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Symptoms and complications

Hepatitis B virus infection may either be acute (self-limiting) or chronic (long-standing). Persons with self-limiting infection clear the infection spontaneously within weeks to months.

Children are less likely than adults to clear the infection. More than 95% of people who become infected as adults or older children will stage a full recovery and develop protective immunity to the virus. However, only 5% of newborns that acquire the infection from their mother at birth will clear the infection. Of those infected between the age of one to six, 70% will clear the infection.[1]

Acute infection with hepatitis B virus is associated with acute viral hepatitis - an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few patients may have more severe liver disease (fulminant hepatic failure), and may die as a result of it. The infection may be entirely asymptomatic and may go unrecognized.

Chronic infection with hepatitis B virus may be either asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (liver cancer). Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer.

Hepatitis D infection can only occur with a concomitant infection with Hepatitis B virus because the Hepatitis D virus uses the Hepatitis B virus surface antigen to form a capsid.[2] Co-infection with hepatitis D increases the risk of liver cirrhosis and liver cancer.[3] Polyarteritis nodosa is more common in people with hepatitis B infection.

Diagnosis

Hepatitis B viral antigens and antibodies detectable in the blood following acute infection.
Hepatitis B viral antigens and antibodies detectable in the blood of a chronically infected person

The tests, called assays, for detection of hepatitis B virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by the host. Interpretation of these assays is complex.[4]

The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. However, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host. The infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of core protein, alternatively known as hepatitis B core antigen, or HBcAg. During this 'window' in which the host remains infected but is successfully clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IgM) may be the only serological evidence of disease.

Shortly after the appearance of the HBsAg, another antigen named as the hepatitis B e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the hepatitis B virus do not produce the 'e' antigen, so this rule does not always hold true. During the natural course of an infection, the HBeAg may be cleared, and antibodies to the 'e' antigen (anti-HBe) will arise immediately afterwards. This conversion is usually associated with a dramatic decline in viral replication.

If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by IgG antibodies to the hepatitis B surface antigen and core antigen, (anti-HBs and anti HBc IgG).[5] A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously.

Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers.[6] Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase levels and inflammation of the liver, as revealed by biopsy. Carriers who have seroconverted to HBeAg negative status, particularly those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others.[7]

More recently, PCR tests have been developed to detect and measure the amount of viral nucleic acid in clinical specimens. These tests are called viral loads and are used to assess a person's infection status and to monitor treatment.[8]

Treatment

Hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously.[9] Early antiviral treatment may only be required in fewer than 1% of patients, whose infection takes a very aggressive course ("fulminant hepatitis") or who are immunocompromised. On the other hand, treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer. Chronically infected individuals with persistently elevated serum alanine aminotransferase, a marker of liver damage, and HBV DNA levels are candidates for therapy.[10]

Although none of the available drugs can clear the infection, they can stop the virus from replicating, and prevent liver damage such as cirrhosis and liver cancer. Treatments include antiviral drugs such as lamivudine, adefovir and entecavir, and immune system modulators such as interferon alpha. However, some individuals are much more likely to respond than others and this might be because of the genotype of the infecting virus or the patient's heredity. The treatment works by reducing the viral load, (the amount of virus particles as measured in the blood), which in turn reduces viral replication in the liver.

On March 29, 2005, the US Food and Drug Administration (FDA) approved Entecavir for the treatment of Hepatitis B.[11] On February 25, 2005, the EU Commission approved Pegasys.[12][13] On October 27, 2006, telbivudine gained FDA approval. It is marketed under the brand name Tyzeka in the US and Sebivo outside the US. It is approved in Switzerland.[14]

Infants born to mothers known to carry hepatitis B can be treated with antibodies to the hepatitis B virus (hepatitis B immune globulin or HBIg). When given with the vaccine within twelve hours of birth, the risk of acquiring hepatitis B is reduced 95%. This treatment allows a mother to safely breastfeed her child.

