easily to filter and desalinate water using nanotubes.

[1] World Community Grid
http://www.worldcommunitygrid.org/research/viewSubmitAProposal.do

[2] Discovering Dengue Drugs - Together
http://www.worldcommunitygrid.org/research/dddt2/overview.do


[3] Bonneau Lab: HPF2 Update - January 2011
http://homepages.nyu.edu/~rb133/wcg/thread_2011_01_31.html

[4] Human Microbiome Project (HMP). The National Institutes of Health NIH
http://commonfund.nih.gov/hmp/

[5] Human Microbiome Jumpstart Reference Strains Consortium: A catalog of reference genomes from the human microbiome. Science. 2010 May 21;328(5981):994-9.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940224/?tool=pubmed

[6] Center for Nano and Micro Mechanics: The Computing for Clean Water Project (C4CW)
http://cnmm.tsinghua.edu.cn/contents/51/263.html


20.02.2011: Leishmaniasis [1]
Leishmaniasis is caused by protozoan parasites of the genus Leishmania. It is transmitted by the bite of sandflies of the genus Phlebotomus.

Only the female sandfly transmits the parasites. Female sandflies need blood for their eggs to develop, and become infected with the Leishmania parasites when they suck blood from an infected person or animal and the Leishmania can develop in the sanfly. Feeding blood from another animal or human the sandfly inoculates the Leishmania, which can than mature.

Sand flies within the genus Lutzomyia serve as the vectors for all species of the protozoan parasite Leishmania. Lutzomyia longipalpis was the predominant species collected within the Pacific plains region of western Nicaragua. Lutzomyia cruciata or Lutzomyia barrettoi majuscula were the species most frequently collected in the central highlands and Atlantic plains regions. [2]

Leishmania protozoans which infect mamals are the Leishmania donovani complex with three species (L. donovani, L. infantum, and L. chagasi), the Leishmania mexicana complex with four species (L. mexicana, L. amazonensis, and L. venezuelensis), Leishmania tropica, Leishmania major, Leishmania aethiopica, and the subgenus Viannia with four important species (L. (V.) braziliensis, L. (V.) guyanensis, L. (V.) panamensis, and L. (V.) peruviana).

The disease may cause cutaneous, mucocutaneous or visceral forms. Cutaneous leishmaniasis is the most common form. Visceral leishmaniasis is the most severe form, in which vital organs of the body are affected. The mucocutaneous form affects the nasopharyngeal tissues with lesions of this tissue. Differention between the different species of Leishmania uses isoenzyme analysis, DNA sequence analysis, or monoclonal antibodies, because there is no difference of morphology between the species.

Cutaneous leishmaniasis is known to be endemic in south-central Texas. Wright et al.2008 report nine cases of cutaneous leishmaniasis in residents of north Texas. The authors warns that the disease may experience a northern spread. [3]

A kind of a symbiosis between Leishmania and virus increasing severity of leishmaniasis [4]
The mucocutaneous form of leishmaniasis affecting the nasopharyngeal tissues was studied by Ives et al. 2011. The authors report that metastasizing parasites are highly infected by a virus, the Leishmania RNA virus–1 (LRV1). This virus interferes with the human immune system sensor protein called Toll-like receptor 3 (TLR3) localised in macrophages of humans. The TLR3 protectve immune pathway is turned to produce proinflammatory cytokines and chemokines triggered by the LRV1 virus.

[1] World Heath Organisation: Leishmaniasis.
http://www.who.int/leishmaniasis/en/

[2] Raymond RW, McHugh CP, Kerr SF: Sand flies of Nicaragua: a checklist and reports of new collections.Mem Inst Oswaldo Cruz. 2010 Nov;105(7):889-94.
http://www.ncbi.nlm.nih.gov/pubmed/21120358

[3] Wright NA, Davis LE, Aftergut KS, Parrish CA, Cockerell CJ: Cutaneous leishmaniasis in Texas: A northern spread of endemic areas. J Am Acad Dermatol. 2008 Apr;58(4):650-2.
http://www.ncbi.nlm.nih.gov/pubmed/18249464

[4] Ives A, Ronet C, Prevel F, Ruzzante G, Fuertes-Marraco S, Schutz F, Zangger H, Revaz-Breton M, Lye LF, Hickerson SM, Beverley SM, Acha-Orbea H, Launois P, Fasel N, Masina S: Leishmania RNA virus controls the severity of mucocutaneous leishmaniasis. Science. 2011 Feb 11;331(6018):775-8. .Doi: 10.1126/science.1199326
http://www.sciencemag.org/content/331/6018/775


19.02.2011: Dietary Guidelines for Americans, 2010 [1]
The Dietary Guidelines for Americans include recommendations for healthy eating and informations about nutrients and food components. The Guidelines are reviewed every 5 years. They contain advice for people 2 years and older about how good dietary habits can promote health and reduce risk for major chronic diseases.
Guidelines Download
The 2010 Dietary Guidelines released on January 2011 recommend to balance intake of calories with physical activity and consume more vegetables, fruits, low-fat dairy products, seafood., beans and peas, and nuts and seeds. Kitchen salt, solid fats, added sugars, and refined grains should be reduced.
Advices to persons with chronic diseases due to the poor diet and physical inactivity resulting in overweight and obesity of the US population were included in the new version of the Guidelines.

Two new chapters were included in the new Guideline: "The Total Diet: Combining Nutrients, Consuming Food" and "Translating and Integrating the Evidence: A Call to Action."

According to the Guidelines Poor diet and physical inactivity are the most important factors contributing to an epidemic of overweight and obesity. In USA 72 percent of men and 64 percent of women are overweight or obese [2]. Poor diet and physical inactivity alone are the major causes of morbidity and mortality.

Daily sodium intake in general population should be less than 2300 mg and less than 1500 mg for people older than50 years and those with hypertension, diabetes, or chronic kidney disease.

[1] Dietary Guidelines for Americans, 2010 (Released 1/31/11) U.S. Department of Agriculture. U.S. Department of Health and Human Services
http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/PolicyDoc.pdf

[2] Flegal KM, Carroll MD, Ogden CL, Curtin LR. Prevalence and trends in obesity among U.S. adults, 1999-2008. JAMA. 2010;303(3):235-241.
http://www.ncbi.nlm.nih.gov/pubmed/20071471


18.02.2011: Antimalarial and hepatoprotective effect of Middle East and Sahara Desert plant [1]
Sobhy et al. 2011 report antimalarial and hepatoprotective effect of the plant Anastatica hierochuntica known in traditional medicine for the treatment of variety of diseases including parasitic disease. The study was performed with mice infected with Plasmodium berghei. The plant extract presented also a hepatoprotective effect against D-glactosamine induced cytotoxicity in vitro.

Plasmodium berghei is a unicellular parasite which infects mammals, such as murine rodents, but it does not infect humans. There are four malaria parasites found in murine rodents which are used in anti-malaria drug research and P berghei was used in the present study.

The authors confirm the effect of traditional medicine use of Anastatic hierochuntica, also known as rose of Jericho, as anti-malaria and hepatoprotective plant.

Hepatoprotective researche was based on Yoshikawa et al. which described in 2003 the flavonoids, anastatins A and B, presenting a benzofuran moiety structure, isolated from the whole plants of Anastatica hierochuntica. These flavonoids presented hepatoprotective effects on D-galactosamine-induced cytotoxicity in mouse hepatocytes. According to Yoshikawa et al.the activity of the anastatins were stronger than commercial flavonoids, such as silybin. [2]

Composition and anti-melanome effect of extract of Anastatica hierochuntica [3]
Nakashima et al. 2010 found that the methanolic extract from the whole plant of Anastatica hierochuntica inhibit melanogenesis in theophylline-stimulated murine B16 melanoma 4A5 cells. The authors describe the composition of the extract stressing the importance of the inibition of tyrosinase activity of silybins and isosilybins. Isosilybins A and B were found by the authors to inhibit the mRNA expression of TRP-2. Silybins A and B enhanced the mRNA expression of tyrosinase and TRP-1 and -2. According to Nakashima et al. the inhibition of phosphorylation of extracellular signal-regulated kinases (ERK1/2) increases the expression of mRNA, similar to that of PD98059.

PD98059 (MEK1 Inhibitor) acts in vivo as a highly selective inhibitor of MEK1 activation and the MAP kinase cascade. [4]

[1] Eman.A.Sobhy, Mukul Tailang, Saleem Benyounes, K.Gauthaman: Antimalarial and hepatoprotective effects of entire plants of Anastatic hierochuntica. Int. J. Res. Phytochem. Pharmacol. 2011, 1(1), 24-27
http://ijrpp.pharmascope.org/jdownloads/Volume%201/Issue%201/04-m4.pdf

[2] Yoshikawa M, Xu F, Morikawa T, Ninomiya K, Matsuda H: Anastatins A and B, new skeletal flavonoids with hepatoprotective activities from the desert plant Anastatica hierochuntica.Bioorg Med Chem Lett. 2003 Mar 24;13(6):1045-9.
http://www.ncbi.nlm.nih.gov/pubmed/12643908

[3] Nakashima S, Matsuda H, Oda Y, Nakamura S, Xu F, Yoshikawa M: Melanogenesis inhibitors from the desert plant Anastatica hierochuntica in B16 melanoma cells. Bioorg Med Chem. 2010 Mar 15;18(6):2337-45.
http://www.ncbi.nlm.nih.gov/pubmed/20189399

[4] Di Paola R, Galuppo M, Mazzon E, Paterniti I, Bramanti P, Cuzzocrea S: PD98059, a specific MAP kinase inhibitor, attenuates multiple organ dysfunction syndrome/failure (MODS) induced by zymosan in mice. Pharmacol Res. 2010 Feb;61(2):175-87.
http://www.ncbi.nlm.nih.gov/pubmed/19819333


17.02.2011: Fish consumption reduces the stroke incidence in women says Swedish study [1]
Larsson, Virtamo and Wolk 2010 examined data of 34.670 women in the Swedish Mammography Cohort. Over 14 years 1680 incident cases of stroke, including 1310 cerebral infarctions, 233 hemorrhagic strokes, and 137 unspecified strokes were registered. The authors found that women who ate more than three servings of fish per week had a 16% lower risk of total stroke than women who ate less than one serving a week, However, cerebral infarction or hemorrhagic stroke were not reduced by diet rich in fish.

Fatty fish like salmon, whitefish, char, herring and mackerel were not significantly associated with risk of stroke. In Sweden salmon and herring are eaten salty. This might cancel the health benefits of the omega 3 PUFAs. Claims of benefits of moderate consumption of fatty fish should therefore still remain valid, say the authors.

