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Livestock Diseases

Infectious diseases of livestock

Disease management of livestock include biosecurity measures, such as controlling animal mixing, controlling entry to farm lots and the use of protective clothing, and quarantining sick animals. Diseases also may be controlled by the use of vaccines and antibiotics. Antibiotics in sub-therapeutic doses may also be used as a growth-promoter such as antibiotic-laced feed increased growth by 10-15%, however, it soon leaded to antibiotics resistance of pathogen bacteria. Disease-free areas often impose quarantine and other measures or even import ban of animals from areas with epidemics.

Leptospirosis [1]

Leptospirosis is caused by a spirochaete bacterium called Leptospira spp. that has at least 5 serovars of importance in the United States and Canada causing disease in dogs (Icterohaemorrhagiae, Canicola, Pomona, Grippotyphosa, and Bratislava).

There are over 200 known serovars of Leptospira, however only few are known to cause the "leptospirosis" disease. The pathogenic bacteria are almost entirely within the Leptospira interrogans genomospecies, serogroup Icterohaemorrhagiae. Risk groups are workers in rice fields, sugar cane plantations, mines, sewer systems, and slaughterhouses; animal caretakers and veterinarians; and travelers to tropical parts of the world involved in recreational activities in fresh water. Recreational exposures can include rafting, kayaking, and swimming, in tropical and temperate climates. [2]

Leptospirosis is transmitted by the urine of an infected animal and is contagious as long as it is still moist. Although rats, mice and moles are important primary hosts, a wide range of other mammals including dogs, deer, rabbits, hedgehogs, cows, sheep, raccoons, possums, skunks, and certain marine mammals are able to carry and transmit the disease as secondary hosts. The type of habitats most likely to carry infective bacteria are muddy riverbanks, ditches, gullies, and muddy livestock rearing areas where there is regular passage of either wild or farm mammals.

Humans become infected through contact with water, food, or soil containing urine from these infected animals. Occupations at risk include veterinarians, slaughterhouse workers, farmers, sewer workers, and people working on derelict buildings. Rowers are also sometimes known to contract the disease.

Co-infection of malaria and leptospirosis [3]

Baliga et al. 2011 report the simultaneous infections of malaria and leptospirosis One was a case of infection with Plasmodium falciparum together with Leptospira serovar icterohaemorrhagiae another case was the simultaneous infection with Plasmodium vivax together with Leptospira serovar batavia. The authors propose that febrile cases presenting hepato-renal dysfunction may be caused by a co-infection of malaria and leptospirosis.


Milk was a frequent vector of tuberculosis. Only after research of Louis Pasteur introducing the technology of pasteurisation milk turned out to be safe.

Bovine TB: Pre-movement testing for all cattle over 42 days old in UK. [4] [5]

Defra wants to reduce the risk of the spread of bovine tuberculosis by TB pre-movement tests as well as routine surveillance tests. The tests were extended beginning with the age of 42 days as it was noted that infection is also being picked up earlier in high-risk herds. With this policy the Defra hopes to prevent 610 new incidents a year. Pre-movement testing was introduced in March 2006 in England and May 2006 in Wales.

To avoid human tuberculosis adquired from infectuous milk consume only pasteurized milk(heat treated milk). [5]

According to FDA [6] more than 300 people in the United States got sick from drinking raw milk or eating cheese made from raw milk in 2001, and nearly 200 became ill from these products in 2002, according to the Centers for Disease Control and Prevention. Some of the diseases that pasteurization can prevent are tuberculosis, diphtheria, polio, salmonellosis, strep throat, scarlet fever, and typhoid fever.

Enzootic bovine leucosis [7]

EBL is a transmissible disease caused by a virus. It can be transmitted both vertically, mother to calf, and horizontally, cow to cow; causing leukaemia and multiple tumours. Only cattle is affected. No transmission to humans are known. Clinical signs are usually apparent in cattle between 4 and 8 years of age and are only rarely seen in animals under 2 years old. In the live animal the disease is characterised by chronic ill health, progressive loss of condition, weakness, anaemia and anorexia, attributable to tumorous infiltration of various organs throughout the body, with serological antibody response. Lymphocytosis occurs, however, not always. Serological evidence of EBL is more specific; it may be demonstrated within a few months after infection. Confirmation of the existence of the disease depends upon laboratory detection of the EBL virus. Under natural conditions the disease is transmitted mainly by milk to the calf. Infected lymphocytes transmit the disease too.

Bovine immunodeficiency virus [8]

The bovine immunodeficiency virus (BIV) was found to cause wasting syndrome suggesting bovine leucosis. The virus is a lentivirus similar to the human immunodeficiency virus (HIV).

Bovine leukemia virus (BLV)

BLV is a bovine virus closely related to HTLV-1, a human tumour virus. BLV is a retrovirus which integrates a DNA intermediate as a provirus into the DNA of B-lymphocytes of blood and milk. It contains an oncogene coding for a protein called Tax.

Council Directive 64/432/EEC as amended on health problems affecting intra-Community trade in bovine animals and swine, and Council Directive 77/391/EEC as amended introducing Community measures for the eradication of brucellosis, tuberculosis and leukosis.

All infected cattle and contacts which have been exposed to infection must be slaughtered. No treatment is allowed.

New case of enzootic bovine leucosis in Germany [9]

According to the OIE immediate notification report 23/12/2010 a case of enzootic bovine leucosis was detected in Germany All cattle for slaughter in Germany are subjected to an ante and post mortem inspection which, in the case of suspicion, includes enzootic bovine leucosis test. Germany still fulfills the requirements of freedom from leucosis according to the chapter 11.9.2. of the OIE Terrestrial Animal Health

Feline leukaemia

The feline leukemia virus (FeLV) is a retrovirus which causes blood cell cancer (leukemia) domestic cats. FeLV can be transmitted between infected cats when the transfer of saliva or nasal secretions is involved. An infected mother cat can transmit the virus to her kittens, either before they are born or while they are nursing. If not defeated by the animal’s immune system, the virus can be lethal. Overwhelming epidemiologic evidence suggests FeLV is not transmissible to either humans or dogs.

Feline immunodeficiency virus (FIV) [10]

Feline immunodeficiency virus (FIV) is a lentivirus that affects domestic cats and causes feline AIDS. FIV differs taxonomically from two other feline retroviruses, feline leukemia virus (FeLV) and feline foamy virus (FFV), and is more closely related to human immunodeficiency virus HIV. FIV is the only non-primate lentivirus to cause an AIDS-like syndrome.FIV and HIV are both lentiviruses; however, neither can infect the other's usual host: humans cannot be infected by FIV nor can cats be infected by HIV. FIV is transmitted primarily through saliva (bites), such as those incurred during territorial battles between males.

Canine distemper [11]

Is caused by paramyxovirus. It is a single-stranded RNA virus of the family paramyxovirus, and thus a close relative of measles and rinderpest.

Human infection Smith 2010 reviewed studies related to human multiple sclerosis (MS) concluded that canine distemper virus (CDV) may be responsible for the causation of multiple sclerosis. However, it is not the only factor in the causal pathway. This implies that CDV may be a necessary factor in the development of MS as could be other infectious agents (bacterial or viral). The authors stresses that an individual's environment, genetics and immune system are other sufficient factors crucial in disease causation.

Rinderpest vaccine provide a lesson for the eradication of measles

Rinderpest (cattle plage) is an ancient viral infection of cattle and other large ruminants, It is caused by a member of the genus morbillivirus, of the Paramyxovirus family closely related to human measles virus and canine distemper virus. The disease is characterized by fever, oral erosions, diarrhea, lymphoid necrosis, and high mortality. [12]

After the Global Rinderpest Eradication Programme (GREP) of the Food and Agriculture Organization of the United Nations (FAO), the last confirmed case of rinderpest was diagnosed in 2001. On 8 August 2011, the United Nations held a ceremony declaring the disease eradicated, making rinderpest the second disease in history to be fully wiped out, following smallpox. [13]

The disease was effectively eradicated by developing a vaccine which could be kept unchilled, solving logistical and financial problems and delivery to the remote areas of Africa and Asia allowing veterinary personnel to interact directly with affected cattle herders. Vaccinations were accompanied by expansive disease surveillance. Blood samples were collected from herds to determine the extent of immunity. But most important, there was a concerted, well-funded, and unparalleled international response to eradicate rinderpest. [14]

Measles is caused by measles virus (MeV). Also member of the genus Morbillivirus. It is a common infection in children. Measles virus is closely related to rinderpest virus (RPV), which is a pathogen of cattle. MeV evolved in an environment where cattle and humans lived in close proximity and is thought to be mutation of the rinderpest virus. According to Furuse et al. 2010, divergence between MeV and RPV occurred around the 11th to 12th centuries, contrary to previous believes it dated of the prehistoric age. [15]


Parvoviruses which causes human and animal diseases are not in the genus Parvovirus, though they are casually called parvoviruses. Parvoviruses are typically linear, non-segmented single-stranded DNA viruses, with an average genome size of 5000 nucleotides. Parvoviruses are some of the smallest viruses and are 18–26 nm in diameter.

The new "Schmallenberg virus" affects European livestock (European Shamonda-like orthobunyavirus)

A new virus, the "Schmallenberg virus" (SBV) was reported in Autumn 2011 affecting livestoch in Europe. The virus has been found in sheep, cattle and goats and has to date infected animals in Belgium, France, Germany, the Netherlands and the United Kingdom. [16]

The "Schmallenberg virus" is a part of the Simbu serogroup of viruses belonging to the Bunyaviridae family, genus Orthobunyavirus. These serogroup viruses have mostly been found in ruminants in Asia, Australia, Africa and the Middle East.

The Friedrich-Loeffler-Institut (FLI) reported on 21 Nov 2011 data of genetic material of an unknown pathogen by means of metagenomic analysis. First comparative investigations indicate that the pathogen is a virus of the genus Orthobunyavirus, which is related with the group of Akabane-like viruses. [17]

Similarly to the bluetongue disease virus, these pathogens are mainly transmitted by biting midges. The virus belongs to the Simbu serogroup (Shamonda, Aina, Akabane viruses). The S segment of Schmallenberg's genome is most closely related to sequences of a different orthobunyavirus called Shamonda virus. The virus could be isolated, cultivated and replicated and named "Schmallenberg virus".

