Johnes disease and Crohn's disease

Gilles R. G. Monif, M.D.
Infectious Diseases Incorporated
Premises are hypotheses awaiting scientific confirmation
Mycobacterium Avium Subspecies Paratuberculosis (Map) is a mycobacterium that is embedded in the food supply of herbivores. In cattle, it infects the gastrointestinal tract and induces transient or chronic enteritis. Using 1990’s statistics, Map had an estimated 1.2 billion dollar adverse impact on producers (due to decreased milk and fat production, decreased slaughter weight, reproductive losses, and early replacement of productive animals). Despite the acknowledged economic losses to the dairy industry, producers have been reluctant to address the issue owing to Map’s presence in unpasteurized milk and what was then deemed a possible causal relationship between Map and Crohn’s disease in humans. USDA initiated a subsidized Map testing on a voluntary basis.  To participate in the program, a producer would have had to pay a small portion of the cost plus potentially exposed unfavorable data about his or her herd. 
Since 2008, Map has been recognized as a zoonotic pathogen for man. Map or its DNA has been demonstrated primarily in diseased tissue from individuals with inflammatory bowel disease. Similarly, Map has been demonstrated to be in the blood and breast milk of predominantly individuals with Crohn’s disease. Governments have been reluctant to respond to the “Map dilemma”, given the importance of milk and milk-based products to the national economies.
In 2002, Infectious Diseases Incorporated (IDI) began work on its patented FUIDI Herd Management Schema (FHMS). FHMS is a system that allows infected animals to remain in production yet reduces the amount of Map entering the human food supply through milk and milk-related products.
To create the FHMS, IDI had to free itself from the prevailing opinions/published literature and develop a number of independent sets of premises from its analysis of relevant observations and from its research in order to formulate the hypothesis that became the foundation block for the FHMS.
Mycobacterium Avium Subspecies Paratuberculosis (Map) and Genomic Variants
1.      Map is present in soil.
2.      Map becomes embedded in the food supply of herbivores.
3.      Map evolved from Mycobacterium avium subspecies avium (Ma).
4.      Between Ma and Map polymorphic variants exist that can cause chronic enteritis in animals.
5.      The older a pathogenic mycobacterium is phylogenically, the less virulence is the species.
6.      Map is A cause of chronic enteritis in herbivores and other animals, but not THE sole cause of disease.
7.      Pathogenicity varies among Map isolates.
8.      Species virulence among pathogenic mycobacterium can be enhanced by current herd management practices that embed and disseminate into the production area environment isolates that have been selected to be effective pathogens for the host species in question.
9.      Once introduced into the pasture or production environment, total elimination is at best very difficult.
10.   Infected animals are not the ultimate reservoir for Map.
11.   Map has the potential to be a zoonotic pathogen for humans.
12.   Not all Map isolates are detected by IS900 direct primers.
13.   Current commercial MAP ELISA tests do not identify all pathogenic mycobacterium that produce enteric disease in herbivores.
Mycobacterium Avium Subspecies Paratuberculosis (Map) and Johne’s Disease
1.       Map is A cause of Johne’s disease.
2.       Host susceptibility is inversely related to age (as in humans).
3.       Map herbivore infection can occur due to organism acquisition by transplacental transmission, in the newborn period, and in adult life (intra-herd dissemination).
4.       The theorized three stage pathogenesis of Map infection cannot with stand scientific challenge.
5.       IDI’s construction of the natural history of Map infection is foundation for the FUIDI Herd Management Schema.
6.       Host containment of Map can be overwhelmed by a combination of factors that alters its immune status.
7.       USDA’s policy of containing Johne’s Disease by testing animal and culling animals with advanced infection reduces the incidence of Johne’s disease, but does not reduce the prevalence of herd infection.
8.       USDA commercially sanctioned Map ELISA test identify but a limited number of infected animals.
9.       Fecal culture is a too insensitive test to anchor epidemiologic studies
10.   The “gold standard” for assessing Map infection is PCR analysis of mesenteric and ileocecal lymph nodes.
11.   The concept of “pass-through” technically and conceptionally is flawed.
12.   Epidemiologic studies predicated upon Map fecal culture and the approved commercial Map ELISA tests are flawed in their foundation premises and are responsible for the current state of confusion concerning Map.
13.   The use of confined production areas selects for propagation of the more virulent subgroup of Map.
14.   Milk is one of the primary vehicles which expose humans to Map in significant numbers.
15.   The virulence of Map isolates in milk are theorized to be greater than Map isolate found in the wild or water not exposed to domesticated herbivores.
16.   Because of its replication in clumps, the use of the quantity of Map in a given fecal sample introduces the potential for significant sample and interpretation errors.
Mycobacterium Avium Subspecies Paratuberculosis (Map) and Crohn’s Disease
1.       Directly or indirectly, Map is a zoonotic pathogen for human beings.
2.       Map and related mycobacterium cause a spectrum of gastrointestinal conditions that include asymptomatic infections, an increase in bowel movements, irritable bowel syndrome, and inflammatory bowel disease.
3.       Article 5.7 of the World Trade Organization’s Agreement on Sanitary and Phytosanity Measures  and Principle 15 of the United Nations’ Rio Declaration on Food Safety render the debate of direct vs. indirect ethically untenable .
4.       Map initiates the production of tumor necrosis factor that is primarily responsible for gastrointestinal tissue damage.
5.       Human beings will be perpetually exposed to Map.
6.       Selected groups are genetically predisposed to developing inflammatory bowel disease.
7.       Specific preventive step are required to protect the most vulnerable human beings (babies and children) without a genetic predisposition.
8.      Voluntary monitoring programs without consequences and defined benefits will not work.
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Comments and questions will be appreciated.


