Billy the Kid

Billy the Kid, also known as William Henry McCarty, Henry Antrim and William H. Bonney (Allegedly November 23, 1859 – c. July 14, 1881) was a 19th-century American frontier outlaw and gunman who participated in the Lincoln County War. According to legend, he killed 21 men, but he is generally accepted to have killed between four and nine.

McCarty (or Bonney, the name he used at the height of his notoriety) was 5 feet 8 inches (173 cm) to 5 feet 9 inches (175 cm) tall with blue eyes, a smooth complexion, and prominent front teeth. He was said to be friendly and personable at times, and many recalled that he was as "lithe as a cat". Contemporaries described him as a "neat" dresser who favored an "unadorned Mexican sombrero".These qualities, along with his cunning and celebrated skill with firearms, contributed to his paradoxical image, as both a notorious outlaw and beloved folk hero.

Relatively unknown during most of his lifetime, Bonney was catapulted into legend a few months before his death by New Mexico's governor, Lew Wallace, who placed a price on his head, and by stories printed in the Las Vegas Gazette (Las Vegas, New Mexico) and the New York Sun. Many other newspapers followed suit and published stories about Billy the Kid's exploits. After his death, several biographies were written that portrayed the Kid in varying lights.

Early life

Little is known about McCarty's origins, but some scholars of western history "contend that he was born on the eve of the Civil War in the bowels of an Irish neighborhood in New York City" (at 70 Allen Street). If indeed his birthplace was New York, no records that can prove beyond a reasonable doubt that he ever lived there have ever been uncovered". While his biological father remains an obscure figure, some researchers have theorized that his name was Patrick McCarty, Michael McCarty, William McCarty, or Edward McCarty. There is clear evidence that his mother's name was Catherine McCarty, although "there have been continuing debates about whether McCarty was her maiden or married name".According to some accounts, McCarty was born as William Henry McCarty, Jr., but his mother preferred to call him "Henry" because she did not wish him to be known as "Junior". It is believed that McCarty's mother was a survivor of the Great Famine. By 1868, Catherine McCarty had moved with her two young sons, Henry and Joseph, to Indianapolis, Indiana. There, she met William Antrim, who was 12 years her junior. In 1873, after several years of moving around the country, the two were married at the First Presbyterian Church in Santa Fe, New Mexico, and settled further south in Silver City. Antrim found sporadic work as a bartender and carpenter but soon became more interested in prospecting and gambling for fortune than in his wife and stepsons. Nevertheless, young McCarty often used the surname "Antrim" when referring to himself.

Faced with a husband who was frequently absent, McCarty's mother reportedly washed clothes, baked pies, and took in boarders in order to provide for her sons. Although she was fondly remembered by onetime boarders and neighbors as "a jolly Irish lady, full of life and mischief", she was already in the final stages of tuberculosis when the family reached Silver City. The following year, on September 16, 1874, Catherine McCarty died; she was buried in the Memory Lane Cemetery in Silver City. At age 14, McCarty was taken in by a neighboring family who operated a hotel where he worked to pay for his keep. The manager was impressed by the youth, contending that he was the only young man who ever worked for him that did not steal anything. One of McCarty's school teachers later recalled that the young orphan was "no more of a problem than any other boy, always quite willing to help with chores around the schoolhouse". Early biographers sought to explain McCarty's subsequent descent into lawlessness by focusing on his habit of reading dime novels that romanticized crime. A more likely explanation, however, was his slender physique, "which placed him in precarious situations with bigger and stronger boys".

Forced to seek new lodgings when his foster family began to experience "domestic problems", McCarty moved into a boarding house and pursued odd jobs. In April 1875, McCarty was arrested by Grant County Sheriff Harvey Whitehill, after McCarty stole some cheese. On September 24, 1875, McCarty was again arrested when he was found in possession of clothing and firearms that a fellow boarder had stolen from a Chinese laundry owner. Two days after McCarty was placed in jail, the teenager escaped by worming his way up the jailhouse chimney. From that point on, McCarty was more or less a fugitive.According to some accounts, he eventually found work as an itinerant ranch hand and shepherd in southeastern Arizona. In 1876, he settled in the vicinity of Fort Grant Army Post in Arizona, where he worked local ranches and tested his skills at local gaming houses. Sheriff Whitehill would later say that he liked the boy, and his acts of theft were more due to necessity than wantonness.

During this time, McCarty became acquainted with John R. Mackie, a Scottish-born ex-cavalry private with a criminal bent. The two men supposedly became involved in the risky, but profitable, enterprise of horse thievery; and McCarty, who targeted local soldiers, became known by the sobriquet of "Kid Antrim".Biographer Robert M. Utley writes that the nickname arose because of McCarty's "slight build and beardless countenance, his young years, and his appealing personality". In 1877, McCarty was involved in an altercation with the civilian blacksmith at Fort Grant, an Irish immigrant named Frank "Windy" Cahill, who took pleasure in bullying young McCarty. On August 17, Cahill reportedly attacked McCarty after a verbal exchange and threw him to the ground. Reliable accounts suggest McCarty retaliated by drawing his gun and shooting Cahill, who died the next day. The coroner's inquest concluded that McCarty's shooting of Cahill was "criminal and unjustifiable". Some of those who witnessed the incident later claimed that McCarty acted in self-defense. Years later, Louis Abraham, who had known McCarty in Silver City but was not a witness, denied that anyone was killed in this altercation.