It is still unclear whether this exotic virus has been newly introduced or whether orthobunyaviruses already have been present in ruminants in Europe for some time. Therefore, further investigations are necessary to assess this virus detection.

In absence of specific data on the new "Schmallenberg virus", analogy was made with knowledge on Akabane virus, another representative of the of the Simbu serogroup. The Akabane virus has previously been reported in cattle in Turkey. It is supposed that the Schmallenberg virus is being transmitted by midges and mosquitoes. However, the possibility of direct animal-to-animal transmission cannot be excluded. The virus causes fever, diarrhoea and reduced milk production for up to a week. If infection occurs in pregnant animals during a short, vulnerable stage of the pregnancy it can result in severe birth defects of the offspring.

There is currently no evidence that the virus could cause illness in humans. As the genetically most related viruses do not cause disease in humans, it is unlikely that this new virus will cause disease in humans but it cannot be excluded at this stage.

It is known that the pathogenic effects of infection with Akabane virus are only seen when the virus exceeds the geographical boundaries of the endemic area and infects susceptible animals in early stage of pregnancy. Such a situation is likely to occur at the edges of an endemic area and may be due to the movement of either infected hosts or infected vectors.

The EFSA developed different scenarios based on the hypothesis that the transmission mode and the vectors transmitting the virus are similar to that of Bluetongue virus (BTV8) model to assess under which conditions SBV could spread into susceptible populations. The number of vectors and the temperature have an impact on the possible spread of the virus. However, it is unknown how likely animals are to become immune. EFSA proposes a coordinated data collection in all Member States related to Schmallenberg virus.

Bluetongue is a non-contagious infection transmitted by midge insects affecting domestic and wild ruminants including sheep, goats and deer. [18]

In Germany animals from 506 holdings have been tested positiv for "Schmallenberg virus" so far. The cases occurred in 15 cattle holdings, 470 sheep holdings and 21 goat holdings. [19] FLI developed a detection method and provides reagents, materials and sequence informations to institutions on request. [20]

Dutch experts expect that the Dutch calves were infected in August / September 2011, and that therefore that the peak of calves infected with the virus will be born during March / April this year. The major negative effect on the production of the virus is the cause of abnormalities of the born animals.

Russia banned import [21]

The Russian Government banned the import of sheep and goats, including related products from Germany and the Netherlands. Mexico banned imports of sperm and embryos of sheep, goats and cattle from the Netherlands. A Russian ban on the import of live cattle, mostly heifers, would have significant trade implications. Another important trade flow is the export of beef from Germany to Russia.

Recommendations of the Friedrich-Loeffler-Institute related to Schmallenberg virus [22]

Control: The Friedrich-Loeffler-Institute recommends for the forthcoming season, the protection of susceptible animals from biting midges/mosquitoes will be the only possibility to reduce the number of cases. A vaccine is not available.

Recommendations for animal holders and veterinarians: If symptoms occurr (drop in milk yield, fever and diarrhoea) in cattle during insect activity, suitable samples should be sent to responsible diagnostic agencies for detection of a possible infection with "Schmallenber virus." The same applies for clinically suspicious newborns.

Risk assessment.of the European Center for Disease Prevention and Control regarding the Schmallenberg virus [23]

Previously, genetically similar orthobunyaviruses have not caused disease in humans. It is therefore unlikely that this virus will cause disease in humans, but it cannot be excluded at this stage. Close collaboration between animal and human health services is necessary to ensure rapid detection of any change in the epidemiology of animals and humans. In particular, the health of farmers and veterinarians in close contact with potentially infected animals should be carefully monitored.

The Schmallenberg virus epidemic in Europe [24]

The German Friedrich-Loeffler-Institut discovered the Schmallenberg virus which caused an undetermined disease in animals in late 2011. Sheep, cattle and goats presented fever, decreased milk production, and diarrhoea, malformed newborn animals and stillborn calves, goats an lambs. A study leaded by Martin Beer used metagenomic analysis to identify the novel orthobunyavirus. The epidemic spread from Germany to the Netherlands, Belgium, Great Britain, France, Italy, Luxembourg and Spain
The Schmallenberg virus is part of the Simbu serogroup of the Bunyaviridae family, genus Orthobunyavirus. Viruses of this group are mostly found in ruminants in Asia, Oceania, Australia, Africa and the Middle East ( Israel). Especially the Simbu serogroup, which includes Akabane, Aino, and Shamonda viruses, can play a role as pathogens of ruminants. They are mainly transmitted by mosquitoes (Culicidae) or midges (Culicoides). Direct transmission from animal to animal has not been demonstrated except trans-placental from a viremic dam to the foetus.

Metagenomic approach to identify the Schmallenberg virus

A newly developed real-time quantitative reverse transcription PCR (RT-qPCR) demonstrated the power of a metagenomic approach to discovering emerging pathogens. Specific and sensitive RT-qPCRs could be developed quickly and used in analysing infected herds. Abdominal fluid was PCR positive for the novel virus, with a $C_{t}$ value of ∼27.

Beer et al. note that some members of the Simbu serogroup, such as the Oropouche virus, are zoonotic. The Schmallenberg virus, however, presents a very low to negligible risk to humans, because of the close relationship to Shamonda virus and the absence of reports of clinical signs in humans,. Nevertheless, clinical and serologic surveillance in humans should be conducted in regions with infected animals to update the risk assessments.

The Schmalleng virus in The Netherlands [25]

Muskens et al 2012 reported that Dutch dairy herds presented sudden decreased milk production, watery diarrhea and sometimes fever. Bacteriological, virological and parasitological testing of the faeces of sick cows did not reveal an infectious cause of the clinical problems, but 36% tested positiv for Schmallenberg virus. This suggests that the Schmallenberg virus was the primary cause of the disease.

Congenital malformation in lamb caused by Schmallenberg virus [26]

Epizootic outbreaks of congenital malformations in sheep was reported in The Netherlands by van den Brom et al. 2012. The main deformations included arthrogryposis, torticollis, scoliosis and kyphosis, brachygnathia inferior, and mild-to-marked hypoplasia of the cerebrum, cerebellum and spinal cord.

Nutritional deficiencies, intoxication, and genetic factors border disease virus, bovine viral diarrhoea virus, and bluetongue virus were excluded as cause of the malformations, The Schmallenberg virus was detected in brain samples of affected animals and is considered to be the cause of the disease.

OIE recommendations on safety precautions related to Schmallenberg virus [27]

Meat: Only clinically healthy animals should be slaughtered. Transmission of the virus is most likely by vectors. Risk of transmission to animals and humans is negligible.
Milk: Milk should only be collected from clinically healthy animals. Risk of transmission to animals and humans is negligible.
Safety recommendations related to semen,embryos, live adult non-pregnant and pregnant animals, and live newborns are available at:

Position of the European Commission [28]

The European Commission notes that there is no evidence that the virus could cause illness in people. The European Centre for Disease Prevention and Control (ECDC) assessed the zoonotic risks and concluded "it is unlikely that this virus can cause disease in humans, but it cannot be completely excluded at this stage".

Recommendations of the Institute in Bilthoven, The Netherlands. 21 Dec 2011 [29]

Zoonotic transmission of Schmallenberg virus can not be excluded but is considered unlikely when considering the vectorial transmission route (most likely midges). However, exposure risk during abortion or delivery of affected ruminants due to Schmallenberg virus is unknown. There have been no reports of unusual illness in humans in the months when the cattle syndrome peaked. However, new outbreaks should be monitored closely from a public health perspective. The institute advices to initiate a monitoring system for diseases among professionals (farmers, veterinarians) that have been in close contact with abortion products or who conducted deliveries of affected calves/lambs.

Schmallenberg virus in Great Britain [30]

Species affected: The Defra notes that the Schmallenberg virus has been detected in the United Kingdom. The virus is known to infect and cause disease in sheep, cattle and goats. Keepers of exotic or wild ruminants, such as the camelid and cervid family (alpacas, llamas and deer) should also be vigilant.

The virus circulates in the blood system of infected animals for two to five days, when biting insects may acquire the virus which they can then transmit to another susceptible animal during blood-feeding. It is likely that initial introduction of the virus to the UK resulted from wind-blown insect vectors.

Risk to humans: An Europe-wide risk assessment has concluded that Schmallenberg virus is unlikely to cause illness in people, no human cases have been detected in any country, and the most closely related viruses only cause animal disease, a gene sequence which carries the ability to infect humans is not present in Schmallenber virus. However, Defra advices farmers and veterinary surgeons to take sensible hygiene precautions when working with livestock and abortion material.

Pregnant women should not have contact with sheep and goats at lambing/kidding time due to risks of exposure to other disease causing organisms.

Schmallenberg virus does not infect humans [31]

Schmallenberg virus (SBV), a novel orthobunyavirus, is spreading, since November 2011, among ruminants, especially sheep, cattle, and goats throughout Europe. Infection causes acute fever, diarrhea, severe congenital malformation, and a high proportion of stillbirths. The virus is transmitted by midges (Culicoides spp.).

The Schmallenberg virus is closely related to the Simbu serogroup of which no zoonotic transmission are known. However, several other close related viruses are also transmitted by culicoids and cause serious outbreaks in humans. High numbers of Schmallenberg virus are found in infected animals and their birth products. Shepherds, assisting lamb births, are therefore strongly exposed.

Ducomble et al 2012 conducted a study to determine whether zoonotic or vector-borne infections occur in humans. The authors used an indirect fluorescent antibody test with antihuman fluorescein isothiocyanate-conjugated secondary antibodies against SBV-specific IgM or IgG.. No evidence of SBV infection among the shepherds was found by molecular and serologic tests, even in highly exposed shepherds.

Participants reported frequent insect bites. Some symptoms experienced by shepherds were compatible with illnesses commonly experienced during the winter caused by respiratory human viruses. The authors concluded that the Schmallenberg virus is unlikely to pose a threat to humans by transmission from infected livestock or from midges.

Impact and prediction of the Schmallenberg virus epidemic [32]

Since its first detection in Germany in 2011, til mid May 2012, the "Schmallenberg" virus (SBV) has been reported in 3745 holdings.