Paratuberculosis and Crohn’s disease: Premises and open questions


K. Hruska and I. Pavlik
OIE Reference Laboratory for Paratuberculosis
Veterinary Research Institute, Brno, Czech Republic

Mycobacteria and some other bacteria are sources of peptidoglycans, the parent compounds for muramyldipeptide (MDP), a potent immunomodulator.

N-glycolyl-MDP (derived from mycobacteria) has a greater NOD2-stimulating activity than N-acetyl MDP (derived from other bacterial species).

The participation of MDPs in immunomodulation (Freund adjuvans), in inflammatory processes and autoimmune and autoinflammatory diseases is well documented.

Paratuberculosis in ruminants differs from similar diseases in non-ruminants, omnivores and primates by virtue of its extraordinarily potent production of huge numbers of mycobacteria. A speculative reason may lie in differing metabolisms, different immunological pathways or different microbioms.

The pathogenesis of both paratuberculosis in ruminants and Crohn’s disease can be triggered by several different pathways in different species and in individuals of the same species. Genetic factors, innate and adaptive immunity are well described; the participation of mycobacteria is hypothesized, with good grounds, but cannot be experimentally proven in humans.

Some other factors may play a role in Crohn’s disease etiology:
• exposure to mycobacteria at different stages of life
• exposure to different species of mycobacteria
• exposure to differing numbers of mycobacteria for differing time spans
• exposure to live or dead mycobacteria
• interval between successive exposures
• coincidence of exposure with other diseases or factors like stress, starvation, gravidity
• differing modes of exposure (ingestion or inspiration) or a combination of different modes

Crohn’s disease can likely be triggered by other bacteria or viruses which interact with the relevant pathogen recognition or NOD-like receptors. Crohn’s disease is hypothesized to be linked with several infectious diseases, in the course of which high numbers of cells can be replicated.

Non-tuberculous mycobacteria including causal agent of paratuberculosis in milk and dairy products, in meat, in water from household plumbing, in bottled table and mineral water, in indoor and open swimming pools, in rivers and lakes, in aerosols inspired during showering, baby swimming or bathing, or in the vicinity of polluted rivers are not yet considered to be a risk. Thus, no legal limits for mycobacteria exist which could at least enable the removal of highly contaminated foods from distribution.

The number of mycobacterial cells in milk, meat, dairy and beef products and in tap water can be in the order of 104 per gram. Eight million cells in one package consumed by a baby over the course of one week, sometimes augmented by mycobacteria from tap water, represent a heavy load of triggers.

A premise of the importance of both live and dead cells as possible triggers of Crohn’s disease does not run counter to prevailing hypotheses regarding the etiology of Crohn’s disease:
• infectious, caused by different pathogens
• hygiene hypothesis, with the availability of hot water from communal distribution
• cold chain hypothesis
• the protective effect of breast feeding as an opposite to formula feeding
• the resistance of some ethnic groups (Canadian Indians, Maoris in New Zealand, Gypsies in Hungary and Palestinians in Israel) or social groups with higher dispositions (city residents, those from higher social strata, immigrants to western countries from countries with a low prevalence) also chimes with the above, given that these groups have different approaches to breast and formula feeding of babies, to burger consumption, to showering and bathing using household plumbing.