Vaccination

Main article: Hepatitis B vaccine
HBsAg

Several vaccines have been developed for the prevention of hepatitis B virus infection. These rely on the use of one of the viral envelope proteins (hepatitis B surface antigen or HBsAg). The vaccine was originally prepared from plasma obtained from patients who had long-standing hepatitis B virus infection. However, currently, these are more often made using recombinant DNA technology, though plasma-derived vaccines continue to be used; the two types of vaccines are equally effective and safe.[15]

Following vaccination Hepatitis B Surface antigen may be detected in serum for several days this is known as vaccine antigenaemia.[16]


Genome

The genome of HBV is made of circular DNA, but it is unusual because the DNA is not fully double-stranded. One end of the full length strand is linked to the viral DNA polymerase. The genome is 3020-3320 nucleotides long (for the full length strand) and 1700-2800 nucleotides long (for the short length strand).[17] The negative-sense, (non-coding), is complementary to the viral mRNA. The viral DNA is found in the nucleus soon after infection of the cell. The partially double-stranded DNA is rendered fully double-stranded by completion of the (+) sense strand and removal of a protein molecule from the (-) sense strand and a short sequence of RNA from the (+) sense strand. Non-coding bases are removed from the ends of the (-)sense strand and the ends are rejoined. There are four known genes encoded by the genome called C, X, P, and S. The core protein is coded for by gene C (HBcAg), and its start codon is preceded by an upstream in-frame AUG start codon from which the pre-core protein is produced. HBeAg is produced by proteolytic processing of the pre-core protein. The DNA polymerase is encoded by gene P. Gene S is the gene that codes for the surface antigen (HBsAg). The HBsAg gene is one long open reading frame but contains three in frame "start" (ATG) codons that divide the gene into three sections, pre-S1, pre-S2, and S. Because of the multiple start codons, polypeptides of three different sizes called large, middle, and small (pre-S1 + pre-S2 + S, pre-S2 + S, or S) are produced.[18] The function of the protein coded for by gene X is not fully understood.[19]


Hepatitis B virus (HBV) is a member of the Hepadnavirus family.[5] The virus particle, (virion) consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of protein. The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse transcriptase activity.[20] The outer envelope contains embedded proteins which are involved in viral binding of, and entry into, susceptible cells. The virus is one of the smallest enveloped animal viruses with a virion diameter of 42nm, but pleomorphic forms exist, including filamentous and spherical bodies lacking a core. These particles are not infectious and are composed of the lipid and protein that forms part of the surface of the virion, which is called the surface antigen (HBsAg), and is produced in excess during the life cycle of the virus.[21]

The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. However, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host. The infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of core protein, alternatively known as hepatitis B core antigen, or HBcAg. During this 'window' in which the host remains infected but is successfully clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IgM) may be the only serological evidence of disease.

Shortly after the appearance of the HBsAg, another antigen named as the hepatitis B e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the hepatitis B virus do not produce the 'e' antigen, so this rule does not always hold true. During the natural course of an infection, the HBeAg may be cleared, and antibodies to the 'e' antigen (anti-HBe) will arise immediately afterwards. This conversion is usually associated with a dramatic decline in viral replication.

If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by IgG antibodies to the hepatitis B surface antigen and core antigen, (anti-HBs and anti HBc IgG).[5] A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously.

Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers.[6] Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase levels and inflammation of the liver, as revealed by biopsy. Carriers who have seroconverted to HBeAg negative status, particularly those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others.[7]

More recently, PCR tests have been developed to detect and measure the amount of viral nucleic acid in clinical specimens. These tests are called viral loads and are used to assess a person's infection status and to monitor treatment.[8] The three standard blood tests for hepatitis B can determine if a person is currently infected with HBV, has recovered, is a chronic carrier, or is susceptible to HBV infection:[22]



For the biology of the animal, see Head louse.
Head lice infestation (pediculosis capitis)
Classification and external resources
File:Fig.4.Louse bites.jpg
Head lice bites on the nape of the neck
ICD-10 B85.0
DiseasesDB 9725
MedlinePlus 000840
eMedicine med/1769 
MeSH D010373

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2]

Overview

Head lice infestation[23] (also known as pediculosis capitis, or as "having nits" or "having cooties")[23] the colonization of the hair by the head louse (Pediculus humanus capitis), typically only involves the head or scalp of the human host. Head lice feed on human blood; itching from lice bites is a common symptom of this condition.[24] Treatment includes application of topical insecticides such as a pyrethrin or permethrin, although a variety of herbal remedies are also common.[25]

Lice infestation in general is known as pediculosis, and occurs in many mammalian and bird species.[26] The term pediculosis capitis, or simply "pediculosis", is sometimes used to refer to the specific human pediculosis due to P. humanus capitis (i.e., head-louse infestation)[citation needed]. Humans are hosts for two other lice as well — the body louse and the crab louse.