In fear of Cahill's friends and associates, McCarty fled Arizona Territory and entered New Mexico Territory. He eventually arrived at the former army post of Apache Tejo, where he joined a band of cattle rustlers who targeted the sprawling herds of cattle magnate John Chisum. During this period, McCarty was spotted by a resident of Silver City, and the teenager's involvement with the notorious gang was mentioned in a local newspaper. It is unclear how long McCarty rode with the gang of rustlers known as the "Jesse Evans Gang", but reliable sources indicate that he soon turned up at Heiskell Jones's house in Pecos Valley, New Mexico. According to this account, Apaches stole McCarty's horse, forcing him to walk many miles to the nearest settlement, which happened to be Jones's home. When he arrived, the young man was supposedly near death, but Mrs. Jones nursed him back to health. The Jones family developed a strong attachment to McCarty and gave him one of their horses. At some point in 1877, McCarty began to refer to himself as "William H. Bonney".

Lincoln County War

In 1877, McCarty (now widely known as William Bonney) moved to Lincoln County, New Mexico, and was first hired by Doc Scurlock and Charlie Bowdre to work in their cheese factory.Through them he met Frank Coe, George Coe and Ab Saunders, three cousins who owned their own ranch near to the ranch of Richard Brewer. After a short stint working on the ranch of Henry Hooker, McCarty began working on the Coe-Saunders ranch.

Late in 1877, McCarty, along with Brewer, Bowdre, Scurlock, the Coes and the Saunders, was hired as a cattle guard by John Tunstall, an English cattle rancher, banker and merchant, and his partner, Alexander McSween, a prominent lawyer. A conflict known today as the Lincoln County War had erupted between the established town merchants, Lawrence Murphy and James Dolan, and competing business interests headed by Tunstall and McSween. Events turned bloody on February 18, 1878, when Tunstall was spotted while driving a herd of nine horses towards Lincoln and murdered by William Morton, Jessie Evans, Tom Hill, and Frank Baker — all members of the Murphy-Dolan faction, and members of a posse sent to attack McSween's holdings.After murdering Tunstall, the gunmen shot down his prized bay horse. "As a wry and macabre joke on Tunstall's great affection for horses, the dead bay's head was then pillowed on his hat", writes Frederick Nolan, Tunstall's biographer. Although members of the Murphy-Dolan faction sought to frame Tunstall's death as a "justifiable homicide", evidence at the scene suggested that Tunstall attempted to avoid a confrontation before he was shot down. Tunstall's murder enraged McCarty and the other ranch hands.

McSween, who abhorred violence, took steps to punish Tunstall's murderers through legal means; he obtained warrants for their arrests from the local justice of the peace John B. Wilson. Tunstall's men formed their own group called the Regulators. After being deputized by Brewer, Tunstall's foreman, who had been appointed a special constable and given the warrant to arrest Tunstall's killers, they proceeded to the Murphy-Dolan store. The wanted men, Bill Morton and Frank Baker, attempted to flee, but they were captured on March 6. Upon returning to Lincoln, the Regulators reported that Morton and Baker had been shot on March 9 near Agua Negra during an alleged escape attempt. During their journey to Lincoln, the Regulators also killed one of their own members, a man named McCloskey, whom they suspected of being a traitor. On the very day that McCloskey, Morton, and Baker were slain, Governor Samuel Beach Axtell arrived in Lincoln County to investigate the ongoing violence. The governor, accompanied by James Dolan and associate John Riley, proved hostile to the faction now headed by McSween. Thus, the Regulators "went from lawmen to outlaws". Notably, Axtell refused to acknowledge the existence of the so-called "Santa Fe Ring", a group of corrupt politicians and business leaders led by U.S. Attorney Thomas Benton Catron. Catron cooperated closely with the Murphy-Dolan faction, which was perceived as part of the notorious "ring".

Unfazed, the Regulators planned to settle a score with Sheriff William J. Brady, who had arrested McCarty and fellow deputy Fred Waite in the aftermath of Tunstall's murder. At the time Brady arrested them, the two men were attempting to serve a warrant on Brady for his suspected role in looting Tunstall's store after the Englishman's death, as well as his posse members for the murder of Tunstall. On April 1, Regulators Jim French, Frank McNab, John Middleton, Fred Waite, Henry Brown and McCarty ambushed Sheriff Brady and his deputy, George W. Hindman, killing them both in Lincoln's main street. McCarty was shot in the thigh while attempting to retrieve a rifle that Brady had seized from him during an earlier arrest. With this move, the McSween faction disillusioned many former supporters, who came to view both sides as "equally nefarious and bloodthirsty".

The connection between McSween and the Regulators was ambiguous, however. McCarty was loyal to the memory of Tunstall, though not necessarily to McSween. There is some doubt as to whether McCarty and McSween were even acquainted at the time of Brady's death.According to a contemporary newspaper account, the Regulators disclaimed "all connection or sympathy with McSween and his affairs" and expressed their sole desire to track down Tunstall's murderers.

On April 4, in what became known as the Gunfight of Blazer's Mills, the Regulators sought the arrest of an old buffalo hunter known as Buckshot Roberts, whom they suspected of involvement in the Tunstall slaying. Roberts refused to be taken alive, even after he suffered a severe bullet wound to the chest. During the gun battle that ensued, Roberts shot and killed the Regulators' leader, Dick Brewer.Four other Regulators were wounded in the skirmish. The incident had the effect of further alienating the public, given that many local residents "admired the way Roberts put up a gutsy fight against overwhelming odds".

