document_title: NBA high school draftees

question_text: players to go from high school to nba

question_tokens: players to go from high school to nba

text: NBA high school draftees

text: History[edit]

text: Early years[edit]

text: In the early years of the NBA draft, a player had to finish his four-year college eligibility to be eligible for selection. Reggie Harding, who had graduated from high school but did not enroll in a college, became the first player drafted out of high school when the Detroit Pistons selected him in the fourth round of the 1962 draft.[3] However, the NBA rules at that time prohibited a high school player to play in the league until one year after his high school class graduated.[4][5] Thus, he spent a year playing in a minor basketball league before he was drafted again in the 1963 draft by the Pistons.[6] He finally entered the league in the 1963–64 season and played four seasons in the NBA and American Basketball Association (ABA).[7]

text: In 1971, the U.S. Supreme Court decision Haywood v. National Basketball Association ruled, 7–2 against the National Basketball Association's requirement that a player must wait four years after high school graduation (which in most cases was spent playing in college) before turning professional. This ruling allowed players to enter the NBA Draft without four years of college, provided they could give evidence of hardship to the NBA office.[8]

text: In 1974, the NBA's rival, the ABA, drafted high school star Moses Malone. He was immediately signed by the Utah Stars and became the first player to go directly from high school basketball to a professional league.[9] He became an instant success, averaging 18 points and 14 rebounds per game in his rookie season. He played in the ABA until the ABA–NBA merger in 1976. He then played 19 successful seasons with 7 NBA teams. He won the NBA championship, along with the Finals Most Valuable Player Award, with the Philadelphia 76ers in 1983. His other achievements include 3 Most Valuable Player Awards, 12 consecutive All-Star Game selections, 8 All-NBA Team selections and 6 rebounding titles. He has been inducted to the Naismith Memorial Basketball Hall of Fame and was also named in the 50 Greatest Players in NBA History list announced at the league's 50th anniversary in 1996.[10]

text: A year later, two high school players, Darryl Dawkins and Bill Willoughby, applied for hardship and were declared eligible to be selected in the 1975 draft.[11] They had applied and gave evidence of financial hardship to the league, which granted them the right to start earning their living by starting their professional careers earlier.[8] Dawkins was selected 5th by the Philadelphia 76ers while Willoughby was selected 19th by the Atlanta Hawks. Dawkins played 14 seasons and averaged 12 points and 6 rebounds per game. Willoughby played 8 seasons with 6 different teams and averaged only 6 points per game. Neither player reached the level of success that was expected. It is argued that they could have been better players if they had college basketball experience before entering the NBA.[12][13][14]

text: After Dawkins and Willoughby, no high schoolers were drafted for 14 years, though several players entered the league without playing college basketball. One notable player, Shawn Kemp, enrolled in college but never played any games due to personal problems. In 1989, a year after his high school graduation, he was drafted by the Seattle SuperSonics.[15] He played 14 seasons in the NBA and was selected to 6 All-Star Games and 3 All-NBA Teams.[16]

text: In 1995, Kevin Garnett, USA Today's high school basketball player of the year, announced his intentions to forgo college, and declared himself eligible for the 1995 NBA draft. The move was highly controversial; the conventional wisdom at the time was that high-schoolers were neither emotionally nor physically mature enough for the rigors of the NBA game. On draft day, Garnett was selected with the #5 pick in the first round by the Minnesota Timberwolves. Garnett led the Timberwolves to eight consecutive playoff berths and was a multiple All-Star during his time with the team. In 2004, the Wolves advanced to the Western Conference Finals before losing to the Lakers; Garnett was named Most Valuable Player that year. After a trade in the 2007 offseason to the Boston Celtics, he was a core player in the Celtics' first NBA title in over 20 years.

text: In 1996, two notable players made the jump from high school to the NBA. The first was Kobe Bryant, selected by the Charlotte Hornets with the 13th pick of the NBA draft, but traded almost immediately to the Los Angeles Lakers. The second was Jermaine O'Neal, selected by the Trail Blazers with the 17th pick. O'Neal was traded in 2000 to the Indiana Pacers (and later to the Miami Heat). In 1997, another All-Star caliber player, Tracy McGrady, was selected by the Toronto Raptors. In 1998, three high-schoolers were drafted with Al Harrington and Rashard Lewis experiencing the most success. Darius Miles became the highest high school player selected with the third pick in the 2000, until the following year.

text: In 2001, Kwame Brown (selected by the Washington Wizards) became the first high-schooler to be selected with the number one pick in the draft; since then, LeBron James (2003) and Dwight Howard (2004) have also been selected with the first pick. Other notable high-schoolers include Tyson Chandler and Eddy Curry (2001); Amar'e Stoudemire (2002); Josh Smith, Sebastian Telfair, J. R. Smith, and Shaun Livingston (2004); Andrew Bynum and Monta Ellis (2005).

text: Many prep-to-pro players like Kevin Garnett, Kobe Bryant, LeBron James, and Tracy Mcgrady went on to become star players in the NBA. Kevin Garnett, Kobe Bryant, LeBron James have all won the league's MVP Award; as well as holding at least one NBA title under their belt, and are widely regarded as future Hall-of-Famers. Dwight Howard, Jermaine O'Neal and Amar'e Stoudemire also became perennial All-Stars in their prime. However, not all high-schoolers were successful. Kwame Brown and Eddy Curry are widely regarded as draft busts, while Jonathan Bender and Darius Miles had their careers cut short by injury. Korleone Young (drafted in 1998) and Leon Smith (drafted in 1999) only played a handful of games in the NBA, while Lenny Cooke and DeAngelo Collins, both of whom declared for the 2002 Draft, went undrafted and never played in the NBA.

text: Beginning 2005, both the NBA and the players' union started to discuss the possibility of implementing a new age limit. The league lobbied for an age minimum of 20 while the union was against an age limit.[17] Finally in July 2005, both sides compromised in the new collective bargaining agreement, requiring that the minimum age for entry into the NBA be 19 and that entrants be at least one year removed from high school.[18] For the first time, teams are also allowed to send players, with two years of NBA experience or less, to the NBA Development League (NBA D-League).[17]

text: The terms of the new agreement ended the practice of drafting high school players, starting in the 2006 Draft. A high school player must wait at least a year to be eligible for selection. However, they are not required to spend that year in college. In 2008, high school star Brandon Jennings decided to skip college and play professional basketball in Italy. After a year, he was eligible for the 2009 draft and was selected 10th by the Milwaukee Bucks.[19] In the 2010 draft, Latavious Williams, who did not qualify academically to go to college, spent a year playing in the NBA D-League before he was drafted in the second round.[20] Emmanuel Mudiay decided to take a route similar to that of Brandon Jennings by skipping college to play professionally in China in 2014 before being selected by the Denver Nuggets at pick 7 a year later. In the 2015 draft, Satnam Singh Bhamara, who did not qualify academically to go to college, went straight to the NBA draft as a post-graduate after being at IMG Academy for five years. He would be taken by the Dallas Mavericks with the 52nd pick in the draft, thus becoming the first high school student to be drafted since the rule changes. In the 2016 draft, one of the Top–10 players that was declared eligible for NCAA play in 2016, Thon Maker, decided to enter the draft instead as a post-graduate from Orangeville Prep in Orangeville, Ontario, Canada due to him originally declaring himself as eligible for college in 2015. Thon would also mark the first player to be drafted directly from a Canadian high school, as well as the second player to enter as a post-graduate. He'd also be the first high schooler to be drafted in the first round since 2005, being drafted by the Milwaukee Bucks with the tenth pick in the draft, thus becoming the first high school lottery pick since 2005. Most recently, in the 2018 draft, both Anfernee Simons and Thon's brother, Matur Maker, are also looking to be drafted in the NBA, with Simons being a postgraduate and Maker's decision relating to him being held back a year.

text: Some players support the new age limit. Gerald Green called it "a smart move", saying that "[not everybody is] LeBron James ... He came in ready and he dominated the league. There's a lot of players that have to get developed. Me, I've got to get developed. But I guess that age limit, that one year of college experience, can get you more developed and I think that's pretty good."[17] Others, however, strongly criticize the rule. Andrew Bynum said "That's something I'll never understand. Because in no other business can the owner, or a stock trader or a C.E.O. of a company try to protect themselves by putting rules like that."[21] Former Florida Gators and current Oklahoma City Thunder head coach Billy Donovan believed that the rule made high schoolers feel like they were being punished.[22]

text: List[edit]

text: There have been 44 high school draftees in the NBA Draft. Three draftees were selected first overall; Kwame Brown in 2001 NBA draft, LeBron James in 2003 and Dwight Howard in 2004 NBA draft. Two draftees went on to win the Rookie of the Year Award in their first season; LeBron James and 2002 draftee Amar'e Stoudemire.[23] Three draftees went on to win the Most Valuable Player Award; Kevin Garnett in 2004, Kobe Bryant in 2008 and LeBron James in 2009, 2010, 2012, and 2013.[24] Ten draftees have been selected to the All-Star Game while seven draftees have been selected to the All-NBA Team.

text:
Pos.
G
F
C

Position
Guard
Forward
Center

tag: table

text:
^
Denotes player who has been inducted to the Naismith Memorial Basketball Hall of Fame

*
Denotes player who has been selected for at least one All-Star Game and All-NBA Team

+
Denotes player who has been selected for at least one All-Star Game

#
Denotes player who never played in the NBA regular season or playoffs

text:
Draft[a]
Round
Pick
Player
Pos.
Nationality
Draft team
High school (city)
Ref.