Head-lice infestation is widely endemic, especially in children. It is a cause of some concern in public health, although, unlike human body lice, head lice are not carriers of other infectious diseases. It has been suggested that in the past, head lice infection has been a mutualistic beneficial condition which helps to defend against the far more dangerous disease-carrying body louse.[27]

Cause

Head lice are generally spread through direct head-to-head contact with an infested person; transmission by sharing bedding or clothing such as headwear is much less common.[28] Body lice are spread through direct contact with the body, clothing or other personal items of a person already carrying lice. Pubic lice are most often spread by intimate contact with an infested person. Head lice occur on the head hair, body lice on the clothing, and pubic lice mainly on the hair near the groin. Human lice do not occur on pets or other animals[citation needed]. Lice do not have wings and cannot jump[citation needed].

From each egg or "nit" may hatch one nymph that will grow and develop to the adult louse[citation needed]. Full-grown lice are found to be the size of a sesame seed. Lice feed on blood 1–8 times each day by piercing the skin with their tiny needle-like mouthparts[citation needed]. Lice cannot burrow into the skin.

Head lice and body lice (Pediculus humanus) are similar in appearance, although the head louse is often smaller.[29] Pubic lice (Pthirus pubis), on the other hand, are quite distinctive. They have shorter bodies and pincer-like claws, and are colloquially known as "crabs"[citation needed]. Head lice are not known to be transmitters of diseases, unlike body lice.

Diagnosis

Lice comb (Bug Buster) wet combing with conditioner for diagnosis and treatment. Head lice can be seen in foam.

The condition is diagnosed by the presence of lice or eggs in the hair, which is facilitated by using a magnifying glass or running a comb through the child's hair. In questionable cases, a child can be referred to a health professional. However, the condition is overdiagnosed, with extinct infestations being mistaken for active ones. As a result, lice-killing treatments are more often used on noninfested than infested children.[30] The use of a louse comb is the most effective way to detect living lice.[31] In cases of children with dirty, long and/or curly/frizzy hair, an alternative method of diagnosis is examination by parting the hair at 2 cm intervals to look for moving lice near the scalp[citation needed]. With both methods, special attention should be paid to the area near the ears and the nape of the neck. The examiner should examine the scalp for at least 5 minutes[citation needed]. The use of a magnifying glass to examine the material collected between the teeth of the comb could prevent misdiagnosis.

The presence of nits alone, however, is not an accurate indicator of an active head louse infestation. Children with nits on their hair have a 35–40% chance of also being infested with living lice and eggs.[31][32] If lice are detected, the entire family needs to be checked (especially children up to the age of 13 years) with a louse comb, and only those who are infested with living lice should be treated. As long as no living lice are detected, the child should be considered negative for head louse infestation. Accordingly, a child should be treated with a pediculicide ONLY when living lice are detected on his/her hair (not because he/she has louse eggs/nits on the hair and not because the scalp is itchy).[33]

Prevention

Examination of the child’s head at regular intervals using a louse comb allows the diagnosis of louse infestation at an early stage. Early diagnosis makes treatment easier and reduces the possibility of infesting others. In times and areas when louse infestations are common, weekly examinations of children, especially those 4–15 yrs old, carried out by their parents will aid control. Additional examinations are necessary if the child came in contact with infested individuals, if the child frequently scratches his/her head, or if nits suddenly appear on the child’s hair. Keeping long hair tidy could be helpful in the prevention of infestations with head lice.

Clothes, towels, bedding, combs and brushes, which came in contact with the infested individual, can be disinfected either by leaving them outside for at least 2 weeks or by washing them at 60°C(140 degrees F) for 30 minutes.[34] This is because adult lice can survive only one to two days without a blood meal, and are highly dependent on human body warmth.[35] An insecticidal treatment of the house and furniture is not necessary.