Escape from Lincoln

McCarty was transported from Fort Sumner to Las Vegas, where he gave an interview to a reporter from the Las Vegas Gazette. Next, the prisoner was transferred to Santa Fe, where he sent four separate letters over the next three months to Governor Wallace seeking clemency. Wallace, however, refused to intervene, and the Kid's trial was held in April 1881 in Mesilla. On April 9, after two days of testimony, McCarty was found guilty of the murder of Sheriff Brady, the only conviction ever secured against any of the combatants in the Lincoln County War. On April 13, he was sentenced by Judge Warren Bristol to hang.

With his execution scheduled for May 13, McCarty was removed to Lincoln, where he was held under guard by two of Garrett's deputies, James Bell and Robert Ollinger, on the top floor of the town courthouse. On April 28, while Garrett was out of town, McCarty stunned the territory by killing both of his guards and escaping. The details of the escape are unclear. Some researchers believe that a sympathizer placed a pistol in a nearby privy that McCarty was permitted to use, under escort, each day. McCarty retrieved the gun, and turned it on Bell when the pair had reached the top of a flight of stairs in the courthouse. Another theory holds that McCarty slipped off his manacles at the top of the stairs, struck Bell over the head with them, grabbed Bell's own gun, and shot him with it.

Bell staggered into the street and collapsed, mortally wounded. McCarty scooped up Ollinger's 10-gauge double-barrel shotgun. Both barrels had been fully loaded with buckshot earlier by Ollinger himself. The kid waited at the upstairs window for his second guard, who had been across the street with some other prisoners, to respond to the gunshot and come to Bell's aid. As Ollinger came running into view, McCarty leveled the shotgun at him, called out "Hello Bob!" and killed him. The Kid's escape was delayed for an hour while he worked free of his leg irons with a pickax and then the young outlaw mounted a horse and rode out of town, reportedly singing. The horse returned two days later.

Death

Sheriff Pat Garrett offered that he responded to rumors that McCarty was lurking in the vicinity of Fort Sumner almost three months after his escape. Garrett and two deputies set out on July 14, 1881, to question one of the town's residents, a friend of McCarty's named Pete Maxwell (son of land baron Lucien Maxwell). Close to midnight, as Garrett and Maxwell sat talking in Maxwell's darkened bedroom, McCarty unexpectedly entered the room.

There are at least two versions of what happened next. One version suggests that as the Kid entered, he failed to recognize Garrett in the poor light. McCarty drew his pistol and backed away, asking "¿Quién es? ¿Quién es?" (Spanish for "Who is it? Who is it?"). Recognizing McCarty's voice, Garrett drew his own pistol and fired twice, the first bullet striking McCarty in the chest just above his heart, killing him. In a second version, McCarty entered carrying a knife, evidently headed to a kitchen area. He noticed someone in the darkness, and uttered the words, "¿Quién es? ¿Quién es?" at which point he was shot and killed in ambush style. Although the popularity of the first story persists, and portrays Garrett in a better light, some historians contend that the second version is probably the accurate one. A markedly different theory, in which Garrett and his posse set a trap for McCarty, has also been suggested. Most recently explored in the 2004 Discovery Channel documentary, Billy the Kid: Unmasked, this theory contends that Garrett went to the bedroom of Pedro Maxwell's sister, Paulita, and bound and gagged her in her bed. When McCarty arrived, Garrett was waiting behind Paulita's bed and shot the Kid.

According to Garrett, McCarty was buried the next day in Fort Sumner's old military cemetery, between his fallen companions Tom O'Folliard and Charlie Bowdre. A single tombstone was later erected over the graves, giving the three outlaws' names (Billy's as "William H. Bonney") and with a one word epitaph of "Pals" also carved into it. The tombstone has been stolen and recovered three times since it was set in place in the 1940s, and the entire gravesite is now enclosed within a steel cage.

In his book, Billy the Kid: A Short and Violent Life, Robert Utley told the story of Pat Garrett's book effort. In the weeks following Garrett's execution of the Kid, he felt the need to tell his side of the story. Many people had begun to talk about the unfairness of the encounter, so Garrett called upon his friend, Marshall Ashmun Upson, to ghost-write a book with him. Ash Upson was a roving journalist who had a gift for graphic prose. Their collaboration led to a book entitled The Authentic Life of Billy the Kid, which was first published in 1882. The book never sold many copies; however, it eventually proved to be an important reference for historians who would later write about the Kid's life.

Posthumous pardon for Billy the Kid

In 2010, the governor of New Mexico, Bill Richardson, considered a posthumous pardon for McCarty, who had been convicted for killing Sheriff William Brady. The pardon was considered to be a follow-through on a purported promise made by then Governor Lew Wallace in 1879. On December 31, 2010, on the last day of his term in office, Bill Richardson announced on Good Morning America his decision not to pardon McCarty. He cited "historical ambiguity" surrounding the conditions of Lew Wallace's pardon.

Selected references in popular culture

Billy the Kid has been the subject and inspiration for many popular works, including:

Literature

Billy The Kid (1958), a serial poem by Jack Spicer.

Billy the Kid was published in 1962 as an episode in the ongoing adventures of Lucky Luke by Goscinny and Morris.

The Collected Works of Billy the Kid: Left-handed Poems, by Michael Ondaatje, 1970 Governor General's Award-winning biography in the form of experimental poetry.

Added as an immortal to Michael Scott's series Secrets of the Immortal Nicholas Flamel during the third book The Sorceress.

The Illegal Rebirth of Billy the Kid is a science fiction novel by Rebecca Ore, published in 1991.

Anything for Billy is a 1988 novel by Larry McMurtry.

Lucky Billy: a novel about Billy the Kid is a 2008 novel by John Vernon, a professor at Binghamton University.