Many authors have noted the parallel increase in the incidence of Crohn’s disease and paratuberculosis. The exact data on Crohn´s disease sufferers are available in the Czech Republic. The index 2011/1995 is 5.0, 4.9 and 11.6 for age categories 0-19, 20-64 and 65+, respectively. Irrespective of age the total number of Crohn’s disease patients has increased 5.3 fold over the course of 16 years. Unfortunately, similarly exact data for paratuberculosis in cattle are not available. However, until 1990 paratuberculosis was unknown due to the near complete isolation of the country from the world animal market. Subsequently, the borders were suddenly opened both for the import of heifers from highly infected western countries and for the import of dairy and meat products including baby foods and dried milk for formula feeding. The paratuberculosis prevalence is now estimated to be similar to western countries.

Paratuberculosis in cattle is in many parameters different from other infectious or emerging diseases:
• Several years can pass from the first contact with an agent which causes either latent infection or some sensitization or immunomodulation, and clinical signs of the disease.
• Shedding of mycobacteria or antibodies in serum is not in direct relation with clinical signs of the disease.
• Paratuberculosis is not thought by farmers and veterinary authorities to be very important despite the economical losses calculated.
• A possible zoonotic link is ignored despite the well documented and published data including meta-analyses on microbial triggers of chronic human illnesses.
• Culture of mycobacteria requires four to six or more months; some strains of causal agents of paratuberculosis are uncultivable in vitro as well. The diagnosis can be shortened using sophisticated expensive instrumentation or molecular methods, which are able not only to detect, but also quantify some mycobacterial species including causal agents of paratuberculosis and avian mycobacteriosis; but they are also rather expensive. Unfortunately, most methods are not sensitive or diagnosis fails due to the irregular shedding of mycobacteria or their ability to lose their cell wall.

Control and eradication of paratuberculosis is possible, but requires a heavy investment of both time and money. The herd must be closed, individual faecal or pooled samples periodically checked and shedders including progenies immediately culled. Alternatively ELISA of milk or blood serum, analysis of milk filters, bulk tank milk, environmental samples or liquid dung can be evaluated.

Complete eradication of mycobacteria from the environment, water and food is not a realistic aim. However, the following should be required:
• To consider paratuberculosis and mycobacteria as real public health threat.
• To develop methods for simple determination of mycobacteria in water, milk, and meat in concentration over the limit and to remove foods contaminated over the limit from distribution.
• To preferentially use milk and beef free from causal agent of paratuberculosis (or contaminated less than some lower than general limit) for the production of baby foods or foods for people at the highest risk (suffering from Crohn’s disease or relatives of such patients).
• To explain the importance of breast feeding for four to six months (mothers suffering from Crohn’s disease should be sure that their milk is mycobacteria-free).
• To widely introduce a method for the determination of mycobacteria in household plumbing and shower heads. If tap water is contaminated a suitable alternative (bottled or filtered water) should be available.
• To prepare legal measures for mycobacterial control of water in bottling plants, in food producing plants and in public swimming pools, especially those also used for babies.

All these issues are very sensitive for public including farmers, producers and market. Well prepared information must be available and public panic should be avoided. Unfortunately, general support from state budgets cannot be expected. Some measures require global understanding and realization, e.g., in baby food production. Producers should be aware that the solving of these problems is also in their own interest and not only in the interest of consumers.

PDF document can be downloaded for printing.

Comments and questions will be appreciated.
Make a request for references


EFSA Science video clips

Watch Understanding Science video clips in which EFSA staff explain scientific concepts.
Chemical contaminants in the food chain
Safety of chemicals in food
What are pesticides and how do they get into our food?
What is antimicrobial resistance? How is it related to food safety?
What are food-borne zoonotic pathogens? Why are they important for public health?
What is Salmonella? How can we control and reduce it?
What are non-food-borne zoonotic diseases? How can they transmit to humans?
What is Campylobacter? Why is food safety important to prevent it?
What are GM animals?
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Independent science
Enjoy the short video clips to self education and learn to listen presentations in English.

Charting a Course for a Successful Research Career


Source: Elsevier Authors Update, Issue 1: Open Access and innovation
Date: 23 March 2012

Elsevier's newly revised “Charting a Course for a Successful Research Career” is a crash course of practical advice on how to plan your career. Written by 30-year research veteran Professor Alan Johnson, this free mentoring booklet—used as a resource in many workshops around the world— provides a detailed map of the important milestones you should reach along the path to a successful research career.

Rich in advice on the do’s and the don’ts along your career path, it shows you the benefits of working smarter, not harder. You’ll learn to make informed decisions, define your goals and measure your success. It also talks about how to make a realistic plan to get where you want to be in 5–10 years.

The booklet provides wide-ranging topics from planning your career to preparing a grant funding application, to selecting a research discipline, supervisor and mentor. It also discuses the importance of getting recognized for the work you do, how to publish research – thinking about this early on is essential – and where to publish.