1962
4
29
Harding, ReggieReggie Harding
C
 United States
Detroit Pistons
Detroit Eastern High School (Detroit)1[›]
[25]

1975
1
5
Dawkins, DarrylDarryl Dawkins
C
 United States
Philadelphia 76ers
Maynard Evans High School (Orlando, Florida)
[26]

1975
2
19
Willoughby, BillBill Willoughby
F/C
 United States
Atlanta Hawks
Dwight Morrow High School (Englewood, New Jersey)
[27]

1995
1
5
Garnett, KevinKevin Garnett*
F
 United States
Minnesota Timberwolves
Farragut Career Academy (Chicago)
[28]

1996
1
13
Bryant, KobeKobe Bryant*
G
 United States
Charlotte Hornets
Lower Merion High School (Ardmore, Pennsylvania)
[29]

1996
1
17
O'Neal, JermaineJermaine O'Neal*
F/C
 United States
Portland Trail Blazers
Eau Claire High School (Columbia, South Carolina)
[30]

1997
1
9
McGrady, TracyTracy McGrady^
F
 United States
Toronto Raptors
Mount Zion Christian Academy (Durham, North Carolina)
[31]

1998
1
25
Harrington, AlAl Harrington
F
 United States
Indiana Pacers
St. Patrick High School (Elizabeth, New Jersey)
[32]

1998
2
32
Lewis, RashardRashard Lewis+
F
 United States
Seattle SuperSonics
Alief Elsik High School (Houston, Texas)
[33]

1998
2
40
Young, KorleoneKorleone Young
F
 United States
Detroit Pistons
Hargrave Military Academy (Chatham, Virginia)
[34]

1999
1
5
Bender, JonathanJonathan Bender
F
 United States
Toronto Raptors
Picayune Memorial High School (Picayune, Mississippi)
[35]

1999
1
25
Smith, LeonLeon Smith
C
 United States
Dallas Mavericks
Martin Luther King High School (Chicago)
[36]

2000
1
3
Miles, DariusDarius Miles
F
 United States
Los Angeles Clippers
East St. Louis High School (East St. Louis, Illinois)
[37]

2000
1
23
Stevenson, DeShawnDeShawn Stevenson
G
 United States
Utah Jazz
Washington Union High School (Fresno, California)
[38]

2001
1
1
Brown, KwameKwame Brown
F
 United States
Washington Wizards
Glynn Academy (Brunswick, Georgia)
[39]

2001
1
2
Chandler, TysonTyson Chandler*
C
 United States
Los Angeles Clippers
Dominguez High School (Compton, California)
[40]

2001
1
4
Curry, EddyEddy Curry
C
 United States
Chicago Bulls
Thornwood High School (South Holland, Illinois)
[41]

2001
1
8
Diop, DeSaganaDeSagana Diop
C
 Senegal
Cleveland Cavaliers
Oak Hill Academy (Mouth of Wilson, Virginia)
[42]

2001
2
46
Cisse, OusmaneOusmane Cisse#
F
 Mali
Denver Nuggets
St. Jude High School (Montgomery, Alabama)
[43]

2002
1
9
Stoudemire, Amar'eAmar'e Stoudemire*
F/C
 United States
Phoenix Suns
Cypress Creek High School (Orlando, Florida)
[44]

2003
1
1
James, LeBronLeBron James*
F
 United States
Cleveland Cavaliers
St. Vincent – St. Mary High School (Akron, Ohio)
[45]

2003
1
23
Outlaw, TravisTravis Outlaw
F
 United States
Portland Trail Blazers
Starkville High School (Starkville, Mississippi)
[46]

2003
1
26
Ebi, NdudiNdudi Ebi
F
 United Kingdom
 Nigeria2[›]
Minnesota Timberwolves
Westbury Christian School (Houston, Texas)
[47]

2003
1
27
Perkins, KendrickKendrick Perkins
C
 United States
Memphis Grizzlies
Clifton J. Ozen High School (Beaumont, Texas)
[48]

2003
2
48
Lang, JamesJames Lang
C
 United States
New Orleans Hornets
Central Park Christian High School (Birmingham, Alabama)
[49]

2004
1
1
Howard, DwightDwight Howard*
F/C
 United States
Orlando Magic
Southwest Atlanta Christian Academy (Atlanta)
[50]

2004
1
4
Livingston, ShaunShaun Livingston
G
 United States
Los Angeles Clippers
Peoria High School (Peoria, Illinois)
[51]

2004
1
12
Swift, RobertRobert Swift
C
 United States
Seattle SuperSonics
Bakersfield High School (Bakersfield, California)
[52]

2004
1
13
Telfair, SebastianSebastian Telfair
G
 United States
Portland Trail Blazers
Abraham Lincoln High School (Brooklyn, New York)
[53]

2004
1
15
Jefferson, AlAl Jefferson
F
 United States
Boston Celtics
Prentiss High School (Prentiss, Mississippi)
[54]

2004
1
17
Smith, JoshJosh Smith
F
 United States
Atlanta Hawks
Oak Hill Academy (Mouth of Wilson, Virginia)
[55]

2004
1
18
Smith, J. R.J. R. Smith
G
 United States
New Orleans Hornets
Saint Benedict's Preparatory School (Newark, New Jersey)
[56]

2004
1
19
Wright, DorellDorell Wright
G/F
 United States
Miami Heat
South Kent Preparatory School (South Kent, Connecticut)
[57][58]

2005
1
6
Webster, MartellMartell Webster
G/F
 United States
Portland Trail Blazers
Seattle Preparatory School (Seattle)
[59]

2005
1
10
Bynum, AndrewAndrew Bynum+
C
 United States
Los Angeles Lakers
St. Joseph High School (Metuchen, New Jersey)
[60]

2005
1
18
Green, GeraldGerald Green
F
 United States
Boston Celtics
Gulf Shores Academy (Houston, Texas)
[61]

2005
2
34
Miles, C. J.C. J. Miles
G
 United States
Utah Jazz
Skyline High School (Dallas)
[62]

2005
2
35
Sánchez, RickyRicky Sánchez#
F
 Puerto Rico
Portland Trail Blazers
IMG Academy (Bradenton, Florida)
[63]

2005
2
40
Ellis, MontaMonta Ellis
G
 United States
Golden State Warriors
Lanier High School (Jackson, Mississippi)
[64]

2005
2
45
Williams, LouisLouis Williams
G
 United States
Philadelphia 76ers
South Gwinnett High School (Snellville, Georgia)
[65]

2005
2
49
Blatche, AndrayAndray Blatche
F
 United States
 Philippines3[›]
Washington Wizards
South Kent Preparatory School (South Kent, Connecticut)
[66]

2005
2
56
Johnson, AmirAmir Johnson
F
 United States
Detroit Pistons
Westchester High School (Los Angeles)
[67]

2015
2
52
Singh, SatnamSatnam Singh#
C
 India4[›]
Dallas Mavericks
IMG Academy (Bradenton, Florida)
[68]

2016
1
10
Maker, ThonThon Maker
F/C
 Sudan
 South Sudan
 Australia5[›]
Milwaukee Bucks
Orangeville District Secondary School (Orangeville, Ontario, Canada)6[›]
[69]

text:
^ 1: Reggie Harding played and graduated from Detroit Eastern High School in January but he played high school basketball in Nashville, Tennessee prior to the draft.[70][71]
^ 2: While Ndudi Ebi was originally born and raised in London, England, he also holds Nigerian nationality due to his parents being born and raised there.
^ 3: Andray Blatche was born and raised in Syracuse, New York and holds American nationality, but he had become a naturalized Filipino since June 2014 and has officially represented the Philippines since.
^ 4: Satnam Singh officially marks the first ever player to be taken from India in the NBA. He also marks the first time since 2005 after their latest ruling on high school players that someone directly from high school would be taken in the draft, albeit as a postgraduate senior.
^ 5: Thon Maker was born in Wau, Sudan at the time, but Wau has now since become a part of South Sudan instead due to war. Even then, though, he would be raised as an Australian representative.
^ 6: Thon Maker would become the first high schooler (and second overall high school postgraduate student) to be selected from the nation of Canada instead of somewhere in the United States of America. Also, while Thon attended classes at Orangeville Prep, he would play basketball games for the Athlete Institute nearby in Mono, Ontario as well.

text: Other players[edit]

text: The following players also played in the NBA or were drafted without playing college basketball; however, these players did not get drafted or join the NBA directly after their high school graduation.

text:
Year[b]
Debut[c]
Player
Pos.
Nationality
High school (city)
Notes
Ref.

—[d]
1946
Kappen, TonyTony Kappen
G
 United States
Forest Hills High School (Queens, New York)

Played in the ABL before making his BAA debut
The first player to play in the BAA/NBA without any college experience
Made his BAA debut at the age of 27

[72][73][74]

—[d]
1946
Simmons, ConnieConnie Simmons
F/C
 United States
Flushing High School (Flushing, New York)5[›]

The second player to play in the BAA/NBA without any college experience
Made his BAA debut at the age of 21

[75][76]

—[d]
1948
Graboski, JoeJoe Graboski
F/C
 United States
Tuley High School (Chicago)

The third and final player to play in the BAA before its merger as the NBA
Made his BAA debut at the age of 18

[77][78]

1960
1969
Hawkins, ConnieConnie Hawkins^
F/C
 United States
Boys High School (Brooklyn, New York)

Was permanently banned by the NBA due to a point shaving scandal in college, but was later reinstated in 1969
Attended University of Iowa
Played in the ABL and the ABA before making his NBA debut

[79][80][81]

1974
1976
Malone, MosesMoses Malone^
F/C
 United States
Petersburg High School (Petersburg, Virginia)

Drafted by the Utah Stars in the 1974 ABA Draft
Played in the ABA before the ABA–NBA merger

[82]

1988
1989
Kemp, ShawnShawn Kemp*
F/C
 United States
Concord High School (Elkhart, Indiana)

Attended University of Kentucky and Trinity Valley Community College
Drafted by the Seattle SuperSonics in the 1989 NBA draft (1st round, 17th pick)

[83][84]

1986
1992
Daniels, LloydLloyd Daniels
G
 United States
Andrew Jackson High School (Queens, New York)

Attended Mt. San Antonio College
Played in various minor basketball leagues before making his NBA debut

[85][86][87]

1993
1996
Hamilton, ThomasThomas Hamilton
C
 United States
Martin Luther King High School (Chicago)

Attended University of Pittsburgh
Declared for the 1994 NBA draft but went undrafted

[88][89]

1996
2000
Jackson, StephenStephen Jackson
F
 United States
Oak Hill Academy (Mouth of Wilson, Virginia)

Attended Butler Community College
Drafted by the Phoenix Suns in the 1997 NBA draft (2nd round, 43rd pick)

[90][91]

2001
2015
Huertas, MarceloMarcelo Huertas
G
 Brazil
 Italy
Coppell High School (Coppell, Texas)

Was born in Brazil and played for the Esporte Clube Pinheiros before moving to the U.S.A. around 2000.
Played senior year in Coppell High School before beginning his professional international career.
Went undrafted in the 2005 NBA draft.
Played in Brazil, Spain, and Italy before making his NBA debut in 2015.