These results suggest that the consumption of fish, especially of lean fish, may reduce risk of stroke in women. Fish is source of omega 3 PUFAs selenium and taurin. Selenium acts as antioxidant and taurin reduces blood pressure and lowers the level of triglycerides in serum.

[1] Larsson SC, Virtamo J, Wolk A: Fish consumption and risk of stroke in Swedish women.Am J Clin Nutr. 2010 Dec 29.
http://www.ajcn.org/content/early/2010/12/29/ajcn.110.002287.abstract


17.02.2011: Health Effects of Energy Drinks on Children [1]
Seifert and colleagues 2011 report that 30% to 50% of adolescents and young adults consume energy drinks contain high and unregulated amounts of caffeine. Serious adverse effects of these drinks have been reported in association with other health risks. In 2007 there were 5448 US cases of caffeine overdoses of which 46% occurred in persons younger than 19 years. According to the authors the use of energy drinks in these young populations should be debated, as they provide no therapeutic benefit, are associated with health risks, many of their ingredients are understudied and not regulated. Seifert and colleagues argue that such drinks present no therapeutic benefit. The toxicity surveillance should be improved, sales and consumptions regulations should be established.

Bigard et al. 2010 reports that the effect of energy drinks on physical and cognitive performances remains controversial. The toxicity of ingredients or ingestion in combination with alcohol may be the cause of related serious effects. Taurine-induced toxic encephalopathy has been cited in some studies, but the taurincontent of energy drinks do not pose a health risk, but the effect of more then 3 gram taurin/day of energy drinks must be studied. Bigard stresses that consumption of energy drinks may increase the risk for caffeine overdose and toxicity in children and teenagers. This group considers energy combined with alcohol a social way to meet people. Such combination was found to reduce subjective perceptions of some symptoms of alcohol intoxication. [2]

The EU Scientific Committee on Food and the European Food Safety Authority (EFSA) [3]
Germany, Australia, and New Zealand have reported adverse effects of energy drinks associated with liver damage, kidney failure, respiratory disorders, agitation, heart disfunctions and deaths. These incidents usually involved improper intake of energy drinks, such as drinking them with alcohol or in greater quantities than recommended.

EU Scientific Committee on Food (SCF) has issued a statement on the safety of energy drinks and their stimulant ingredients in 1999, and supplemented this statement in 2003. This opinion says that the caffeine content of energy drinks is not so high that intake of caffeine as a result of moderate consumption of energy drinks would be detrimental to a healthy adult. However, energy drinks are not recommended to children and pregnant women. A daily intake of 300 mg is safe for pregnant women. Because of most recent research results, setting the safe limit at 200 mg has been considered.

European Food Safety Authority (EFSA) gave in 2009 an opinion on taurine and glucuronolactone, stating that frequent intake of energy drinks is not a matter of safety concern.
However, the EFSA's committee stressed the acute health concerns including accidents causing death that have been reported for young people that consume excessive amounts of energy drinks combined either with physical stress or as in most cases the use of alcohol.

The committee considers it not probable that taurine and caffeine carry a combined impact on the fluid and sodium losses of the body. Glucuronolactone probably has no combined impact with the effects of caffeine, taurine, alcohol or physical stress. Recommended though is that energy drinks not be used in combination with excessive use of alcohol or as drinks to quench thirst. [4]

Drug interactions and dose-dependent effects remain largely unknown, although the current study reports that the ingredients 5-hydroxy tryptophan, vinpocetine, yohimbine, and ginseng have the potential for drug interactions that could result in adverse effects. Such combination is found in JetFuel. [5]

Energy drinks labelled as nutritional supplements in USA [6]
Energy drinks are categorized as nutritional supplements in order to avoid the limit of 71 mg caffeine per 12 fluid ounces set by the FDA for soda, but also evade pharmaceutical safety testing and labelling in USA. Actually these drinks contain 75 to 400 mg caffeine per container, and guarana, kola nut, yerba mate, and cocoa adds a lot more not yet included in the .declaration of the label.

USA has the the most lax regulatory requirements on energy drinks compared with any other country. These drinks vary from 50 mg to 505 mg per unit. Reissig et al. 2009 state that the absence of regulatory opened to doors to aggressive marketing of energy drinks targeted toward young males, for psychoactive, performance-enhancing and stimulant drug effects, resulting in increasing cases of caffeine intoxication and caffeine dependence and withdrawal in children and adolescents. According to the authors, there are signs that combined use of caffeine and alcohol may increase the rate of alcohol-related injury and provide a gateway to other forms of drug dependence. [7]

Aggressive marketing of energy drinks [8]
Howland et al. 20011 report that marketing promotes mixing caffeinated 'energy' drinks with alcoholic beverages, such as Red Bull with vodka. Young drinkers are brought to expect that these drinks might reduce the effects of alcohol and enhance alertness, leading to increased risk in traffic.
Tests performed by the authors performed demonstrate that alcohol significantly impaired driving and sustained attention/reaction time. No improvement of driving performance was obtained with the addition of caffeine. The authors concluded that energy drinks or caffeine alone does not influence the effects of alcohol related to driving.

Health Canada's New Recommendations [9]
For children age 12 and under, Health Canada recommends a maximum daily caffeine intake of no more than 2.5 milligrams per kilogram of body weight. Based on average body weights of children, this means a daily caffeine intake of no more than:

• 45 mg for children aged 4 - 6;
• 62.5 mg for children aged 7 - 9; and
• 85 mg for children aged 10 - 12.

For women of childbearing age, the recommendation is a maximum daily caffeine intake of no more than 300 mg, or a little over two 8-oz (237 ml) cups of coffee (Nawrot et al. 2003) [10]. For the rest of the general population of healthy adults, Health Canada advises a daily intake of no more than 400 mg. The organisation provides a list of foods and caffeine contents [11]

[1] Seifert SM, SchaechterJL, Hershorin ER, Lipshultz SE: Health Effects of Energy Drinks on Children, Adolescents, and Young Adults. Pediatrics. 2011;127:511-528.
http://pediatrics.aappublications.org/cgi/content/abstract/peds.2009-3592v1

[2] Bigard AX: Risks of energy drinks in youths. Arch Pediatr. 2010 Nov;17(11):1625-31.
http://www.ncbi.nlm.nih.gov/pubmed/20926266

[3] Opinion on Additional information on “energy” drinks. EU Scientific Committee on Food. SCF. 05.03.2003
http://ec.europa.eu/food/fs/sc/scf/out169_en.pdf

[4] EFSA adopts opinion on two ingredients commonly used in some energy drinks. 12.02.2009
http://www.efsa.europa.eu/en/press/news/ans090212.htm

[5] Supplement News: German American Technologies JetFuel - Product Review.
http://www.supplementnews.org/German_American_Technologies/JetFuel

[6] Does the government regulate supplements? Consumer Reports Health.org
http://www.consumerreports.org/health/free-highlights/manage-your-health/supplements_questions.htm?AFFID=HNARSIC5

[7] Reissig CJ, Strain EC, Griffiths RR: Caffeinated energy drinks--a growing problem. Drug Alcohol Depend. 2009 Jan 1;99(1-3):1-10.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735818/?tool=pubmed

[8] Howland J, Rohsenow DJ, Arnedt JT, Bliss CA, Hunt SK, Calise TV, Heeren T, Winter M, Littlefield C, Gottlieb DJ: The acute effects of caffeinated versus non-caffeinated alcoholic beverage on driving performance and attention/reaction time. Addiction. 2011 Feb;106(2):335-41. doi: 10.1111/j.1360-0443.2010.03219.x
http://onlinelibrary.wiley.com/doi/10.1111/j.1360-0443.2010.03219.x/abstract

[9] Healthy living: Caffeine. Health Canada. 2010-03-29
http://www.hc-sc.gc.ca/hl-vs/iyh-vsv/food-aliment/caffeine-eng.php

[10] Nawrot P, Jordan S, Eastwood J, Rotstein J, Hugenholtz A, Feeley M: Effects of caffeine on human health. Food Addit Contam. 2003 Jan;20(1):1-30.
http://www.ncbi.nlm.nih.gov/pubmed/12519715

[11] Sources of Caffeine. Health Canada. 2010-03-19
http://www.hc-sc.gc.ca/fn-an/securit/addit/caf/food-caf-aliments-eng.php
15.02.2011: Rift Valley Fever [1]
Rift valley fever is a disease of domestic livestock and humans. It is spread by the bite of infected mosquitoes, such as Aedes or Culex genera. The disease is caused by the RVF virus, a member of the genus Phlebovirus (family Bunyaviridae). RVF outbreaks occur across sub-Saharan Africa. An outbreak in Egypt in 1977-78, several million people were infected and thousands died.

More than 400 deaths were registrated in Kenya in 1998. Small outbreaks in 2006 and 2007 forced the closure of livestock markets hitting the economy of the region. In September 2000 an outbreak was confirmed in Saudi Arabia and Yemen). In April 2010 fatal human cases of the disease were reported, together with ongoing outbreaks of Rift Valley Fever Virus infection affecting sheep, goats, cattle and wildlife on farms in South Africa with massive livestock deaths.

Rift valley fever is able to infect many species of animals including cattle, sheep, camels and goats. Sheep appear to be more susceptible than cattle or camels. Age is a factor in the animal's susceptibility to the severe form of the disease: over 90% of lambs infected with RVF die, whereas mortality among adult sheep can be as low as 10%. Infection of livestock during pregnancy leads to abortion of all foetuses.

Stable flies may play a role in the spread of rift valley fever [2]
Turell et al. 2010 analysed the possibility of the transmission of the rift valley fever virus byt he house flies (Musca domestica), and stable flies (Stomoxys calcitrans). The disease is known to be transmitted by mosquitoes. It is of importance to know whether other insects are also capable to replicate the virus. The authors found that house flies and stable flies could not support the replication, but Stomoxis calcitrans, the stable fly, could mechanically transmit the virus to hamsters. The authors stress therefore that the stable fly and other Stomoxys may play a role in a rapid spread of the disease, due to their close association with a possible contaminated livestock.

African swine fever [3]
African swine fever (ASF) is a hemorrhagic fever in domestic pigs that causes serious economic losses and high mortality rates in countries in sub-Saharan Africa, the island of Sardinia, Europe , Brazil, the Caribbean region and island of Mauritius. There is no vaccine against ASF, and disease control relies on rapid diagnosis and implementation of quarantine and slaughter policies. African swine fever virus (ASFV) is a large, icosahedral, cytoplasmic, double-stranded DNA virus. It is the only member of the family Asfaviridae, although it shares similarities with other virus families in the superfamily of nucleo-cytoplasmic large DNA viruses.