Film

Billy the Kid, 1930 widescreen film directed by King Vidor and starring Johnny Mack Brown as Billy and Wallace Beery as Pat Garrett

Billy the Kid Returns, 1938: Roy Rogers plays a dual role, Billy the Kid and his dead-ringer lookalike who shows up after the Kid has been shot by Pat Garrett.

Billy the Kid, 1941 remake of the 1930 film, starring Robert Taylor and Brian Donlevy

Buster Crabbe played Billy the Kid in a serial series during 1942 and 1943. The thirteen films included Blazing Frontier, The Renegade, Cattle Stampede, and Western Cyclone (1943).

The Outlaw, Howard Hughes' 1943 motion picture starring Jack Buetel as Billy and featuring Jane Russell in her breakthrough role as the Kid's fictional love interest

The Kid from Texas (1950, Universal International) film starring Audie Murphy--location of title character's place of origin changed to appeal to Texans and capitalize on Murphy association with that state

The Law vs. Billy the Kid (1954, Columbia Pictures Corporation) starring Scott Brady as the Kid, James Griffith as Pat Garrett, Betta St. John as Nita Maxwell, and Alan Hale, Jr. as Bob Ollinger

The Left Handed Gun, Arthur Penn's 1958 motion picture based on a Gore Vidal teleplay, starring Paul Newman as Billy and John Dehner as Garrett

The Boy from Oklahoma (1954), with Tyler MacDuff in the role of Billy the Kid

One-Eyed Jacks (1961), is the only film directed by Marlon Brando, who also played its lead character, Rio. This story is from an adaptation by Rod Serling of a Charles Neider novelization of Billy the Kid's life, with a later revision among others by Sam Peckinpah.

Billy the Kid vs. Dracula (1966), a film starring John Carradine, which strangely pits McCarty against a vampire. Billy the Kid is portrayed as an almost innocent gunslinger and uses his alias William H. Bonney.

Chisum is a 1970 movie starring John Wayne as John Chisum, which deals with Billy the Kid's involvement in the Lincoln County War. Billy is portrayed by Geoffrey Deuel.

Dirty Little Billy,[136] Stan Dragoti's 1972 film starring Michael J. Pollard

Pat Garrett and Billy the Kid, Sam Peckinpah's 1973 motion picture with Kris Kristofferson as Billy, James Coburn as Pat Garrett, and with a soundtrack by Bob Dylan, who also appears in the movie

Young Guns, Christopher Cain's 1988 motion picture starring Emilio Estevez as Billy and Patrick Wayne, son of John Wayne as Pat Garrett

Bill & Ted's Excellent Adventure, 1989 time travel movie featuring Dan Shor as Billy the Kid

Gore Vidal's Billy the Kid, Gore Vidal's 1989 film starring Val Kilmer as Billy and Duncan Regehr as Pat Garrett

Young Guns II, Geoff Murphy's 1990 motion picture starring Emilio Estevez as Billy and William Petersen as Pat Garrett

Purgatory, Uli Edel's 1999 made-for-TV movie starring Donnie Wahlberg as Deputy Glen/Billy The Kid

Requiem for Billy the Kid, Anne Feinsilber's 2006 motion picture starring Kris Kristofferson.

Birth of a Legend, a 2011 film in two parts based on Frederick Nolan's book The Lincoln County War: A Documentary History directed by Andrew Wilkinson

Music

"Billy the Kid", a folk song in the public domain, was published in John A. Lomax and Alan Lomax's American Ballads and Folksongs, and also their Cowboy Songs and Other Frontier Ballads.

"Billy the Kid" folksong sung by Woody Guthrie, recorded by Alan Lomax in 1940 for the Library of Congress (#3412 B2), with a melody Guthrie later used for his song "So Long, it's Been Good to Know You". He also recorded it in 1944 for Moe Asch's Asch/Folkways label (MA67).

Aaron Copland's Billy the Kid, a ballet that premiered in 1938.

Bob Dylan's album Pat Garrett and Billy the Kid, soundtrack of the 1973 film by Sam Peckinpah.

Jon Bon Jovi's album Blaze of Glory, used as part of the soundtrack for Young Guns II, and featured the song "Billy Get Your Gun".

Marty Robbins' song "Billy the Kid" from the album Gunfighter Ballads & Trail Songs Volume 3.

Marty Robbins' song "Fastest Gun Around" from the 1963 album Return of the Gunfighter.

Dave Stamey's "The Skies of Lincoln County", which features the deceased Bonney as narrator, answering historical distortions by Pat Garrett.

Ry Cooder recorded the folk song "Billy the Kid", on the album Into The Purple Valley, with his own melody and instrumental. It was also on Ry Cooder Classics Volume II.

Billy Joel's song "The Ballad of Billy the Kid", a historically inaccurate re-telling of Billy the Kid's life, off of his 1973 album Piano Man

American composer Mark Nichols (American Composer/Playwright) wrote a popular score for Michael Ondaatje 1992 play, The Collected Works of Billy the Kid.

The Charlie Daniels Band recorded the song "Billy The Kid" (Daniels, Dean, Wilson) on their 1976 album High Lonesome.

UK rock band Loungetree recorded a song "William Child" on their 2009 album Seasons with inspiration drawn from the name and legend of Billy the Kid.

Country singer Billy Dean co-wrote and recorded a song called "Billy the Kid," which was subsequently a hit single on the country charts in 1992. It has since gone on to become Dean's signature song.

"Las Cruces Jail" is a song by the band Two Gallants about Billy the Kid's imprisonment near Las Cruces, New Mexico.

"Billy the Kid Strikes Back" is a song by ambient/dub producer Ott from his album Blumenkraft.

Indie-rap outfit WHY? uses the tongue-twister "Billy the Kid did what he did and he died" in "Song of the Sad Assassin" on their album Alopecia.