The impact of this animal disease on holdings does not exceed 4% for sheep or 2% for cattle in member states Goats and a bison. SBV were also infected. SBV antibodies have been detected in deer but no other species. It is unlikely that SBV poses a risk to humans.

The EFSA assumes that animals in previous affected regions aquire imunity. Should the virus survive the winter, EFSA's geographical spread model predicts that SBV is most likely to re-emerge between mid-April and the end of May and is likely to affect regions previously unaffected, that is, south and east of the affected areas.

Novel duck reovirus, DRV-TH11, caused Pekin ducks disease in 2011 [33]

In 2011, an unidentified disease in Pekin ducks (Anas platyrhynchos) was reported in China. The infection caused unstable gait, weakness in legs, diarrhea.and death in 40% of flocks. At necropsy, large necrotic foci were observed in the spleens and alterations in liver.

All classical endemic viruses such as duck enteritis virus, duck hepatitis virus, duck flavivirus, duck parvovirus, and avian influenza virus, could be excluded as the causative agent by PCR and serologic methods. The authors isolated a novel duck-pathogenic avian orthoreovirus (ARVs) of the family Reoviridae, genus Orthoreovirus.

ARVs also have been isolated from the Muscovy duck (Cairina moschata). Muscovy duck reovirus infection caused illness in 30% and death in 20% of ducks on poultry farms in Israel. In China, reovirus infection has been reported in Muscovy ducklings, however, the Muscovy duck reovirus isolate was nonpathogenic for Pekin ducks. Since 2007, three isolates of orthoreovirus were confirmed in Pekin ducks from several duck farms in China. However, experiment infection with the isolates did not cause death.

The disease of Pekin ducks in 2011 was found to be caused by a virus with 10 dsRNA segments in 3 size classes (L1-3, M1-3, and S1-4). The isolate was designated as novel duck reovirus, DRV-TH11. The sequence of S2 gene is distinct but clusters closely with sequences from all 3 Pekin duck isolates within the ARVs serogroup, which suggests that the novel virus is an ARV-like virus within the genus Orthoreovirus.

The authors concluded that the duck reovirus, DRV-TH11 is a highly transmissible infectious agent of high mortality. They call for further studies to determine the role of the virus in the 2011 epidemic and their prevention and control.

Fungal diseases

Fungi are eukaryotic microorganisms which can occur as yeasts, molds, or as a combination of both forms. Yeasts are microscopic fungi consisting of solitary cells that reproduce by budding. Molds occur in long filaments known as hyphae, which grow by apical extension. Hyphae may present septa and several nuclei. Fungi are all heterotrophic and digest their food externally by releasing hydrolytic enzymes into their surroundings.Fungi are associated with allergies and diseases.

Histoplasma capsulatum

Histoplasma capsulatum was found by Dias and colleagues 2010 in bats living in Brazilian urban areas. The authors stress the epidemiological importance of data regarding Histoplasma casulatum which is included in the mandatory disease notification system. Bats living in caves, attics, ceilings, and roofs increase the risk of human infection with the Histoplasma. [34]

Fungus present the ability to convert from hyphal cells to yeast forms. This capacity is called dimorphism. Dimorphism in Histoplasma capsulatum involves three stages and is induced by an increase in temperature. The conversion of terminal or intercalary hyphal cells to a yeast form requires 3 to 14 days. [35]

Human infections by Histoplasma capsulatum is very common in United States. In Africa infections by Histoplasma. capsulatum and Histoplasma duboisii were reported. Dietrich and colleagues 1987 describe a fatal case of disseminated histoplasmois due to Histoplasma capsulatum. [36]
Inhalation of conidial forms present in dust of caves where bats live and soils inhabited by chickens is often the source of infection. Histoplasmosis represents one of the most important systemic mycosis in the Americas, with broad distribution in all regions of Brazil.

Vaccine against three main human fungal infections [37]

Wuethrich and colleagues 2011 report a rise of systemic fungal infections by Coccidioides posadasii, Histoplasma capsulatum, and Blastomyces dermatitidis. The authors reports that vaccine-induced Th17 cells were necessary and sufficient to protect against the three major systemic mycoses in North America. The vaccine immunity required the adapter molecule Myd88 but not the fungal pathogen recognition receptor Dectin-1. The authors recommend to design vaccines to be effective against these three fungal infections.

Candida albicans

Candida albicans may form a budding yeast, pseudohyphae, germ tubes, true hyphae, and chlamydospores. The transition between a yeast and a mold is triggered by either low temperature or pH. Substances such as biotin, cysteine, serum transferrin, and zinc stimulate dimorphism in Candida albicans. [35]


Coccidiosis is caused by protozoan parasites. Coccidiosis in goats can cause ill thrift, severe diarrhoea and sometimes death. It is most often seen in kids and stressed animals. Good husbandry practices are required to minimise its occurrence.

Brucellosis in pigs

Brucellosis in pigs is caused by the Brucella suis (B. suis) bacterium. Infection of feral pigs has been reported in Northern Australia, and a number of human infections have been reported in people who hunt and handle tissues from feral pigs. Brucellosis is endemic in Asia, Sub-Saharan Africa, some countries of Latin America, the Middle East and the Mediterranean and South Eastern Europe Region.

Cvetnić and colleagues 2009 found that several pig herds in Croatia tested positive for antibodies against brucellosis. Almost every positive herd was reared outdoors. Brucella suis biovar 2 and biovar 3 could be isolated from pigs with positive sera, and the same biovars were identified in wild boars. The authors concluded that wild boars represent a brucellosis reservoir for free-range pig farms in Croatia and other countries of Central and Western Europe. [38]

Control and Prevention of Brucellosis

According to Dr Trish Holyoake Brucella suis is usually introduced into a herd via an infected animal or through the introduction of infected semen. Herds should be avoided to contact feral pigs. The author recommends the construction of pig-proof fences with electric wire, and control the feral pig populations. Transmission of Brucella suis to pigs may also occur eating contaminated feedstuffs, usually birth and/or abortion products and uterine discharges.

Human infection occurs by contacting infected animals or parts of those animals. Hunters were reported to become sick after contacting infected wild boars. [39]

Nicoletti stresses that there are no easy solutions to control brucellosis, widespread vaccination is the most rapid, efficient and effective procedure in addition to hygiene, and test and slaughter of infected animals. He recommends to increase thhe research on alternative strategies in vaccines and their usage, diagnostic tests, and treatments. [40]

Safe disposal of carcasses and manure

Safe disposal of carcasses for control of infectious disease outbreak in livestock [41]

Usually infectious material is incinerated, however, alternatives must be developed in case pandemics exceed capacities. Reuter and colleagues 2010 developed a bio-contained mortality composting procedure and tested its efficacy for bovine tissue degradation and microbial deactivation. The implementation of the composting system used materials available on-farm or purchasable from local farm supply stores. Carcass composting can take place at the site of a disease outbreak, when large number of diseased animals and manure must be safely discarded.

A bunker is constructed using barley straw bales lined with heavy black silage plastic sheeting. The bunker was loaded with 40-cm loose straw, carcasses overlaid with 1,6 m moist aerated feedlot manure and sealed with the plastic foil. Temperatures exceeded 55 degrees C for more than one month. Infectious agents in beef cattle carcasses and manure were inactivated within 14 days of composting. After 147 days, carcasses were almost completely degraded. The authors suggest composting as a rapid-response disposal method for infected carcasses, manure and soil.

Composting of FMD virus of infected pig carcasses [42]

Guan and colleagues 2010 report the inactivation and degradation of foot-and-mouth disease (FMD) virus during composting of infected pig carcasses, covered with a mixture of chicken manure and wood shavings in a biocontainment level 3 facility. The FMD virus was inactivated in 10 days when temperature reached 50 degrees C. The viral RNA was degraded in skin and organs after 21 days of composting and temperatures reached 70 degrees C. The virus and the RNA survived composting at temperatures near 20 degree C. The authors concluded that composting of FMD carcasses is safe under the mentioned conditions.

Poultry and livestock waste treatment [43]

Sakar and colleagues reviewed studies related to poultry and livestock waste treatment under anaerobic conditions between 25 and 35 degrees C.
Poultry manure wastewater Up-flow anaerobic sludge blanket (UASB) is indicated to treat poultry manure wastewater and the liquid fraction of hen manure.
Cattle manure Different systems were considered to be effective, such as such as fixed-film reactor, attached-film bioreactor, anaerobic rotating biological reactor, batch reactors, downflow anaerobic filter, fixed dome plant, UASB, continuously stirred tank reactor (CSTR), up-flow anaerobic filter (UAF), temperature-phased anaerobic digestion (TPAD), anaerobic hybrid reactor (AHR), and two-stage anaerobic systems are well suited to anaerobic processing of cattle manure.
Swine manure Up-flow anaerobic sludge blanket, anaerobic baffled reactors, continuously stirred tank reactor, and anaerobic sequencing batch reactor are used in mesophilic or thermophilic systems to precess swine manure.


A zoonosis or zoonose is any infectious disease that can be transmitted from animals to humans or from humans to animals (reverse zoonosis or anthroponosis). The interdisciplinary field of conservation medicine, integrating human and veterinary medicine, and environmental sciences, is largely concerned with zoonoses.

Bats as disease vectors

Viruses of bats which can infect animals and humans [44]

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. [45]

Surveillance still necessary despite low incidence of rabies in Swiss bats [46]

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.

Rabis in German bats identified as European Bat Lyssavirus (EBLV-2) [47]

In Europe, rabies in bats is caused by European Bat Lyssavirus (EBLV) type 1 (EBLV-1) or type 2 (EBLV-2) which form two distinct genotypes (gt 5 and 6) within the genus Lyssavirus of the family of Rhadoviridae.Fatal human rabis were reported.

German bats were found to be infected with the EBLV-1 variant. In The Netherlands and the United Kingdom the EBLV-2 was found. Freuling and colleagues 2008 detected one bat infected with EBLV-2 in Germany in a Daubenton's bat (Myotis daubentonii) in August 2007.

Bat guano virome acquired through diet of insects and plants [48]

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 [49]

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 [50]

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 [51]

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.