Treatment

Main article: Treatment of human head lice

Except for recent studies on neem seed extract,[36] there is no product or method which assures 100% destruction of the eggs and hatched lice after a single treatment. However, there are a number of treatment modalities that can be employed with varying degrees of success. These methods include chemical treatments, natural products, combs, shaving, hot air,[37] and silicone-based lotions;[38] however all effective treatments require a two-fold process of killing both the adult lice and the eggs. Generally the eggs (nits) need to be manually picked off one by one in order to ensure all live eggs are removed.

Lice on the hair and body are usually treated with medicated shampoos or cream rinses. Nit combs can be used to remove lice and nits from the hair. Laundering clothes using high heat can eliminate body lice. Efforts to treat should focus on the hair or body (or clothes), and not on the home environment[citation needed].

Some lice have become resistant to certain (but not all) insecticides used in commercially available anti-louse products. A physician or pharmacist can prescribe or suggest treatments. Empty eggs of head lice may remain attached to the hair shaft long after the lice have been eliminated[citation needed], but rarely are adult lice seen even with an active infestation. Since there is no way to determine whether each egg is alive or dead, chemical treatment (which may not kill the eggs) should be considered only when live (crawling) lice are discovered in order to kill the adults. Instead, nitpicking, which is checking each hair strand for eggs and picking off each egg, should be used to prevent the possibility of an egg hatching resulting in reinfestation.

Tea tree oil is one of the few natural ingredients that have been proven to be effective in laboratory tests,[39] but The National Pediculosis Association recommends caution when using tea tree oil for the treatment of pregnant women and young children because of safety concerns.[40] Other home remedies such as putting vinegar, isopropyl alcohol, olive oil, mayonnaise, or melted butter under a shower cap have been disproven.[41] Similarly, the CDC claims that swimming has no effect on treating lice, and can in fact harm the treatment by commercial products.[42]

Epidemiology

Template:Rquote The number of cases of human louse infestations (or pediculosis) has increased worldwide since the mid-1960s, reaching hundreds of millions annually.[43]

Despite improvements in medical treatment and prevention of human diseases during the 20th century, head louse infestation remains stubbornly prevalent. In 1997, 80% of American elementary schools reported at least one outbreak of lice.[44] Lice infestation during that same period was more prevalent than chicken pox.[44]

About 6–12 million children between the ages of 3 and 11 are treated annually for head lice in the United States alone.[28] High levels of louse infestations have also been reported from all over the world including Israel, Denmark, Sweden, U.K., France and Australia.[33][45]

The number of children per family, the sharing of beds and closets, hair washing habits, local customs and social contacts, healthcare in a particular area (e.g. school) and socioeconomic status were found to be significant factors in head louse infestation[citation needed]. Girls are 2–4 times more frequently infested than boys[citation needed]. Children between 4 and 13 years of age are the most frequently infested group.[46] In the U.S., African-American children have lower rates of infestation.[28]

The United Kingdom's National Health Service[citation needed] and many American health agencies [3][4][5] report that lice "prefer" clean hair because it's easier to attach eggs and to cling to the strands; however, this is often contested.

Head lice (Pediculus humanus capitis) infestation is most frequent on children aged 3–10 and their families.[47] Females get head lice twice as often as males,[47] and infestation in persons of Afro-Caribbean or other black descent is rare because of hair consistency.[47] But these children may have nits that hatch and the live lice could be transferred by head contact to other children.[48]