In 2007 a new outbreak of ASF was confirmed in the Republic of Georgia. The Georgia 2007/1isolate was closely related to isolates of genotype II, which has been identified in Mozambique, Madagascar, and Zambia. Chapman et al. 2011 report the complete genomic coding sequence of the Georgia 2007/1 isolate and compared it with other strains.
Phylogeny based on concatenated sequences of 125 conserved ORFs showed that this isolate clustered most closely with the Mkuzi 1979 isolate. Some ORFs clustered differently, suggesting that recombination may have occurred. Results provide a baseline for monitoring genomic changes in this virus.

In the Russian Federation, the deaths of near 48,000 animals and a loss of US$ 1 billion were reported in 2009. The authors stress the risk of African swine fever for pig farming worldwide which may result from a rapid spread of the virus.

Risk of African swine fever in the European Union [4]
The risk that African Swine Fever virus (ASFV) remains endemic in the Trans Caucasian Countries and the Russian Federation is moderate, while the risk of its spread in these regions is high. The resulting risk of introduction from these regions into the EU is moderate most likely through food waste.

Within the EU, mainly domestic pigs in the free range (FR) and the limited biosecurity sector (LB) are likely to be exposed to African Swine Fever virus via swill feeding, with low risk. Once infected, the risk of spread from the LB and FR sectors prior detection is high, mainly due to movement of pigs, people and vehicles and moderate from the High Biosecurity (HB) sector.

Because of their long life, ticks of the Ornithodoros erraticus complex can be important in maintaining local foci of African Swine Fever virus, where pigs are kept under traditional systems. Ticks do not, play an active role in the geographical spread of the virus. Wild boar have never been found infested because they do not rest inside burrows potentially infested by ticks.

West Nile virus (WNV) [5]
West Nile virus is a member of the family Flaviviridae. It mainly infects wild birds, but is known to infect humans, horses, dogs, cats, bats, chipmunks, skunks, squirrels, and domestic rabbits. The main route of human infection is through the bite of an infected mosquito. Approximately 90% of West Nile Virus infections in humans are without any symptoms.It is found in Africa, Middle East, United States, Italy and spreads Asia.
The genetic material of WNV is a positive-sense, single strand of RNA, which is between 11,000 and 12,000 nucleotides long; these genes encode seven non-structural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12 kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral glycoproteins.

The most effective method to detect risk of West Nile fever to humans and horses is sampling of sick or dead birds and test for the virus.
Yeh et al. 2011 say that West Nile fever has not been detected in South Korea so far, however the disease may spread to the country because many Russian migratory birds share flyways over South Korea and Japan. The authors refer to recent findings of the virus in cinereous vulture and cattle egrets in the Russian region , which is adjacent to the Korean peninsula. Flavivirus antibodies were already detected in migrating birds in Japan. The spread of the West Nile virus from Russia to South Korea and Japan is therefore possible due to the migration of infected birds to their breeding places.

Chikungunya virus [6]
Chikungunya virus (CHIKV) is an insect-borne virus, of the genus Alphavirus, that is transmitted to humans by virus-carrying female Aedes aegypti or Aedes albopictus mosquitos. There have been recent breakouts of CHIKV associated with severe illness. CHIKV causes an illness with symptoms similar to dengue fever. CHIKV manifests itself with an acute febrile phase of the illness lasting only two to five days, followed by a prolonged arthralgic disease that affects the joints of the extremities. The pain associated with CHIKV infection of the joints persists for weeks or months, or in some cases years.

Chikungunya virus is indigenous to tropical Africa and Asia, where it is transmitted to humans by the bite of infected mosquitoes, usually of the genus Aedes. Chikungunya virus belongs to alphavirus genus of the Togaviridae family. It is an "Arbovirus" (Ar-arthropod, bo-borne). CHIK fever epidemics are sustained by human-mosquito-human transmission. The word "chikungunya" is thought to derive from description in local dialect of the contorted posture of patients afflicted with the severe joint pain associated with this disease. The main virus reservoirs are monkeys, but other species can also be affected, including humans.

Although CHIK is endemic in Africa/Southeast Asia, recent outbreaks during 2004–2007 have reached new geographical areas where cases are now reported in Europe, Hong-Kong, Canada, Taiwan and the USA. In some cases, these are directly associated with the return of infected tourists from India and islands of the Indian Ocean. Moreover, in 2007, the first CHIK outbreak was recorded in a temperate region of North Eastern of Italy with Aedes albopictus mosquitos as vector.

Chikungunya Fever in in Singapore [7]
Ho et al. 2011 reviewed the epidemiological control of the Chikungunya Fever in Singapore. Some cases were related to Aedes aegypti as vector. Another rapid spread was due to a mutant viral strain (A226V) introduced from India and Malaysia with Aedes albopictus as primary vector. The authors report that the number of new cases declined due to aggressive control of the vector Aedes albopictus, however mosquito control program must be maintained to prevent recurrence of the disease.

[1] WHO: Rift Valley fever. Fact sheet Nr 207. WHO Media Centre 2010
http://www.who.int/mediacentre/factsheets/fs207/en/

[2] Turell MJ, Dohm DJ, Geden CJ, Hogsette JA, Linthicum KJ: Potential for stable flies and house flies (Diptera: Muscidae) to transmit Rift Valley fever virus. J Am Mosq Control Assoc. 2010 Dec;26(4):445-8.
http://www.ncbi.nlm.nih.gov/pubmed/21290943

[3] Chapman DAG, Darby AC, Da Silva M, Upton C, Radford AD, Dixon LK. Genomic analysis of highly virulent isolate of African swine fever virus. Emerg Infect Dis. 2011 Apr; Doi: 10.3201/eid1704.101283
http://www.cdc.gov/eid/content/17/4/pdfs/10-1283.pdf

[4] Scientific Opinion on African Swine Fever. EFSA Journal 2010; 8(3):1556 (149 pp.)
http://www.efsa.europa.eu/en/efsajournal/pub/1556.htm

[5] Yeh JY, Kim HJ, Nah JJ, Lee H, Kim YJ, Moon JS, Cho IS, Choi IS, Song CS, Lee JB: Surveillance for west nile virus in dead wild birds, South Korea, 2005-2008. Emerg Infect Dis. 2011 Feb;17(2):299-301.
http://www.cdc.gov/eid/content/17/2/299.htm

[6] Stock I: Chikungunya fever--expanded distribution of a re-emerging tropical infectious disease. Med Monatsschr Pharm. 2009 Jan;32(1):17-26.
http://www.ncbi.nlm.nih.gov/pubmed/19205134

[7] Ho K, Ang LW, Tan BH, Tang CS, Ooi PL, James L: Epidemiology and Control of Chikungunya Fever in Singapore. J Infect. 2011 Feb 8.
http://www.ncbi.nlm.nih.gov/pubmed/21315108


12.02.2011: STARI (Southern Tick-Associated Rash Illness)
STARI is transmitted via bites from the lone star tick (Ambylomma americanum), found in the southeastern and eastern U.S. It is also called Master Disease. [1]

This illness is a tick-borne disease carried by the Lone Star Tick Amblyomma americanum, which is caused, according to some authors, by the spirochaete bacterium Borrelia lonestari, but it fails to be detected this in most cases of STARI. The CDC says, therefore, that the pathogen of the disease is still unknown.

Erythema migrans (EM) is an annular, erythematous, expanding rash that is characteristic of early Lyme disease. Many cases of EM seem to have an aetiology different from that of Lyme disease and are called Southern tick-associated rash illness.

Microbiologists from the Centers for Disease Control and Prevention contacted the North Carolina Network Consortium, a statewide consortium of practice-based research networks joined to identify the aetiological agents of the STARI. Vaughn et al. 2010 describe the practice-based research network used to identify patients and collect specimens for clinical research. [2]

CDC recommendations on prevention of tick-borne diseases [3]
CDC recommends to avoid tick habitat (dense woods and brushy areas), to use insect repellents containing DEET or permethrin, wear long pants and socks, and perform tick checks and promptly removing ticks after outdoor activity. After tick bites it is important to monitor the onset of a rash, fever, headache, joint or muscle pains, or swollen lymph nodes within 30. In this case a doctor should be consulted immediately. According to the CDC in most circumstances, treating persons who only have a tick bite is not recommended.

Tickborne relapsing fever (TBRF) is transmitted to humans through the bite of infected soft ticks, feeding on rodents. TBRF is found primarily in Africa, Spain, Saudi Arabia, Asia, and certain areas in the Western U.S. and Canada. It is associated with sleeping in rustic cabins and vacation homes. Relapsing infections are acquired from other Borrelia species, such as Borrelia hermsii, Borrelia recurrentis, Borrelia parkeri and Borrelia duttoni, transmitted by the soft-bodied African tick Ornithodoros moubata.

The Eurasia strains of Tick-borne relapsing fever [4]
Tick-borne relapsing fever in Eurasia is attributed mainly to Borrelia persica with Ornithodoros tholozani as important tick vector, in India and Kashmir, the southern countries of the former USSR, Iran, Iraq, Syria, Jordan, Turkey, Israel, Egypt, and Cyprus. It inhabits caves, ruins, houses, cowsheds and burrows of rodents and small mammals, with an incubation period is 5-9 days. Borrelia caucasica, Borrelia latyschewii, Borrelia microtii, and Borrelia baltazardi were also described. To clear taxonomic confusion 16S rRNA and flaB genes were used. Sequencing of Israeli TBRF flaB genes identifies the Eurasia strains, the New World cluster and the Old World cluster.

Louse-borne relapsing fever [5]
Borrelia recurrentis is one of three pathogens (along with Rickettsia prowazekii and Bartonella quintana) of which the body louse, or Pediculus humanus humanus is a vector.Louse-borne relapsing fever is more severe than the tick-borne variety and occurs in epidemics in poor regions in the developing world, such as Ethiopia and Sudan. Mortality rate is 1% with treatment; 30-70% without treatment.

Borrelia organisms multiply in the gut of the louse. The bacterium can infect humans when the louse is crushed by the victim or by scratches. The transmission occurs from person to person using the louse, no animal reservoir exists.

The number of cases or relapsing fever, once a worldwide epidemic disease, is now diminishing, because of improvements in housings and insecticides reducing body louse incidence. Cutler , Abdissa and Trape2009 report that the infection is caused by a louse-adapted variant of Borrelia duttonii, transmitted by Ornithodoros moubata 'soft' ticks in East Africa, and recently by Borrelia crocidurae, transmitted by Ornithodoros sonrai ticks.