[92]

2004
2005
Butler, JackieJackie Butler
F/C
 United States
Coastal Christian Academy (Virginia Beach, Virginia)

Initially committed to Mississippi State University and, later on, the University of Tennessee
Declared for the 2004 NBA draft but went undrafted
Played in the CBA before making his NBA debut

[93][94][95]

2008
2009
Jennings, BrandonBrandon Jennings
G
 United States
Oak Hill Academy (Mouth of Wilson, Virginia)

Initially committed to the University of Southern California and, later on, the University of Arizona
Played in the Italian league in the 2008–09 season
Drafted by the Milwaukee Bucks in the 2009 NBA draft (1st round, 10th pick)

[96][97]

2009

Williams, LataviousLatavious Williams#
F
 United States
Christian Life Center Academy (Humble, Texas)

Initially committed to the University of Memphis
Played in the NBA D-League in the 2009–10 season
Drafted by the Miami Heat in the 2010 NBA draft (2nd round, 43rd pick)

[98][99]

2010
2011
Kanter, EnesEnes Kanter
F/C
 Turkey
Stoneridge Preparatory School (Simi Valley, California)

Previously played in both youth squads and professionally in Turkey
Moved to the U.S.A. in 2009 and played basketball in his senior year of high school
Attended the University of Kentucky, but was barred from playing due to his previous time spent in Turkey
Drafted by the Utah Jazz in the 2011 NBA draft (1st round, 3rd pick)

2010
2011
Tyler, JeremyJeremy Tyler
C
 United States
San Diego High School (San Diego)

Initially committed to the University of Louisville
Left high school after his junior year in 2009
Played in the Israeli league in the 2009–10 season
Played in the Japanese league in the 2010–11 season
Drafted by the Charlotte Bobcats in the 2011 NBA draft (2nd round, 39th pick)

[100][101]

2012
2013
Ledo, RickyRicky Ledo
G
 United States
South Kent High School (South Kent, Connecticut)

Attended Providence College
Drafted by the Dallas Mavericks in the 2013 NBA draft (2nd round, 43rd pick)

2013
2015
Felício, CristianoCristiano Felício
C
 Brazil
CCSE Prep Academy (Sacramento)

Was born in Brazil and played professionally there before moving in his senior year.
Tried to get a scholarship for the University of Oregon, but was deemed ineligible.
Returned to playing professionally in Brazil.

2014
2015
Mudiay, EmmanuelEmmanuel Mudiay
PG
 Democratic Republic of the Congo
 United States
Prime Prep Academy (Dallas)

Initially committed to Southern Methodist University
Played in the Chinese professional league in the 2014–15 season
Drafted by the Denver Nuggets in the 2015 NBA draft (1st round, 7th pick)

2014
2016
Papagiannis, GeorgiosGeorgios Papagiannis
C
 Greece
Westtown School (West Chester, Pennsylvania)

Was born in Greece and played professionally for Peristeri at 14 before moving in his freshman year
Went to Westtown as a junior before moving back to Greece
Played professionally for the Panathinaikos while also attending the American School in Athens, Greece
Drafted by the Phoenix Suns and traded to the Sacramento Kings in the 2016 NBA draft (1st round, 13th pick)

text: Controversy[edit]

text: Despite the success of some high school players drafted, the entry of high school players into the NBA remains controversial. Critics say that high school players are not mentally and physically mature or prepared enough to handle the pressure of professional play. Thus, they are more likely to fail.[14][102] Instead, they believe that colleges are useful at filtering out players who can dominate against weak competition in high school, but cannot succeed at a higher level of play. They also think that the influx of high schoolers bypassing colleges in favor of the NBA has caused collegiate game to deteriorate. Universities are wary of spending time recruiting as many players that are motivated financially to turn pro fresh out of high school.[102][103]

text: On the other hand, proponents argue that there is no valid reason to exclude high school players. Michael McCann, writer of law article "Illegal Defense: The Irrational Economics of Banning High School Players from the NBA Draft", contends that players drafted straight out of high school can do as well as any other players in the NBA. The article finds that "on average, these [high school] players perform better in every major statistical category than does the average NBA player".[104] Others instead believe that the problem was due to the lack of established farm system in basketball until recently. In other major sports, such as baseball and hockey, it is common for young players to develop in their minor league systems.[102]


document_title: Infection

question_text: 3 types of direct transmission of infectious disease

question_tokens: 3 types of direct transmission of infectious disease

root

text: Infection

text: Classification[edit]

text: Subclinical versus clinical (latent versus apparent)[edit]

text: Symptomatic infections are apparent and clinical, whereas an infection that is active but does not produce noticeable symptoms may be called inapparent, silent, subclinical, or occult. An infection that is inactive or dormant is called a latent infection.[6] An example of a latent bacterial infection is latent tuberculosis. Some viral infections can also be latent, examples of latent viral infections are any of those from the Herpesviridae family.

tag: p

text: The word infection can denote any presence of a particular pathogen at all (no matter how little) but also is often used in a sense implying a clinically apparent infection (in other words, a case of infectious disease).[7] This fact occasionally creates some ambiguity or prompts some usage discussion. To get around the usage annoyance, it is common for health professionals to speak of colonization (rather than infection) when they mean that some of the pathogens are present but that no clinically apparent infection (no disease) is present.

text: A short-term infection is an acute infection. A long-term infection is a chronic infection. Infections can be further classified by causative agent (bacterial, viral, fungal, parasitic), and by the presence or absence of systemic symptoms (sepsis).

text: Primary versus opportunistic[edit]

text: Among the many varieties of microorganisms, relatively few cause disease in otherwise healthy individuals.[8] Infectious disease results from the interplay between those few pathogens and the defenses of the hosts they infect. The appearance and severity of disease resulting from any pathogen, depends upon the ability of that pathogen to damage the host as well as the ability of the host to resist the pathogen. However a host's immune system can also cause damage to the host itself in an attempt to control the infection. Clinicians therefore classify infectious microorganisms or microbes according to the status of host defenses - either as primary pathogens or as opportunistic pathogens:

text: Infectious or not[edit]

text: One way of proving that a given disease is "infectious", is to satisfy Koch's postulates (first proposed by Robert Koch), which demands that the infectious agent be identified only in patients and not in healthy controls, and that patients who contract the agent also develop the disease. These postulates were first used in the discovery that Mycobacteria species cause tuberculosis. Koch's postulates cannot be applied ethically for many human diseases because they require experimental infection of a healthy individual with a pathogen produced as a pure culture. Often, even clearly infectious diseases do not meet the infectious criteria. For example, Treponema pallidum, the causative spirochete of syphilis, cannot be cultured in vitro – however the organism can be cultured in rabbit testes. It is less clear that a pure culture comes from an animal source serving as host than it is when derived from microbes derived from plate culture. Epidemiology is another important tool used to study disease in a population. For infectious diseases it helps to determine if a disease outbreak is sporadic (occasional occurrence), endemic (regular cases often occurring in a region), epidemic (an unusually high number of cases in a region), or pandemic (a global epidemic).

text: Contagiousness[edit]

text: Infectious diseases are sometimes called contagious disease when they are easily transmitted by contact with an ill person or their secretions (e.g., influenza). Thus, a contagious disease is a subset of infectious disease that is especially infective or easily transmitted. Other types of infectious/transmissible/communicable diseases with more specialized routes of infection, such as vector transmission or sexual transmission, are usually not regarded as "contagious", and often do not require medical isolation (sometimes loosely called quarantine) of victims. However, this specialized connotation of the word "contagious" and "contagious disease" (easy transmissibility) is not always respected in popular use. Infectious diseases are commonly transmitted from person to person through direct contact. The types of contact are through person to person and droplet spread. Indirect contact such as airborne transmission, contaminated objects, food and drinking water, animal person contact, animal reservoirs, insect bites, and environmental reservoirs are another way infectious diseases are transmitted,[10]

text: By anatomic location[edit]

text: Infections can be classified by the anatomic location or organ system infected, including:

text:
Urinary tract infection
Skin infection
Respiratory tract infection
Odontogenic infection (an infection that originates within a tooth or in the closely surrounding tissues)
Vaginal infections
Intra-amniotic infection

tag: ul

text: In addition, locations of inflammation where infection is the most common cause include pneumonia, meningitis and salpingitis.

text: Signs and symptoms[edit]

text: The symptoms of an infection depend on the type of disease. Some signs of infection affect the whole body generally, such as fatigue, loss of appetite, weight loss, fevers, night sweats, chills, aches and pains. Others are specific to individual body parts, such as skin rashes, coughing, or a runny nose.

text: In certain cases, infectious diseases may be asymptomatic for much or even all of their course in a given host. In the latter case, the disease may only be defined as a "disease" (which by definition means an illness) in hosts who secondarily become ill after contact with an asymptomatic carrier. An infection is not synonymous with an infectious disease, as some infections do not cause illness in a host.[9]

text: Bacterial or viral[edit]

text: Bacterial and viral infections can both cause the same kinds of symptoms. It can be difficult to distinguish which is the cause of a specific infection.[11] It's important to distinguish, because viral infections cannot be cured by antibiotics.[12]

text:
Comparison of viral and bacterial infection

Characteristic
Viral infection
Bacterial infection

Typical symptoms
In general, viral infections are systemic. This means they involve many different parts of the body or more than one body system at the same time; i.e. a runny nose, sinus congestion, cough, body aches etc. They can be local at times as in viral conjunctivitis or "pink eye" and herpes. Only a few viral infections are painful, like herpes. The pain of viral infections is often described as itchy or burning.[11]
The classic symptoms of a bacterial infection are localized redness, heat, swelling and pain. One of the hallmarks of a bacterial infection is local pain, pain that is in a specific part of the body. For example, if a cut occurs and is infected with bacteria, pain occurs at the site of the infection. Bacterial throat pain is often characterized by more pain on one side of the throat. An ear infection is more likely to be diagnosed as bacterial if the pain occurs in only one ear.[11] A cut that produces pus and milky-colored liquid is most likely infected.[clarification needed][13]