Pigs may transmit ebolavirus to other animals and humans [52]

Reston ebolavirus, an ebolavirus which is not pathogen to humans, was detected in pigs in the Philippines, and specific antibodies were found in pig farmers which did not develop the disease.

Kobinger et al 2011, found that the human highly pathogen Zaire ebolavirus may infect pigs, replicate, cause disease of the respiratory tract and is transmitted to other animals. Shedding of the virus from nasal mucosa was detected for up to 14 days post-infection, and severe lung disease was observed. Human outbreaks of Ebola hemorrhagic fever, caused by the Zaire ebolavirus (ZEBOV) has a fatality rate as high as 90 percent in humans. The findings of the authors suggest that pigs may be able to transmit virulent ebolavirus to humans as well.

The authors stress that in primates Zaire ebolavirus affects multiple organs, leading to shock and death, but in pigs the virus causes respiratory syndromes which may be mistaken for other porcine respiratory diseases.

Dogs and cats as disease vectors

Dogs and cats as vectors of human diseases in Italy [53]

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 [54]

Rickettsia massiliae DNA was 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, described by Beati and Raoult 1993. [55]


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. [56]

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. [57]

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. [58]

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. [59] [60]

The Ixodes ricinus tick removed from dogs in Warsawm (Poland) were found infected by Babesia microti, demonstrating their presence in ticks in Poland. [61]

Human pathogens in ticks living on birds [62]

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.

Anaplasmosis in hoses in Brazil [63]

Equine Granulocytic Anaplasmosis - EGA (formerly Equine Granulocytic Ehrlichiosis, EGE) is a disease affecting horses. EGA infection is suspected when horses present symptoms of ehrlichiosis but do not respond to piroplasmosis treatment. (Equine piroplasmosis may be caused by Babesia caballi and Babesia equi)

Salvagni et al. 2010 found horse serum samples from the central West region of Brazil 65% positive for Anaplasma phagocytophilum and 85% positive for Theileria equi by ELISAe of EGA and equine piroplasmosis in central West Brazil.

Coexistence of Borrelia spp. and Babesia spp. in ticks [64]

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

[65] 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.


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.[66]

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. [67]

Anaplasma phagocytophilum [68]

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 [69]

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) [70]

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. The disease was previously knowm as human granulocytotropic ehrlichiosis [71]. 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. [72]

Ehrlichia chaffeensis as human pathogen [73]

The Ehrlichia chaffeensis is an obligately intracellular bacterium lives in mononuclear phagocytes. It causes the human monocytotropic ehrlichiosis. Thomas, Popov and Walker 2010 studied the infection mechanism of ehrlichiosis using Ehrlichia muris and Ixodes ovatus Ehrlichia (IOE) as mouse models of the disease. The authors found that Ehrlichia was transported through the filopodia of macrophages during early stages of infection. Cytochalasin could inhibit the formation of filopodia, preventing the transport of the bacteria to the interior of the macrophages. The erlichia cells are released when the cell membrane of the macrophage ruptures in a late phase of the disease.

Advice to prevent outdoor vector-borne diseases in USA [74]

Hayes 2010 advises travellers visit the United States to practice personal protection against arthropod bites, including appropriate use of insect repellents, especially when visiting rural and suburban areas during the warm months, to prevent Lyme disease, anaplasmosis and babesiosis in the northeast and north central States, West Nile virus disease in western plains States, and Rocky Mountain spotted fever and tularemia in the southeast of the USA.

Ehrlichiosis and anaplsmosis disease in dogs and cats in USA [75]

Ehrlichia canis is known since 1935, however, and was found in the United States for the first time in 1962. It may infect dogs and sometimes cats. Little 2010 describes the transmission, diagnosis, and management of ehrlichiosis and anaplasmosis in these animals.

Determination of Anaplasma phagocytophilum clusters using ankA gene [76]

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 [77]

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 [78]

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.

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 [79]

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 [80]

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.

Low risk of tick-borne disease in the Netherlands [81]

Tiisse-Klasen et al.2011 determined the risk of developing tick-borne diseases. They collected Ixodes ricinus ticks and found PCR positive for Borrelia burgdorferi s.l (60%), Rickettsia spp.(19%), Ehrlichia/Anaplasma spp.(12%), and Babesia spp.(10%). After six month following a tick bite, the participants of the study reported reddening at the bite site (8.3%) and systemic symptoms (4.1%). However, no association between symptoms and tick-borne microorganisms was found. The authors concluded that the risk in the Netherlands of contracting acute Lyme borreliosis, rickettsiosis, babesiosis or ehrlichiosis from a single tick bite was less than 1%.

Failing to develop a Lyme vaccine [82]

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. [83] Nardelli et al. 2009 call for the development of a new vaccine, because Lyme disease cases increase and diagnoses is difficult. [84]

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. [85]

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. [86]

CDC recommendations on prevention of tick-borne diseases [87]

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 [88]

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

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 [89]

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. [90]

Chlorine disinfection of Francisella tularensis in drinking water [91]

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.


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. [92]

Evaluation of disease caused by Rickettsia 364D [93]

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. [94]

Diseases transmitted by ticks in Swizerland [95]

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 [96]

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

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 [97]

The northernmost tick-borne encephalitis (TBE) focus is in Simo, Finnish Lapland. Four TBE cases were confirmed during 2008-2009 by Jääskeläinen et al. 2011. 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.

Jääskeläinen 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. [98]

Complete genome sequences of two Korean strains of the tick-borne encephalitis virus [99]

Yun at al. 2011report 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.

Rift Valley Fever [100]

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. Over 400 persons died 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 [101]

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 [102]

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

[103] 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 [104]

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 [105]

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 [106]

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.

Clenbuterol in pork

Clenbuterol is a beta-2 agonist and sympathomimetic amine that is used to treat breathing disorders. When fed to livestock it accelerates growth and increases the proportion of lean meat. In 2002 China banned the use of clenbuterol in feed after complaints of consumers suffering from nausea, dizziness, hypertension and hyperglycemia after eating pork raised with such feed.
Image Clenbuterol
In March 2011 Shuanghui, largest meat producer of China was cited to produce meat tainted with illegal clenbuterol. People producing, selling or using clenbuterol were arrested. All meat product sales of Shuanghui have been suspended.

Pleadin et al. 2010 determined the concentration of clenbuterol in meat of pigs which were fed a growth-promoting dose of clenbuterol of 20 microg/kg body mass per day during 28 days. Residues of Clenbuterol in meat is found up to 7 days after treatment discontinuation.The chemical could not be detected only after 14 days of cessation of clenbuterol administration. [107]

Clenbuterol has also been used as a performance-enhancing drug and a number of athletes were banned after using the drug in 2008 to 2010. Traces of the amine from meat in the diet is regularly turning up in athletes' blood. A lab in Cologne, Germany, found that 22 of 28 travellers returning from China tested positive for low levels of clenbuterol, probably from food contamination. This may also affect athletes travelling to China. [108]

Veterinary professionals say the number of tests for clenbuterolin pig is to low because these tests are too costly. They call for the development of easier, cheaper, more convenient and wider-spectrum testing methods for regular food products. Liu and colleagues 2011 report the development of a method to determine 20 illegal residual beta-agonists in pork tissues, including muscle and liver simultaneously. [109]

Monocultures of non-edible oil plants for Biodiesel endanger native bees [110]

Castor bean (Ricinus communis) is largely cultivated in the region of northeastern Brazil for the production of biodiesel. Assessing the toxicity of pollen samples of Ricinus communis to honey bees de Assis Junior and colleagues 2011 found that the survival of honey bees were significantly reduced if they had access to castor bean pollen. The authors concluded that expansion of castor bean plantations in Brazilian may endanger native and domestic honey bees. The authors call for more studies on the effect of non-edible oil plants to honey bees.

Honey containing pollen of GM plants will be ruled under the GM legislation [111]

The attorney general of the Court of Justice of the European Union, Yves Bot ruled that honey containing pollen derived from GM maize requires approval to be marketed within the Community. Pollen is a genetic modified organism which bears genetic informations of the plant of origin and must be ruled according to genetic engineering legislation [112]. Under this legislation it is irrelevant how the pollen found its way to the honey and if it is fertile or not. If this rule comes into effect honey containing pollen of not allowed GM plants, such as the Canadian rapeseed honey needs to be approved by regulators before it can be sold in the European Union. [113]

Traces of genetically-modified pollen from a Monsanto maize crop (MON 810) in honey samples ignited the debate on how to reform the GM approval system. More than one third of crop plants depend on the pollination by honeybees. Interests of beekeepers are therefore of vital importance for agriculture.

Honey with traces of GMO pollen must be labelled as GM produce and be submitted to safety authorisation [114]

Honey with traces of GMO pollen must be labelled as GM produce and be submitted to safety authorisation, following new ruling by the European Court of Justice. The ruling stated that GM pollen produced by MON810 maize and present in honey falls under the scope of Regulation 1829/2003 on GM food and feed and is therefore subject to authorisation prior to placement on the market.

MON810 pollen in honey was not included in the original scope of the authorisation application for maize MON810, meaning that honey containing the GM pollen became illegal following the court ruling. The decision will have an impact on the 140,000 tonnes/y honey which the EU imports from Argentina and China, both GM-friendly countries.

Production of GM-free honey will be endangered by the activities of biotech corporations and law makers

The decision will also collide with he EU regulation of July 2011 which permits traces of GMOs in animal feed without safety review. [115]
The regulation of 24/06/2011 which came for low level presence of non-EU approved genetically modified organisms (GMOs) in feed sets a 0.1% threshold replacing the former zero tolerance level for unapproved GMOs. It applies for GM material authorised for commercialisation in a third country, and for which the EU approval procedure has been pending for more than three months, and certain GMOs for which the authorisation has expired. [116]

Heavy pressure of biotech on Vatican and on EU countries says a WikiLeak report [117]

Craig Stapleton US ambassador in Paris urged Washington to penalise the EU after France moved to ban a Monsanto GM corn variety.
Catholic bishops in developing countries have been opposed to the GM crops, because peasant could not pay the seeds and additional chemicals. The US embassy in the Vatican believed that the pope might support biotech and order these bishops to accept GM crops. The embassy lobbied the Cardinal Renato Martino which is the adviser of the pope. The Cardinal, trying to keep good relations to the US government, cooperated with biotech to compensate the Vatican refusal of the Iraq war. "Recently, however, the Cardinal no longer feels the need to take this approach," says the US embassy cable.