Food-borne tularemia in Bulgaria [6]
Tularemia is caused by the bacterium Francisella tularensis. A Gram-negative, nonmotile coccobacillus, the bacterium has several subspecies with varying degrees of virulence. The most important of those is F. tularensis tularensis (Type A), which is found in lagomorphs in North America and is highly virulent in humans and domestic rabbits. F. tularensis palaearctica (Type B) occurs mainly in aquatic rodents (beavers, muskrats) in North America and in hares and small rodents in northern Eurasia. It is less virulent for humans and rabbits. The primary vectors are ticks and deer flies Chrysops discalis, but the disease can also be spread through other arthropods. Rodents, rabbits, and hares often serve as reservoir hosts,

Tularemia may also be spread by direct contact with contaminated animals or material, by ingestion of poorly cooked flesh of infected animals or contaminated water, or by inhalation.

Komitova et al. 2010 describe the outbreak of tularemia in Bulgaria and its reemerging in 2003. Francisella tularensis (F. tularensis) was detected by PCR. The authors concluded that the tularemia outbreak was probably food-borne and was associated with a surge in the rodent population. [7]

Chlorine disinfection of Francisella tularensis in drinking water [8]
O'Connell et al. 2011 determined the resistance to chlorine of live vaccine strain (LVS) and wild-type strains of Francisella tularensis. The authors found that free available chlorine residual concentrations routinely maintained in drinking water distribution systems would require up to two hours to reduce all F. tularensis strains by 4 log10. LVS should not be used for disinfection studies, because this strain dies earlier compared with the wild type strain.

364D Rickettsiosis
Evaluation of disease caused by Rickettsia 364D [9]
364D Rickettsiosis (Rickettsia phillipi, proposed) is transmitted to humans by the Pacific Coast tick (Dermacentor occidentalis ticks). This is a new disease that has been found in California.
Shapiro et al. 2010 report that "spotless" Rocky Mountain spotted fever may be associated with the spotted fever group rickettsiae SFGR 364D, transmitted by the tick Dermacentor occidentalis. The authors stress that possible infection with 364D or other SFGR should be confirmed through molecular techniques in patients who present with "spotless" Rocky Mountain spotted fever or have serum antibodies to R. rickettsii with group-specific assays.

Wikswo et al.2008 provided molecular data on the prevalence and species identification of spotted fever group SFG rickettsiae circulating in populations of southern California ticks. They stress that neither Dermacentor variabilis nor R. rickettsii were often found, 364D should therefore be evaluated further as a potential cause of human SFG rickettsioses. [10]

Members of the order Rickettsiales (alpha-proteobacteria), transmitted by ticks, include the genera Rickettsia and Ehrlichia. The Mediterranean Spotted Fever (MSF), caused by Rickettsia conorii, the pathogens Rickettsia helvetica and Rickettsia slovaca Rickettsia monacensis and Rickettsia sp. IRS4 are frequent disease agents in Europe.

Lo et al. 2004 describe a novel alphaproteobacterium IricES1 found in the tick Ixodes ricinus. This bacterium can existing within the mitochondria, as well as the cytoplasm, of ovarian cells. The authors found that the bacterium enters mitochondria between the inner and outer membranes, and then proceeds to consume the inner mitochondrial matrix. [11]

Diseases transmitted by ticks in Swizerland [12]
Gern et al. 2010 report that Ixodes ricinus is the most frequent tick in Switzerland which transmit Lyme borreliosis (Borrelia burgdorferi group) and tick-borne encephalitis (TBE), the major tick-borne diseases transmitted to human. According to the authors there are several factors which influence infection, such as stage of the vector, the multiple hosts, the pathogenic agent, as well as human behaviour in nature, and the presence of co-infection agents in ticks such as Anaplasma, Babesia and Rickettsia. The authors call to evaluate the importance of such infections.

Spotted Fever Rickettsioses in Poland [13]
Podsiadły et al. 2010 found antibodies to specific Spotted Fever Rickettsioses rickettsiae antibodies in 14.7% of tested Poland forest workers, whereas most of these cases were due to Rickettsia massiliae. No antibodies to Rickettsia helvetica and Rickettsia slovaca in human sera were found, despite the presence of such bacteria in local ticks. Antibodies to Borrelia burgdorferi was most often found, isolated or in coinfection with Bartonella spp.

The authors stress that no infections with spotted fever group rickettsiae have been reported, however, monitoring of any changes is necessary, because of the local presence of the bacteria in ticks and specific antibodies in humans.

Tick-borne encephalitis [14]
Tick-borne encephalitis (TBE) is a central nervous system infection caused by a flavivirus [tick-borne encephalitis virus (TBEV). It is transmitted by the bite of several species of infected ticks, including Ixodes scapularis, Ixodes ricinus and Ixodes persulcatus, or (rarely) through the non-pasteurized milk of infected cows. The virus can infect the brain (encephalitis), the meninges (meningitis) or both.

The disease is caused by the tick-borne encephalitis virus, a member of the genus Flavivirus in the family Flaviviridae. Mortality is 1% to 2%, with deaths occurring 5 to 7 days after the onset of neurologic signs. Three virus sub-types are described: European or Western tick-borne encephalitis virus, Siberian tick-borne encephalitis virus, and Far-Eastern tick-borne encephalitis virus (formerly known as Russian Spring Summer encephalitis virus). Russia and Europe report about 5,000-7,000 human cases annually.

Tick-borne encephalitis moves northward triggered by climate change [15]
The northernmost tick-borne encephalitis (TBE) focus is in Simo, Finnish Lapland. Four TBE cases were confirmed during 2008-2009. The virus has 3 subtypes: European (TBEV-Eur), Siberian (TBEV-Sib), and Far Eastern (TBEV-FE). TBEV-Eur is mainly transmitted by Ixodes ricinus ticks (sheep ticks) and the 2 other subtypes by Ixodes persulcatus ticks (taiga ticks). Tick-borne encephalitis seems to be moving northward in Europe and shifting upward to higher elevations in the mountains, apparently influenced by climate change and an unusual combination of the TBEV-Eur strain and Ixodes persulcatus ticks.

Jääskelainen et al. 2010 describe two European-subtype strains from human serum samples containing tick-borne encephalitis virus (TBEV) RNA. The authors also analysed the variations within European-subtype strains, Siberian-subtype strains and Far Eastern-subtype strains using TBEV E and NS3 gene sequences. [16]

Complete genome sequences of two Korean strains of the tick-borne encephalitis virus [17]
Yun at al. 2011report the the complete genome sequences of two Korean strains of the tick-borne encephalitis virus (TBEV), designated KrM 93 and KrM 213. The data of the study demonstrates that the Korean TBEV strains clustered with the Western subtype rather than with Far-Eastern or Siberian subtypes.


[1] Masters EJ, Grigery CN, Masters RW: STARI, or Masters disease: Lone Star tick-vectored Lyme-like illness. Infect Dis Clin North Am. 2008 Jun;22(2):361-76, viii.
http://www.ncbi.nlm.nih.gov/pubmed/18452807

[2] Vaughn MF, Sloane PD, Knierim K, Varkey D, Pilgard MA, Johnson BJ: Practice-Based Research Network Partnership with CDC to Acquire clinical specimens to study the etiology of southern tick-associated rash illness (STARI): J Am Board Fam Med. 2010 Nov-Dec;23(6):720-7.
http://www.jabfm.org/cgi/content/full/23/6/720

[3] Southern Tick-Associated Rash Illness. Centers for Disease Control and Prevention CDC. Division of Vector-Borne Infectious Diseases
http://www.cdc.gov/ncidod/dvbid/stari/

[4] Assous MV, Wilamowski A: Relapsing fever borreliosis in Eurasia-forgotten, but certainly not gone! Clin Microbiol Infect. 2009 May;15(5):407-14.
http://www.ncbi.nlm.nih.gov/pubmed/19489923

[5] Cutler SJ, Abdissa A, Trape JF: New concepts for the old challenge of African relapsing fever borreliosis. Clin Microbiol Infect. 2009 May;15(5):400-6.
http://www.ncbi.nlm.nih.gov/pubmed/19489922

[6] Wikipedia: Tularemia
http://en.wikipedia.org/wiki/Tularemia

[7] Komitova R, Nenova R, Padeshki P, Ivanov I, Popov V, Petrov P: Tularemia in bulgaria 2003-2004.
Infectious Diseases Departnment, University Hospital, Pleven, Bulgaria. J Infect Dev Ctries. 2010 Nov 24;4(11):689-94.
http://www.ncbi.nlm.nih.gov/pubmed/21252445

[8] O'Connell HA, Rose LJ, Shams AM, Arduino MJ, Rice EW: Chlorine disinfection of Francisella tularensis. Lett Appl Microbiol. 2011 Jan;52(1):84-6.
http://www.ncbi.nlm.nih.gov/pubmed/21189486

[9] Shapiro MR, Fritz CL, Tait K, Paddock CD, Nicholson WL, Abramowicz KF, Karpathy SE, Dasch GA, Sumner JW, Adem PV, Scott JJ, Padgett KA, Zaki SR, Eremeeva ME: Rickettsia 364D: a newly recognized cause of eschar-associated illness in California. Clin Infect Dis. 2010 Feb 15;50(4):541-8.
http://www.ncbi.nlm.nih.gov/pubmed/20073993

[10] Wikswo ME, Hu R, Dasch GA, Krueger L, Arugay A, Jones K, Hess B, Bennett S, Kramer V, Eremeeva ME: Detection and identification of spotted fever group rickettsiae in Dermacentor species from southern California. J Med Entomol. 2008 May;45(3):509-16.
http://www.ncbi.nlm.nih.gov/pubmed/18533446

[11] Lo N, Beninati T, Sacchi L, Genchi C, Bandi C: Emerging rickettsioses. Parassitologia. 2004 Jun;46(1-2):123-6.
http://www.ncbi.nlm.nih.gov/pubmed/15305700

[12] Gern L, Lienhard R, Péter O: Diseases and pathogenic agents transmitted by ticks in Switzerland. Rev Med Suisse. 2010 Oct 13;6(266):1906-9.
http://www.ncbi.nlm.nih.gov/pubmed/21089555

