the new forest were seropositive, as were between 2% and 4–5% of the general local population of the area. tests on pet dogs carried out throughout the country in 2009 indicated that around 2.5% of ticks in the uk may be infected, considerably higher than previously thought. it is speculated that global warming may lead to an increase in tick activity in the future, as well as an increase in the amount of time that people spend in public parks, thus increasing the risk of infection. however no published research has proven this to be so. north america many studies in north america have examined ecological and environmental correlates of the number of people affected by lyme disease. a 2005 study using climate suitability modelling of i. scapularis projected that climate change would cause an overall 213% increase in suitable vector habitat by 2080, with northward expansions in canada, increased suitability in the central u.s., and decreased suitable habitat and vector retraction in the southern u.s. a 2008 review of published studies concluded that the presence of forests or forested areas was the only variable that consistently elevated the risk of lyme disease whereas other environmental variables showed little or no concordance between studies. the authors argued that the factors influencing tick density and human risk between sites are still poorly understood, and that future studies should be conducted over longer time periods, become more standardized across regions, and incorporate existing knowledge of regional lyme disease ecology. canada the range of ticks able to carry lyme disease has expanded from a limited area of ontario to include areas of southern quebec, manitoba, northern ontario, southern new brunswick, southwest nova scotia and limited parts of saskatchewan and alberta, as well as british columbia. cases have been reported as far east as the island of newfoundland. a model-based prediction by leighton et al. (2012) suggests that the range of the i. scapularis tick will expand into canada by 46 km/year over the next decade, with warming climatic temperatures as the main driver of increased speed of spread. mexico a 2007 study suggests borrelia burgdorferi infections are endemic to mexico, from four cases reported between 1999 and 2000. united states cdc map showing the risk of lyme disease in the united states, particularly its concentration in the northeast megalopolis and western wisconsin lyme disease is the most common tick-borne disease in north america and europe, and one of the fastest-growing infectious diseases in the united states. of cases reported to the united states cdc, the ratio of lyme disease infection is 7.9 cases for every 100,000 persons. in the ten states where lyme disease is most common, the average was 31.6 cases for every 100,000 persons for the year 2005. although lyme disease has been reported in all states due to travel-associated infections, about 99% of all reported cases are confined to just five geographic areas (new england, mid-atlantic, east-north central, south atlantic, and west north-central). cdc implemented national surveillance of lyme disease cases in 1991. since then, reporting criteria has been modified multiple times. the 2022 surveillance case definition classifies cases as confirmed, probable, and suspect. cdc emphasizes that, while surveillance data has limitations, it is useful due to "uniformity, simplicity, and timeliness." while cases are under-reported in high-incidence areas, over-reporting is likely in low-incidence areas. additionally, surveillance cases are reported by county of residence and not where an infection was necessarily contracted. the number of reported cases of the disease has been increasing, as are endemic regions in north america. for example, b. burgdorferi sensu lato was previously thought to be hindered in its ability to be maintained in an enzootic cycle in california, because it was assumed the large lizard population would dilute the number of people affected by b. burgdorferi in local tick populations; this has since been brought into question, as some evidence has suggested lizards can become infected. except for one study in europe, much of the data implicating lizards is based on dna detection of the spirochete and has not demonstrated that lizards are able to infect ticks feeding upon them. as some experiments suggest lizards are refractory to infection with borrelia, it appears likely their involvement in the enzootic cycle is more complex and species-specific. while b. burgdorferi is most associated with ticks hosted by white-tailed deer and white-footed mice, borrelia afzelii is most frequently detected in rodent-feeding vector ticks, and borrelia garinii and borrelia valaisiana appear to be associated with birds. both rodents and birds are competent reservoir hosts for b. burgdorferi sensu stricto. the resistance of a genospecies of lyme disease spirochetes to the bacteriolytic activities of the alternative complement pathway of various host species may determine its reservoir host association. several similar but apparently distinct conditions may exist, caused by various species or subspecies of borrelia in north america. a regionally restricted condition that may be related to borrelia infection is southern tick-associated rash illness (stari), also known as masters disease. amblyomma americanum, known commonly as the lone-star tick, is recognized as the primary vector for stari. in some parts of the geographical distribution of stari, lyme disease is quite rare (e.g., arkansas), so people in these regions experiencing lyme-like symptoms—especially if they follow a bite from a lone-star tick—should consider stari as a possibility. it is generally a milder condition than lyme and typically responds well to antibiotic treatment. in recent years there have been 5 to 10 cases a year of a disease similar to lyme occurring in montana. it occurs primarily in pockets along the yellowstone river in central montana. people have developed a red bull's-eye rash around a tick bite followed by weeks of fatigue and a fever. lyme disease effects are comparable among males and females. a wide range of age groups is affected, though the number of cases is highest among 10- to 19-year-olds. for unknown reasons, lyme disease is seven times more common among asians. south america in brazil, a lyme-like disease known as baggio–yoshinari syndrome was identified, caused