US authorities have asked Turkey to change their legislation on GMO which demands 5 years prison for GMO foods importers in Turkey. The request was launched in exchange to a Turkish request to . to ease customs regulations for importing fruits and vegetables to the U.S. market. Negotiations ended without results on both sides. [118]

Biotech disapproved by most consumers

Most people disapprove GM food and avoid it whenever the products are clearly labelled and there are alternatives. The strategy of corporations introducing GM foods is to blur the boundaries between GM-NonGM crops starting with GMO contaminated animal feeds or staple foods, leaving the consumer without choice. [119]

Peru approves GMO ban [120]

In 5 November 2011 the Congress of Peru approved a 10-year moratorium on imports of genetically modified organisms, including seeds, livestock, and fish in order to safeguard the country's biodiversity. Peru is one of the world's leading exporters of organic food, including coffee and cocoa. The country has 40,000 certified producers.

The Gates Foundation embraces biotech instead of agroecological techniques disregarding sustainability [121]

The Gates Foundation collaborates with agri-biotechnology companies including Monsanto, BASF, Du Pont, Dow and the Syngenta Foundation in projects to develop GM seeds and promote fertilisers, pesticides and hybrid seeds to small African farmers, says a GM Freeze report of October 2011. According to the report the strategy of the Gates Foundation relies on input of petrochemicals and GMO plants. This may lead to degradation of soils, water supplies and biodiversity. The report urges the Gates Foundation to re-assess their approach and focus on developing agroecological techniques that have already been demonstrated as effective at providing environmental, social and economic solutions.

New Porcine Calicivirus in US Swine []

Wang and colleagues report that new St-Valerien-like porcine caliciviruses are prevalent in up to 80% in finisher pigs in North Carolina. One strain, NC-WGP93C, shares over 89 genomic nucleotide identity with Canadian strains. The authors could not say whether these strains are pathogenic for animals or humans or may affect food safety.

The caliciviruses have been found in humans, cattle, pigs, cats, chickens, reptiles, dolphins and amphibians.Viruses in the family Caliciviridae are nonenveloped, polyadenylated, single-stranded, positive-sense RNA viruses with 5 genera (Norovirus, Sapovirus, Vesivirus, Lagovirus, and Nebovirus). The nonhuman primate Tulane virus and the porcine St-Valerien-like viruses, may become a new genera in the Caliciviridae family.

St-Valerien-like viruses have been detected in Canada, the United States, and Italy. In order to support the classification of St-Valerien-like viruses as a member of Casliciviridae it is important to demonstrate the presence of the virus in other regions and determine the genetic differences between strains. St-Valerien-like viruses are close to Tulane virus and human noroviruses, and more data may may help to clear if an interspecies transmission may take place, and find the bst way to control the spread of the new viruses.

Chronic and visceral botulism may impact birds, cattle and humans [122]

Böhnel, Schwagerick and Gessler 2001 describe a bovine disease in lower Saxony, Germany and named it "visceral botulism". The symptoms are constipation alternating with diarrhoea, non-infectious chronic laminitis, engorged veins, oedemas, retracted abdomen, emaciation and apathy. Unexpected death, delayed growth and wasting in heifers, and decreasing milk yield are reported. The authors found Clostridium botulinum bacteria, their spores and toxins in animals of affected farms. Free botulinum toxin was found in lower sections of the intestine. In farms with healthy animals all tests were negative. According to Professor Dr. Helge Böhnel of the University of Göttingen and his colleagues, long-lasting absorption of low quantities of botulinum toxin may interfere with the neurological control of intestinal physiology.

Botulinum neurotoxin and Sudden Infant Death Syndrome [123]

Böhnel et al 2001 studied case of unexpected infant death up to 12 months of age. Free botulinum neurotoxin (BoNT) and bacterial forms were detected. Toxin neutralisation revealed the definite presence of BoNT/BoNT producing bacteria (mainly type E). The authors found a remarkable incidence of infant botulism hidden as sudden infant death. They suggest to systematically search for botulism in cases of sudden infant death.

Clostridium botulinum produce botulinum neurotoxin (BoNT) which acts by blocking the neural transmission in the cholinergic synapses. Ingesting food contaminated by BoNT toxin botulismus symptom may arise, ranging from asymptomatic, mild with subtle paralysis ("failure to thrive") oder severe with generalized paralysis or sudden death may occur (Sudden Infant Death Syndrome). Fischer et al. 2004 report two cases which shows that botulism is a potential cause of unexpected infant deaths. The study of Fischer supports the Botulinum/Sudden Infant Death Syndrome hypothesis of Böhnel. [124]

Infant botulism sudden infant death syndrome linked to ingestion of spores of Clostridium botulinum [125]

Infant botulism results of the ingestion of spores of Clostridium botulinum leading to germination of the organism and neurotoxin production in the intestine. Symptoms typically develop gradually in contrast to classical food botulism in which an acute onset of symptoms shortly after the ingestion of preformed toxin in a food is characteristic. The toxin irreversibly blocks the release of acetylcholin in the nerve synapses resulting in muscle weakness and paralysis. depending on the amount of toxin produced and may cause sudden infant death, says Bartram and Singer 2004.

Plastic-wrapped and nonacidified silage as cattle feed increase risk of botulism [126]

Lindström et al 2010 report botulism outbreaks in cattle due to the use of plastic-wrapped and nonacidified silage as cattle feed. Clostridium botulinum in silage and in the gastrointestinal tract of cattle with botulism has been reported. The authors warns of human contamination with spores of Clostridium botulinum in dairy products. The standard milk pasteurization treatment does not eliminate these spores. Outbreaks in dairy products may be initiated by failures during production and lack of adequate quality control of ingredients.

Chronic visceral botulism from biogas plants [127]

Since the studies related to chronic botulismus were made public, the citizens living in the proximitiy of biogas plant became worried about the residue from biogas plants containing botulism bacteria which threatens domestic, wild animals and humans- chronic botulism.

In the German region of Vogtland in Lower Saxony, Germany, cows diseased of what Professor Dr. Helge Böhnel of the University of Góttingen called, chronic and visceral botulism. Bóhnel studied diseased cows at the farm of Hermann Bormann. These animals present chronic botulism.

The researcher says that slaughterhouse waste and other meat, such as old hens, along with manure slurry, are used as raw material of biogas plants. At temperature of 40° anaerobic bacteria, such as Chlostridium are bred. Their spores survive the hygienisation process of heating to 70° . The waste material is used as fertilizer spreading the spores in the environment. Grazing animals ingest such spores which evolve to toxins producing bacteria in the digestive tract. The spores are spread all over the landscape as dust transported by wind and are ingested by grazing animals.

Dead birds of chicken farms and slaughterhouse waste are added to the raw material of biogas plants and are excellent growth conditions for Chlostridium. Carcasses should not be used as raws material but no regulation limits "unintentional" carcasses content of raw material for biogas plants. [128]

Study found no Chlostridium botulinum in biogas plants and their wastes [129]

Gerhard Breves of the veterinary school Hannover believes that there is no great potential risk coming from biogas plants. He found no botulismus bacteria in biogas plant contents and waste. He says that he does not want to generalise his findings, but he considers safety risk of biogas plants as small. Chicken dunghill at chicken farms: Feathers and carcasses of birds should not be added to chicken dunghill.

Silage: Experts urge to keep dead wild birds, small wild animals and rats out of silage as it may increase the risk of growth of Chlostridium botulinum and death of livestock. Horses are very sensitive to botulismus toxins. Therefore silage is not used as feed for horses by some animal owners. It is being recommended to avoid fertilise grass field with liquid manure and chicken dung shortly before harvest. Dry matter should not be below 30% to avoid noxious fermentation. [130]

Brazilian Lupinus albus protein isolates lower blood cholesterol and reduce liver steatosis in hamsters [131]

Diets from lupin protein isolate and whole lupin seed promoted a significant reduction of total cholesterol and non-HDL cholesterol in the plasma of hamsters, as compared to a control group fed with casein. The liver revealed that animals, fed on both lupin diets, present reduced steatosis (abnormal retention of fat within the liver cels) steatosis as compared to the ones fed on casein as protein diet. Fontanari et al. 2012, authors of the study, suggest that whole lupin and its protein isolate lowers serum cholesterol and reduces the risk of hepatic steatosis.

Lupin protein as feed for broiler produce better meas as compared to soybean feed [132]

Laudadio et al. 2011 report that dehulled-micronised lupin meal in diet for broiler chickens provides better lipid profile and quality, with no adverse effects on productive parameters as compared to defatted soybean meal diet.

Micronised-dehulled lupin (Lupinus albus L. cv. Multitalia) diet did not result in lower growth rates of chickens, nore negative effect on carcass meat was noted. However, a reduction of abdominal fat content was reported. The lupin diet reduced fat content and increased the total collagen and water-holding capacity values of the meat of the birds. Saturated fatty acid content was reduced, while total PUFA and monounsaturated fatty acids levels were increased, improving heart disease prevention factors.

White lupin based diet produced healthier meat as obtained with sunflower meal [133]

Whole white lupin (Lupinus albus cv. Amiga) seed diet (WL) was found by Volek and Marounek 2011 to contain less saturated fatty acids and polyunsaturated fatty acids (PUFAs) but more monounsaturated fatty acids than sunflower meal diet. The meat of rabbits fed with whole white lupin diet presented a significant decreased saturated fats, reduced PUFAs content, and healthier PUFA n-6/PUFA n-3 ratio and saturation, atherogenic and thrombogenic indexes as compared to rabbits fed with the sunflower meal. The authors concluded white lupin seed diet result in healthier meat as obtained with sunflower meal diet for rabbits.