William Bonney is a midwestern emo/screamo band that takes their name from Billy the Kid's alternative name, William H. Bonney.

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History Lyme disease

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. 

This is 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 Reverend Dr 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 (in) 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 colour 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 immigrated 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 early European studies of what is now known as Lyme disease described its skin manifestations. The first study dates to 1883 in Wrocław, Poland (then known as Breslau, Free State of Prussia), where physician Alfred Buchwald described a man who had suffered for 16 years with 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.

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 patient 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 patient 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. The recognition that the patients 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, elements of B. burgdorferi sensu lato infection were called or known as tick-borne meningopolyneuritis, Garin-Bujadoux syndrome, Bannwarth syndrome, Afzelius' 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 adult patients 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 scapularis from Shelter Island, NY, a known Lyme-endemic area as part of an ongoing investigation of Rocky Mountain spotted fever. In examining the ticks for rickettsiae, Burgdorfer noticed “poorly stained, rather long, irregularly coiled spirochetes.” Further examination revealed spirochetes in 60% of the ticks. Burgdorfer credited his familiarity with the European literature for his realization that the spirochetes might be the “long-sought cause of ECM and Lyme disease.” Benach supplied him with more ticks from Shelter Island and sera from patients diagnosed with Lyme disease. University of Texas Health Science Center researcher Alan Barbour “offered his expertise to culture and immunochemically characterize the organism.” Burgdorfer subsequently confirmed his discovery by isolating from patients with Lyme disease spirochetes identical to those found in ticks. In June 1982 he published his findings in Science, and the spirochete was named Borrelia burgdorferi in his honor.

After the identification of B. burgdorferi as the causative agent of Lyme disease, antibiotics were selected for testing, guided by in vitro antibiotic sensitivities, including tetracycline antibiotics, amoxicillin, cefuroxime axetil, intravenous and intramuscular penicillin and intravenous ceftriaxone. The mechanism of tick transmission was also the subject of much discussion. B. burgdorferi spirochetes were identified in tick saliva in 1987, confirming the hypothesis that transmission occurred via tick salivary glands.

Jonathan Edlow, Professor of Medicine at Harvard Medical School, quotes the late Ed Masters (discoverer of STARI, a Lyme-like illness) in his book Bull's-Eye, on the history of Lyme disease. Edlow writes:

Masters points out that the "track record" of the "conventional wisdom" regarding Lyme disease is not very good: "First off, they said it was a new disease, which it wasn't. Then it was thought to be viral, but it isn't. Then it was thought that sero-negativity didn't exist, which it does. They thought it was easily treated by short courses of antibiotics, which sometimes it isn't. Then it was only the Ixodes dammini tick, which we now know is not even a separate valid tick species. If you look throughout the history, almost every time a major dogmatic statement has been made about what we 'know' about this disease, it was subsequently proven wrong or underwent major modifications.

Society and culture

Urbanization and other anthropogenic factors can be implicated in the spread of Lyme disease to humans. In many areas, expansion of suburban neighborhoods has led to gradual deforestation of surrounding wooded areas and increased border contact between humans and tick-dense areas. Human expansion has also resulted in reduction of predators that hunt deer as well as mice, chipmunks and other small rodents – the primary reservoirs for Lyme disease. As a consequence of increased human contact with host and vector, the likelihood of transmission of the disease has greatly increased. Researchers are investigating possible links between global warming and the spread of vector-borne diseases, including Lyme disease.

The deer tick (Ixodes scapularis, the primary vector in the northeastern U.S.) has a two-year life cycle, first progressing from larva to nymph, and then from nymph to adult. The tick feeds only once at each stage. In the fall, large acorn forests attract deer, as well as mice, chipmunks and other small rodents infected with B. burgdorferi. During the following spring, the ticks lay their eggs. The rodent population then "booms". Tick eggs hatch into larvae, which feed on the rodents; thus the larvae acquire infection from the rodents. At this stage, tick infestation may be controlled using acaricides (miticides).

Adult ticks may also transmit disease to humans. After feeding, female adult ticks lay their eggs on the ground, and the cycle is complete. On the West Coast of the United States, Lyme disease is spread by the western black-legged tick (Ixodes pacificus), which has a different life cycle.

The risk of acquiring Lyme disease does not depend on the existence of a local deer population, as is commonly assumed. New research suggests eliminating deer from smaller areas (less than 2.5 ha or 6 acres) may in fact lead to an increase in tick density and the rise of "tick-borne disease hotspots".

Harassment of researchers

In 2001, the New York Times Magazine reported that Allen Steere, chief of immunology and rheumatology at Tufts Medical Center and a codiscoverer and leading expert on Lyme disease, had been harassed, stalked, and threatened by patients and patient advocacy groups angry at his refusal to substantiate their diagnoses of chronic Lyme disease and endorse long-term antibiotic therapy. Because this intimidation included death threats, Steere was assigned security guards. Paul G. Auwaerter, director of infectious disease at Johns Hopkins School of Medicine, cited the political controversy and high emotions as contributing to a "poisonous atmosphere" around Lyme disease, which he believes has led to doctors trying to avoid having Lyme patients in their practice.

Media

A 2004 study in The Pediatric Infectious Disease Journal stated 9 of 19 Internet websites surveyed contained what were described as major inaccuracies. Websites described as providing inaccurate information included several with the word "lyme" in their domain name (e.g. lymenet.org), as well as the website of the International Lyme And Associated Diseases Society. A 2008 article in the New England Journal of Medicine argued media coverage of chronic Lyme disease ignored scientific evidence in favor of anecdotes and testimonials:

The media frequently disregard complex scientific data in favor of testimonials about patients suffering from purported chronic Lyme disease and may even question the competence of clinicians who are reluctant to diagnose chronic Lyme disease. All these factors have contributed to a great deal of public confusion with little appreciation of the serious harm caused to many patients who have received a misdiagnosis and have been inappropriately treated.