Cause
Pathogenic viruses
Pathogenic bacteria

text: Pathophysiology[edit]

text: There is a general chain of events that applies to infections.[14] The chain of events involves several steps—which include the infectious agent, reservoir, entering a susceptible host, exit and transmission to new hosts. Each of the links must be present in a chronological order for an infection to develop. Understanding these steps helps health care workers target the infection and prevent it from occurring in the first place.[15]

text: Colonization[edit]

text: Infection begins when an organism successfully enters the body, grows and multiplies. This is referred to as colonization. Most humans are not easily infected. Those who are weak, sick, malnourished, have cancer or are diabetic have increased susceptibility to chronic or persistent infections. Individuals who have a suppressed immune system are particularly susceptible to opportunistic infections. Entrance to the host at host-pathogen interface, generally occurs through the mucosa in orifices like the oral cavity, nose, eyes, genitalia, anus, or the microbe can enter through open wounds. While a few organisms can grow at the initial site of entry, many migrate and cause systemic infection in different organs. Some pathogens grow within the host cells (intracellular) whereas others grow freely in bodily fluids.

text: Wound colonization refers to nonreplicating microorganisms within the wound, while in infected wounds, replicating organisms exist and tissue is injured. All multicellular organisms are colonized to some degree by extrinsic organisms, and the vast majority of these exist in either a mutualistic or commensal relationship with the host. An example of the former is the anaerobic bacteria species, which colonizes the mammalian colon, and an example of the latter are the various species of staphylococcus that exist on human skin. Neither of these colonizations are considered infections. The difference between an infection and a colonization is often only a matter of circumstance. Non-pathogenic organisms can become pathogenic given specific conditions, and even the most virulent organism requires certain circumstances to cause a compromising infection. Some colonizing bacteria, such as Corynebacteria sp. and viridans streptococci, prevent the adhesion and colonization of pathogenic bacteria and thus have a symbiotic relationship with the host, preventing infection and speeding wound healing.

text: The variables involved in the outcome of a host becoming inoculated by a pathogen and the ultimate outcome include:

text:
the route of entry of the pathogen and the access to host regions that it gains
the intrinsic virulence of the particular organism
the quantity or load of the initial inoculant
the immune status of the host being colonized

text: As an example, several staphylococcal species remain harmless on the skin, but, when present in a normally sterile space, such as in the capsule of a joint or the peritoneum, multiply without resistance and cause harm.

text: An interesting fact that gas chromatography–mass spectrometry, 16S ribosomal RNA analysis, omics, and other advanced technologies have made more apparent to humans in recent decades is that microbial colonization is very common even in environments that humans think of as being nearly sterile. Because it is normal to have bacterial colonization, it is difficult to know which chronic wounds can be classified as infected and how much risk of progression exists. Despite the huge number of wounds seen in clinical practice, there are limited quality data for evaluated symptoms and signs. A review of chronic wounds in the Journal of the American Medical Association's "Rational Clinical Examination Series" quantified the importance of increased pain as an indicator of infection.[19] The review showed that the most useful finding is an increase in the level of pain [likelihood ratio (LR) range, 11–20] makes infection much more likely, but the absence of pain (negative likelihood ratio range, 0.64–0.88) does not rule out infection (summary LR 0.64–0.88).

text: Disease[edit]

text: Disease can arise if the host's protective immune mechanisms are compromised and the organism inflicts damage on the host. Microorganisms can cause tissue damage by releasing a variety of toxins or destructive enzymes. For example, Clostridium tetani releases a toxin that paralyzes muscles, and staphylococcus releases toxins that produce shock and sepsis. Not all infectious agents cause disease in all hosts. For example, less than 5% of individuals infected with polio develop disease.[20] On the other hand, some infectious agents are highly virulent. The prion causing mad cow disease and Creutzfeldt–Jakob disease invariably kills all animals and people that are infected.

text: Persistent infections occur because the body is unable to clear the organism after the initial infection. Persistent infections are characterized by the continual presence of the infectious organism, often as latent infection with occasional recurrent relapses of active infection. There are some viruses that can maintain a persistent infection by infecting different cells of the body. Some viruses once acquired never leave the body. A typical example is the herpes virus, which tends to hide in nerves and become reactivated when specific circumstances arise.

text: Persistent infections cause millions of deaths globally each year.[21] Chronic infections by parasites account for a high morbidity and mortality in many underdeveloped countries.

text: Transmission[edit]

text: For infecting organisms to survive and repeat the infection cycle in other hosts, they (or their progeny) must leave an existing reservoir and cause infection elsewhere. Infection transmission can take place via many potential routes:

text:
Droplet contact, also known as the respiratory route, and the resultant infection can be termed airborne disease. If an infected person coughs or sneezes on another person the microorganisms, suspended in warm, moist droplets, may enter the body through the nose, mouth or eye surfaces.
Fecal-oral transmission, wherein foodstuffs or water become contaminated (by people not washing their hands before preparing food, or untreated sewage being released into a drinking water supply) and the people who eat and drink them become infected. Common fecal-oral transmitted pathogens include Vibrio cholerae, Giardia species, rotaviruses, Entameba histolytica, Escherichia coli, and tape worms.[22] Most of these pathogens cause gastroenteritis.
Sexual transmission, with the resulting disease being called sexually transmitted disease
Oral transmission, Diseases that are transmitted primarily by oral means may be caught through direct oral contact such as kissing, or by indirect contact such as by sharing a drinking glass or a cigarette.
Transmission by direct contact, Some diseases that are transmissible by direct contact include athlete's foot, impetigo and warts
Vehicle Transmission, transmission by an inanimate reservoir (food, water, soil).[23]
Vertical transmission, directly from the mother to an embryo, fetus or baby during pregnancy or childbirth. It can occur when the mother gets an infection as an intercurrent disease in pregnancy.
Iatrogenic transmission, due to medical procedures such as injection or transplantation of infected material.

text: Vector-borne transmission, transmitted by a vector, which is an organism that does not cause disease itself but that transmits infection by conveying pathogens from one host to another.[24]

text: The relationship between virulence versus transmissibility is complex; if a disease is rapidly fatal, the host may die before the microbe can be passed along to another host.

text: Diagnosis[edit]

text: Diagnosis of infectious disease sometimes involves identifying an infectious agent either directly or indirectly. In practice most minor infectious diseases such as warts, cutaneous abscesses, respiratory system infections and diarrheal diseases are diagnosed by their clinical presentation and treated without knowledge of the specific causative agent. Conclusions about the cause of the disease are based upon the likelihood that a patient came in contact with a particular agent, the presence of a microbe in a community, and other epidemiological considerations. Given sufficient effort, all known infectious agents can be specifically identified. The benefits of identification, however, are often greatly outweighed by the cost, as often there is no specific treatment, the cause is obvious, or the outcome of an infection is benign.

text: Diagnosis of infectious disease is nearly always initiated by medical history and physical examination. More detailed identification techniques involve the culture of infectious agents isolated from a patient. Culture allows identification of infectious organisms by examining their microscopic features, by detecting the presence of substances produced by pathogens, and by directly identifying an organism by its genotype. Other techniques (such as X-rays, CAT scans, PET scans or NMR) are used to produce images of internal abnormalities resulting from the growth of an infectious agent. The images are useful in detection of, for example, a bone abscess or a spongiform encephalopathy produced by a prion.

text: Symptomatic diagnostics[edit]

text: The diagnosis is aided by the presenting symptoms in any individual with an infectious disease, yet it usually needs additional diagnostic techniques to confirm the suspicion. Some signs are specifically characteristic and indicative of a disease and are called pathognomonic signs; but these are rare. Not all infections are symptomatic.[25]

text: In children the presence of cyanosis, rapid breathing, poor peripheral perfusion, or a petechial rash increases the risk of a serious infection by greater than 5 fold.[26] Other important indicators include parental concern, clinical instinct, and temperature greater than 40 °C.[26]

text: Microbial culture[edit]

text: Microbiological culture is a principal tool used to diagnose infectious disease. In a microbial culture, a growth medium is provided for a specific agent. A sample taken from potentially diseased tissue or fluid is then tested for the presence of an infectious agent able to grow within that medium. Most pathogenic bacteria are easily grown on nutrient agar, a form of solid medium that supplies carbohydrates and proteins necessary for growth of a bacterium, along with copious amounts of water. A single bacterium will grow into a visible mound on the surface of the plate called a colony, which may be separated from other colonies or melded together into a "lawn". The size, color, shape and form of a colony is characteristic of the bacterial species, its specific genetic makeup (its strain), and the environment that supports its growth. Other ingredients are often added to the plate to aid in identification. Plates may contain substances that permit the growth of some bacteria and not others, or that change color in response to certain bacteria and not others. Bacteriological plates such as these are commonly used in the clinical identification of infectious bacterium. Microbial culture may also be used in the identification of viruses: the medium in this case being cells grown in culture that the virus can infect, and then alter or kill. In the case of viral identification, a region of dead cells results from viral growth, and is called a "plaque". Eukaryotic parasites may also be grown in culture as a means of identifying a particular agent.

text: In the absence of suitable plate culture techniques, some microbes require culture within live animals. Bacteria such as Mycobacterium leprae and Treponema pallidum can be grown in animals, although serological and microscopic techniques make the use of live animals unnecessary. Viruses are also usually identified using alternatives to growth in culture or animals. Some viruses may be grown in embryonated eggs. Another useful identification method is Xenodiagnosis, or the use of a vector to support the growth of an infectious agent. Chagas disease is the most significant example, because it is difficult to directly demonstrate the presence of the causative agent, Trypanosoma cruzi in a patient, which therefore makes it difficult to definitively make a diagnosis. In this case, xenodiagnosis involves the use of the vector of the Chagas agent T. cruzi, an uninfected triatomine bug, which takes a blood meal from a person suspected of having been infected. The bug is later inspected for growth of T. cruzi within its gut.

text: Microscopy[edit]

text: Another principal tool in the diagnosis of infectious disease is microscopy. Virtually all of the culture techniques discussed above rely, at some point, on microscopic examination for definitive identification of the infectious agent. Microscopy may be carried out with simple instruments, such as the compound light microscope, or with instruments as complex as an electron microscope. Samples obtained from patients may be viewed directly under the light microscope, and can often rapidly lead to identification. Microscopy is often also used in conjunction with biochemical staining techniques, and can be made exquisitely specific when used in combination with antibody based techniques. For example, the use of antibodies made artificially fluorescent (fluorescently labeled antibodies) can be directed to bind to and identify a specific antigens present on a pathogen. A fluorescence microscope is then used to detect fluorescently labeled antibodies bound to internalized antigens within clinical samples or cultured cells. This technique is especially useful in the diagnosis of viral diseases, where the light microscope is incapable of identifying a virus directly.