See more at SciVal Failure to plan is a plan to fail

Charting a Course for a Successful Research Career
A Guide for Early Career Researchers, 2nd Edition
Professor Alan M Johnson
Elsevier 2011, 117 pp

Foreword by Jay Katzen 2
Introduction 4
1. Career Planning 7
2. Selecting a Research Discipline Area 11
3. Selecting a Supervisor 19
4. Selecting a Mentor 25
5. Research Collaboration 29
6. Networking 35
7. Ethics and Research Integrity 39
8. Choosing Your Publication’s Style and Format 43
9. Where to Publish 49
10. Preparing a Grant Funding Application 61
11. Collaborating with Industry and Academia 69
12. Attending Conferences 75
13. Society Membership 81
14. Selling Your Accomplishments 85
15. Curriculum Vitae 93
16. Applying for Fellowships 97
17. Applying for a Job or Promotion 101
References 106
About Professor Alan Johnson 116

CGNI 2012-03-24-043

The evolving threat of antimicrobial resistance – Options for Action

CGNI 2012-03-13-037
World Health Organization – March 2012
Full text (125 pages) available online


Chapter 1 - The evolving threat of antimicrobial resistance - Introduction
Chapter 2 - Surveillance to track antimicrobial use and resistance in bacteria
Chapter 3 - Measures to ensure better use of antibiotics
Chapter 4 - Reducing antimicrobial use in animal husbandry
Chapter 5 - Infection prevention and control in health-care facilities
Chapter 6 - Fostering innovation to combat antimicrobial resistance
Chapter 7 - The way forward: political commitment to enable options for action


Antimicrobial resistance (AMR) is not a recent phenomenon, but it is a critical health issue today. Over several decades, to varying degrees, bacteria causing common infections have developed resistance to each new antibiotic, and AMR has evolved to become a worldwide health threat. With a dearth of new antibiotics coming to market, the need for action to avert a developing global crisis in health care is increasingly urgent.

In addition to a substantial financial burden that national health-care budgets can ill afford, AMR has economic consequences far beyond the health sector, such as damaging repercussions on international travel and trade resulting from the cross-border spread of resistant infections. The cost of not acting against AMR needs to be considered when deciding resource allocation and assessing interventions.

We know how and why AMR develops, what factors favour its emergence and spread, and what measures can be taken to limit it. Why then are we now facing an impending crisis in the treatment of many infections? This book describes the context of the problem, some of the progress made in recent years to tackle it, and what more should be done. Without question, more information and new tools are needed, but available strategies and interventions can go a long way towards minimizing the scale and impact of AMR, and maximizing the effective lifespan of existing antibiotics. Much more could be achieved by better and more widespread application of these measures, and there are many promising opportunities for innovation in this area.

Infections which are increasingly resistant to antibiotics together account for a heavy disease burden, often affecting developing countries disproportionately. The use of vast quantities of antibiotics in food-producing animals adds another dimension to a complex situation. Several sectors and services are involved and each, from public health to animal husbandry, has an important role to play in counteracting AMR. Responsibility needs to be shared, and coordination of the separate necessary inputs requires determined leadership, additional resources, and solid commitment at many levels.

The World Health Organization (WHO) has long recognized AMR as a growing global health threat, and the World Health Assembly, through several resolutions over two decades, has called upon Member States and the international community to take measures to curtail the emergence and spread of AMR. The WHO Global Strategy for Containment of Antimicrobial Resistance, published in 2001, set out a comprehensive set of recommendations for AMR control which remain valid today. This book examines the experiences with implementing some of those recommendations ten years on, the lessons learnt along the way and the remaining gaps. On World Heath Day 2011, WHO again highlighted AMR and urged countries to commit to a comprehensive financed national plan to combat AMR, engaging all principal stakeholders including civil society.

I am pleased to present this book during the campaign year chosen by WHO for special emphasis on the importance of AMR. It testifies to the Organization’s commitment to promoting and facilitating global action to contain AMR and ensuring that effective antibiotics will be available worldwide in the future.

Dr Marie-Paule Kieny
Assistant Director-General

Innovation, Information, Evidence and Research
orld Health Organization

EFSA Fact Sheets on food-borne pathogens


Antimicrobial Resistance
Zoonotic E. coli
Food borne zoonoses

For other EU, FAO and WHO scientific documents visit also Reports  and Documents

CGNI 2011-11-26-192
K. Hruska

Shiga toxin-producing Escherichia coli (STEC)

EFSA Panel on Biological Hazards (BIOHAZ):
Scientific Opinion on the risk posed by Shiga toxin-producing Escherichia coli (STEC) and other pathogenic bacteria in seeds and sprouted seeds
EFSA Journal 2011;9(11):2424. [101 pp.]. doi:10.2903/j.efsa.2011.2424.
Available as contents only (two pages)
Available as full text document (101 pages)