The 2008 Oscar finalist documentary film Under Our Skin: The Untold Story of Lyme Disease opened June 19, 2009 in New York City. This documentary, made by a director whose sister contracted the disease, argues that chronic Lyme disease exists. Lyme disease was also the focus of a major feature in The Times (London) in February 2010 which detailed the impact the disease had had on British author Alex Wade.

Tags:  Lyme disease in world , Lyme disease

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Lyme disease in world

Africa

In northern Africa, B. burgdorferi sensu lato has been identified in Morocco, Algeria, Egypt and Tunisia.

Lyme disease in sub-Saharan Africa is presently unknown, but evidence indicates it may occur in humans in this region. The abundance of hosts and tick vectors would favor the establishment of Lyme infection in Africa. In East Africa, two cases of Lyme disease have been reported in Kenya.

Asia

B. burgdorferi sensu lato-infested ticks are being found more frequently in Japan, as well as in northwest China and far eastern Russia. Borrelia has been isolated in Mongolia, as well.

Australia

In Australia, there is no definitive evidence for the existence of B. burgdorferi or for any other tick-borne spirochete that may be responsible for a local syndrome being reported as Lyme disease. Cases of neuroborreliosis have been documented in Australia, but are often ascribed to travel to other continents. The existence of Lyme disease in Australia is controversial.

Canada

Due to changing climate, 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, the Maritimes and parts of the Prairie provinces, as well as British Columbia.

Europe

In Europe, cases of B. burgdorferi sensu lato-infected ticks are found predominantly in central Europe, particularly in Slovenia and Austria, but have been isolated in almost every country on the continent. Incidence in southern Europe, such as Italy and Portugal, is much lower.

South America

In South America, tick-borne disease recognition and occurrence is rising. Ticks carrying B. burgdorferi sensu lato, as well as canine and human tick-borne disease, have been reported widely in Brazil, but the subspecies of Borrelia has not yet been defined. The first reported case of Lyme disease in Brazil was made in 1993 in Sao Paulo. B. burgdorferi sensu stricto antigens in patients have been identified in Colombia and Bolivia.

United States

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 49 of 50 states in the U.S, 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). New 2008 CDC Lyme case definition guidelines are used to determine confirmed CDC surveillance cases. Effective January 2008, the CDC gives equal weight to laboratory evidence from 1) a positive culture for B. burgdorferi; 2) two-tier testing (ELISA screening and Western blot confirming); or 3) single-tier IgG (old infection) Western blot. Previously, the CDC only included laboratory evidence based on (1) and (2) in their surveillance case definition. The case definition now includes the use of Western blot without prior ELISA screen.

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 prevalence of 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 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.
Tags: History Lyme disease ,  Lyme disease

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Lyme disease

Lyme disease, or Lyme borreliosis, is an emerging infectious disease caused by at least three species of bacteria belonging to the genus Borrelia. Borrelia burgdorferi sensu stricto is the main cause of Lyme disease in the United States, whereas Borrelia afzelii and Borrelia garinii cause most European cases. The disease is named after the town of Lyme, Connecticut, USA, where a number of cases were identified in 1975. Although Allen Steere realized Lyme disease was a tick-borne disease in 1978, the cause of the disease remained a mystery until 1981, when B. burgdorferi was identified by Willy Burgdorfer.

Lyme disease is the most common tick-borne disease in the Northern Hemisphere. Borrelia is transmitted to humans by the bite of infected ticks belonging to a few species of the genus Ixodes ("hard ticks"). 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. In most cases, the infection and its symptoms are eliminated by antibiotics, especially if the illness is treated early. Delayed or inadequate treatment can lead to the more serious symptoms, which can be disabling and difficult to treat. Lyme disease is a biosafety level 2 disease.

Signs and symptoms

Lyme disease can affect multiple body systems and produce a range of symptoms. Not all patients with Lyme disease will have all symptoms, and many of the symptoms are not specific to Lyme disease, but can occur with other diseases, as well. The incubation period from infection to the onset of symptoms is usually one to two weeks, but can be much shorter (days), or much longer (months to years). Symptoms most often occur from May through September, because the nymphal stage of the tick is responsible for most cases. Asymptomatic infection exists, but occurs in less than 7% of infected individuals in the United States. Asymptomatic infection may be much more common among those infected in Europe.

Early localized infection

The classic sign of early local infection with Lyme disease is a circular, outwardly expanding rash called erythema chronicum migrans (also erythema migrans or EM), which occurs at the site of the tick bite three to thirty days after the tick bite. The rash is red, and may be warm, but is generally painless. Classically, the innermost portion remains dark red and becomes indurated; the outer edge remains red; and the portion in between clears, giving the appearance of a bullseye. However, partial clearing is uncommon, and the bullseye pattern more often involves central redness.

EM is thought to occur in about 80% of infected patients. Patients can also experience flu-like symptoms, such as headache, muscle soreness, fever, and malaise. Lyme disease can progress to later stages even in patients who do not develop a rash.

Early disseminated infection

Within days to weeks after the onset of local infection, the Borrelia bacteria may begin to spread through the bloodstream. EM may develop at sites across the body that bear no relation to the original tick bite. Another skin condition, which is apparently absent in North American patients, but occurs in Europe, is borrelial lymphocytoma, a purplish lump that develops on the ear lobe, nipple, or scrotum. Other discrete symptoms include migrating pain in muscles, joint, and tendons, and heart palpitations and dizziness caused by changes in heartbeat.