Nutritional effects on fat composition of animal products [134]

Kouba and Mourot in a review in 2011 report healthy outcomes of fatty acid composition of eggs, milk and meat in response to feed containing fish meal or linseed. The effect of these diets are stronger in monogastrics such as pigs, poultry and rabbits than in ruminants, where dietary fatty acids are hydrogenated in the rumen. The authors stress that short-term diet manipulation is sufficient to increase PUFA content of the final product. The linseed-supplemented diets is not needed to be maintained for a long time as PUFA content of the products increase promptly.

Lupinosis [135]

Lupinosis is a mycotoxicosis caused by the ingestion of toxins produced by the fungus Diaporthe toxica (Phomopsis leptostromiformis) which grows on lupin plants. Allen and Randall 1993 found that in addition to being an hepatotoxicity, lupinosis also resulted in injury to muscle, kidney and adrenal cortex.

Isolation of phomopsin the poison of lupinosis [136]

Lupinosis was first recognised in Germany in 1872 and is being reported in the United States of America, Poland, New Zealand, Australia and South Africa. Sheep are particularly susceptible and cause high economic losses. Two metabolites of P. leptostromijormis (phomopsins A and B) have been isolated as a crystalline mixture from a culture of the fungus on lupin seed. The mixture has been shown to be capable of inducing lupinosis in sheep and in young rats.

Varieties of lupin [137]

Lupinus angustifolius breeding has been by far the major focus in Australia. Lupinus albus and Lupinus luteus have received more attention in Europe and the former USSR but breeding of Lupinus angustifolius is increasing. The most important disease of the narrow-leaf lupin (Lupinus angustifolius) in Victoria is brown leaf spot which is caused by the fungus Pleiochaeta setosa.

Albus lupin variety Kiev [138]

The management of sheep grazing Albus lupin (Lupinus albus) stubble is similar to those grazing narrow leafed lupins. However, the seed is almost three times bigger and consequently sheep select and eat the seed much more quickly. Albus have a higher protein and energy content than narrow leafed lupins. In addition, Albus varieties such as Kiev are less prone to Phomopsis infection than narrow leafed lupins.

Lupin stubble paddocks provide a valuable feed source. Careful management reduces the risk of lupinosis which can cause deaths, reduced twining and conception rates at joining, weight loss, poor wool growth and pregnancy toxaemia.

An outbreak of natural lupinosis in lambs in Caceres, Spain was described by Soler Rodrigues et al. in 1991. [139] Lupinosis is a result of livestock grazing lupin stems or lupin seed infected by the fungus Diaporthe toxica, formerly known as Phomopsis leptostromiformis. New lupin varieties have some resistance to the fungus, however, danger still remains as favourable conditions are likely to result in the fungus being present in all varieties.

The Western Australian Department of Agriculture and Food recommends to ensure there is other more digestible feed available and stocking rates are below 15 sheep per hectare to reduce grazing pressure. This reduces the need for sheep to graze lupin stems.
Livestock are removed of the pasture when the grain falls below four grains per ten square centimetres and before the green weeds run out, as lupin stubbles on their own provide poor nutrition and the risk of Lupinosis greatly increases as the animals are more likely to graze the stems. [140]

Weather [138]

Temperature, rainfall, humidity and dew all influence the production of toxin by the fungus. Rainfall, high humidity or consistent dews when daily maximum temperatures are about 25C create ideal conditions for toxin production in stubble. Lupinosis most commonly occurs in the first few days following more than 10 mm of summer rain.

Serine-Endopeptidase specificity to twin-arginine pairs in lupin seed may be associated with germination [141]

Magni et al. 2012 describe a novel serine-endopeptidase activity with cleavage specificity to twin-arginine pairs (-R-R-) in mature dry Lupinus albus seeds. The authors suggest that the activity of the novel endopeptidase is essential for degradation at germination and generates polypeptide fragments with specific biological activity.

Prioritization of diseases of food-producing animals [142]

Humblet et al 2012 prioritized 100 animal diseases and zoonoses in Europe using 57 prioritization criteria. The method of disease prioritization has been defined as the "organization of listed diseases into a hierarchy, considering their respective impacts". Five aspects of a pathogen were considered: epidemiology, prevention/control, effects on economy/trade, zoonotic characteristics, and effect on society.

Prioritization of diseases has acquired major interest within the past few years, especially from a prevention point of view and in the sector of public health. Such a method is needed within the context of emerging diseases because it is not known how severe socioeconomic consequences of outbreaks will be. This study included zoonoses and transmissible diseases common to humans and animals and reportable animal diseases, and involves interdisciplinary work of animal and human epidemiologists; chief veterinary officers; experts in agricultural economics, animal welfare, and biodiversity; and experts on societal aspects of diseases.

The new model presented by the authors enables adaptations (vaccination becoming available, increased knowledge of a pathogen, viral mutations or genetic reassortments increasing host specificity). It may be applied to diseases affecting domestic (dogs, cats) pets or exotic pets (reptiles).

Classification of 100 diseases of food-producing animals and zoonoses into 4 subgroups

Classification and regression tree analysis showing grouping of diseases of food-producing animals and zoonoses into 4 subgroups by using overall weighted scores per disease as input, Europe. A) High importance and significant importance. B) Moderate importance and relatively low importance. See the Classification tree:




Baliga KV, Uday Y, Sood V, and Nagpal A.
Acute febrile hepato-renal dysfunction in the tropics: co-infection of malaria and leptospirosis.
J Infect Chemother, 2 2011.

More: Defra, UK: Bovine TB: pre-movement testing extended to younger animals.

See also: Defra: Bovine TB pages.

US FDA: Got Milk? Make Sure It's Pasteurized. FDA Consumer Magazine; September-October 2004.

Enzootic bovine leukosis (ebl).
DEFRA, 1 2010.

Corredor AG, St-Louis MC, and Archambault D.
Molecular and biological aspects of the bovine immunodeficiency virus.
Curr HIV Res., 8(1):2-13, 1 2010.

Immediate notification report. report reference: Ebl 2010, ref oie: 10089, report date: 23/12/2010 , country: Germany.
OIE, 12 2010.

Feline immunodeficiency virus.

Smith TC.
Can your pet dog make you sick? multiple sclerosis and canine distemper virus. april 29, 2010.

C áceres sb: The long journey of cattle plague.
Can Vet J, 52(10):1140, 10 2011.

de Swart RL, Duprex WP, and Osterhaus AD.
Rinderpest eradication: lessons for measles eradication?
Curr Opin Virol, 2(3):330-4, 6 2012.

Jeffrey C, Mariner JC, House JA, Mebus CA, Sollod AE, Chibeu D, Jones BA Roeder PL, Admassu B, and van 't Klooster GGM.
Rinderpest eradication: Appropriate technology and social innovations.
Science, 337(6100):1309-1312, 9 2012.

Furuse Y, Suzuki A, and Oshitani H.
Origin of measles virus: divergence from rinderpest virus between the 11th and 12th centuries.
Virol J, 4(7):52, 3 2010.

"schmallenberg" virus: likely epidemiological scenarios and data needs. efsa 6 feb 2012.

Evidence for presence of a new virus in cattle in germany. friedrich-loeffler-institut (fli). press release 21 nov 2011.

Efsa publishes report on likely scenarios for spread of "schmallenberg" virus in ruminants. efsa 8 feb 2012.

Schmallenberg virus. current information on "schmallenberg virus". friedrich-loeffler-institut.14th feb 2012.

Schmallenberg virus: Distribution of virus samples, information on virus genome and protocol for genome detection. friedrich-loeffler-institut (fli). 10 jan 2012.

Gain: Schmallenberg virus found in cattle. 30 jan 2012.

Information of the friedrich-loeffler-institut on "schmallenberg virus" (european shamonda-like orthobunyavirus) 31 jan 2012.

Risk assessment: New orthobunyavirus isolated from infected cattle and small livestock - potential implications for human health. european centre for disease, prevention and control. 22 dez 2011.

Hoffmann B, Scheuch M, Höper D, Jungblut R, Holsteg M, Schirrmeier H, and et al.
Novel orthobunyavirus in cattle, europe 2011.
Emerg Infect Dis, 3 2012.

Muskens J, Smolenaars AJ, van der Poel WH, Mars MH, van Wuijckhuise L, Holzhauer M, van Weering H, and Kock P.
Diarrhea and loss of production on dutch dairy farms caused by the schmallenberg virus.
Tijdschr Diergeneeskd, 137(2):112-5, 2 2012.

van den Brom R, Luttikholt SJ, Lievaart-Peterson K, Peperkamp NH, Mars MH, van der Poel WH, and Vellema P.
Epizootic of ovine congenital malformations associated with schmallenberg virus infection.
137(2):106-11, 2 2012.

Schmallenberg virus: Recommendations as endorsed by the oie scientific commission for animal diseases on 16 february 2012 (will be updated when relevant).

European commission: Schmallenberg virus.

Risk profile humaan schmallenbergvirus. national institute of public health and the environment, bilthoven, the netherlands. 21 dez 2011.

Schmallenberg virus. information for farmers and vets in great britain. animal health and veterinary laboratories agency.
3 2012.

Ducomble T, Wilking H, Stark K, Takla A, Askar M, Schaade L, and et al.
Lack of evidence for schmallenberg virus infection in highly exposed persons. germany, 2012.
Emerg Infect Dis, 8 2012.

Efsa assesses impact of schmallenberg virus in eu. efsa press release 14 jun 2012.

Chen Z, Zhu Y, Li C, and Liu G.
Outbreak-associated novel duck reovirus, china, 2011 [letter].
EID Journal, 18(7), 2012.

Dias MA, Oliveira RM, Giudice MC, Netto HM, Grigorio IM Jordao LR, Rosa AR, Amorim J, Nosanchuk JD, Travassos LR, and Taborda CP.
Isolation of histoplasma capsulatum from bats in the urban area of são paulo state, brazil.
Epidemiol Infect, pages 1-3, 12 2010.

Michael R, McGinnis, and Stephen K. Tyring.
Introduction to mycology. medical microbiology. 4th edition.galveston (tx.
University of Texas Medical Branch at Galveston, 1996.

Dietrich PY, Bille J, Fontolliet C, and Regamey C.
Disseminated histoplasmosis due to histoplasma capsulatum in a patient with acquired immunodeficiency syndrome (aids).
Schweiz Med Wochenschr, 117(35):1289-96, 8 1987.