Sprouted seeds are young seedlings obtained from the germination of seeds. They are ready-to-eat foods which have caused large outbreaks. The bacterial pathogens most frequently associated with illness due to contaminated sprouted seeds are Salmonella and to a lesser extent STEC. Bacillus cereus, Listeria monocytogenes, Staphylococcus aureus and Yersinia enterocolitica have also been transmitted by sprouted seeds, albeit very rarely. Dry seed contaminated with bacterial pathogens has been identified as the most likely initial source of sprout-associated outbreaks; although other routes of contamination (e.g. during production due to poor practices) may also occur. In some outbreaks, contamination of seeds with as low as 4 Salmonella per kg was sufficient for the sprouts to cause disease. Seeds purchased by sprouts producers are usually not grown specifically for this purpose. They may be contaminated during production, harvest, storage and transport, and there may be difficulties in traceability of seeds from production to sprouting. Bacterial pathogens on seeds may survive for long periods during seed storage. There is so far no guarantee of a bactericidal step which is able to control contamination of seeds with bacterial foodborne pathogens acquired prior to germination. Due to the high humidity and the favourable temperature during sprouting, bacterial pathogens present on dry seeds can multiply on the sprouts. Contamination with pathogenic bacteria must be minimized by identification of seed crops intended for sprouted seeds production before planting, and application of GAP, GHP, GMP, HACCP principles at all steps of the production chain. The relevance of decontamination treatments of seeds and of microbiological criteria is also discussed.

CGNI 2011-11-24-187
K. Hruska

EFSA Manual for Reporting on Zoonoses,

Manual for Reporting on Zoonoses, Zoonotic Agents and Antimicrobial Resistance in the framework of Directive 2003/99/EC and of some other pathogenic microbiological agents for information derived from the year 2010
Question number: EFSA-Q-2011-00155
Issued: 31 March 2011


This Reporting Manual provides guidance for reporting on zoonoses, zoonotic agents and antimicrobial resistance in animals, food and feed under the framework of Directive 2003/99/EC. Some advice is also given on reporting of other pathogenic microbiological agents in food. The objective is to harmonise and streamline the reporting made by the Member States in a way that the data collected would be relevant and easy to be analysed at the European Union level. The manual is in particular intended to be used when reporting the data through the web reporting application run by the European Food Safety Authority.

The manual covers all the agents and items included by the current data collection through the web-based reporting system. This includes animal populations, antimicrobial resistance as well as bovine tuberculosis, bovine, ovine and caprine brucellosis, Salmonella, Campylobacter, Listeria, Yersinia, verotoxigenic Escherichia coli, MRSA, Q fever, Trichinella, Echinococcus, Toxoplasma, Cysticercus, and rabies, in animals, food and feed. Also data on some microbiological contaminants, such as staphylococcal enterotoxins, Cronobacter sakazakii and histamine, is covered by the manual.

Detailed guidelines are provided for reporting of the data in the tables and text forms of the web reporting application. This guidance typically applies to the agents, animal species and food categories to be reported on. Advice is also provided on the agent species, serotypes and serovars to be included in the reporting as well as on the reporting on antimicrobial resistance.

Instructions are given on description of the sampling and monitoring schemes as well as analyses of the results in the national reports. Special reference is made to fields were following of trends would be desirable at the European Union level and where Member States are encouraged to provide data on a regular basis.

This manual is specifically aimed to guide the reporting of the information deriving from the year 2010.
Published: 4 April 2011

Emerging and major infectious diseases of livestock

Transnational call for proposals (EMIDA ERA-Net)

The 2nd joint call for transnational research projects of the EMIDA ERA‐Net initiative will open on March 7th, 2011 with a total budget in the region of €20 million. This announcement will provide you with the relevant information on call topics, project eligibility criteria, timeline, application procedure, forms, guidelines, etc. and a detailed description of the activity lines and specific topics.

The 2nd joint call for transnational research projects of EMIDA includes the following 8 activity lines with several specific topics each. Activity lines address broader research areas while the associated topics particularly focus on more specific research needs. Funders may ask for proposals on the level of activity lines and/or specific topics.* Project consortia are invited to apply accordingly. Each subject will be funded by different combinations of countries (funders), according to a distributed pot scheme. (Please refer to ANNEX for detailed descriptions.)

Applications will involve a two step submission procedure with a pre-proposal and a full proposal. All proposals must be submitted electronically to the EMIDA ERA-Net call office as the central communication point. Pre-proposals will be checked by the partners from each of the counties involved to ensure, that they comply with the national eligibility criteria, to be published in the EMIDA ERA-Net 2nd call guidelines). The project description may not exceed three (3) pages in total: a two (2) pages project description plus a one (1) page project summary. The deadline for submitting pre-proposals in May 3rd, 2011, 1 p.m.