Various acute neurological problems, termed neuroborreliosis, appear in 10–15% of untreated patients. These include facial palsy, which is the loss of muscle tone on one or both sides of the face, as well as meningitis, which involves severe headaches, neck stiffness, and sensitivity to light. Radiculoneuritis causes shooting pains that may interfere with sleep, as well as abnormal skin sensations. Mild encephalitis may lead to memory loss, sleep disturbances, or mood changes. In addition, some case reports have described altered mental status as the only symptom seen in a few cases of early neuroborreliosis.

Late persistent infection

After several months, untreated or inadequately treated patients may go on to develop severe and chronic symptoms that affect many parts of the body, including the brain, nerves, eyes, joints and heart. Many disabling symptoms can occur, including permanent paraplegia in the most extreme cases.

Chronic neurologic symptoms occur in up to 5% of untreated patients. A polyneuropathy that involves shooting pains, numbness, and tingling in the hands or feet may develop. A neurologic syndrome called Lyme encephalopathy is associated with subtle cognitive problems, such as difficulties with concentration and short-term memory. These patients may also experience profound fatigue. However, other problems, such as depression and fibromyalgia, are no more common in people who have been infected with Lyme than in the general population.Chronic encephalomyelitis, which may be progressive, can involve cognitive impairment, weakness in the legs, awkward gait, facial palsy, bladder problems, vertigo, and back pain. In rare cases untreated Lyme disease may cause frank psychosis, which has been mis-diagnosed as schizophrenia or bipolar disorder. Panic attack and anxiety can occur, also delusional behavior, including somatoform delusions, sometimes accompanied by a depersonalization or derealization syndrome, where the patients begin to feel detached from themselves or from reality.

Diffuse white matter pathology can disrupt grey matter connections, and could account for deficits in attention, memory, visuospatial ability, complex cognition, and emotional status. White matter disease may have a greater potential for recovery than gray matter disease, perhaps because neuronal loss is less common. Resolution of MRI white matter hyperintensities after antibiotic treatment has been observed.

Lyme arthritis usually affects the knees. In a minority of patients, arthritis can occur in other joints, including the ankles, elbows, wrist, hips, and shoulders. Pain is often mild or moderate, usually with swelling at the involved joint. Baker's cysts may form and rupture. In some cases, joint erosion occurs.

Acrodermatitis chronica atrophicans (ACA) is a chronic skin disorder observed primarily in Europe among the elderly. ACA begins as a reddish-blue patch of discolored skin, often on the backs of the hands or feet. The lesion slowly atrophies over several weeks or months, with the skin becoming first thin and wrinkled and then, if untreated, completely dry and hairless.

Cause

Lyme disease is caused by Gram-negative, spirochetal bacteria from the genus Borrelia. At least 11 Borrelia species have been discovered, three of which are known to be Lyme-related. The Borrelia species that cause Lyme disease are collectively known as Borrelia burgdorferi sensu lato, and show a great deal of genetic diversity.

The group Borrelia burgdorferi sensu lato, made up of three closely related species, are probably responsible for the large majority of cases: B. burgdorferi sensu stricto (predominant in North America, but also present in Europe), B. afzelii, and B. garinii (both predominant in Eurasia). Some studies have also proposed B. bissettii and B. valaisiana may sometimes infect humans, but these species do not seem to be important causes of disease.

Transmission

Lyme disease is classified as a zoonosis, as it is transmitted to humans from a natural reservoir among rodents by ticks that feed on both sets of hosts. Hard-bodied ticks of the genus Ixodes are the main vectors of Lyme disease.Most infections are caused by ticks in the nymphal stage, as they are very small and may feed for long periods of time undetected. Larval ticks are very rarely infected. Tick bites often go unnoticed because of the small size of the tick in its nymphal stage, as well as tick secretions that prevent the host from feeling any itch or pain from the bite. However, transmission is quite rare, with only about 1% of recognized tick bites resulting in Lyme disease; this may be because an infected tick must be attached for at least a day for transmission to occur.

In Europe, the vector is Ixodes ricinus, which is also called the sheep tick or castor bean tick. In China, Ixodes persulcatus (the taiga tick) is probably the most important vector. In North America, the black-legged tick or deer tick (Ixodes scapularis) is the main vector on the east coast. The lone star tick (Amblyomma americanum), which is found throughout the Southeastern United States as far west as Texas, is unlikely to transmit the Lyme disease spirochete Borrelia burgdorferi, though it may be implicated in a related syndrome called southern tick-associated rash illness, which resembles a mild form of Lyme disease. On the West Coast of the United States, the main vector is the western black-legged tick (Ixodes pacificus). The tendency of this tick species to feed predominantly on host species such as lizards that are resistant to Borrelia infection appears to diminish transmission of Lyme disease in the West.

While Lyme spirochetes have been found in insects as well as ticks, reports of actual infectious transmission appear to be rare. Lyme spirochetes have been found in semen and breast milk,but transmission has not been known to take place through sexual contact. Transmission across the placenta during pregnancy has not been demonstrated, and no consistent pattern of teratogenicity or specific "congenital Lyme borreliosis" has been identified. As with a number of other spirochetal diseases, adverse pregnancy outcomes are possible with untreated infection; prompt treatment with antibiotics reduces or eliminates this risk. Pregnant Lyme-disease patients cannot be treated with the first-choice antibiotic, doxycycline (see below), as it is potentially harmful for the fetus. Instead, erythromycin is usually given; it is less effective against the disease but harmless for the fetus.