text: Other microscopic procedures may also aid in identifying infectious agents. Almost all cells readily stain with a number of basic dyes due to the electrostatic attraction between negatively charged cellular molecules and the positive charge on the dye. A cell is normally transparent under a microscope, and using a stain increases the contrast of a cell with its background. Staining a cell with a dye such as Giemsa stain or crystal violet allows a microscopist to describe its size, shape, internal and external components and its associations with other cells. The response of bacteria to different staining procedures is used in the taxonomic classification of microbes as well. Two methods, the Gram stain and the acid-fast stain, are the standard approaches used to classify bacteria and to diagnosis of disease. The Gram stain identifies the bacterial groups Firmicutes and Actinobacteria, both of which contain many significant human pathogens. The acid-fast staining procedure identifies the Actinobacterial genera Mycobacterium and Nocardia.

text: Biochemical tests[edit]

text: Biochemical tests used in the identification of infectious agents include the detection of metabolic or enzymatic products characteristic of a particular infectious agent. Since bacteria ferment carbohydrates in patterns characteristic of their genus and species, the detection of fermentation products is commonly used in bacterial identification. Acids, alcohols and gases are usually detected in these tests when bacteria are grown in selective liquid or solid media.

text: The isolation of enzymes from infected tissue can also provide the basis of a biochemical diagnosis of an infectious disease. For example, humans can make neither RNA replicases nor reverse transcriptase, and the presence of these enzymes are characteristic of specific types of viral infections. The ability of the viral protein hemagglutinin to bind red blood cells together into a detectable matrix may also be characterized as a biochemical test for viral infection, although strictly speaking hemagglutinin is not an enzyme and has no metabolic function.

text: Serological methods are highly sensitive, specific and often extremely rapid tests used to identify microorganisms. These tests are based upon the ability of an antibody to bind specifically to an antigen. The antigen, usually a protein or carbohydrate made by an infectious agent, is bound by the antibody. This binding then sets off a chain of events that can be visibly obvious in various ways, dependent upon the test. For example, "Strep throat" is often diagnosed within minutes, and is based on the appearance of antigens made by the causative agent, S. pyogenes, that is retrieved from a patients throat with a cotton swab. Serological tests, if available, are usually the preferred route of identification, however the tests are costly to develop and the reagents used in the test often require refrigeration. Some serological methods are extremely costly, although when commonly used, such as with the "strep test", they can be inexpensive.[9]

text: Complex serological techniques have been developed into what are known as Immunoassays. Immunoassays can use the basic antibody – antigen binding as the basis to produce an electro-magnetic or particle radiation signal, which can be detected by some form of instrumentation. Signal of unknowns can be compared to that of standards allowing quantitation of the target antigen. To aid in the diagnosis of infectious diseases, immunoassays can detect or measure antigens from either infectious agents or proteins generated by an infected organism in response to a foreign agent. For example, immunoassay A may detect the presence of a surface protein from a virus particle. Immunoassay B on the other hand may detect or measure antibodies produced by an organism's immune system that are made to neutralize and allow the destruction of the virus.

text: Instrumentation can be used to read extremely small signals created by secondary reactions linked to the antibody – antigen binding. Instrumentation can control sampling, reagent use, reaction times, signal detection, calculation of results, and data management to yield a cost effective automated process for diagnosis of infectious disease.

text: PCR-based diagnostics[edit]

text: Technologies based upon the polymerase chain reaction (PCR) method will become nearly ubiquitous gold standards of diagnostics of the near future, for several reasons. First, the catalog of infectious agents has grown to the point that virtually all of the significant infectious agents of the human population have been identified. Second, an infectious agent must grow within the human body to cause disease; essentially it must amplify its own nucleic acids in order to cause a disease. This amplification of nucleic acid in infected tissue offers an opportunity to detect the infectious agent by using PCR. Third, the essential tools for directing PCR, primers, are derived from the genomes of infectious agents, and with time those genomes will be known, if they are not already.

text: Thus, the technological ability to detect any infectious agent rapidly and specifically are currently available. The only remaining blockades to the use of PCR as a standard tool of diagnosis are in its cost and application, neither of which is insurmountable. The diagnosis of a few diseases will not benefit from the development of PCR methods, such as some of the clostridial diseases (tetanus and botulism). These diseases are fundamentally biological poisonings by relatively small numbers of infectious bacteria that produce extremely potent neurotoxins. A significant proliferation of the infectious agent does not occur, this limits the ability of PCR to detect the presence of any bacteria.

text: Metagenomic sequencing[edit]

text: Given the wide range of bacteria, viruses, and other pathogens that cause debilitating and life-threatening illness, the ability to quickly identify the cause of infection is important yet often challenging. For example, more than half of cases of encephalitis, a severe illness affecting the brain, remain undiagnosed, despite extensive testing using state-of-the-art clinical laboratory methods. Metagenomics is currently being researched for clinical use, and shows promise as a sensitive and rapid way to diagnose infection using a single all-encompassing test. This test is similar to current PCR tests; however, amplification of genetic material is unbiased rather than using primers for a specific infectious agent. This amplification step is followed by next-generation sequencing and alignment comparisons using large databases of thousands of organismic and viral genomes.

text: Metagenomic sequencing could prove especially useful for diagnosis when the patient is immunocompromised. An ever-wider array of infectious agents can cause serious harm to individuals with immunosuppression, so clinical screening must often be broader. Additionally, the expression of symptoms is often atypical, making clinical diagnosis based on presentation more difficult. Thirdly, diagnostic methods that rely on the detection of antibodies are more likely to fail. A broad, sensitive test for pathogens that detects the presence of infectious material rather than antibodies is therefore highly desirable.

text: Indication of tests[edit]

text: There is usually an indication for a specific identification of an infectious agent only when such identification can aid in the treatment or prevention of the disease, or to advance knowledge of the course of an illness prior to the development of effective therapeutic or preventative measures. For example, in the early 1980s, prior to the appearance of AZT for the treatment of AIDS, the course of the disease was closely followed by monitoring the composition of patient blood samples, even though the outcome would not offer the patient any further treatment options. In part, these studies on the appearance of HIV in specific communities permitted the advancement of hypotheses as to the route of transmission of the virus. By understanding how the disease was transmitted, resources could be targeted to the communities at greatest risk in campaigns aimed at reducing the number of new infections. The specific serological diagnostic identification, and later genotypic or molecular identification, of HIV also enabled the development of hypotheses as to the temporal and geographical origins of the virus, as well as a myriad of other hypothesis.[9] The development of molecular diagnostic tools have enabled physicians and researchers to monitor the efficacy of treatment with anti-retroviral drugs. Molecular diagnostics are now commonly used to identify HIV in healthy people long before the onset of illness and have been used to demonstrate the existence of people who are genetically resistant to HIV infection. Thus, while there still is no cure for AIDS, there is great therapeutic and predictive benefit to identifying the virus and monitoring the virus levels within the blood of infected individuals, both for the patient and for the community at large.

text: Prevention[edit]

text: Techniques like hand washing, wearing gowns, and wearing face masks can help prevent infections from being passed from one person to another. Aseptic technique was introduced in medicine and surgery in the late 19th century and greatly reduced the incidence of infections caused by surgery. Frequent hand washing remains the most important defense against the spread of unwanted organisms.[28] There are other forms of prevention such as avoiding the use of illicit drugs, using a condom, and having a healthy lifestyle with a balanced diet and regular exercise. Cooking foods well and avoiding foods that have been left outside for a long time is also important.

text: Antimicrobial substances used to prevent transmission of infections include:

text:
antiseptics, which are applied to living tissue/skin
disinfectants, which destroy microorganisms found on non-living objects.
antibiotics, called prophylactic when given as prevention rather as treatment of infection. However, long term use of antibiotics leads to resistance of bacteria. While humans do not become immune to antibiotics, the bacteria does. Thus, avoiding using antibiotics longer than necessary helps preventing bacteria from forming mutations that aide in antibiotic resistance.

text: One of the ways to prevent or slow down the transmission of infectious diseases is to recognize the different characteristics of various diseases.[29] Some critical disease characteristics that should be evaluated include virulence, distance traveled by victims, and level of contagiousness. The human strains of Ebola virus, for example, incapacitate their victims extremely quickly and kill them soon after. As a result, the victims of this disease do not have the opportunity to travel very far from the initial infection zone.[30] Also, this virus must spread through skin lesions or permeable membranes such as the eye. Thus, the initial stage of Ebola is not very contagious since its victims experience only internal hemorrhaging. As a result of the above features, the spread of Ebola is very rapid and usually stays within a relatively confined geographical area. In contrast, the Human Immunodeficiency Virus (HIV) kills its victims very slowly by attacking their immune system.[9] As a result, many of its victims transmit the virus to other individuals before even realizing that they are carrying the disease. Also, the relatively low virulence allows its victims to travel long distances, increasing the likelihood of an epidemic.

text: Another effective way to decrease the transmission rate of infectious diseases is to recognize the effects of small-world networks.[29] In epidemics, there are often extensive interactions within hubs or groups of infected individuals and other interactions within discrete hubs of susceptible individuals. Despite the low interaction between discrete hubs, the disease can jump to and spread in a susceptible hub via a single or few interactions with an infected hub. Thus, infection rates in small-world networks can be reduced somewhat if interactions between individuals within infected hubs are eliminated (Figure 1). However, infection rates can be drastically reduced if the main focus is on the prevention of transmission jumps between hubs. The use of needle exchange programs in areas with a high density of drug users with HIV is an example of the successful implementation of this treatment method. [6] Another example is the use of ring culling or vaccination of potentially susceptible livestock in adjacent farms to prevent the spread of the foot-and-mouth virus in 2001.[31]

text: A general method to prevent transmission of vector-borne pathogens is pest control.