From research to farm: ex ante evaluation of strategic deworming in pig finishing


Van Meensel et al., Veterinarni Medicina 55, 2010, in press

This paper upgrades generic and partial information from parasitological research for farm-specific decision support, using two methods from managerial sciences: partial budgeting and frontier analysis. The analysis focuses on strategic deworming in pig finishing and assesses both effects on economic performance and nutrient efficiency. The application of partial budgeting and frontier analysis is based on a production-theoretical system analysis which is necessary to integrate parasitological research results to assess aggregate economic and environmental impacts. Results show that both statistically significant and insignificant parasitological research results have to be taken into account. Partial budgeting and frontier analysis appear to be complementary methods: partial budgeting yields more discriminatory and communicative results, while frontier methods provide additional diagnostics through exploring optimization possibilities and economic-environmental trade-offs. Strategic deworming results in a win-win effect on economic and environmental performances. Gross margin increases with 3 to 12 € per average present finisher per year, depending on the cyclic pig price conditions. The impact on the nutrient balance ranges from +0.2 to -0.5 kg nitrogen per average present finisher per year. The observed efficiency improvements are mainly technical and further economic and environmental optimizations can be achieved through input re-allocation. A user-friendly spreadsheet is provided to translate the generic experimental information to farm-specific conditions. 


Global policy recommendations (WHO Publications Series)

Increasing access to health workers in remote and rural areas through improved retention
Global policy recommendations

World Health Organization WHO - 2010 - ISBN: 9789241564014
CGNI 2010-09-06-189
Available on-line PDF [80p.]

“…….Globally, approximately one half of the population lives in rural areas, but less than 38% of the
nurses and less than 25% of the physicians work there. While getting and keeping health workers in
rural and remote areas is a challenge for all countries, the situation is worse in the 57 countries that
have an absolute shortage of health workers.
After a year-long consultative effort, this document proposes sixteen evidence-based
recommendations on how to improve the recruitment and retention of health workers in underserved
areas. It also offers a guide for policy makers to choose the most appropriate interventions, and to
implement, monitor and evaluate their impact over time….”

Tables of contents
Executive Summary
1. Introduction
1.1 Rationale
1.2 Objective
1.3 Target audience
1.4 Scope
1.4.1 Types of health workers targeted
1.4.2 Geographical areas covered
1.4.3 Categories of interventions covered
1.5 Process for formulating the global recommendations
1.6 Dissemination process
1.7 Methodology
1.8 Structure of the report
2. Principles to guide the formulation of national policies to improve retention of health workers in
remote and rural areas
2.1 Focus on health equity
2.2 Ensure rural retention policies are part of the national health plan
2.3 Understand the health workforce
2.4 Understand the wider context
2.5 Strengthen human resource management systems
2.6 Engage with all relevant stakeholders from the beginning of the process
2.7 Get into the habit of evaluation and learning 3. Evidence-based recommendations to improve
attraction, recruitment and retention of health workers in remote and rural areas
3.1 Education
3.1.1 Get the “right” students
3.1.2 Train students closer to rural communities
3.1.3 Bring students to rural communities
3.1.4 Match curricula with rural health needs
3.1.5 Facilitate professional development
3.2 Regulatory interventions
3.2.1 Create the conditions for rural health workers to do more
3.2.2 Train more health workers faster to meet rural health needs
2 3.2.3 Make the most of compulsory service
3.2.4 Tie education subsidies to mandatory placements
3.3 Financial incentives
3.3.1 Make it worthwhile to move to a remote or rural area
3.4 Personal and professional support
3.4.1 Pay attention to living conditions
3.4.2 Ensure the workplace is up to an acceptable standard
3.4.3 Foster interaction between urban and rural health workers
3.4.4 Design career ladders for rural health workers
3.4.5 Facilitate knowledge exchange
3.4.6 Raise the profile of rural health workers 4. Measuring results: how to select, implement and
evaluate rural retention policies 35
4.1 Relevance: which interventions best respond to national priorities and the expectations of health
workers and rural communities?
4.2 Acceptability: which interventions are politically acceptable and have the most stakeholder
4.3 Affordability: which interventions are affordable?
4.4 Effectiveness: have complementarities and potential unintended consequences between various
interventions been considered?
4.5 Impact: what indicators will be used to measure impact over time?
5. Research gaps and research agenda
5.1 Research gaps
5.1.1 Study all types of health workers
5.1.2 More research in low-income countries
5.1.3 More well-designed evaluations
5.1.4 Quality of the evidence – not only “what works”, but also “why” and “how”
5.2 Research agenda
6. Deciding on the strength of the recommendations Methodology List of participants References
:: Annex 1 – Grade evidence profiles [pdf 151kb]
:: Annex 2 – Descriptive evidence profiles [pdf 220kb]

RELATED LINK:: WHO Global Code of Practice on the International Recruitment of Health

Resolution WHA63.16 is included as Annex 3 in the CD attached to the printed version of the global
policy recommendations.