[13] Podsiadły E, Chmielewski T, Karbowiak G, Kędra E, Tylewska-Wierzbanowska S: The Occurrence of Spotted Fever Rickettsioses and Other Tick-Borne Infections in Forest Workers in Poland. Vector Borne Zoonotic Dis. 2010 Nov 17.
http://www.ncbi.nlm.nih.gov/pubmed/21083370

[14] Süss, J: Tick-borne encephalitis in Europe and beyond – the epidemiological situation as of 2007. Eurosurveillance, Volume 13, Issue 26, 26 June 2008 http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=18916

[15].Jääskeläinen AE, Tonteri E, Sironen T, Pakarinen L, Vaheri A, Vapalahti O: European Subtype Tick-borne Encephalitis Virus in Ixodes persulcatus Ticks. Emerg Infect Dis. 2011 Feb;17(2):323-5
http://www.cdc.gov/eid/content/17/2/323.htm

[16] Jääskeläinen AE, Sironen T, Murueva GB, Subbotina N, Alekseev AN, Castrén J, Alitalo I, Vaheri A, Vapalahti O: Tick-borne encephalitis virus in ticks in Finland, Russian Karelia and Buryatia. J Gen Virol. 2010 Nov;91(Pt 11):2706-12.
http://www.ncbi.nlm.nih.gov/pubmed/20660147

[17] Yun SM, Kim SY, Ju YR, Han MG, Jeong YE, Ryou J: First complete genomic characterization of two tick-borne encephalitis virus isolates obtained from wild rodents in South Korea. Virus Genes. 2011 Feb 1.
http://www.ncbi.nlm.nih.gov/pubmed/21286797


11.02.2011: Lyme disease
Lyme disease, or Lyme borreliosis is an infectious disease caused by Borrelia bacteria.Borrelia burgdorferi sensu stricto causes Lyme disease in the United States. In Europa Borrelia afzelii and Borrelia garinii are the cause of Lyme disease. Borrelia is transmitted to humans by the bite of infected ticks belonging to a few species of the genus Ixodes ("hard ticks"). For the transmission of the disease, the presence of ticks is a prerequisite. Early symptoms may include fever, headache, fatigue, depression, and a characteristic circular skin rash called erythema migrans. Left untreated, later symptoms may involve the joints, heart, and central nervous system.

Lyme neuroborreliosis in horses [1]
Imai et al. 2011 describe Lyme disease in horses with progressive neurologic symptoms. Borrelia burgdorferi sensu stricto was identified by polymerase chain reaction amplification of B burgdorferi sensu stricto-specific gene targets (ospA, ospC, flaB, dbpA, arp). Spirochaetes were found in tissues with inflammation, including spinal cord, muscle, and joint capsule. Sequence analysis was identical to a human isolate of Borrelia burgdorferi strain 297, demonstrating inter-species infectivity of neuroborreliosis.

Borrelia burgdorferi in tick and dogs in Serbia [2]
Savić et al. 2010 studied Ixodes ricinus ticks and dogs in Serbia. The authors found 22.12% of ticks infected with Borrelia burgdorferi s.l and specific antibodies were determined in 25.81% of dogs.
The authors stress the actual risk of Borrelia to infect other animals and humans, because ticks and dogs of Serbia represent a reservoir of the disease agent.

Failing to develop a Lyme vaccine [3]
According to Poland 2011 the withdrawal of the 1998 FDA approved Lyme vaccine resulted from safety concerns suggesting that the vaccine antigen was arthritogenic, produced high costs, the vaccination had a difficult schedule, might need boosters, risk of the disease was uncertain, and there was low public demand. Poland deplores that no protection from Lyme disease will be available as no US vaccine will be developed in near future. A new vaccine should overcome such hurdles.

According to Shen, Mead and Beard 2011 the Lyme disease preventions include area acaricides, landscape management, host-targeted interventions, management of deer populations, use of insect repellent and tick checks. However, rates of compliance are poor. [4]

Nardelli et al. 2009 call for the development of a new vaccine, because Lyme disease cases increase and diagnoses is difficult. [5]

[1] Imai DM, Barr BC, Daft B, Bertone JJ, Feng S, Hodzic E, Johnston JM, Olsen KJ, Barthold SW: Lyme Neuroborreliosis in 2 Horses. Vet Pathol. 2011 Feb 1.
http://www.ncbi.nlm.nih.gov/pubmed/21285382

[2] Savić S, Vidić B, Lazić S, Lako B, Potkonjak A, Lepsanović Z: Borrelia burgdorferi in ticks and dogs in the province of Vojvodina, Serbia. Parasite. 2010 Dec;17(4):357-61.
http://www.ncbi.nlm.nih.gov/pubmed/21275243

[3] Poland GA: Vaccines against Lyme disease: What happened and what lessons can we learn? Clin Infect Dis. 2011 Feb;52 Suppl 3:s253-8.
http://www.ncbi.nlm.nih.gov/pubmed/21217172

[4] Shen AK, Mead PS, Beard CB: The lyme disease vaccine--a public health perspective. Clin Infect Dis. 2011 Feb;52 Suppl 3:s247-52.
http://www.ncbi.nlm.nih.gov/pubmed/21217171

[5]Nardelli DT, Munson EL, Callister SM, Schell RF: Human Lyme disease vaccines: past and future concerns. Future Microbiol. 2009 May;4(4):457-69.
http://www.ncbi.nlm.nih.gov/pubmed/19416014


10.02.2011: Anaplasmosis [1]
The Anaplasma marginale (Rickettsiales: Anaplasmataceae) is an obligate intraerythrocytic rickettsial gram-negative bacterium which infects cattle causing a mild to severe hemolytic disease. Anaplasmosis is responsible for dairy and beef industries losses. Cattle becomes infected through bites of ticks, biting flies or blood-cotaminated fomites. Intradermal needles, ear tagging, dehorning and castration equipment may also spread the disease.Determining msp1alpha Distribution and the evolution of Anaplasma marginale is being studied by determining msp4 and msp1alpha genotypes. Vaccines may prevented clinical anaplasmosis in cattle but are unable to avoid infection. Kocan et al. 2010 call for vaccines which prevent clinical disease and also prevent infection in cattle and ticks.

Fever, anemia, jaundice, weakness, and/or respiratory distress in infected animals and milk production decline in dairy cattle are reported. Clinically affected dairy cattle may also have a rapid decline in milk production. Anaplasmosis is a global disease of ruminants which presents clinical signs only in cattle. Anaplasmosis poses no direct human health or food safety. Howden et al. 2010 report that Dermacentor andersoni and Dermacentor variabilis are vector ticks in Canada. [2]

Severity of anaplasmosis in cattle increases with age. Anaplasma marginale can be detected on stained blood smears from animals during the acute phase, but is not always found in pre-symptomatic or carrier animals, when serology of antibodies and molecular detection methods are necessary. According to Aubry and Geale 2011 the role of wild ruminants in the epidemiology of bovine anaplasmosis is needed to be further evaluated. The authors cite the maintenance of Anaplasma-free herds, vector control, administration of antibiotics and vaccination as actual control measures for bovine anaplasmosis. [3]

Anaplasma phagocytophilum [4]
The bacterium Anaplasma phagocytophilum is known to infect sheep, goat, cattle, horse, dog, cat, roe deer, reindeer and humans in Europe, with Ixodes ricinus as vector. It may cause high fever, cytoplasmatic inclusions in phagocytes and severe neutropenia, but is seldom fatal unless complicated by other infections. The predisposing factor of anaplasmosis for other infections is very relevant, especially in sheeps. Stuen 2007 reports that several variants based on 16S rRNA gene sequences may exist in the same herd or even in the same animal.

Inadequate vector control of Bovine anaplasmosis in Costa Rica [5]
Bovine anaplasmosis in dairy farms of Costa Rica was determined by Oliveira et al., using recombinant truncated MSP-5 (rMSP-5) enzyme-linked immunosorbent assay (ELISA). Herd seroprevalence ranged from 20.0 to 72.0%. The authors stress that the endemic situation is due to inadequate vector control associated, among others, with rainy season, presence of tabanids and stable flies.

Human granulocytic anaplasmosis (HGA) [6]
Anaplasma phagocytophilum cause human granulocytic anaplasmosis (HGA) in USA, Europe and the Far East of Russia, with ticks as the main vector and mammalian species as reservoirs. Ixodes ricinus ticks from Estonia, Belarus and the European part of Russia were found to be infected by Anaplasma phagocytophilum. Katargina et al. 2011 assigned these strains to different groESL lineages and 16S rRNA gene variants with variable numbers of repetitive elements within ankA gene.

The tick-borne fever (TBF) and pasture fever in sheep, ruminants, horses and humans are caused by variants of Anaplasma phagocytophilum. The diseases present high fever, recurrent bacteremia, neutropenia, lymphocytopenia, thrombocytopenia, general immunosuppression, and secondary infections such as tick pyemia, pneumonic pasteurellosis, listeriosis, and enterotoxemia. Vector is the hard tick Ixodes ricinus, and possibly other ticks. Some cases of human granulocytic anaplasmosis (HGA) have been reported in Europe, but Woldehiwet 2006 stresses that it is not yet cleared if there is a difference between the variants causing HGA and those causing TBF in ruminants. [7]

Determination of Anaplasma phagocytophilum clusters using ankA gene [8]
Scharf et al.sequenced the 16S rRNA and ankA genes of Anaplasma. phagocytophilum strains from humans and several animal species to explain host preference and epidemiological diversity. The authors stress that analysis using 16S rRNA gene sequences is not sufficient to determine clusters of Anaplasma phagocytophilum, therefore ankA gene should be included in such determinations.

Diagnosis of anaplasmosis in dogs [9]
Ravnik et al. report that antibody titre and haematological parameters are not sufficient to confirm the clinical relevance of exposure to Anaplasmosis phagocytophilum. The authors suggest to include additional diagnostic tools, such as PCR in the diagnosis of such infections.

Fatal bovine anaplasmosis outbreak in Hungary [10]
Hornok et al. 2010 studied the occurrence of a fatal outbreak of bovine anaplasmosis in Hungary . An Anaplasma-carrier state of 92% of the cattle and cases of concurrent infections with Mycoplasma wenyonii, 'CandidatusMycoplasma haemobos' and rickettsaemia were reported by the authors. This outbreak was associated with divergent Anaplasma marginale genotypes and concurrent 'Candidatus Mycoplasma haemobos' infection, as well as of an Anaplasma ovis strain in ticks.