Wuethrich M, Gern B, Hung CY, Ersland K, Rocco N, Pick-Jacobs J, Galles K, Filutowicz H, Warner T, Evans M, Cole G, and Klein B.
Vaccine-induced protection against 3 systemic mycoses endemic to north america requires th17 cells in mice.
J Clin Invest, 121(2):554-68, 2 2011.

Cvetnić Z, Spicić S, Toncić J, Majnarić D, Benić M, Albert D, Thiébaud M, Garin-Bastuji B: Brucella suis infection in domestic pigs and wild boar in Croatia.Rev Sci Tech. 2009 Dec;28(3):1057-67.


Nicoletti P: Brucellosis: Past, Present and Future. Prilozi. 2010 Jul;31(1):21-32.

Reuter T, Xu W, Alexander TW, Gilroyed BH, Inglis GD, Larney FJ, Stanford K, and McAllister TA.
Biocontained carcass composting for control of infectious disease outbreak in livestock.
J Vis Exp, 6(39):pii 1946, 5 2010.

Guan J, Chan M, Grenier C, Brooks BW, Spencer JL, Kranendonk C, Copps J, and Clavijo A.
Degradation of foot-and-mouth disease virus during composting of infected pig carcasses.
Can J Vet Res, 74(1):40-4, 1 2010.

Sakar S, Yetilmezsoy K, and Kocak E.
Anaerobic digestion technology in poultry and livestock waste treatment-a literature review.
Waste Manag Res, 27(1):3-18, 2 2009.

van der Poel WH, Lina PH, and Kramps JA.
Public health awareness of emerging zoonotic viruses of bats: a european perspective.
Vector Borne Zoonotic Dis, 6(4):315-24, 2006.

Klug BJ, Turmelle AS, Ellison JA, Baerwald EF, and 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, 47(1):64-77, 1 2011.

Megali A, Yannic G, Zahno ML, Brügger D, Bertoni G, Christe P, and Zanoni R.
Surveillance for european bat lyssavirus in swiss bats.
Arch Virol, 155(10):1655-62, 10 2010.

Freuling C, Grossmann E, Conraths FJ, Schameitat A, Kliemt J, Auer E, Greiser-Wilke I, and Müller T.
First isolation of eblv-2 in germany.
Vet Microbiol, 131(1-2):26-34, 9 2008.

Li L, Victoria JG, Wang C, Jones M, Fellers GM, Kunz TH, and Delwart E.
Bat guano virome: predominance of dietary viruses from insects and plants plus novel mammalian viruses.
84(14):6955-65, 7 2010.

Rihtaric D, Hostnik P, Steyer A, Grom J, and Toplak I.
Identification of sars-like coronaviruses in horseshoe bats (rhinolophus hipposideros) in slovenia.
Arch Virol, 155(4):507-14, 4 2010.

Foley J, Clifford D, Castle K, Cryan P, and Ostfeld RS.
Investigating and managing the rapid emergence of white-nose syndrome, a novel, fatal, infectious disease of hibernating bats.
Conserv Biol, 2 2011.

Wong S, Lau S, Woo P, and Yuen KY.
Bats as a continuing source of emerging infections in humans.
Rev Med Virol, 17(2):67-91, Mar-Apr 2007.

Kobinger GP, Leung A, Neufeld J, Richardson JS, Falzarano D, Smith G, Tierney K, Patell A, and Weingart HM.
Replication, pathogenicity, shedding, and transmission of zaire ebolavirus in pigs.
Journal of Infectious Diseases, 2011.

Otranto D and Dantas-Torres F.
Canine and feline vector-borne diseases in italy: current situation and perspectives.
Parasit Vectors, 3(2), 1 2010.

Beeler E, Abramowicz KF, Zambrano ML, Sturgeon MM, Khalaf N, Hu R, Dasch GA, and Eremeeva ME.
A focus of dogs and rickettsia massiliae-infected rhipicephalus sanguineus in california.
Am J Trop Med Hyg, 84(2):244-9, 2 2011.

Beati L and Raoult D.
New spotted fever group rickettsia rickettsia massiliae sp. nov., a new spotted fever group rickettsia.
International Journal of Systematic Bacteriology, 43(4):839-840, 1993.

Dvoraková HM and Dvorácková M.
Babesiosis, a little known zoonosis.
Epidemiol Mikrobiol Imunol, 56(4):176-80, 11 2007.

Irwin PJ.
Canine babesiosis.
Vet Clin North Am Small Anim Pract, 40(6):1141-56, 11 2010.

Ramharter M, Walochnik J, Lagler H, Winkler S, Wernsdorfer WH, Stoiser B, and Graninger W.
Clinical and molecular characterization of a near fatal case of human babesiosis in austria.
J Travel Med, 17(6):416-8, 11-12 2010.

Hamaguchi K, Ike K, Yamazaki Y, Morita T, and Imai S.
Influence of zinc deficiency to the mice infected with babesia microti.
J Vet Med Sci, 19 2010.

Hamaguchi K, Ike K, Yamamoto R, Morita T, and Imai S.
Influence of zinc deficiency to the rats infected with babesia rodhaini.
J Vet Med Sci, 71(8):1085-8, 8 2009.

Zygner W, Baska P, Wiśniewski M, and Wedrychowicz H.
The molecular evidence of babesia microti in hard ticks removed from dogs in warsaw (central poland).
Pol J Microbiol, 59(2):95-7, 2010.

Franke J, Meier F, Moldenhauer A, Straube E, Dorn W, and Hildebrandt A.
Established and emerging pathogens in ixodes ricinus ticks collected from birds on a conservation island in the baltic sea.
Med Vet Entomol, 24(4):425-32, 12 2010.

Salvagni CA, Dagnone AS, Gomes TS, Mota JS, Baldani CD Andrade G AND, and Machado RZ.
Serologic evidence of equine granulocytic anaplasmosis in horses from central west brazil.
Rev Bras Parasitol Vet, 19(3):135-40, Jul-Sep 2010.

Hildebrandt A, Pauliks K, Sachse S, and Straube E.
Coexistence of borrelia spp. and babesia spp. in ixodes ricinus ticks in middle germany.
Vector Borne Zoonotic Dis, 10(9):831-7, 11 2010.

Iori A, Gabrielli S, Calderini P, Moretti A, Pietrobelli M, Tampieri MP, Galuppi R, and Cancrini G.
Tick reservoirs for piroplasms in central and northern italy.
Vet Parasitol, 170(3-4):291-6, 6 2010.

Howden KJ, Geale DW, Paré J, Golsteyn-Thomas EJ, and Gajadhar AA.
An update on bovine anaplasmosis (anaplasma marginale) in canada.
Can Vet J., 51(8):, 8 2010.

Aubry P and Geale DW.
A review of bovine anaplasmosis:.
Transbound Emerg Dis, 58(1):1-30, 2 2011.

Anaplasma phagocytophilum - the most widespread tick-borne infection in animals in europe.
Vet Res Commun, Suppl 1:79-84, 8 207.

Oliveira JB, Montoya J, Romero JJ, Urbina A, Soto-Barrientos N, Melo ES, Ramos CA, and Araújo FR.
Epidemiology of bovine anaplasmosis in dairy herds from costa rica.
Vet Parasitol, 12 2010.

Katargina O, Geller J, Alekseev A, Dubinina H, Efremova G, Mishaeva N, Vasilenko V, Kuznetsova T, Järvekülg L, Vene S, Lundkvist A, and Golovljova I.
Identification of anaplasma phagocytophilum in tick populations in estonia, european part of russia and belarus.
Clin Microbiol Infect, 1 2011.

Ismail N, Bloch KC, and McBride JW.
Human ehrlichiosis and anaplasmosis.
Clin Lab Med, 30(1):261-92, 3 2010.

Woldehiwet Z.
Anaplasma phagocytophilum in ruminants in europe.
Ann N Y Acad Sci, 1078:446-60, 10 2006.

Thomas S, Popov VL, and Walker DH.
Exit mechanisms of the intracellular bacterium ehrlichia.
PLoS One, 5(12):e15775, 12 2010.

Hayes EB.
Looking the other way: preventing vector-borne disease among travellers to the united states.
Travel Med Infect Dis, 8(5):277-84, 9 2010.

Little SE.
Ehrlichiosis and anaplasmosis in dogs and cats.
Vet Clin North Am Small Anim Pract, 40(6):1121-40, 11 2010.

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, and von Loewenich FD.
Distinct host species correlate with anaplasma phagocytophilum anka gene.
J Clin Microbiol, 12 2010.

Ravnik U, Tozon N, Smrdel KS, and Zupanc TA.
Anaplasmosis in dogs: The relation of haematological, biochemical and clinical alterations to antibody titre and pcr confirmed infection.
Vet Microbiol, 10 2010.

Hornok S, Micsutka A, Fernández de Mera IG, Meli ML, Gönczi E, Tánczos B, Mangold AJ, Farkas R, Lutz H, Hofmann-Lehmann R, and de la Fuente J.
Fatal bovine anaplasmosis in a herd with new genotypes of anaplasma marginale, anaplasma ovis and concurrent haemoplasmosis.
Res Vet Sci, 11 2010.

Imai DM, Barr BC, Daft B, Bertone JJ, Feng S, Hodzic E, Johnston JM, Olsen KJ, and Barthold SW.
Lyme neuroborreliosis in 2 horses.
Vet Pathol, 2 2011.

Savić S, Vidić B, Lazić S, Lako B, Potkonjak A, and Lepsanović Z:.
Borrelia burgdorferi in ticks and dogs in the province of vojvodina, serbia.
Parasite, 17(4):357-61, 12 2010.

Tijsse-Klasen E, Jacobs JJ, Swart A, Fonville M, Reimerink JH, Brandenburg AH, van der Giessen JW, Hofhuis A, and Sprong H.
Small risk of developing symptomatic tick-borne diseases following a tick bite in the netherlands.
Parasit Vectors, 4(1):17, 2 2011.

Poland GA.
Vaccines against lyme disease: What happened and what lessons can we learn?
Clin Infect Dis, 52(suppl 3):s253-8, 2 2011.