Ruggiero, Mrs. Ana Lucia

Results of the monitoring of dioxin levels in food and feed


Scientific Report of EFSA, EFSA Journal 2010; 8(3):1385 (35 pp)
Question number: EFSA-Q-2009-00869
Adopted: 28 February 2010

Dioxins and dioxin-like compounds include a range of toxic and environmentally persistent substances. The terms most often refer to 29 congeners of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and dioxin-like polychlorinated biphenyls (PCB). Dioxin and furan congeners are formed as unintentional by-products during combustion processes such as waste incineration and forest fires, as well as during some industrial processes such as paper pulp bleaching and the manufacturing of chlorinated pesticides. PCBs are synthesised by direct chlorination of biphenyl and can be divided into different groups according to their biochemical and toxicological properties. Non-ortho and mono-ortho substituted PCBs show toxicological properties that are similar to dioxins. They are therefore often termed ‘dioxin-like PCBs’.  The other PCBs don’t exhibit a dioxin-like toxicological profile and are therefore termed ‘non-dioxin-like PCBs’. PCBs have been used in a variety of applications such as dielectric fluids in transformers and as heat transfer fluids because of their non-flammability and electrical insulation properties. The production and use of PCBs have been discontinued in most countries since a ban on their manufacturing, processing and distribution was introduced in 1985, but large amounts remain in electrical equipment, plastic products and buildings.

While the amount of dioxins and dioxin-like compounds in the environment has declined since the late 1970s, there is a continued concern about the safety of the food supply and the potential adverse health effects of exposure to this group of substances. Because of their lipophilicity, together with their persistency in the environment, dioxins have accumulated in the food chain, particularly in animal fat, dairy products, and fish.

The presence of dioxins and dioxin-like PCBs is expressed as toxic equivalents (TEQ) after multiplication of congener-specific concentration levels with toxicity equivalency factors (TEF) developed based on their relative toxicity compared to 2,3,7,8-TCDD. The current European legislation is based on TEFs set by the World Health Organisation (WHO) in 1998 with the results expressed as TEQWHO98. New TEFs were suggested in 2005 with the results expressed as TEQWHO05.

In 2002 the European Commission prescribed a list of actions to further reduce the presence of dioxins and dioxin-like PCBs and later introduced regular monitoring by Member States of food and feed, including, if possible, also non-dioxin-like PCBs. Data on the presence of 17 congeners of dioxins and furans, and 12 congeners of dioxin-like PCBs in food and feed have been reported on a regular basis to the Commission. In April 2008 the Commission handed the collected information to the European Food Safety Authority (EFSA) for assessment.

A total of 7,270 samples collected in the period 1999-2008 from 19 Member States, Norway and Iceland were analysed in detail. The percentage of samples below the limit of quantification (LOQ) varied considerably at the congener level. Overall, the percentages of censoring, defined as the proportion of non-quantified (<LOQ) observations, varied sizeably depending on how results were expressed: on a fat basis (about 40%), on a whole weight basis (about 30%), or for feed on ‘12% moisture’ basis (about 60%).

The highest mean levels of dioxins and dioxin-like PCBs in food were observed for ‘Fish liver and products thereof’ (32.6 pg TEQWHO98/g) and ‘Muscle meat eel’ (6.7 pg TEQWHO98/g) expressed on whole weight basis, and for ‘Liver and products thereof from terrestrial animals’ (5.7 pg TEQWHO98/g) expressed on fat basis. The highest level in feed was found in ‘Fish oil’ (10.0 pg TEQWHO98/g) expressed on 12% moisture basis. 