[1] Kocan KM, de la Fuente J, Blouin EF, Coetzee JF, Ewing SA. The natural history of Anaplasma marginale. Vet Parasitol. 2010 Feb 10;167(2-4):95-107
http://www.ncbi.nlm.nih.gov/pubmed/19811876

[2] Howden KJ, Geale DW, Paré J, Golsteyn-Thomas EJ, Gajadhar AA: An update on bovine anaplasmosis (Anaplasma marginale) in Canada. Can Vet J. 2010 Aug;51(8):837-40.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905000/?tool=pubmed

[3] Aubry P, Geale DW: A review of bovine anaplasmosis: Transbound Emerg Dis. 2011 Feb;58(1):1-30. doi: 10.1111/j.1865-1682.2010.01173.x.
http://www.ncbi.nlm.nih.gov/pubmed/21040509

[4] Stuen S: Anaplasma phagocytophilum - the most widespread tick-borne infection in animals in Europe. Vet Res Commun. 2007 Aug;31 Suppl 1:79-84.
http://www.ncbi.nlm.nih.gov/pubmed/17682851

[5] Oliveira JB, Montoya J, Romero JJ, Urbina A, Soto-Barrientos N, Melo ES, Ramos CA, Araújo FR. Epidemiology of bovine anaplasmosis in dairy herds from Costa Rica. Vet Parasitol. 2010 Dec 14.
http://www.ncbi.nlm.nih.gov/pubmed/21236580

[6] Katargina O, Geller J, Alekseev A, Dubinina H, Efremova G, Mishaeva N, Vasilenko V, Kuznetsova T, Järvekülg L, Vene S, Lundkvist A, Golovljova I. Identification of Anaplasma phagocytophilum in tick populations in Estonia, European Part of Russia and Belarus. Clin Microbiol Infect. 2011 Jan 2. doi: 10.1111/j.1469-0691.2010.03457.x.
http://www.ncbi.nlm.nih.gov/pubmed/21199155

[7] Woldehiwet Z: Anaplasma phagocytophilum in ruminants in Europe. Ann N Y Acad Sci. 2006 Oct;1078:446-60.
http://www.ncbi.nlm.nih.gov/pubmed/17114753

[8] Scharf W, Schauer S, Freyburger F, Petrovec M, Schaarschmidt-Kiener D, Liebisch G, Runge M, Ganter M, Kehl A, Dumler JS, Garcia-Perez AL, Jensen J, Fingerle V, Meli ML, Ensser A, Stuen S, von Loewenich FD.Distinct host species correlate with Anaplasma phagocytophilum ankA gene J Clin Microbiol. 2010 Dec 22.clusters.
http://www.ncbi.nlm.nih.gov/pubmed/21177886

[9] Ravnik U, Tozon N, Smrdel KS, Zupanc TA: Anaplasmosis in dogs: The relation of haematological, biochemical and clinical alterations to antibody titre and PCR confirmed infection. Vet Microbiol. 2010 Oct 16.
http://www.ncbi.nlm.nih.gov/pubmed/21112165

[10] Hornok S, Micsutka A, Fernández de Mera IG, Meli ML, Gönczi E, Tánczos B, Mangold AJ, Farkas R, Lutz H, Hofmann-Lehmann R, de la Fuente J: Fatal bovine anaplasmosis in a herd with new genotypes of Anaplasma marginale, Anaplasma ovis and concurrent haemoplasmosis. Res Vet Sci. 2010 Nov 19.
http://www.ncbi.nlm.nih.gov/pubmed/21094505


10.02.2011: Babesiosis
Babesiosis is tick borne zoonotic disease caused by invasion of the red cells of the blood by parasites of the genus Babesia in free-living animals, such as rodents, carnivores, and cattle. This fact increases the concern about the emerging zoonosis. Babesia microti and Babesia divergens cause human infections which vary from silent infection to a fulminant, malaria-like disease.
Babesia is a protozoan parasite of the blood causing hemolytic disease known as Babesiosis. There exist many Babesia, however, only few are pathogenic. [1]

Canine babesiosis is an important disease of dogs all over the world, resulting in anemia, thrombocytopenia varying from nonspecific illness to peracute collapse and death. Human infectios should be considered, in connection to travel or blood transfusion history. [2]

A case of malaria-like babesiosis after a travel to Nicaragua,confirmed by molecular characterization by polymerase chain reaction and sequence analysis was reported in Austria. [3]

Zinc deficiency induces a wide range of disorders including immunodeficiency which rises the risk of bacterial infections. Hamaguch and colleagues found that zinc deficiency increased the severity of Babesia microti and Babesia rodhaini infections of mice, resulting growth retardation, reduction of immunity and the decrease in Packed cell volume (PCV). PCV is a measure of the proportion of blood volume that is occupied by red blood cells. [4] [5]

The Ixodes ricinus tick removed from dogs in Warsawm (Poland) were found infected by
Babesia microti, demonstrating their presence in ticks in Poland. [6]

Human pathogens in ticks living on birds [7]
Franke and colleagues 20101 found European Ixodes ricinus (Acari: Ixodidae) ticks infected by Borrelia spp., Anaplasma phagocytophilum, Rickettsia spp. and Babesia spp. The majority of birds with ticks testing positive were European robins and thrushes.
Data of this study suggest that birds may also serve as host for Borrelia afzelii. Rickettsia monacensis and Rickettsia helvetica were also found. The authors found Babesia divergens and Babesie microti in ticks living on infected birds. This demonstrates that birds may infect ticks with Ricketsia spp.

Coexistence of Borreliaspp. and Babesia spp. in ticks [8]
Hildebrandt and et al. 2010 determined the infection of Ixodes ricinus ticks with borrelia spp. (ospA gene) and Babesia spp18S rRNA gene) in Middle Germany. Borrelia garinii was detected most frequently, but mixed infections occurred. Frequency of species and OspA types are described. Some ticks were infected with a combination of Borrelia spp. and Babesia microti, Babesia divergens. The authors stress the importance of the knowledge of the population of Borrelia species and OspA types, development of diagnostic tests and vaccines.

Ticks as hosts of piroplasm parasites in Italy [9]
Piroplasms are protozoan parasite which divide by binary fission and as sporozoan parasites they possess sexual and asexual phases. They include the tick parasites Babesia and Theileria.
Ticks, collected in central and northern Italy from pets, livestock, wild animals and the environment act as a reservoir for piroplasms such as Theileria equi and Babesia species.

Ixodes ricinus hosted the highest number of piroplasm species, although the highest infection rate was recorded in Hyalomma marginatum Dermacentor marginatus, Rhipicephalus turanicus and Rhipicephalus sanguineus were also found infected with the pathogens.

[1] Dvoraková HM, Dvorácková M: Babesiosis, a little known zoonosis. Epidemiol Mikrobiol Imunol. 2007 Nov;56(4):176-80.
http://www.ncbi.nlm.nih.gov/pubmed/18072299

[2] Irwin PJ .Canine babesiosis. Vet Clin North Am Small Anim Pract. 2010 Nov;40(6):1141-56.
http://www.ncbi.nlm.nih.gov/pubmed/20933141

[3] Ramharter M, Walochnik J, Lagler H, Winkler S, Wernsdorfer WH, Stoiser B, Graninger W: Clinical and molecular characterization of a near fatal case of human babesiosis in Austria. J Travel Med. 2010 Nov-Dec;17(6):416-8. doi: 10.1111/j.1708-8305.2010.00446.x.
http://www.ncbi.nlm.nih.gov/pubmed/21050324

[4] Hamaguchi K, Ike K, Yamazaki Y, Morita T, Imai S: Influence of Zinc Deficiency to the Mice Infected with Babesia microti. J Vet Med Sci. 2010 Oct 12.
http://www.jstage.jst.go.jp/article/jvms/advpub/0/advpub_1010050346/_article

[5] Hamaguchi K, Ike K, Yamamoto R, Morita T, Imai S: Influence of zinc deficiency to the rats infected with Babesia rodhaini. J Vet Med Sci. 2009 Aug;71(8):1085-8.
http://www.jstage.jst.go.jp/article/jvms/71/8/71_1085/_article

[6] Zygner W, Baska P, Wiśniewski M, Wedrychowicz H The molecular evidence of Babesia microti in hard ticks removed from dogs in Warsaw (central Poland). Pol J Microbiol. 2010;59(2):95-7.
http://www.pjm.microbiology.pl/archive/vol5922010095.pdf

[7] Franke J, Meier F, Moldenhauer A, Straube E, Dorn W, Hildebrandt A: Established and emerging pathogens in Ixodes ricinus ticks collected from birds on a conservation island in the Baltic Sea. Med Vet Entomol. 2010 Dec;24(4):425-32. doi: 10.1111/j.1365-2915.2010.00905.x
http://www.ncbi.nlm.nih.gov/pubmed/20868431

[8] Hildebrandt A, Pauliks K, Sachse S, Straube E: Coexistence of Borrelia spp. and Babesia spp. in Ixodes ricinus ticks in Middle Germany. Vector Borne Zoonotic Dis. 2010 Nov;10(9):831-7.
http://www.ncbi.nlm.nih.gov/pubmed/20420533

[9] Iori A, Gabrielli S, Calderini P, Moretti A, Pietrobelli M, Tampieri MP, Galuppi R, Cancrini G: Tick reservoirs for piroplasms in central and northern Italy. Vet Parasitol. 2010 Jun 24;170(3-4):291-6.
http://www.ncbi.nlm.nih.gov/pubmed/20304560


09.02.2011: Alginate based nanoparticles for transport of Vitamin D3 in aqueous systems [1]
Li and colleagues 2011 report the development of nanoparticles prepared from hydrophobic alginate derivative obtained by acid chloride reaction using oleoyl chloride without organic solvents used in other configurations. These nanoparticles maintained their structural in gastric fluid and intestinal fluid conditions and could transport vitamin D3 as a model for other lipidic nutraceuticals in solutions based on water. The nanostructures released release vitamin D3 at a appropriate rate under sustained gastrointestinal conditions. These nanoparticle system may thus be used as oral transporter of vitamin D3.

[1] Li Q, Liu CG, Huang ZH, Xue FF. Preparation and Characterization of Nanoparticles Based on Hydrophobic Alginate Derivative as Carriers for Sustained Release of Vitamin D(3). J Agric Food Chem. 2011 Feb 2.Doi: 10.1021/jf1020347
http://www.ncbi.nlm.nih.gov/pubmed/21288023


09.02.2011: Connection between diet and behaviour in attention-deficit hyperactivity disorder (ADHD) children [1]
As part of the Impact of Nutrition on Children with ADHD (INCA) study Pelsser and colleagues found that a 5 week restricted elimination diet consisting mainly of hypoallergenic foods such as rice, turkey, lamb, a range of vegetables (lettuce, carrots, cauliflower, cabbage and beet), pears and water. The hipoallergic diet reduced the ADHS symptoms by at least 40% in 78% of the children, compared with a control group. Diets were composed of high-IgG or low-IgG foods, based on every child's individual IgG blood test results. Children which returned to high allergic diet had a relapse in symptoms with no difference in the immunologic responses immunological response to the different diets.
The authors concluded that food sensitivity plays a part in ADHD, but it is not caused by an allergic reaction, and diets on the basis of IgG blood tests should be discouraged.