See also

References

  1. ↑ Kerkar N (2005). "Hepatitis B in children: complexities in management". Pediatric transplantation. 9 (5): 685–91. doi:10.1111/j.1399-3046.2005.00393.x. PMID 16176431.
  2. ↑ Taylor JM (2006). "Hepatitis delta virus". Virology. 344 (1): 71–6. doi:10.1016/j.virol.2005.09.033. PMID 16364738.
  3. ↑ Oliveri F, Brunetto MR, Actis GC, Bonino F (1991). "Pathobiology of chronic hepatitis virus infection and hepatocellular carcinoma (HCC)". The Italian journal of gastroenterology. 23 (8): 498–502. PMID 1661197.
  4. ↑ Bonino F, Chiaberge E, Maran E, Piantino P (1987). "Serological markers of HBV infectivity". Ann. Ist. Super. Sanita. 24 (2): 217–23. PMID 3331068.
  5. ↑ 5.0 5.1 5.2 Zuckerman AJ (1996). Hepatitis Viruses. In: Baron's Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
  6. ↑ 6.0 6.1 Lok AS, McMahon BJ (2007). "Chronic hepatitis B". Hepatology. 45 (2): 507–39. doi:10.1002/hep.21513. PMID 17256718.
  7. ↑ 7.0 7.1 Chu CM, Liaw YF (2007). "Predictive factors for reactivation of hepatitis B following hepatitis B e antigen seroconversion in chronic hepatitis B". Gastroenterology. 133 (5): 1458–65. doi:10.1053/j.gastro.2007.08.039. PMID 17935720.
  8. ↑ 8.0 8.1 Zoulim F (2006). "New nucleic acid diagnostic tests in viral hepatitis". Semin. Liver Dis. 26 (4): 309–17. doi:10.1055/s-2006-951602. PMID 17051445.
  9. ↑ Hollinger FB, Lau DT (2006). "Hepatitis B: the pathway to recovery through treatment". Gastroenterol. Clin. North Am. 35 (4): 895–931. doi:10.1016/j.gtc.2006.10.002. PMID 17129820.
  10. ↑ Lai CL, Yuen MF (2007). "The natural history and treatment of chronic hepatitis B: a critical evaluation of standard treatment criteria and end points". Ann. Intern. Med. 147 (1): 58–61. PMID 17606962.
  11. ↑ U.S. Food and Drug Administration. March 30, 2005. FDA Talk Paper: FDA Approves New Treatment for Chronic Hepatitis B. fda.gov. Retrieved on September 11, 2007.
  12. ↑ Hui CK, Lau GK (2005). "Peginterferon-alpha2a (40 kDa) (Pegasys) for hepatitis B". Expert review of anti-infective therapy. 3 (4): 495–504. doi:10.1586/14787210.3.4.495. PMID 16107195.
  13. ↑ February 25, 2005. [http://www.roche.com/med-cor-2005-02-25 Pegasys approved in the European Union for the treatment of chronic hepatitis B: Only pegylated interferon approved for the treatment of chronic hepatitis B Retrieved on September 11, 2007.
  14. ↑ October 27, 2006. FDA Approves Telbivudine for Treatment of Chronic Hepatitis B. hivandhepatitis.com. Retrieved on September 11, 2007.
  15. ↑ Zuckerman JN (2006). "Vaccination against hepatitis A and B: developments, deployment and delusions". Curr. Opin. Infect. Dis. 19 (5): 456–9. doi:10.1097/01.qco.0000244051.23511.09. PMID 16940869.
  16. ↑ Martín-Ancel A, Casas ML, Bonet B (2004). "Implications of postvaccination hepatitis B surface antigenemia in the management of exposures to body fluids". Infect Control Hosp Epidemiol. 25 (7): 611–3. PMID 15301037.
  17. ↑ Kay A, Zoulim F (2007). "Hepatitis B virus genetic variability and evolution". Virus Res. 127 (2): 164–76. PMID 17383765.
  18. ↑ Beck J, Nassal M (2007). "Hepatitis B virus replication". World J. Gastroenterol. 13 (1): 48–64. PMID 17206754.
  19. ↑ Bouchard MJ, Schneider RJ (2004). "The enigmatic X gene of hepatitis B virus". J. Virol. 78 (23): 12725–34. doi:10.1128/JVI.78.23.12725-12734.2004. PMID 15542625.
  20. ↑ Locarnini S (2004). "Molecular virology of hepatitis B virus". Semin. Liver Dis. 24 Suppl 1: 3–10. doi:10.1055/s-2004-828672. PMID 15192795.
  21. ↑ Howard CR (1986). "The biology of hepadnaviruses". J. Gen. Virol. 67 ( Pt 7): 1215–35. PMID 3014045.
  22. ↑ "Hepatitis B".
  23. ↑ 23.0 23.1 Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0.
  24. ↑ Burgess IF (1995). "Human lice and their management". Advances in Parasitology. Advances in Parasitology. 36 (6): 271–342. doi:10.1016/S0065-308X(08)60493-5. ISBN 9780120317363. PMID 7484466. |first2= missing |last2= in Authors list (help); |first3= missing |last3= in Authors list (help)
  25. ↑ Burkhart CG, Burkhart CN, Burkhart KM (June 1998). "An assessment of topical and oral prescription and over-the-counter treatments for head lice". J. Am. Acad. Dermatol. 38 (6 Pt 1): 979–82. doi:10.1016/S0190-9622(98)70163-X. PMID 9632008.
  26. ↑ "Lice (Pediculosis)". The Merck Veterinary Manual. Whitehouse Station, NJ USA: Merck & Co. 2008. Retrieved 2008-10-08.