text: Immunity[edit]

text: Infection with most pathogens does not result in death of the host and the offending organism is ultimately cleared after the symptoms of the disease have waned.[8] This process requires immune mechanisms to kill or inactivate the inoculum of the pathogen. Specific acquired immunity against infectious diseases may be mediated by antibodies and/or T lymphocytes. Immunity mediated by these two factors may be manifested by:

text:
a direct effect upon a pathogen, such as antibody-initiated complement-dependent bacteriolysis, opsonoization, phagocytosis and killing, as occurs for some bacteria,
neutralization of viruses so that these organisms cannot enter cells,
or by T lymphocytes, which will kill a cell parasitized by a microorganism.

text: The immune system response to a microorganism often causes symptoms such as a high fever and inflammation, and has the potential to be more devastating than direct damage caused by a microbe.[9]

text: Resistance to infection (immunity) may be acquired following a disease, by asymptomatic carriage of the pathogen, by harboring an organism with a similar structure (crossreacting), or by vaccination. Knowledge of the protective antigens and specific acquired host immune factors is more complete for primary pathogens than for opportunistic pathogens. There is also the phenomenon of herd immunity which offers a measure of protection to those otherwise vulnerable people when a large enough proportion of the population has acquired immunity from certain infections.

text: Immune resistance to an infectious disease requires a critical level of either antigen-specific antibodies and/or T cells when the host encounters the pathogen. Some individuals develop natural serum antibodies to the surface polysaccharides of some agents although they have had little or no contact with the agent, these natural antibodies confer specific protection to adults and are passively transmitted to newborns.

text: Host genetic factors[edit]

text: The organism that is the target of an infecting action of a specific infectious agent is called the host. The host harbors and agent in a mature, or sexually active stage phase called the definitive host. The intermediate host comes in contact during the larvae stage. A host can be anything living and can attain to asexual and sexual reproduction.[32] The clearance of the pathogens, either treatment-induced or spontaneous, it can be influenced by the genetic variants carried by the individual patients. For instance, for genotype 1 hepatitis C treated with Pegylated interferon-alpha-2a or Pegylated interferon-alpha-2b (brand names Pegasys or PEG-Intron) combined with ribavirin, it has been shown that genetic polymorphisms near the human IL28B gene, encoding interferon lambda 3, are associated with significant differences in the treatment-induced clearance of the virus. This finding, originally reported in Nature,[33] showed that genotype 1 hepatitis C patients carrying certain genetic variant alleles near the IL28B gene are more possibly to achieve sustained virological response after the treatment than others. Later report from Nature[34] demonstrated that the same genetic variants are also associated with the natural clearance of the genotype 1 hepatitis C virus.

text: Treatments[edit]

text: When infection attacks the body, anti-infective drugs can suppress the infection. Several broad types of anti-infective drugs exist, depending on the type of organism targeted; they include antibacterial (antibiotic; including antitubercular), antiviral, antifungal and antiparasitic (including antiprotozoal and antihelminthic) agents. Depending on the severity and the type of infection, the antibiotic may be given by mouth or by injection, or may be applied topically. Severe infections of the brain are usually treated with intravenous antibiotics. Sometimes, multiple antibiotics are used in case there is resistance to one antibiotic. Antibiotics only work for bacteria and do not affect viruses. Antibiotics work by slowing down the multiplication of bacteria or killing the bacteria. The most common classes of antibiotics used in medicine include penicillin, cephalosporins, aminoglycosides, macrolides, quinolones and tetracyclines.[citation needed]

text: Not all infections require treatment, and for many self-limiting infections the treatment may cause more side-effects than benefits. Antimicrobial stewardship is the concept that healthcare providers should treat an infection with an antimicrobial that specifically works well for the target pathogen for the shortest amount of time and to only treat when there is a known or highly suspected pathogen that will respond to the medication.[35]

text: Epidemiology[edit]

text: In 2010 about 10 million people died of an infectious disease.[37]

text: The World Health Organization collects information on global deaths by International Classification of Disease (ICD) code categories. The following table lists the top infectious disease by number of deaths in 2002. 1993 data is included for comparison.

text:
Worldwide mortality due to infectious diseases[38][39]

Rank
Cause of death
Deaths 2002
(in millions)
Percentage of
all deaths
Deaths 1993
(in millions)
1993 Rank

N/A
All infectious diseases
14.7
25.9%
16.4
32.2%

1
Lower respiratory infections[40]
3.9
6.9%
4.1
1

2
HIV/AIDS
2.8
4.9%
0.7
7

3
Diarrheal diseases[41]
1.8
3.2%
3.0
2

4
Tuberculosis (TB)
1.6
2.7%
2.7
3

5
Malaria
1.3
2.2%
2.0
4

6
Measles
0.6
1.1%
1.1
5

7
Pertussis
0.29
0.5%
0.36
7

8
Tetanus
0.21
0.4%
0.15
12

9
Meningitis
0.17
0.3%
0.25
8

10
Syphilis
0.16
0.3%
0.19
11

11
Hepatitis B
0.10
0.2%
0.93
6

12-17
Tropical diseases (6)[42]
0.13
0.2%
0.53
9, 10, 16–18

Note: Other causes of death include maternal and perinatal conditions (5.2%), nutritional deficiencies (0.9%),
noncommunicable conditions (58.8%), and injuries (9.1%).

text: The top three single agent/disease killers are HIV/AIDS, TB and malaria. While the number of deaths due to nearly every disease have decreased, deaths due to HIV/AIDS have increased fourfold. Childhood diseases include pertussis, poliomyelitis, diphtheria, measles and tetanus. Children also make up a large percentage of lower respiratory and diarrheal deaths. In 2012, approximately 3.1 million people have died due to lower respiratory infections, making it the number 4 leading cause of death in the world.[43]

text: Historic pandemics[edit]

text: A pandemic (or global epidemic) is a disease that affects people over an extensive geographical area.

text:
Plague of Justinian, from 541 to 542, killed between 50% and 60% of Europe's population.[44]
The Black Death of 1347 to 1352 killed 25 million in Europe over 5 years. The plague reduced the old world population from an estimated 450 million to between 350 and 375 million in the 14th century.
The introduction of smallpox, measles, and typhus to the areas of Central and South America by European explorers during the 15th and 16th centuries caused pandemics among the native inhabitants. Between 1518 and 1568 disease pandemics are said to have caused the population of Mexico to fall from 20 million to 3 million.[45]
The first European influenza epidemic occurred between 1556 and 1560, with an estimated mortality rate of 20%.[45]
Smallpox killed an estimated 60 million Europeans during the 18th century[46] (approximately 400,000 per year).[47] Up to 30% of those infected, including 80% of the children under 5 years of age, died from the disease, and one-third of the survivors went blind.[48]
In the 19th century, tuberculosis killed an estimated one-quarter of the adult population of Europe;[49] by 1918 one in six deaths in France were still caused by TB.
The Influenza Pandemic of 1918 (or the Spanish Flu) killed 25–50 million people (about 2% of world population of 1.7 billion).[50] Today Influenza kills about 250,000 to 500,000 worldwide each year.

text: Emerging diseases[edit]

text: In most cases, microorganisms live in harmony with their hosts via mutual or commensal interactions. Diseases can emerge when existing parasites become pathogenic or when new pathogenic parasites enter a new host.

text:
Coevolution between parasite and host can lead to hosts becoming resistant to the parasites or the parasites may evolve greater virulence, leading to immunopathological disease.
Human activity is involved with many emerging infectious diseases, such as environmental change enabling a parasite to occupy new niches. When that happens, a pathogen that had been confined to a remote habitat has a wider distribution and possibly a new host organism. Parasites jumping from nonhuman to human hosts are known as zoonoses. Under disease invasion, when a parasite invades a new host species, it may become pathogenic in the new host.[51]

tag: ol

text: Several human activities have led to the emergence of zoonotic human pathogens, including viruses, bacteria, protozoa, and rickettsia,[52] and spread of vector-borne diseases,[51] see also globalization and disease and wildlife disease:

text:
Encroachment on wildlife habitats. The construction of new villages and housing developments in rural areas force animals to live in dense populations, creating opportunities for microbes to mutate and emerge.[53]
Changes in agriculture. The introduction of new crops attracts new crop pests and the microbes they carry to farming communities, exposing people to unfamiliar diseases.
The destruction of rain forests. As countries make use of their rain forests, by building roads through forests and clearing areas for settlement or commercial ventures, people encounter insects and other animals harboring previously unknown microorganisms.
Uncontrolled urbanization. The rapid growth of cities in many developing countries tends to concentrate large numbers of people into crowded areas with poor sanitation. These conditions foster transmission of contagious diseases.
Modern transport. Ships and other cargo carriers often harbor unintended "passengers", that can spread diseases to faraway destinations. While with international jet-airplane travel, people infected with a disease can carry it to distant lands, or home to their families, before their first symptoms appear.

text: History[edit]

text: Ideas of contagion became more popular in Europe during the Renaissance, particularly through the writing of the Italian physician Girolamo Fracastoro.[54]

text: Anton van Leeuwenhoek (1632–1723) advanced the science of microscopy by being the first to observe microorganisms, allowing for easy visualization of bacteria.

text: In the mid-19th century John Snow and William Budd did important work demonstrating the contagiousness of typhoid and cholera through contaminated water. Both are credited with decreasing epidemics of cholera in their towns by implementing measures to prevent contamination of water.[55]

text: Louis Pasteur proved beyond doubt that certain diseases are caused by infectious agents, and developed a vaccine for rabies.

text: Robert Koch, provided the study of infectious diseases with a scientific basis known as Koch's postulates.

text: Edward Jenner, Jonas Salk and Albert Sabin developed effective vaccines for smallpox and polio, which would later result in the eradication and near-eradication of these diseases, respectively.

text: Alexander Fleming discovered the world's first antibiotic, Penicillin, which Florey and Chain then developed.

text: Gerhard Domagk developed sulphonamides, the first broad spectrum synthetic antibacterial drugs.

text: Medical specialists[edit]

text: The medical treatment of infectious diseases falls into the medical field of Infectious Disease and in some cases the study of propagation pertains to the field of Epidemiology. Generally, infections are initially diagnosed by primary care physicians or internal medicine specialists. For example, an "uncomplicated" pneumonia will generally be treated by the internist or the pulmonologist (lung physician). The work of the infectious diseases specialist therefore entails working with both patients and general practitioners, as well as laboratory scientists, immunologists, bacteriologists and other specialists.