The same authors, in a foregoing study, report significant reductions of complaints of these children related to three domains: headaches or bellyaches, unusual thirst or unusual perspiration, and sleep complaints were significantly reduced by hypoallergenic diet, but these reductions were independent of the behavioural changes. An elimination diet may be an effective instrument to reduce aforementioned physical complaints in children with ADHD, [2]

[1] Pelsser LM, Frankena K, Toorman J, Savelkoul HF, Dubois AE, Pereira RR, Haagen TA, Rommelse NN, Buitelaar JK: Effects of a restricted elimination diet on the behaviour of children with attention-deficit hyperactivity disorder (INCA study): a randomised controlled trial. Lancet. 2011 Feb 5;377(9764):494-503.
http://www.ncbi.nlm.nih.gov/pubmed/21296237

[2] Pelsser LM, Frankena K, Buitelaar JK, Rommelse NN: Effects of food on physical and sleep complaints in children with ADHD: a randomised controlled pilot study. Eur J Pediatr. 2010 Sep;169(9):1129-38. Epub 2010 Apr 17.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2908441/?tool=pubmed


07.02.2011: Viruses of bats which can infect animals and humans [1]
Bats species hosts viruses which can infect animals and humans, such as rabies viruses. (Lyssaviruses) of different genotypes which have emerged from bats in America (Genotype 1 rabies virus; RABV), Europe (European bat lyssavirus; EBLV), and Australia (Australian bat lyssavirus; ABLV), Hendra virus and Marburg virus. Nipah virus is the most important recent disease of bat origin in Asia. SARS coronavirus is being found in insectivorous bat, and Ebola virus has been detected in some fruit bats. The implementation of an European surveillance systems for EBLVs in bats. a rapid response system is being suggested by van der Poel, Lina and Kramps 2006 to enhance publik health awareness related to viruses of bats.

The migratory tree-roosting hoary bat and silver-haired bat are hots of rabies in North America. Klung and colleagues found that the prevalence of rabies was about 1 percent, which is significantly lower than reported in previous studies. [2]

Surveillance still necessary despite low incidence of rabies in Swiss bats [3]
Rabies remains a residual risk to public health in Western Europe due to bat-specific viruses, such as European bat lyssaviruses (EBLVs). European bat lyssavirus types 1 and 2. A survey in 2009 by Megali and colleagues detected RNA corresponding to EBLV-2 in one western Switzerland bat, resembling findings of Geneva 2002. However, no infectious virus was found. Three bats were found to be seropositive. The authors stress the importance of continuous management and surveillance are required to avoid any risk to public health, even with a low incidence of rabies in bat population.

Bat guano virome acquired through diet of insects and plants [4]
Contact between bats, humans, and other animal species increases the possibility exists for cross-species transmissions. Li and colleagues 20101 describe full and partial viral genomes identified using metagenomics in the guano of bats from California and Texas. The characterization of the bat guano virome is a metagenomic analysis which found the presence of previously unidentified viral species, genera, and possibly families. The viral metagenomic data describes the viromes in bat guano, and may help to detect zoonotic viruses in bat and A better knowledge concerning the distribution of pathogens in bat may preserve their population.

SARS-like Coronavirus in bats [5]
Viruses closely related to members of the genus Coronavirus associated with severe acute respiratory syndrome (SARS) were detected in faeces of horseshoe bat species in Slovenia. The related virus sequence in GenBank was SARS bat isolate Rp3/2004 (DQ071615) within the SARS-like CoV cluster. Rihtaric and colleagues 2010 underline the risk of a new group of bat coronaviruses as a reservoir for human respiratory infections and call for epidemiological studies.

White-nose syndrome [6]
White-nose syndrome is a fatal disease of hibernating bats with a mortality higher than 95%. It is caused by the fungus Geomyces destructans under low temperatures and humid conditions of caves. Foley and colleagues 2011 gathered new informations on the pathogenesis of Geomyces destructans and white-nose syndrome, using descriptive and analytical epidemiology, which includes epidemiology and disease ecology. The infection has also been confirmed in European bats, however, no epidemic similar to USA has been registered. Instead of culling affected populations of bats the group around Foley try to conserve the genetic diversity of bat populations, combined with a program of public educating of cave tourists.

Bats as source of human infections [7]
Bats are known to host 60 viral species, of which 59 may generate RNA viruses capable of infecting humans. The most important are lyssaviruses and Henipavirus. Human infections with Nipah, Hendra, SARS coronavirus and Ebola virus may involve intermediate hosts such as pigs, horses, civets and primates.

Wong and colleagues 2007, authors of the study, warn that cross-infection between bat species may generate new viruses which can infect humans more easily. According to the authors Pteropodidae, Molossidae, Phyllostomidae, and Vespertilionidae bats are the most frequent hosts of human pathogens.

[1] van der Poel WH, Lina PH, Kramps JA: Public health awareness of emerging zoonotic viruses of bats: a European perspective. Vector Borne Zoonotic Dis. 2006 Winter;6(4):315-24.
http://www.ncbi.nlm.nih.gov/pubmed/17187565

[2] Klug BJ, Turmelle AS, Ellison JA, Baerwald EF, Barclay RM.Rabies prevalence in migratory tree-bats in alberta and the influence of roosting ecology and sampling method on reported prevalence of rabies in bats. J Wildl Dis. 2011 Jan;47(1):64-77.
http://www.ncbi.nlm.nih.gov/pubmed/21269998

[3] Megali A, Yannic G, Zahno ML, Brügger D, Bertoni G, Christe P, Zanoni R. Surveillance for European bat lyssavirus in Swiss bats. Arch Virol. 2010 Oct;155(10):1655-62.
http://www.ncbi.nlm.nih.gov/pubmed/20803042

[4] Li L, Victoria JG, Wang C, Jones M, Fellers GM, Kunz TH, Delwart E. Bat guano virome: predominance of dietary viruses from insects and plants plus novel mammalian viruses.J Virol. 2010 Jul;84(14):6955-65.
http://www.ncbi.nlm.nih.gov/pubmed/20463061

[5] Rihtaric D, Hostnik P, Steyer A, Grom J, Toplak I.Arch Virol. Identification of SARS-like coronaviruses in horseshoe bats (Rhinolophus hipposideros) in Slovenia.2010 Apr;155(4):507-14
http://www.ncbi.nlm.nih.gov/pubmed/20217155

[6] Foley J, Clifford D, Castle K, Cryan P, Ostfeld RS. Investigating and Managing the Rapid Emergence of White-Nose Syndrome, a Novel, Fatal, Infectious Disease of Hibernating Bats. Conserv Biol. 2011 Feb 1. doi: 10.1111/j.1523-1739.2010.01638.x.
http://www.ncbi.nlm.nih.gov/pubmed/21284732

[7] Wong S, Lau S, Woo P, Yuen KY. Bats as a continuing source of emerging infections in humans.Rev Med Virol. 2007 Mar-Apr;17(2):67-91. Doi 10.1002/rmv.520
http://www.ncbi.nlm.nih.gov/pubmed/17042030


07.02.2011: Dogs and cats as vectors of human diseases in Italy [1]
Otranto D, Dantas-Torres highlight the risk of dogs and cats infection in Italy. Various vectors of disease agents were identified, such as ticks, fleas, phlebotomine sand flies, and mosquitoes. Of human concern are Anaplasma phagocytophilum, Borrelia burgdorferi, Dipylidium caninum, Leishmania infantum, Dirofilaria immitis, and Dirofilaria repens. Fleas are recognised as vectors of pathogens transmissible to humans, such as Rickettsia felis. The authors stress that control strategies based on acaricides and insecticides should consider the vector behaviour during seasons of the year and use it accordingly. In Italy ticks and fleas are present throughout the year in certain regions, and phlebotomine sand flies are most active during the summer.

Rickettsia massiliae in brown dog ticks in California [2]
Rickettsia massiliae DNA was detected.in brown dog tick (Rhipicephalus sanguineus) in southern California by Beeler and colleagues 2011. Serum samples from adogs of the property contained antibodies reactive with R. massiliae, R. rhipicephali, R. rickettsii, and 364D Rickettsia but no rickettsial DNA was detected, with Rickettsia massiliae being the probable causative agent of the seroposivity.
The brown dog tick Rhipicephalus sanguineus also hosts the Rocky Mountain spotted fever, a tickborne disease caused by the bacterium Rickettsia rickettsii. [3]

[1] Otranto D, Dantas-Torres F.Canine and feline vector-borne diseases in Italy: current situation and perspectives. Parasit Vectors. 2010 Jan 11;3:2.
http://www.ncbi.nlm.nih.gov/pubmed/21227500

[2] Beeler E, Abramowicz KF, Zambrano ML, Sturgeon MM, Khalaf N, Hu R, Dasch GA, Eremeeva ME A Focus of Dogs and Rickettsia massiliae-Infected Rhipicephalus sanguineus in California.Am J Trop Med Hyg.2011 Feb;84(2):244-9.
http://www.ncbi.nlm.nih.gov/pubmed/21292893

[3] New Spotted Fever Group Rickettsia Rickettsia massiliae sp. nov., a New Spotted Fever Group Rickettsia International Journal of Systematic Bacteriology 1993, p. 839-840Vol. 43, No. 4
http://ijs.sgmjournals.org/cgi/reprint/43/4/839.pdf


03.02.2011: Reintroducing native Buffel grass in Emirate [1]
The United Arab Emirates aim to reintroduce indigenous grasses on farms. The programme would reduce water waste and combat the transformation of habitable land into desert.