  27. ↑ Rozsa, Lajos; Apari P. (2012). "Why infest the loved ones – inherent human behaviour indicates former mutualism with head lice" (PDF). Parasitology. 139 (6): in press. doi:10.1017/S0031182012000017. On-line full text available at link
  28. ↑ 28.0 28.1 28.2 Division of Parasitic Diseases (DPD), National Center for Zoonotic, Vector-Borne, and Enteric Diseases (ZVED) (May 16, 2008). "Head lice fact sheet". Centers for Disease Control and Prevention website. Atlanta, GA: Department of Health and Human Services, US Government. Retrieved 28 May 2010.
  29. ↑ Bacot A (1917). "Contributions to the bionomics of Pediculus humanus (vestimenti) and Pediculus capitis". Parasitology. 9 (2): 228–258. doi:10.1017/S0031182000006065.
  30. ↑ Pollack RJ, Kiszewski AE, Spielman A (2000). "Overdiagnosis and consequent mismanagement of head louse infestations in North America". The Pediatric Infectious Diseases Journal. 19 (8): 689–93. doi:10.1097/00006454-200008000-00003. PMID 10959734.
  31. ↑ 31.0 31.1 Mumcuoglu KY, Friger M, Ioffe-Uspensky I, Ben-Ishai F, Miller J (2001). "Louse comb versus direct visual examination for the diagnosis of head louse infestations". Pediatric dermatology. 18 (1): 9–12. doi:10.1046/j.1525-1470.2001.018001009.x. PMID 11207962.
  32. ↑ Williams LK, Reichert A, MacKenzie WR, Hightower AW, Blake PA (2001). "Lice, nits, and school policy". Pediatrics. 107 (5): 1011–5. doi:10.1542/peds.107.5.1011. PMID 11331679.
  33. ↑ 33.0 33.1 Mumcuoglu, Kosta Y.; Barker CS; Burgess IF; Combescot-Lang C; Dagleish RC; Larsen KS; Miller J; Roberts RJ; Taylan-Ozkan A. (2007). "International Guidelines for Effective Control of Head Louse Infestations". Journal of Drugs in Dermatology. 6 (4): 409–14. PMID 17668538.
  34. ↑ Kidshealth.org – Head lice, page-3
  35. ↑ University of Florida Dept of Entomology Circular 175
  36. ↑ "Efficacy of a single treatment of head lice with a neem seed extract: an in vivo and in vitro study on nits and motile stages". Parasitology Research. Springer Science+Business Media. 110 (1): 277–280. 2012-01-01. doi:10.1007/s00436-011-2484-3. Retrieved 2013-12-30.
  37. ↑ Goates BM, BM; Atkin, JS; Wilding, KG; Birch, KG; Cottam, MR; Bush, SE; Clayton, DH; et al. (5 November 2006). "An Effective Nonchemical Treatment for Head Lice: A Lot of Hot Air" (PDF). Pediatrics. American Academy of Pediatrics. 118 (5): 1962–1970. doi:10.1542/peds.2005-1847. PMID 17079567. Retrieved 2010-08-02.
  38. ↑ Ian F Burgess, Medical Entomology Centre, Insect Research & Development Limited (2009). "The mode of action of dimeticone 4% lotion against head lice, Pediculus capitis". BMC Pharmacol. 9: 3. doi:10.1186/1471-2210-9-3. PMC 2652450. PMID 19232080.
  39. ↑ "Activity of tea tree oil and nerolidol alone or in combination against Pediculus capitis (head lice) and its eggs". Parasitology Research. Springer Science+Business Media. 111 (1): 1985–1992. 2012-11-01. doi:10.1007/s00436-012-3045-0. Retrieved 2013-12-30.
  40. ↑ Eisenhower C, Farrington EA (2012). "Advancements in the treatment of head lice in pediatrics". J Pediatr Health Care (Review). 26 (6): 451–61, quiz 462–4. doi:10.1016/j.pedhc.2012.05.004. PMID 23099312.
  41. ↑ "Home Remedies to Control Head Lice: Assessment of Home Remedies to Control the Human Head Louse, Pediculus humanus capitis (Anoplura: Pediculidae)". Pediatric Nursing (journal). Elsevier. 19 (6): 393–398. December 2004. doi:10.1016/j.pedn.2004.11.002. PMID 15637580. Retrieved 2013-12-30.
  42. ↑ http://www.cdc.gov/healthywater/swimming/faq/#get_lice
  43. ↑ Norman G. Gratz (1998). "Human lice: Their prevalence, control and resistance to insecticides. A review 1985–1997" (PDF). Geneva, Switzerland: World Health Organization. Retrieved 2008-01-02.
  44. ↑ 44.0 44.1 "A modern scourge: Parents scratch their heads over lice". Consumer Reports. February 1998. pp. 62–63. Retrieved 2008-10-10.
  45. ↑ Ian Burgess (2004). "Human Lice and their Control". Annual Review of Entomology. Annual Reviews. 49: 457–481. doi:10.1146/annurev.ento.49.061802.123253. PMID 14651472.
  46. ↑ Mumcuoglu KY, Miller J, Gofin R; et al. (September 1990). "Epidemiological studies on head lice infestation in Israel. I. Parasitological examination of children". International Journal of Dermatology. 29 (7): 502–6. doi:10.1111/j.1365-4362.1990.tb04845.x. PMID 2228380.
  47. ↑ 47.0 47.1 47.2 Nutanson I.; et al. (2008). "Pediculus humanus capitis: an update" (PDF). Acta Dermatoven. 17 (4): 147–59.
  48. ↑ James GH Dinulos (September 2008). "Lice (Pediculosis)". The Merck Manual. Merck & Co., Inc. Retrieved 2008-12-27.