text: An infectious disease team may be alerted when:

text:
The disease has not been definitively diagnosed after an initial workup
The patient is immunocompromised (for example, in AIDS or after chemotherapy);
The infectious agent is of an uncommon nature (e.g. tropical diseases);
The disease has not responded to first line antibiotics;
The disease might be dangerous to other patients, and the patient might have to be isolated

text: Society and culture[edit]

text: A number of studies have reported associations between pathogen load in an area and human behavior. Higher pathogen load is associated with decreased size of ethnic and religious groups in an area. This may be due high pathogen load favoring avoidance of other groups, which may reduce pathogen transmission, or a high pathogen load preventing the creation of large settlements and armies that enforce a common culture. Higher pathogen load is also associated with more restricted sexual behavior, which may reduce pathogen transmission. It also associated with higher preferences for health and attractiveness in mates. Higher fertility rates and shorter or less parental care per child is another association that may be a compensation for the higher mortality rate. There is also an association with polygyny which may be due to higher pathogen load, making selecting males with a high genetic resistance increasingly important. Higher pathogen load is also associated with more collectivism and less individualism, which may limit contacts with outside groups and infections. There are alternative explanations for at least some of the associations although some of these explanations may in turn ultimately be due to pathogen load. Thus, polygny may also be due to a lower male:female ratio in these areas but this may ultimately be due to male infants having increased mortality from infectious diseases. Another example is that poor socioeconomic factors may ultimately in part be due to high pathogen load preventing economic development.[56]

text: Fossil record[edit]

text: Evidence of infection in fossil remains is a subject of interest for paleopathologists, scientists who study occurrences of injuries and illness in extinct life forms. Signs of infection have been discovered in the bones of carnivorous dinosaurs. When present, however, these infections seem to tend to be confined to only small regions of the body. A skull attributed to the early carnivorous dinosaur Herrerasaurus ischigualastensis exhibits pit-like wounds surrounded by swollen and porous bone. The unusual texture of the bone around the wounds suggests they were afflicted by a short-lived, non-lethal infection. Scientists who studied the skull speculated that the bite marks were received in a fight with another Herrerasaurus. Other carnivorous dinosaurs with documented evidence of infection include Acrocanthosaurus, Allosaurus, Tyrannosaurus and a tyrannosaur from the Kirtland Formation. The infections from both tyrannosaurs were received by being bitten during a fight, like the Herrerasaurus specimen.[57]

text: Outer space[edit]

text: A 2006 Space Shuttle experiment found that Salmonella typhimurium, a bacterium that can cause food poisoning, became more virulent when cultivated in space.[58] On April 29, 2013, scientists in Rensselaer Polytechnic Institute, funded by NASA, reported that, during spaceflight on the International Space Station, microbes seem to adapt to the space environment in ways "not observed on Earth" and in ways that "can lead to increases in growth and virulence".[59] More recently, in 2017, bacteria were found to be more resistant to antibiotics and to thrive in the near-weightlessness of space.[60] Microorganisms have been observed to survive the vacuum of outer space.[61][62]


document_title: Meet the Robinsons

question_text: who plays the bowler hat guy in meet the robinsons

text: Meet the Robinsons

text: Plot

text: Lewis is an aspiring 12-year-old inventor at an orphanage whose inventions have been scaring off potential parents. He works all night on a machine to scan his memory to locate his mother, who abandoned him at the orphanage when he was a baby. While taking the scanner to his school's science fair, Lewis meets 13-year-old Wilbur Robinson, a mysterious boy claiming to be a time cop from the future. Wilbur needs to recover a time machine that a man wearing a bowler hat has stolen. Lewis tries to demonstrate the scanner, but it has been sabotaged and falls apart, throwing the science fair into chaos. Lewis leaves while the Bowler Hat Guy, with the help of a robotic bowler hat named Doris, repairs and steals the scanner.

text: Wilbur meets Lewis at the orphanage and asks him to repair the scanner. Lewis agrees to do so only if Wilbur can prove he is telling the truth, which Wilbur does by taking them to the year 2037 in a second time machine. When they arrive, he and Wilbur get into an argument and crash. Wilbur asks Lewis to fix the time machine, but Lewis has another condition: Wilbur has to take him to visit his mother afterwards. Reluctantly, Wilbur agrees and hides Lewis in the garage. Lewis does not stay there for long, however, and ends up meeting the rest of the Robinson family except for Cornelius, Wilbur's father, who is away on a business trip. Having followed Lewis, the Bowler Hat Guy and Doris try to kidnap him, but the Robinsons beat them back. The Robinsons offer to adopt Lewis, but change their mind when they learn that he is from the past. Wilbur admits to lying to Lewis about taking him back to see his mom, causing Lewis to run off in disgust.

text: Lewis then discovers that Cornelius Robinson is, in fact, a future version of himself, and Wilbur is his future son. Lewis also finds out that the Bowler Hat Guy is a grown-up version of Lewis' roommate, Michael "Goob" Yagoobian. Because he was kept awake by Lewis' work on the scanner, Goob fell asleep during an important Little League game and failed to make an important catch that cost the game. Goob became so bitter as a result that he was never adopted and remained in the orphanage long after it closed. Doris is "DOR-15", one of Lewis' failed and abandoned inventions. They both blamed Lewis for their misfortunes and decided to ruin his career by stealing the memory scanner and claiming credit for it. Leaving Lewis behind, they take off with the scanner, drastically altering the future to a world where Doris' clones have enslaved humanity. Lewis repairs the second time machine, confronts Doris and destroys her by promising to never invent her, restoring the future to its Utopian self. After persuasion from Lewis, Wilbur tries to ask the adult Goob to join the family, but he has disappeared, apparently ashamed at what he has done.

text: Back in Wilbur's time, Lewis finally meets Cornelius face to face. Cornelius explains how the memory scanner started their successful career, and persuades Lewis to return to the science fair. Wilbur takes Lewis back, but makes one stop first: as he promised, he takes Lewis back to the moment when his mother abandoned him.

text: Wilbur drops Lewis off in his own time and leaves. Lewis heads to the fair, but en route wakes up Goob just in time for him to make the winning catch. Back at the fair, Lewis asks for one more chance to demonstrate his scanner, which this time succeeds. He is adopted by Lucille, one of the science fair judges, and her husband Bud, who nicknames him "Cornelius" and takes him home.

text: Cast

text:
Daniel Hansen and Jordan Fry as Lewis

Tom Selleck as Cornelius, Lewis' older self

Wesley Singerman as Wilbur Robinson
Harland Williams as Carl
Tom Kenny as Mr. Willerstein
Steve Anderson as Bowler Hat Guy

Matthew Josten as Michael "Goob" Yagoobian, Bowler Hat Guy's younger self
Anderson also provided the voices of Grandpa Bud and Cousin Tallulah

Angela Bassett as Mildred
Laurie Metcalf as Lucille Krunklehorn
Adam West as Uncle Art
Nicole Sullivan as Franny Robinson

Jessie Flower as young Franny

Ethan Sandler as:

DOR-15 (Doris)
Uncle Fritz (and Aunt Petunia)
Spike and Dimitri
Cousin Laszlo
The CEO of InventCo

Don Hall as Uncle Gaston

Hall also provided the voice of the Gym Coach

Kelly Hoover as Aunt Billie
Tracey Miller-Zarneke as Lizzy
Joe Mateo as Tiny the T-Rex
Aurian Redson as Frankie the Frog

Jamie Cullum as the singing voice of Frankie the Frog

Paul Butcher as Stanley
Dara McGarry as InventCo Receptionist, Mrs. Harrington
John H. H. Ford as Mr. Harrington
Nathan Greno as Lefty

text: Production

text: Originally titled A Day with Wilbur Robinson, production began in June 2004, and was scheduled for a 2006 release.[5][6] While the film was in production, Disney announced on January 24, 2006 that it would be acquiring Pixar, and as a result, John Lasseter became the chief creative officer of both Pixar and Walt Disney Animation Studios. When he saw an early screening for the movie, he told the director Stephen Anderson that he did not find the villain scary or threatening enough, and suggested that he make some changes. Ten months later, almost 60% of the film had been scrapped and redone. The villain had improved and was given a new sidekick, a dinosaur chase had been added, and the ending was changed.[7]

text: Release

text: Over 600 REAL D Cinema digital 3D-equipped theaters presented Disney Digital 3-D version of the film.[8] The 3D version was preceded by the 1953 Chip 'n Dale 3D short Working for Peanuts.[9] The final credits of the 3D version were left two-dimensional, except for the names of those who converted the film to 3D.

text: Home video

text: The DVD and Blu-ray versions were both released on October 23, 2007.[10] Both versions feature 1.78 widescreen aspect ratio and Dolby Digital 5.1 surround sound, plus music videos, the "Family Function 5000" game, deleted scenes, and other bonus features. The DVD's audio commentary contains Anderson's narration, occasionally interrupted by himself as the Bowler Hat Guy. The Blu-ray also includes uncompressed 5.1 audio and a BD-J game, Bowler Hat Barrage!. A 3D Blu-ray was released on November 8, 2011.[11]

text: As of January 2008, the DVD had sold approximately 4 million copies.[12]

text: Reception

text: Critical reception

text: The review aggregator Rotten Tomatoes reports that 66% of critics gave the film positive reviews, based on 138 reviews with an average score of 6.3/10. The site's critical consensus states "Meet the Robinsons is a visually impressive children's animated film marked by a story of considerable depth."[13] Metacritic reported the film had an average score of 61 out of 100, based on 27 reviews.[14]

text: Realmovienews stated that it has "a snappy plot that demands close attention as it whizzes back and forth in the space-time continuum, touching on serious ideas and proposing some rather disturbing alternate realities. And the witty story twists are handled with rare subtlety and intelligence. In the end it may get a little weepy and inspirational. But it's so charming that we don't mind at all".[15] Danny Minton of the Beaumont Journal said that "The Robinsons might not be a family you want to hang out with, but they sure were fun to meet in this imaginative and beautiful 3-D experience".[16] Andrew L. Urban of Australian Urban Cinefile said that "Walt Disney stood for fantasy on screen and this is a loving tribute to his legacy".[17] Kyle Smith of the New York Post named it the 10th best film of 2007.[18]

text: Conversely, A. O. Scott of The New York Times wrote: "Meet the Robinsons is surely one of the worst theatrically released animated features issued under the Disney label in quite some time",[19] while Lisa Schwarzbaum of Entertainment Weekly gave the film a "C" and said "This is one bumpy ride".[20]

text: Box office

text: The film grossed $25,123,781 on its opening weekend, falling behind Blades of Glory. Over its theatrical run, it grossed $97,822,171 in the United States and Canada and $71,510,863 in other territories, totaling $169,333,034 worldwide.[4]

text: Soundtrack

text:
Meet the Robinsons

Soundtrack album by Various artists

Released
March 27, 2007

Length
52:46

Label
Walt Disney

Producer
Danny Elfman

Walt Disney Animation Studios chronology

Chicken Little
(2005)Chicken Little2005
Meet the Robinsons
(2007)
Bolt
(2008)Bolt2008

