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Clinical Updates

Michel Develoux, MD

Head Lice: Epidemiology and Resistance to Pediculicides

Michel Develoux

Wednesday, August 13, 2008

Pediculosis capitis (head lice) is a common ectoparasitosis worldwide. The majority of epidemiologic data come from schoolchildren surveys. Most papers highlight the increased prevalence in head lice over the past decade. Such increase can be explained by the resistance to insecticides and poor response to nonchemical treatments.

Epidemiology of Pediculosis capitis infestations

There are few recent data concerning head lice prevalence in developed countries. Of 21,556 school children surveyed in the United Kingdom, 2.03% had head lice at the time of examination and overall the annual prevalence apperared to be 37.4%. In Ghent, Belgium, in a total of 6,169 school children aged 2.5 to 12 years, the prevalence of head lice was 8.9%.2 More recent studies have come from Denmark and France, where 14.4% and 3.3% of screened schoolchildren, respectively, were infested.3,4 Data from less developed countries are fewer. In school children from Abidjan, Ivory-Coast, the prevalence of head lice was 18.5%,5 and among Argentinean schoolchildren, this figure was as high as 61.4%.6 In developing countries, persistent head lice infestation has an important morbidity with scalp infection, impetigo that may provoke psychological disturbances. It is difficult to compare the results of prevalence studies because of the use of different methods (questionnaire based-surveys or examination of children). Furthermore, diagnostic criteria and detecting methods vary in accordance with the study authors. Currently, the standard diagnosis is finding living lice using an adapted comb.

Community-based studies are lacking. In Brazil, the prevalence of head lice in a representative population of an urban slum was 43.4%, and in a fishing community, 28.1%.7 Most frequently, affected children are aged between 5 and 9 years, after which the prevalence declines. Direct close contact is more frequent among young children, which explains the spread of head lice in this age group. Nevertheless, in some reports, older children have a higher prevalence.5,7 Adults can also be infested but data are few. An important degree of infestation in adults was found in resource-poor communities in Brazil.7 A higher prevalence in females is well known worldwide. All socio-economic groups are affected by head lice; however, social condition is a modifier of head lice prevalence. Children from families with a lower socio-economical status are particularly at risk of getting head lice.2 This finding has also been reported in developing countries. In the study conducted in the Ivory Coast, the monthly incomes of the schoolchildren parents and the collective use of washing facilities and bedding affected the prevalence of head lice.5 In an Argentinean study, the highest prevalence and degrees of parasitism were found in the schools close to the very poor neighbourhoods.6

In the USA, a lower prevalence of head lice has been noted in African American children. It has been suggested that African American children have oval-shaped hair shafts that are harder for lice to grasp. The hypothesis of a specific lice strain adapted to Negroid hair was not demonstrated. Two factors were invocated by Downs and Oxley: the difficulty to comb curly hair with a louse detector comb could have underestimated the prevalence of head lice and/or the frequent use of hair gel by African Americans may participate to suffocate head lice.8 The role of hair characteristics as a predisposing factor has been discussed. A higher prevalence of head lice infestation was found in children with brown hair, and longer hair could allow lice to move more easily from one head to another.7

Seasonal variation of head lice has been noted but differs according to countries and populations. Usually, the incidence is higher during the warmer months. Transmission occurs mainly through direct head-to-head contact. In school surveys it has been shown that clustering of children is the most important factor for the risk of head lice.2 Recently, fomite transmission by adult lice, instars and eggs was confirmed.9 Indirect transmission could occur more frequently than been previously believed. It involves screening of the entourage of the parazited individual and environmental interventions. Washing done with a water temperature of at least 50°C or drying is necessary to decontaminate washable clothes, linens and fomites.10

Resistance of head lice to insecticides

The primary treatments for head lice are insecticides, especially malathion, pyrethrins and pyrethroids. Increasing resistance to these insecticides has been observed in various countries3,11-15 but treatment failures can also be the result of non-compliance, inappropriate application of products, or reinfestation. These possibilities must be considered before thinking of resistance. Resistance should be suspected in cases of lice living 24 hrs after application while lice living 12 days later would rather reflect the poor ovicidal effect of the product. Two applications 7-12 days apart should be systematically performed.

Resistance reflects the wide use of chemical pediculides in several countries with therapeutic pressure against lice. A study in 1999 evaluated the efficacy of permethrin in head lice populations from the USA and Borneo. Resistance to permethrin was high in lice collected in the USA, where there was repeated product exposure, but was not observed in Borneo children who had never received chemical products. In the USA, malathion was withdrawn from the local market and reintroduced 5 years later. Malathion then appeared to be the fastest acting pediculicide in this country. Recently, a low level of resistance to malathion was found in head lice from Florida and California.15 Studies on insecticide resistance using in-vivo methods are, unfortunately, not standardized.

Biochemical and molecular methods have recently been performed. Mechanisms of resistance are the same as those observed with other insects: metabolic detoxification of insecticides or alteration of the insecticide binding site (knock-down resistance [kdr]). Permethrin resistance is linked to a kdr mechanism. Several studies showed that the knock-down resistance head louse population were associated with mutations in the voltage-sensitive sodium channel α subunit gene.3,15  Esterase-based resistance is the likely mechanism for malathion resistance. Resistance to permethrin is established in the following countries: UK, France, Denmark, Czech Republic, Israel, USA, and Australia. Cross-resistance among pyrethroids is frequent. Malathion resistance was described in the UK in 1995 and later confirmed. It was also reported in France, Australia, Czech Republic, Denmark and parts of Africa. Double resistance to permethrin and malathion has also been confirmed in the UK.