External links

Template:Pediculosis, acariasis and other infestations


Treatment

General recommendations for treatment

Main article: Treatment of human head lice

The number of cases of human louse infestations (or pediculosis) has increased worldwide since the mid-1960s, reaching hundreds of millions annually.[1] There is no product or method which assures 100% destruction of the eggs and hatched lice after a single treatment. However, there are a number of treatment modalities that can be employed with varying degrees of success. These methods include chemical treatments, natural products, combs, shaving, hot air, and silicone-based lotions.

Ancient lice - Use in archaeogenetics

Lice are also important in the field of Archaeogenetics. Because most "modern" human diseases have in fact recently jumped from animals into humans through close agricultural contact, and also given fact that Neolithic human populations were too scattered to support contagious "crowd" diseases, lice (along with such parasites as intestinal tapeworms) are considered to be one of the few ancestral disease infestations of humans and other hominids. As such, analysis of mitochondrial lice DNA has been used to map early human and archaic human migrations and living conditions. Because lice can only survive for a few hours or days without a human host, and because lice species are so specific to certain species or areas of the body, the evolutionary history of lice reveals much about human history. It has been demonstrated, for example, that some varieties of human lice went through a population bottleneck about 100,000 years ago (supporting the Single origin hypothesis), and also that hominid lice lineages diverged around 1.18 million years ago (probably infesting Homo erectus) before re-uniting around 100,000 years ago. This recent merging seems to argue against the Multi-regional origin of modern human evolution and argues instead for a close proximity replacement of archaic humans by a migration of anatomically modern humans, either through inter-breeding, fighting, or being more fit to use available resources.

  1. ↑ Gratz, N. (1998). "Human lice, their prevalence and resistance to insecticides". Geneva: World Health Organization (WHO). Check date values in: |date= (help); |access-date= requires |url= (help)
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