||Clinical manifestations of infections by encephalomyocarditis virus (EMCV), belonging to the genus cardiovirus of the family Picomaviridae, emerged in European pig farms in the nineties. Two types of clinical disease were noticed, acute myocarditis, usually in young piglets, and reproductive failure in sows. To understand its relevance in pigs and develop hypotheses on the origin, cause and nature of infection, the occurrence of EMCV infections was studied in domestic pigs in several European countries. In addition, virus spread in pigs and rats as well as risk factors for clinical appearance of EMCV in domestic pig farms were studied to increase our knowledge of the disease and support its prevention and control. Although outbreaks appeared to be clustered in endemic areas, infection usually was restricted to individual farms. The seroprevalence varied considerably among farms, age categories and countries, while sub-clinical infection with EMCV was quite common. The variable clinical picture in pigs in literature was ascribed to the pathogenicity of the EMCV strains, the available infectious dose and/or the susceptibility of the pigs (age, breed). Local rodent populations were often suggested responsible for the observed clustering and re-occurrence in farms. A matched case-control study on risk factors inducing clinical EMCV revealed the presence of mice (OR = 8.3) as a risk factor. The transmission of a myocardial EMC V-strain in fattening piglets was quantified by the basic reproduction ratio (R0) both from experiments (Ro=1.24, 95%-CI = 0.39 - 4.35) and field data (Ro=1.36, 95%-CI 0.93-2.23). Although these results suggested that EMCV transmission among pigs in most cases will be limited (Ro close to 1), both studies remained inconclusive with respect to the threshold value of R0=l. Therefore it could not be concluded whether EMCV could persist in a pig population by pig-to-pig transmission alone (i.e. Ro>l). To estimate the transmission in a compartmentalised house setting without possible interference of multiple transmission routes (field), a stochastic simulation model was developed to extrapolate the experimental results to a compartmentalised pig house setting with 22 pens. The introduction of virtual fences in itself already reduced EMCV spread by avoiding random mixing and for any R0<1.24 the probability to observe outbreaks affecting at least 50% of the pens(major outbreaks) remained below 0.10. When contact transmission was limited by an increasing fence effect (reducing contacts between pens), the probability to observe major outbreaks was reduced to about 0.50 for any Ro<2.7. These results indicated that pigs should not be considered the main reservoir host for EMCV in compartmentalised pig farms. Additionally, EMCV transmission in rats was experimentally quantified at R0>9.9. These findings indicated that the virus can spread and persist easily within a rat population by horizontal rat-to-rat transmission alone, which made the rat population to a potential reservoir for EMCV and a probable transmitter of EMCV into domestic pig farms. In conclusion, multiple EMCV introductions by e.g. rodents or indirect transmission routes (by manure, farmer, rodents) most probably are required to explain major outbreaks divided over many pens in commercial pig houses. Therefore the observed (temporary) emergence of EMCV in domestic pig farms most likely had a multi factorial cause mediated by the EMCV-strain type involved, the infection status of local rodent populations, the contact structure between local rodent populations and domestic pigs and individual pig factors (susceptibility due to age or breed). To prevent or control future EMCV outbreaks in pig farms, farmers should avoid contacts between potentially infected rodent populations (active rodent control), maintain high levels of bio security and isolate diseased pigs immediately.