Resistance of P. capitis concerns other chemical pediculicides. Lindane is an organochloride considered to be a second-line treatment with decreasing efficacy. It is not recommended anymore due to its adverse reactions. Carbaryl is an alternative treatment available on prescription in the UK, but resistance appears to be emerging in some parts of the country and it is carcinogenic in rodents.12 Results on insecticide resistance must be cautiously interpreted. Resistance to an insecticide can vary in the same country from region to region, and even from school to school in the same town.13 Second, resistance to one formulation does not inevitably mean resistance to all formulations. British head lice resistant to malathion were killed by Ovide, a US formulation of malathion with excipients that have pediculocide properties.16

Most authors recommend malathion in areas where there is a marked resistance to pyrethroids. Otherwise, permethrin can be considered as first-line treatment because of its favorable tolerability. Alternative treatments for head lice are needed due to the problem of resistance among head lice to these two classes of insecticides. Some conventional insecticides could form a new generation of pediculicides.17 Physical or chemophysical methods represent another therapeutic approach: wet-combing kit, bug buster technique, hot air, exoskeleton integrity dehydration pediculicide, and dry-on suffocation-based pediculicide. However, initial results of studies using intervention with the Bug Buster kit or pediculicide treatment were considered too biased and unreliable18  and must be confirmed by randomized trials.

Conclusion

Recent data concerning the prevalence of head lice and resistance to commonly used pediculicides are lacking in most parts of the world. Nevertheless, resistance to permethrin is well established. Resistance to malathion is lower but increasing. Other therapeutic agents are clearly needed; new chemical agents and chemophysical methods are currently being evaluated and will probably change the treatment approach to head lice.

References

  1. Harris J, Crawshaw JG, Millership S. Incidence and prevalence of head lice in a district health authority area. Commun Dis Public Health. 2003;6:246-249.
  2. Willems S, Lapeere H, Haedens N, et al. The importance of socio-economic status and individual characteristics on the prevalence of head lice in schoolchildren. Eur J Dermatol.  2005;15:387-392.
  3. Durand R, Millard B, Bouges-Michel C, et al. Detection of pyrethroid resistance gene in head lice in schoolchildren from Bobigny, France. J Med Entomol. 2007;44:796-798.
  4. Kristensen M, Knorr M, Rasmussen AM, et al. Survey of permethrin and malathion resistance in human lice populations from Denmark. J Med Entomol. 2006;43:533-538.
  5. Menan EI, N'Guessan G, Kiki-Barro PC, et al. Scalp pediculosis in school environment in the city of Abidjan: prevalence and influence of socioeconomic conditions. Sante. 1999;9:32-37.
  6. Catalá S, Junco L, Vaporaky R. Pediculus capitis infestation according to sex and social factors in Argentina. Rev Saúde Pública. 2005;39:438-443.
  7. Heukelbach J, Wilke T, Winter B, et al. Epidemiology and morbidity of scabies and Pediculosis capitis in resource-poor communities in Brazil. Brit J Dermatol. 2005;153:150-156.
  8. Downs AM, Oxley J. Head lice infestations in different ethnic groups. Int J Dermatol. 2001;40:237-238.
  9. Burkhart CN, Burkhart C G. Fomite transmission in head lice. J Am Acad Dermatol. 2007;56:1044-1047.
  10. Izri A, Chosidow O. Efficacy of machine laundering to eradicate head lice: recommendations to decontaminate washable clothes, linens, and fomites. CID. 2006;42:e9-e10.
  11. Chosidow O, Chastang C, Brue C. Controlled study of malathion and d-phenothrin lotions for Pediculus humanus var capitis-infested school children. Lancet. 1994;344:1724-1727.
  12. Downs AM, Strafford KA, Hunt LP, et al. Widespread insecticide resistance in head lice to the over-the-counter pediculocides in England, and the emergence of carbaryl resistance. Br J Dermatol. 2002;146:88-93.
  13. Hunter JA, Barker SC. Susceptibility of head lice (Pediculus humanus capitis) to pediculicides in Australia. Parasitol Res.  2003;90:476-478.
  14. Yoon KS, Gao JR, Lee SH, et al. Permethrin-resistant human head lice, Pediculus capitis, and their treatment. Arch Dermatol.  2003;139:994-1000.
  15. Yoon KS, Gao JR, Lee SH, et al. Resistance and cross-resistance to insecticides in human head lice from Florida and California. Pestic Biochem Physiol. 2004;80:192-2001.
  16. Downs AM, Narayan S, Stafford KA, et al. Effectiveness of ovide against malathion-resistant head lice. Arch Dermatol.  2005;14:1318.
  17. Hill N. Control of head lice: past, present and future. Expert Rev Anti Infect Ther. 2006;4:887-894.
  18. Chosidow O. Bug Buster for head lice. Is it effective? Arch Dermatol. 2006;142:1635-1637.
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