The Ministry of Environment and Water, and the International Centre for Agricultural Research in the Dry Areas (Icarda) are trying to reintroduce Buffel grass which uses only a fifth of water needed for Rhodes grass and has similar nutritional content. Six hours a day watering of grass could thus be reduced to 20 minutes. Icarda is planning to develop seed facilities in the UAE, Oman and Saudi Arabia to check seed health to avoid anyspread of disease.
Rhodes grass had been imported from Africa and became the leading grass as feed. Rhodes grass needs high amounts of water Most farmers in the UAE plant Rhodes grass as livestock forage. [2]

Buffel Grass [3]
Buffel Grass or African Foxtail Grass (Cenchrus ciliaris) is a species of grass native to most of Africa, southern Asia (east to India), Southern Iran, Middle East, Indonesia and the extreme south of Europe (Sicily). Introduced to Australia and the New World such as the Sonoran Desert Region and southern Arizona, it became invasive. Easy to ignite it became a fire hazzard, regrowing where other plants were ultimately destroyed by fire. In some US regions buffel grass is being controlled by manual pulling and herbicides.
Buffel grass is still valued as livestock forage, however it is not nearly as economically viable as first thought, because of its limited life of pastures. Buffel grass impoverishes the soil and evenually dies, leaving behind a sterile wasteland.

Rhodes Grass [4]
Rhodes grass (Chloris gayana) was imported from Africa and became the leading grass as feed. Rhodes grass needs high amounts of water. It has a vigourous root system, capable of extracting water from more than 4m deep which delivers some degree of drought tolerance, but it grows best in 600-1000mm rainfall regions and is highly salt tolerant. It contains low oxalate levels making it safe for horses to graze.

[1] Farmers told to plant 'greener' grass. The National. 30.01.2011.
http://www.thenational.ae/news/uae-news/environment/farmers-told-to-plant-greener-grass

[2] Indigenous grasses to reduce water waste. The National. 29.01.2011.
http://www.thenational.ae/news/uae-news/environment/indigenous-grasses-to-reduce-water-waste

[3] Buffelgrass (Pennisetum ciliare)
http://www.desertmuseum.org/invaders/invaders_buffelgrass.php

[4] Rhodes Grass
http://www.regalseeds.com.au/rhodes.pdf


02.02.2011: Comparative genomics identifies drug targets against fungal pathogens [1]
Abadio and colleagues 201, using comparative genomics, selected 10 genes present in pathogenic fungi which are absent in the human genome and may be used as anti-fungal drug target. The authors concentrated their researches on trr1 that encodes for thioredoxin reductase, rim8 that encodes for a protein involved in the proteolytic activation of a transcriptional factor in response to alkaline pH, kre2 that encodes for alpha-1,2-mannosyltransferase and erg6 that encodes for delta (24)-sterol C-methyltransferase. Drug side effects are not expected because these genes are not present in the human genome, stress the authors.

[1] Abadio AK, Kioshima ES, Teixeira MM, Martins NF, Maigret B, Felipe MS. Comparative genomics allowed the identification of drug targets against human fungal pathogens. BMC Genomics. 2011 Jan 27;12(1):75.
http://www.ncbi.nlm.nih.gov/pubmed/21272313


02.02.2011: Cryptococcus gattii, a pathogenic yeast [1]
Cryptococcus gattii, formerly known as Cryptococcus neoformans var gattii, is an encapsulated yeast found primarily in tropical and subtropical climates. It causes the human diseases of pulmonary cryptococcosis, basal meningitis, and cerebral cryptococcomas. Occasionally, the fungus is associated with skin, soft tissue, lymph node, bone, and joint infections. The infection is caused by inhaling spores. The fungus is not transmitted from person to person or from animal to person. A person with cryptococcal disease is not contagious.

Human infections by Cryptococcus gattii are found in Papua New Guinea, Northern Australia. British Columbia, Canada, Brazil, India and the Pacific. The fungus also infects animals, such as dogs, koalas and dolphins. Cryptococcus gattii spreads to Oregon and Washington. The highly virulent strain VGIIc is related to a high mortility.
Macdougall 2010 reports that had the largest number of infections with Cryptococcus gattii worldwide. The most frequent ailments were respiratory illness or lung cryptococcoma. The older persons, and those who had central nervous system disease. [2]

Cryptcoccus gattii may infect healthy persons, however several immunosuppressive and pulmonary conditions seem to be risk factors, such as oral steroids, pneumonia, and other lung conditions, age of 50 years and higher, current smokers, infected with HIV, or have a history of invasive cancer were associated which increased number of infections.

Cryptococcus gattii ability to survive in human body
To cause infection in humans, Cryptococcus gatti must have a gene that encodes the Cryptococcus gatti calcineurin A catalytic subunit. Calcineurin is a serine-threonine specific phosphatase that is activated by Ca(2)-calmodulin and is involved in stress responses in yeasts. Odom and colleagues 1997 found that calcineurin A is a basic requirement for Cryptococcus gattii to survive in the host at 37 °C and factor for the pathogenicity of the organism. [3]

The ability to survive and proliferate at the human body temperature is controlled in part by the Ca(2)-calcineurin pathway, which senses and utilizes cytosolic calcium for signaling. Kmetzsch and colleagues 2010 identified the Cryptococcus neoformans gene VCX1, which encodes a vacuolar calcium exchanger and acts in parallel with calcineurin. [4]

[1] MacDougall L, Fyfe M, Romney M, Starr, Galanis E. Risk factors for Cryptcoccus gattii infection, British Columbia, Canada. Emerg Infect Dis. 2011 Feb.DOI: 10.3201/eid1702.101020 http://www.cdc.gov/EID/content/17/2/193.htm

[2] Galanis E, Macdougall L. Epidemiology of Cryptococcus gattii, British Columbia, Canada, 1999-2007. 2010 Feb;16(2):251-7.Emerg Infect Dis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958008

[3] Odom A, Muir S, Lim E, Toffaletti DL, Perfect J, Heitman J. Calcineurin is required for virulence of Cryptococcus neoformans. EMBO J 1997;16:2576-89.
http://www.nature.com/emboj/journal/v16/n10/full/7590243a.html

[4] Kmetzsch L, Staats CC, Simon E, Fonseca FL, de Oliveira DL, Sobrino L, Rodrigues J, Leal AL, Nimrichter L, Rodrigues ML, Schrank A, Vainstein MH: The vacuolar Ca(2+) exchanger Vcx1 is involved in calcineurin-dependent Ca²(+) tolerance and virulence in Cryptococcus neoformans. Eukaryot Cell. 2010 Nov;9(11):1798-805.
http://www.ncbi.nlm.nih.gov/pubmed/20889719


02.02.2011: Reassortment may increased pathogenicity of pandemic (H1N1) [1]
Schrauwen and colleagues 2011 report that three influenza A viruses (seasonal (H3N2), seasonal (H1N1), and pandemic (H1N1) 2009) were found to be circulating during the swine flue pandemic which started in 2009. The authors are concerned with the possibility of genetic reassortment between these viruses. The resulting strains my present increased pathogenicity. The authors tested four reassortant viruses determining their replication kinetics in vitro and pathogenicity and transmission in ferrets.

Pandemic (H1N1) 2009 with neuraminidase of seasonal (H3N2) virus resulted in increased virus replication and produced severe pulmonary lesions, while pandemic (H1N1) 2009 viruses containing basic polymerase 2 alone or in combination with acidic polymerase of seasonal (H1N1) virus were attenuated in ferrets.

The authors concluded that pandemic (H1N1) 2009 virus has the potential to reassort with seasonal influenza viruses, which may increase its pathogenicity and maintains the abillity of transmission through the aerosols or respiratory droplets.

[1] Schrauwen EJA, Herfst S, Chutinimitkul S, Bestebroer TM, Rimmelzwaan GF, Osterhaus ADME, et al. Possible increased pathogenicity of pandemic (H1N1) 2009 influenza virus upon reassortment. Emerg Infect Dis [serial on the Internet]. 2011 Feb [date cited]. http://www.cdc.gov/EID/content/17/2/200.htm Doi: 10.3201/eid1702.101268
http://www.cdc.gov/eid/content/17/2/200.htm?source=govdelivery


01.02.2010: The Transition Town Totnes and Transition Network [1]
The aim of this community project is to equip communities for the dual challenges of climate change and peak oil. The Transition Towns movement is an example of socioeconomic localisation. The main aim of the project is to raise awareness of sustainable living and build local ecological resilience in the near future. Communities are encouraged to seek out methods for reducing energy usage as well as reducing their reliance on long supply chains that are totally dependent on fossil fuels for essential items. Initiatives created community gardens to grow food; business waste exchange, which seeks to match the waste of one industry with another industry that uses this waste; and even simply repairing old items rather than throwing them away.

Rob Hopkins is the co-founder of Transition Town Totnes and of the Transition Network.
He teaches natural buildings and permaculture. Permaculture is the design of human settlements and agricultural systems that are modeled on the relationships found in natural ecologies. Hopkins organised the first 2 year full-time permaculture course in the world, at Kinsale Further Education College in Ireland. He also developed the first eco-village in Ireland. [2]

Totnes' Energy Descent Action Plan [3]
A key concept within transition is to reduce the dependence on fossil fuels and reduce carbon footprint, moving away from fossil fuels. Key players of the plans are local people, local institutions, local agencies and the local council.

Energy Descent Action Plan: An Energy Descent Action Plan is a guide to reduce dependence on fossil fuels and carbon footprint over the next 20 years. Waiting for governments to do this, it will be too late. Individual actions will not be enough to avoid serious If we try and do it all on our own, it will be too little. But by organising with friends, neighbours and our community, it may just be enough, and it may just be in time.

Resilience
Resilience of Totnes is focused on the economy that cycles more money locally, creates more local jobs, is less at the mercy of major employers. It is more diverse, in terms of skills, livelihoods, land use, businesses, housing provision and so on. Totnes uses local currencies and local investment mechanisms to enable more money to be invested in the immediate area. See pictures on change of Totnes to resilience. [4] Pictures of Totnes

These plans are good activities for specific communities living embedded in a global industrialised economy. Such community needs inputs from an established economy to satisfy the high demands and lifestyle of modern society in high demographic regions. Nobody will accept to return to an alternative lifestyle of Vincent van Gock's “The Potato Eaters”. (Picture source: Wikipedia)

The “Transition” is an excellent tool to introduce the idea of sustainability, however, it needs further solutions for the global energy demands of United States, China and the developing countries. Additional to wind energy, solar energy may become carbon-free energy producing electricity and hydrogen as fuel for transportation and as energy storage.

[1] Transition Town Totnes.
http://www.transitiontowntotnes.org/

[2] Transition culture.
http://transitionculture.org/about/

[3] Rob Hopkins helps "unleash" the Transition Town Totnes Energy Descent Action Plan
by Rob Hopkins
http://www.energybulletin.net/node/52762

[4] Visual Journey in Totnes
http://totnesedap.org.uk/book/part2/totnes-past-present-future-visual-journey/