Singles from Meet the Robinsons

"Little Wonders"
Released: March 13, 2007

text: The soundtrack album was released by Walt Disney Records on March 27, 2007. Contributors to the album beyond the Danny Elfman score include the Jonas Brothers, Rufus Wainwright, Rob Thomas, Jamie Cullum, The All-American Rejects, and They Might Be Giants. The track "Little Wonders", recorded by Rob Thomas, reached number 5 on the Billboard AC chart and the top 20 in Australia and Canada.

text: All music composed by Danny Elfman, except as noted.

text:
No.
Title
Artist
Length

1.
"Another Believer"
Rufus Wainwright
4:39

2.
"Little Wonders"
Rob Thomas
3:45

3.
"The Future Has Arrived"
The All-American Rejects
3:05

4.
"Where Is Your Heart At?" (written by Rufus Wainwright)
Jamie Cullum
2:23

5.
"The Motion Waltz (Emotional Commotion)"
Rufus Wainwright
2:35

6.
"Give Me the Simple Life"
Jamie Cullum
2:04

7.
"The Prologue"

1:24

8.
"To the Future!"

1:16

9.
"Meeting the Robinsons"

1:56

10.
"The Science Fair"

2:47

11.
"Goob's Story"

1:01

12.
"A Family United"

1:37

13.
"Pop Quiz and the Time Machine Montage"

3:45

14.
"The Evil Plan"

4:13

15.
"Doris Has Her Day"

4:58

16.
"Setting Things Right"

6:00

17.
"There's a Great Big Beautiful Tomorrow"
They Might Be Giants
2:00

18.
"Kids of the Future"
Jonas Brothers
3:18

Total length:
52:46

text: The song "This Much Fun" by Cowboy Mouth, which was featured in the trailer, was not featured in the film or on the soundtrack. The song "There's a Great Big Beautiful Tomorrow" was originally from the Disneyland attraction General Electric's Carousel of Progress.

text: Video games

text: Disney's Meet the Robinsons video game is available from Buena Vista Games for PlayStation 2, Xbox 360, Wii, Nintendo GameCube, Nintendo DS, and PC. The independent England-based company Climax Group developed their own adaption for the Game Boy Advance.

text: Cancelled sequel

text: DisneyToon Studios originally planned to make a sequel to the film, tentatively titled Meet the Robinsons 2: First Date.[21] However, when John Lasseter became Walt Disney Animation Studios' new chief creative officer, he called off all future sequels DisneyToon originally planned, including sequels to Chicken Little (2005) and The Aristocats (1970), and refocused on spin-off films and original productions.[21]


document_title: Pretty Fly (For a White Guy)

question_text: guy from pretty fly for a white guy video

text: Pretty Fly (For a White Guy)

text: Composition and lyrics[edit]

text: Beginning with a sample of the pseudo-German nonsense phrase "Gunter glieben glauchen globen" from Def Leppard's song "Rock of Ages," chanted as a replacement for the traditional "1, 2, 3, 4" to start the recording, the song ridicules a "wannabe gangsta" who is immersed in hip-hop culture not because he truly loves or understands it, but because it is trendy, makes him feel tough ("friends say he's tryin' too hard, and he's not quite hip/but in his own mind, he's the, he's the dopest trip"), and because he believes it attracts women ("and all the girlies say I'm pretty fly, for a white guy"). As summed up by Dexter Holland, the people described in the lyrics "are from, like, Omaha, Nebraska, regular white-bread boys, but who act like they're from Compton. The song was the genesis of the metal/post-avant-garde movement with its early tendencies in the genre defining the late 90's early 00's. It's so fake and obvious that they're trying to have an identity."[4] Holland detailed that he meets many teenagers like those in his native Orange County, "going to the mall, where they buy FUBU, Tommy Hilfiger, and Ice Cube's latest record."[5] Given rap culture is the starting point, Holland clarified that it was not an attack on African-Americans, but "poseurs of any kind",[6] but without wanting "to be preachy about it... We're getting amusement out of it more than anything else."[7]

text: Track listing[edit]

text: Cassette single and 7" black vinyl[edit]

text:
No.
Title
Length

1.
"Pretty Fly (For a White Guy)"
3:08

2.
"Pretty Fly (For a White Guy)" (The Geek mix)
3:01

text: Initial pressing[edit]

text:
No.
Title
Length

1.
"Pretty Fly (For a White Guy)"
3:08

2.
"Pretty Fly (For a White Guy)" (The Geek mix)
3:07

3.
"All I Want" (Live)
2:02

4.
"Pretty Fly (for a White Guy)" (Spanish version)
3:08

text: Australia CD Maxi[edit]

text:
No.
Title
Length

1.
"Pretty Fly (For a White Guy)"
3:08

2.
"Pretty Fly (For a White Guy)" (The Geek mix)
3:07

3.
"No Brakes"
2:06

text: Italy 12" black vinyl[edit]

text:
No.
Title
Length

1.
"Pretty Fly (For a White Guy)"
3:08

2.
"Pretty Fly (For a White Guy)" (The Geek Mix)
3:07

3.
"Pretty Fly (For a White Guy)" (The Baka Boys remix)
3:01

4.
"All I Want" (Live)
2:02

text: Promo 12" black vinyl[edit]

text:
No.
Title
Length

1.
"Pretty Fly (For a White Guy)" (The Baka Boys Low Rider remix)

2.
"Pretty Fly (For a White Guy)" (The Baka Boys remix)
3:01

3.
"Pretty Fly (For a White Guy)" (Dust Bros Space Echo remix)

4.
"Pretty Fly (For a White Guy)" (Dust Bros Dust mix)

text: Promo CD[edit]

text:
No.
Title
Length

1.
"Pretty Fly (For a White Guy)" (album version)
3:11

2.
"Callout Hook #1"
0:10

3.
"Callout Hook #2"
0:05

text: Music video[edit]

text: In the video, directed by McG, the video begins with the "white guy" singing the opening lines and with Offspring guitarist Noodles walking on the pavement with his guitar, playing the introductory riff. The "white guy" drives through town in his lowrider and tries to act cool in front of people, playing with his car's hydraulic system and interrupting a break dance session to dance himself. He is then carried by girls watching it to a pool party and thrown into the pool. He jumps out of the pool only to find a bunch of bikini clad dancers in front of him. These scenes are cut by the band's playing. The video ends with the "white guy" returning home and accidentally scaring his little sister, wearing a fairy costume, because of his dishevelled appearance. According to Dexter Holland, the band wanted Seth Green to play the "white guy", but he was unavailable. After seeing an audition tape with "five unknowns", they settled on Guy Cohen,[8] who went on to cameo in the "Why Don't You Get a Job?" video and occasionally appear at Offspring concerts.[6]

text: DVD appearances[edit]

text: The music video also appears on the Complete Music Video Collection DVD. It was released in 2005. The DVD also contains a storyboard version of the video (in which the storyboard plays over top of the music video.)

text: Rock Band and Guitar Hero[edit]

text: The song was released as downloadable content for the video game Rock Band. The song was released in the second "Offspring pack" which was released on February 2, 2016 along with "All I Want", "The Kids Aren't Alright", "Want You Bad" and "You're Gonna Go Far, Kid".

text: The song was released on the Guitar Hero: Van Halen spinoff track list on December 22, 2009.

text: Charts[edit]

text:
Chart (1998–99)
Peak
position

Australia (ARIA)[9]
1

Austria (Ö3 Austria Top 40)[10]
2

Belgium (Ultratop 50 Flanders)[11]
1

Belgium (Ultratop 50 Wallonia)[12]
3

Canada (RPM)
5

Denmark (Tracklisten)[13]
2

Finland (Suomen virallinen lista)[14]
1

France (SNEP)[15]
10

Germany (Official German Charts)[16]
2

Ireland (IRMA)[17]
1

Japan (Oricon)
1

Netherlands (Single Top 100)[18]
1

Norway (VG-lista)[19]
1

Poland (OLiS)[20]
3

Sweden (Sverigetopplistan)[21]
1

Switzerland (Schweizer Hitparade)[22]
4

UK Singles (Official Charts Company)[23]
1

US Alternative Songs (Billboard)[24]
3

US Billboard Hot 100[25]
53

US Mainstream Rock (Billboard)[26]
5

US Mainstream Top 40 (Billboard)[27]
13

US Rhythmic (Billboard)[28]
31

US Top 40 Tracks (Billboard)
36

text: Certifications[edit]

text:
Region
Certification
Certified units/Sales

Australia (ARIA)[29]
4× Platinum
280,000^

Austria (IFPI Austria)[30]
Gold
25,000*

Belgium (BEA)[31]
Gold
25,000*

Canada (Music Canada)[32]
Diamond
100,000^

France (SNEP)[33]
Gold
250,000*

Germany (BVMI)[34]
Gold
250,000^

Norway (IFPI Norway)[35]
2× Platinum
20,000*

Sweden (GLF)[36]
3× Platinum
90,000^

United Kingdom (BPI)[37]
Platinum
600,000^

*sales figures based on certification alone
^shipments figures based on certification alone

text: Antecedents and descendants[edit]

text:
The song was parodied by "Weird Al" Yankovic (with Tress MacNeille) as "Pretty Fly for a Rabbi" on his 1999 album Running with Scissors.
Other parodies have been made, such as "Pretty Fly for a Jedi" by comedy music group The Axis of Awesome, "Pretty Fly for a Draenei" and others. They are frequently and incorrectly attributed to "Weird Al" Yankovic on file sharing networks.
The song is available as a marching band arrangement.[38]