Tick-borne coinfections

Ticks that transmit B. burgdorferi to humans can also carry and transmit several other parasites, such as Theileria microti and Anaplasma phagocytophilum, which cause the diseases babesiosis and human granulocytic anaplasmosis (HGA), respectively. Among early Lyme disease patients, depending on their location, 2–12% will also have HGA and 2–40% will have babesiosis. Ticks in certain regions, including the landscapes along the eastern Baltic Sea, also transmit tick-borne encephalitis.

Coinfections complicate Lyme symptoms, especially diagnosis and treatment. It is possible for a tick to carry and transmit one of the coinfections and not Borrelia, making diagnosis difficult and often elusive. The Centers for Disease Control studied 100 ticks in rural New Jersey, and found 55% of the ticks were infected with at least one of the pathogens.

Pathophysiology

Borrelia burgdorferi can spread throughout the body during the course of the disease, and has been found in the skin, heart, joint, peripheral nervous system, and central nervous system. Many of the signs and symptoms of Lyme disease are a consequence of the immune response to the spirochete in those tissues.

B. burgdorferi is injected into the skin by the bite of an infected Ixodes tick. Tick saliva, which accompanies the spirochete into the skin during the feeding process, contains substances that disrupt the immune response at the site of the bite. This provides a protective environment where the spirochete can establish infection. The spirochetes multiply and migrate outward within the dermis. The host inflammatory response to the bacteria in the skin causes the characteristic circular EM lesion. Neutrophils, however, which are necessary to eliminate the spirochetes from the skin, fail to appear in the developing EM lesion. This allows the bacteria to survive and eventually spread throughout the body.

Days to weeks following the tick bite, the spirochetes spread via the bloodstream to joints, heart, nervous system, and distant skin sites, where their presence gives rise to the variety of symptoms of disseminated disease. The spread of B. burgdorferi is aided by the attachment of the host protease plasmin to the surface of the spirochete. If untreated, the bacteria may persist in the body for months or even years, despite the production of B. burgdorferi antibodies by the immune system. The spirochetes may avoid the immune response by decreasing expression of surface proteins that are targeted by antibodies, antigenic variation of the VlsE surface protein, inactivating key immune components such as complement, and hiding in the extracellular matrix, which may interfere with the function of immune factors.

In the brain, B. burgdorferi may induce astrocytes to undergo astrogliosis (proliferation followed by apoptosis), which may contribute to neurodysfunction. The spirochetes may also induce host cells to secrete products toxic to nerve cells, including quinolinic acid and the cytokines IL-6 and TNF-alpha, which can produce fatigue and malaise. Both microglia and astrocytes secrete IL-6 and TNF-alpha in the presence of the spirochete. This cytokine response may contribute to cognitive impairment.

A developing hypothesis is that the chronic secretion of stress hormones as a result of Borrelia infection may reduce the effect of neurotransmitters, or other receptors in the brain by cell-mediated proinflammatory pathways, thereby leading to the dysregulation of neurohormones, specifically glucocorticoids and catecholamines, the major stress hormones. This process is mediated via the hypothalamic-pituitary-adrenal axis. Additionally tryptophan, a precursor to serotonin, appears to be reduced within the central nervous system (CNS) in a number of infectious diseases that affect the brain, including Lyme. Researchers are investigating if this neurohormone secretion is the cause of neuropsychiatric disorders developing in some patients with borreliosis.

Tags: History Lyme disease , Lyme disease in world 

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The Green River Killer (film)

Green River Killer is a 2005 American crime film starring George Kiseleff, Jaquelyn Aurora (as Jacquelyn Horrell), Georgina Donovan, Shannon Leade, Naidra Dawn Thomson, and Shawn G. Smith. 

Synopsis

It is based upon the crimes of serial killer Gary Ridgway.

Plot

Based on the true story of serial murderer Gary Ridgway, the film depicts how he would approach prostitutes in bars, then take them to his homes and brutally kill them. Then he'd throw the corpses into the Green River, which is where the name "Green River Killer" comes from. Soon the investigating police officers are on his track.

Cast

George Kiseleff - Gary Ridgway

Jaquelyn Aurora - Hedy

Georgina Donovan

Shannon Leade - Anna

Naidra Dawn Thomson - Irene

Shawn G. Smith - Coworker #1

Kimko - Coworker #2

Sebastien Szumilas - Kevin

Bud Watson - Defense Attorney

Carsten Frank - Boris

Filming

The documentary footage is of the real Gary Ridgway confessing to the killings.

The flashback of Ridgway's fictional "mentor," Boris, has a distinctly different look and atmosphere compared with the rest of the movie. That is because the footage was not shot by director Ulli Lommel but by German actor-director "Marian Dora," a pseudonym for the physician who began making gory horror films around the same time Lommel directed Green River Killer. Dora made Cannibal – Aus dem Tagebuch des Kannibalen, for example. Dora, who also worked on Lommel's Zombie Nation, in this flashback directs actor Carsten Frank as he strangles a woman.

Green River Killer was the second in a series of direct-to-DVD titles directed by Lommel and released by Lionsgate Entertainment under its Artisan label. The first was Zodiac Killer (2005). Green River Killer would soon to be followed by BTK Killer (2005) and Killer Pickton (2005). Other direct-to-DVD movies directed by Lommel and featuring serial killers would follow in 2007 and 2008.

Ridgway's home in the movie, which is a residence located in Marina Del Rey, California, was also the house inhabited by "Producer McCoon" in Black Dahlia (2006).