by microorganisms that do not belong to the b. burgdorferi sensu lato complex and transmitted by ticks of the amblyomma and rhipicephalus genera. the first reported case of bys in brazil was made in 1992 in cotia, são paulo. etymology lyme disease was diagnosed as a separate condition for the first time in 1975 in lyme, connecticut. outside of the us and english-speaking world, the disease is known as borreliosis. history the evolutionary history of borrelia burgdorferi genetics has been the subject of recent studies. one study has found that prior to the reforestation that accompanied post-colonial farm abandonment in new england and the wholesale migration into the mid-west that occurred during the early 19th century, lyme disease was present for thousands of years in america and had spread along with its tick hosts from the northeast to the midwest. john josselyn, who visited new england in 1638 and again from 1663 to 1670, wrote "there be infinite numbers of ticks hanging upon the bushes in summertime that will cleave to man's garments and creep into his breeches, eating themselves in a short time into the very flesh of a man. i have seen the stockings of those that have gone through the woods covered with them." this is also confirmed by the writings of peter kalm, a swedish botanist who was sent to america by linnaeus, and who found the forests of new york "abound" with ticks when he visited in 1749. when kalm's journey was retraced 100 years later, the forests were gone and the lyme bacterium had probably become isolated to a few pockets along the northeast coast, wisconsin, and minnesota. perhaps the first detailed description of what is now known as lyme disease appeared in the writings of john walker after a visit to the island of jura (deer island) off the west coast of scotland in 1764. he gives a good description both of the symptoms of lyme disease (with "exquisite pain the interior parts of the limbs") and of the tick vector itself, which he describes as a "worm" with a body which is "of a reddish color and of a compressed shape with a row of feet on each side" that "penetrates the skin". many people from this area of great britain emigrated to north america between 1717 and the end of the 18th century. the examination of preserved museum specimens has found borrelia dna in an infected ixodes ricinus tick from germany that dates back to 1884, and from an infected mouse from cape cod that died in 1894. the 2010 autopsy of ötzi the iceman, a 5,300-year-old mummy, revealed the presence of the dna sequence of borrelia burgdorferi making him the earliest known human with lyme disease. the early european studies of what is now known as lyme disease described its skin manifestations. the first study dates to 1883 in breslau, germany (now wrocław, poland), where physician alfred buchwald described a man who for 16 years had had a degenerative skin disorder now known as acrodermatitis chronica atrophicans. at a 1909 research conference, swedish dermatologist arvid afzelius presented a study about an expanding, ring-like lesion he had observed in an older woman following the bite of a sheep tick. he named the lesion erythema migrans. the skin condition now known as borrelial lymphocytoma was first described in 1911. the modern history of medical understanding of the disease, including its cause, diagnosis, and treatment, has been difficult. neurological problems following tick bites were recognized starting in the 1920s. french physicians garin and bujadoux described a farmer with a painful sensory radiculitis accompanied by mild meningitis following a tick bite. a large, ring-shaped rash was also noted, although the doctors did not relate it to the meningoradiculitis. in 1930, the swedish dermatologist sven hellerström was the first to propose em and neurological symptoms following a tick bite were related. in the 1940s, german neurologist alfred bannwarth described several cases of chronic lymphocytic meningitis and polyradiculoneuritis, some of which were accompanied by erythematous skin lesions. carl lennhoff, who worked at the karolinska institute in sweden, believed many skin conditions were caused by spirochetes. in 1948, he used a special stain to microscopically observe what he believed were spirochetes in various types of skin lesions, including em. although his conclusions were later shown to be erroneous, interest in the study of spirochetes was sparked. in 1949, nils thyresson, who also worked at the karolinska institute, was the first to treat aca with penicillin. in the 1950s, the relationship among tick bite, lymphocytoma, em and bannwarth's syndrome was recognized throughout europe leading to the widespread use of penicillin for treatment in europe. in 1970, a dermatologist in wisconsin named rudolph scrimenti recognized an em lesion in a person after recalling a paper by hellerström that had been reprinted in an american science journal in 1950. this was the first documented case of em in the united states. based on the european literature, he treated the person with penicillin. the full syndrome now known as lyme disease was not recognized until a cluster of cases originally thought to be juvenile rheumatoid arthritis was identified in three towns in southeastern connecticut in 1975, including the towns lyme and old lyme, which gave the disease its popular name. this was investigated by physicians david snydman and allen steere of the epidemic intelligence service, and by others from yale university, including stephen malawista, who is credited as a co-discover of the disease. the recognition that the people in the united states had em led to the recognition that "lyme arthritis" was one manifestation of the same tick-borne condition known in europe. before 1976, the elements of b. burgdorferi sensu lato infection were called or known as tick-borne meningopolyneuritis, garin-bujadoux syndrome, bannwarth syndrome, afzelius's disease, montauk knee or sheep tick fever. since 1976 the disease is most often referred to as lyme disease, lyme borreliosis or simply borreliosis. in 1980, steere, et al., began to test antibiotic regimens in adults with lyme disease. in the same year, new york state health dept. epidemiologist jorge benach provided willy burgdorfer, a researcher at the rocky mountain biological laboratory, with collections of i. dammini from shelter island, new york, a known lyme-endemic area as part of an ongoing