Ad hoc analyses were conducted for the groups ‘Meat and meat products ruminants’, ‘Muscle meat fish and fish products excluding eel’, ‘Raw milk and dairy products including butter’, and ‘Hen eggs and egg products’ to evaluate the influence of species, geographical or production differences. No clear conclusion could be drawn for the ruminant meat group because of low sample numbers for some species. For the food group muscle meat of fish and fish products excluding eel there were differences in dioxins and dioxin-like PCBs between the different sub-groups, with mean values ranging from 1.20 (‘Farmed trout’) to 7.99 (‘Salmon’) pg TEQWHO98/g expressed on whole weight basis. Mean levels of dioxins and dioxin-like PCBs in herring were overall higher for samples collected in countries from the Baltic Sea area (8.64 pg TEQWHO98/g) compared to countries outside the Baltic area (2.30 pg TEQWHO98/g). In the food group milk and dairy products, slightly lower mean levels of dioxins and dioxin-like PCBs were found when moving from farm (1.27 pg TEQWHO98/g) and bulk milk (1.30 pg TEQWHO98/g) to retail milk (0.95 pg TEQWHO98/g) expressed on fat basis. This could be related to a slight dilution effect at retail level in the mixing of milk from different origins or to a targeting of possible suspect samples at farm level. Too few egg samples had been assigned a specific production method to serve as a basis for any detailed analysis.

The percentage of results exceeding different maximum levels for dioxins and dioxin-like PCBs set by legislation was on average 8% with a further 4% exceeding some action levels, but there were large variations between groups. Overall, a lower percentage of results exceeded maximum levels set for feed than for food. It is important to bear in mind that a varying proportion of product testing reflects targeted and not random monitoring. This has the potential of introducing a degree of uncertainty and bias in the evaluation of background levels of dioxins and dioxin-like PCBs in food and feed, as higher total values are expected in targeted compared to random samples.

The impact of changing the basis for the calculation of TEQ from TEFWHO98 to TEFWHO05 was evaluated with levels of dioxins and dioxin-like PCBs using the latter being overall 14% lower than levels using the former. This difference was mainly due to changes in TEFs for mono-ortho PCB and furan congeners with little change in dioxin and non-ortho PCB congeners. However, there were large variations observed for different food and feed categories and between products within food and feed categories.

Dioxin and furan congeners comprised between 30% and 74% of the total concentration of dioxins and dioxin-like PCBs depending on the food or feed group. There was considerable variation within food and feed groups. Mono-ortho PCBs comprised between 15% and 45% of the concentration of dioxin-like PCBs. This proportion was considerably lower when using the TEFWHO05 rather than TEFWHO98 as the basis for calculating the TEQ.

The current results clearly include results from both random and targeted monitoring although not specifically stated and should be interpreted with some caution. The lack of such sampling information and the irregular coverage of food and feed groups over time did unfortunately not allow for a time trend analysis to be performed. To improve the validity of any assessment of the presence of dioxins and dioxin-like PCBs in food and feed in Europe random testing and separate reporting of a sufficient number of samples in each food and feed group is important. Targeted sampling during contamination incidences should be clearly indicated as such in the reporting.
Published: 31 March 2010

Bovine tuberculosis in the EU

Working Document on Eradication of Bovine Tuberculosis in the EU accepted by the Bovine tuberculosis subgroup of the Task Force on monitoring animal disease eradication

The purpose of this document is:  

to review the general principles that constitute the basis for strategic planning for the future 
to propose short term measures in order to accelerate the progress of eradication
to draw conclusions on perspectives on eradication 
to stimulate discussion on future strategy

The proposed measures must be explored and assessed based on the individual situation in
each Member State (MS) running an eradication programme for bovine tuberculosis.

Statistical considerations for the safety evaluation of GMOs

The European Food Safety Authority (EFSA) asked its Panel on Genetically Modified Organisms (GMO) to investigate whether more detailed guidance could be provided regarding the performance of field trials and the analysis of data using appropriate statistical models, with the objective of ensuring a more uniform approach and greater transparency in risk assessment of GMOs. In order to carry out this investigation, the GMO Panel has convened a dedicated statistics Working Group who addressed the issue. A draft document was published on EFSA website from 21 July 2008 until 21 September 2008 for a 2-month period of public consultation. At the deadline EFSA had received 98 submissions, from 9 stakeholders. The table of all received comments together with a summarized response to the most relevant ones is published on the EFSA web site: Following the public consultation, the draft document was revised taking into account all the scientific comments that helped enhancing scientific quality and clarity (opinion adopted on 21 April 2009). Subsequently the adopted opinion was identified to have an incomplete statistical formula used to calculate equivalence limits. Further to adjusting the statistical formula the order of the various sections of the opinion was revised to improve logic flow. The present opinion was amended by the GMO Panel on 2 December 2009. Last updated:May 20, 2010

Scientific Opinion on Statistical considerations for the safety evaluation of GMOs (CGN100526A)
EFSA Journal 2010; 8(1):1250

Statistical considerations for the safety evaluation of GMOs:response to the public consultation (CGN100526B)
EFSA Journal 2009; 340: 1

Presentation of the full statistical code used for the example (CGN100526C)

Source: EFSA Scientific Opinion (EFSA-Q-2006-080)