Shen AK, Mead PS, and Beard CB.
The lyme disease vaccine-a public health perspective.
Clin Infect Dis, 52(Suppl 3):s247-52, 2 2011.

Nardelli DT, Munson EL, Callister SM, and Schell RF.
Human lyme disease vaccines: past and future concerns.
Future Microbiol, 4(4):457-69, 5 2009.

Masters EJ, Grigery CN, and Masters RW.
Stari or masters disease: Lone star tick-vectored lyme-like illness.
Infect Dis Clin North Am, 22(2):361-76,vii, 6 2008.

Vaughn MF, Sloane PD, Knierim K, Varkey D, Pilgard MA, and 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, 23:720-7, Nov-Dec 2010.

Southern tick-associated rash illness.
Centers for Disease Control and Prevention CDC.

Assous MV and Wilamowski A.
Relapsing fever borreliosis in eurasia-forgotten, but certainly not gone!
Clin Microbiol Infect, 15(5):407-14, 5 2009.


Komitova R, Nenova R, Padeshki P, Ivanov I, Popov V, and Petrov P.
Tularemia in bulgaria 2003-2004.
J Infect Dev Ctries, 4(11):689-94, 11 2010.

O'Connell HA, Rose LJ, Shams AM, Arduino MJ, and Rice EW.
Chlorine disinfection of francisella tularensis.
Lett Appl Microbiol, 52(1):84-6, 1 2011.

Lo N, Beninati T, Sacchi L, Genchi C, and Bandi C.
Emerging rickettsioses.
Parassitologia, 46(1-2):123-6, 6 2004.

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, and Eremeeva ME.
Rickettsia 364d: a newly recognized cause of eschar-associated illness in california.
Clin Infect Dis, 50(4):541-8, 2 2010.

Wikswo ME, Hu R, Dasch GA, Krueger L, Arugay A, Jones K, Hess B, Bennett S, Kramer V, and Eremeeva ME.
Detection and identification of spotted fever group rickettsiae in dermacentor species from southern california.
J Med Entomol, 45(3):509-16, 5 2008.

Gern L, Lienhard R, and Péter O.
Diseases and pathogenic agents transmitted by ticks in switzerland.
Rev Med Suisse, 6(266):1906-9, 10 2010.


Jääskeläinen AE, Tonteri E, Sironen T, Pakarinen L, Vaheri A, and Vapalahti O.
European subtype tick-borne encephalitis virus in ixodes persulcatus ticks.
Emerg Infect Dis, 17(2):323-5, 2 2011.

Jääskeläinen AE, Sironen T, Murueva GB, Subbotina N, Alekseev AN, Castrén J, Alitalo I, Vaheri A, and Vapalahti O:.
Tick-borne encephalitis virus in ticks in finland, russian karelia and buryatia.
J Gen Virol, (Pt 11):2706-12, 11 2010.

Yun SM, Kim SY, Ju YR, Han MG, Jeong YE, and Ryou J.
First complete genomic characterization of two tick-borne encephalitis virus isolates obtained from wild rodents in south korea.
Virus Genes, 2 2011.

Rift valley fever. fact sheet nr 207.
WHO Media Centre, 2010.

Turell MJ, Dohm DJ, Geden CJ, Hogsette JA, and Linthicum KJ.
Potential for stable flies and house flies (diptera: Muscidae) to transmit rift valley fever virus.
J Am Mosq Control Assoc, 26(4):445-8, 12 2010.

Chapman DAG, Darby AC, Da Silva M, Upton C, Radford AD, and Dixon LK.
Genomic analysis of highly virulent isolate of african swine fever virus.
Emerg Infect Dis, 4 2011.

Scientific opinion on african swine fever.
EFSA Journal, 8(3):1556(149pp.), 2010.

Yeh JY, Kim HJ, Nah JJ, Lee H, Kim YJ, Moon JS, Cho IS, Choi IS, Song CS, and Lee JB.
Surveillance for west nile virus in dead wild birds, south korea, 2005-2008.
Emerg Infect Dis, 17(2):299-301, 2 2011.

Stock I.
Chikungunya fever-expanded distribution of a re-emerging tropical infectious disease.
Med Monatsschr Pharm, 32(17-26):1, 1 2009.

Ho K, Ang LW, Tan BH, Tang CS, Ooi PL, and James L.
Epidemiology and control of chikungunya fever in singapore.
J Infect, 2 2011.

Pleadin J, Vulić A, Persi N, and Vahcić N.
Clenbuterol residues in pig muscle after repeat administration in a growth-promoting dose.
Meat Sci, 86(3):733-7, 11 2010.

Wada seeks tainted beef info from china. 24.12.2011.
China Post.

Liu C, Ling W, Xu W, and Chai Y.
Simultaneous determination of 20 beta-agonists in pig muscle and liver by high-performance liquid chromatography/tandem mass spectrometry.
J AOAC Int, 94(2):420-7, Mar-Apr 2011.

Eudmar Marcolino de Assis Junior, Ismael Malaquias dos Santos Fernandes, Caio Sérgio Santos, Luciene Xavier de Mesquita, Rogério Aparecido Pereira, Patrício Borges Maracajá, and Benito Soto-Blanco.
Brazil- toxicity of castor bean (ricinus communis) pollen to honeybees.
Agriculture, Ecosystems and Environment, 141(1-2):221-223, 4 2011.

Honey containing gm needs approval before sale. european voice. 09.02.2011.. .

Das deutsche gentechnikrecht. bundesministerium für ernährung, landwirtschaft und verbraucherschutz.

Honig. unverkäuflich durch gen-tech-pollen? ökotest.

Honey and food supplements containing pollen derived from a gmo are foodstuffs produced from gmos which cannot be marketed without prior authorisation. court of justice of the european union. press release no 79/11 luxembourg, 6 september 2011.

Eu bans gm-contaminated honey from general sale.07 sep 2011. bavarian beekeepers forced to declare their honey as genetically modified because of contamination from nearby monsanto crops.
The Guardian.

Memo/11/451 date 24/06/2011 europa rapid press.

Wikileaks: Us targets eu over gm crops the guardian. 03 jan 2011.

Us asks turkey to change gmo regulation, daily says daily news 29 november 2011.

The uk needs a labelling scheme for gm-free meat products.

Peru bans gmo.

Gates foundation "swimming against a tide of informed opinion" 31 oct 2011.

Böhnel H, Schwagerick B, and Gessler F.
Visceral botulism - a new form of bovine clostridium botulinum toxication.
J Vet Med A Physiol Pathol Clin Med, 48(6):373-83, 8 2001.

Böhnel H, Behrens S, Loch P, Lube K, and Gessler F.
Is there a link between infant botulism and sudden infant death? bacteriological results obtained in central germany.
Eur J Pediatr, 160(19):623-8, 10 2001.

Fischer D, Freislederer A, and Jorch G.
Sudden death of twins: botulism because of contamination by pap vegetables.
Klin Padiatr, 216(1):31-5, Jan-Feb 2004.

Bartram U and Singer D.
Infant botulism and sudden infant death syndrome.
Klin Padiatr, 216(1):26-30, Jan-Feb 2004.

Lindström M, Myllykoski J, Sivelä S, and Korkeala H.
Clostridium botulinum in cattle and dairy products.
Crit Rev Food Sci Nutr, 50(4), 4 2010.

Botulismus: Wie gefährlich ist hühnertrockenkot? ndr 06 feb 2012.

Botulismus krank durch biogas. ein gespräch mit dem tiermediziner und agrarwissenschaftler professor helge böhnel dradio. 09.06.2011.

Von biogasanlagen geht keine botulismus-gefahr aus. 13 dez 2011.
Fleckvieh, 1, 12 2011.

Botulismus. ballensilage. com.

Fontanari GG, Batistuti JP, da Cruz RJ, Saldivan PHN, and Ar$\hat{e}$as JAG.
Cholesterol-lowering effect of whole lupin (Lupinus albus) seed and its protein isolate, 132(3):1521-1526, 6 2012.

Laudadio V and Tufarelli V.
Dehulled-micronised lupin (lupinus albus l. cv. multitalia) as the main protein source for broilers: influence on growth performance, carcass traits and meat fatty acid composition.
J Sci Food Agric, 91(11):2081-7, 8 2011.

Volek Z and Marounek M.
Effect of feeding growing-fattening rabbits a diet supplemented with whole white lupin (lupinus albus cv. amiga) seeds on fatty acid composition and indexes related to human health in hind leg meat and perirenal fat.
Meat Sci, 87(1):40-5, 1 2011.

Kouba M and Mourot J.
A review of nutritional effects on fat composition of animal products with special emphasis on n-3 polyunsaturated fatty acids.
Biochimie, 93(1):13, 1 2011.

Allen JG and Randall AG.
The clinical biochemistry of experimentally produced lupinosis in the sheep.
Aust Vet J, pages 283-8, 8 1993.

Culvenor CC, Beck AB, Clarke M, Cockrum PA, Edgar JA, Frahn JL, Jago MV, Lanigan GW, Payne AL, Peterson JE, Petterson DS, Smith LW, and White RR.
Isolation of toxic metabolites of phomopsis leptostromiformis responsible for lupinosis.
Aust J Biol Sci, 30(4):269-77, 8 1977.

137 resource portal for lupins.

13 lupinosis.

Soler Rodriguez F, Miguez Santiyan MP, Pedrera Zamorano JD, and Roncero Cordero V.
An outbreak of lupinosis in sheep.
Vet Hum Toxicol, 33(5):492-4, 10 1991.

Lupinosis is a risk to stock. the rural 03 feb, 2011.

Magni C, Sessa F, Tedeschi G, Negri A, Scarafoni A, Consonni A, and Duranti M.
Identification in lupin seed of a serine-endopeptidase activity cleaving between twin arginine pairs and causing limited proteolysis of seed storage proteins.
Mol Plant, 1 2012.

Humblet MF, Vandeputte S, Albert A, Gosset C, Kirschvink N, Haubruge E, Fecher-Bourgeois F, Pastoret PP, and Saegerman C.
Multidisciplinary and evidence-based method for prioritizing diseases of food-producing animals and zoonoses.
Emerg Infect Dis, 18(4), 4 2012.

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