How prevalent are head lice?

Parasitology Today,vol. 5, no. 5, 1989

135

This M o n t h The genetics of human resistance to disease is as yet poorly understood although it is a highly ac~:ive area of research. Of parasites, it might be expected that malaria would be an important agent of natural selection for humans because it causes high mortality. The situation is complicated by the degree of antigenic diversity displayed by this parasite and there remains much controversy about the respective contribution of host and parasite polymorphism in the co-evolution of both humans and their malaria parasites (see pp 138 and 143).

Circumsporozoite Protein Polymorphism The argument for variation in the circumsporozoite (CS) protein of malaria being sustained by natural selection (p. 143) is that if the CS protein varies even by as little as a single point mutation then it will avoid stimulating T-cells and evade the selective pressure of an immune response. However, the other view (p. 138) is that because the type of mutation seen in malaria proteins seems to be a general feature of mararia, then polymorphism cannot have arisen from natural selection mediated by the immune response, as it would mean that there would have to be a mechanism by which the parasite can choose which mutation to use. So, from this argument it would be necessary to invoke an as yet unknown, and unique, mechanism that causes polymorphism in malaria.

Variation in the MII-IC Conversely, the selection target of malaria would be the genes that govern the cellular immune response and are involved with antigen processing and presentation: the major histocompatibility complex (MHC). Until recently j, there has been no coherent framework for understanding the evolution of the human MHC. The MHC is highly polymorphic with loci of up to 50 alleles in some species, compared with other 'polymorphic' genes which may have two or three alleles. Nevertheless, on an evolutionary scale the MHC is very stable; contemporary alleles are 3-10 million years old. The problem therefore, is to reconcile the rapid evolution and huge diversity seen in malaria, with the slow pace of change and the rela~) 1989,ElsevierSciencePublishersLtd, (UK)0165-6147/89/$02.00

tively limited variation of the MHC. But the situation is further complicated. It should be remembered that 70-90% of any protein antigen is not seen by T-cell receptors because of failure in antigen presentation 2. Likewise, redundancy occurs in the host because immunity to a digested (processed) antigen will not necessarily have any protective value; it may even generate inappropriate cell interactions, and will not be of any selective advantage 3. Zoltan Nagy's ~ proposals may help to unravel this problem. He suggests that immune evasion by infectious organisms acts as a negative selection pressure that cannot drive the MHC toward polymorphism because it tends to select for (I) MHC molecules with broad binding specificity, and ( 2 ) i f some parasites evade more than one MHC molecule then pairs of alleles will be selected against. 'The emerging rule is that a linear increase in the number of [MHC] alleles will decrease exponentially the fraction of unsuccessful homozygotes; whereas a linear increase in the number of MHC-alleleproducts that are escaped by a pathogen will increase the fraction of unfit homozygotes linearly 'L. This is known as heterozygote advan-

tage and eventually this would give rise to polygenism in the MHC. Nagy goes on to propose that molecular mimicry of the host by the parasite is a stronger selection pressure than immune evasion by point mutation, and the only retaliation possible by the host would be to maintain polymorphism of self molecules balanced by the complex mechanisms operating in self-tolerance. This would explain the relatively limited polymorphism of the MHC. One consequence of molecular mimicry is autoimmune disease4. The only thing that seems clear about the molecular evolution of host and parasite is that it is a very complex subject, which will only be resolved as we learn more about the respective roles of antigen presentation, immune evasion, molecular mimicry and the discrimination of self from non-self.

Caroline Ash References I Nagy, Z.A. et al. (1989) Immunology Today 10, 132-138 2 Adonini, L. et al, (I 988)Proc, NatlAcad Sci. USA 85,5181-5185 3 Walker, E. ( 1982)J. Immunol. 128, 2164-2169 4 Petty, K. and Eisen, H. (1989) Parasitology Today

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are H e a d Lnce? A recent preliminary study indicates a much higher prevalence of head lice (Pediculosis capitis) among school-age children in the UK than do the official DHSS figures. Many District Health Authorities have reduced routine checking for head lice by school nurses, but head lice in schools may be a greater problem than they think. Positive cases of head lice infestation can be divided into two categories: 'live' (active insects or eggs found within I cm of the root of the hair shaft); and 'treated' [empty egg shells (nits) or eggs more than I cm from scalp]. J. Maunder has proposed measuring the ratio between live and treated infestations as a means to assessthe success of health education aimed at eradicating head lice. However, the implementation of this proposal is problematic as the Department of Health and Social Security (DHSS) has no

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standard procedure for collecting data, from checks carried out by school nurses, for statistical analysis.

Past Surveys The most recent extensive survey of samples from the whole population was in 1952. The results from this and from Mellanby's surveys in the 1940s suggested a peak of incidence in young children and are still used as a justification for monitoring only 4-6year-old schoolchildren, in the face of Health Service cutbacks.

Survey by Questionnaire In 1984, using a new method that involved sending out questionnaires to ~) 1989,ElsevierSciencePublishersLtd, (UK)0165~* 147/89/$02.00

Parasitology Today,vol. 5, no. 5, 1989

136 parents, S. Davies and S. King ~found that 33% of pupils in primary and junior schools suffered head lice infestations at least once a year. Joanna Ibarra 2, the Programme Coordinator of Community Hygiene Concern, used this method in her preliminary studies in 1986. The questionnaires asked members of households to recall any infestations of any family members within the past year and so also reached pre-school-age siblings of pupils. She found an overall incidence of head lice infestation of 63% in one school (A) and 21% in another (B), and a pattern of repeated infestation of the same individual. These results show a huge discrepancy with the 1986 DHSS figures, which state that 1.6% of 5-14year-olds are infested.

much lower than Mellanby's figure of 37%. In 1988, Ibarra found that 3% of a sample of O-3-year-olds attending play groups not under regular nurse surveillance had head lice during a 4-month study period. The number of infestations rises steeply when children begin to attend full-day schooling and falls offas children reach 12. The high incidence among the under-4's, which Mellanby recorded, seems no longer to exist; this may be the result of increased household/infant hygiene. The new evidence suggests that the peak of incidence has now shifted to the time when children take over their own hair care, between the ages of 4 and I I. It also highlights reinfestation as a major problem.

C u r r e n t Epidemiological P a t t e r n

Control

Ibarra's study found an incidence of head lice in pre-school children of 6%,

Although these studies are not conclusive, they indicate a changing epidemi-

ology and an unacceptably high incidence in schoolchildren from about age 5 to age 12. In both schools involved in Ibarra's 1986 study, routine head inspections by nurses had been discontinued a long time previously, but school B had a nurse regularly available to give advice, and the Education and Health Authorities in District B had a policy of encouraging parents to report cases so that outbreaks could be dealt with. Professional help and health education are most usefully channelled through schools, but the family questionnaire method emphasizes the need for a control programme that penetrates the community. References I Davies, S. and King, S. (1985) in Louse Alert! (Magowan, R., ed.), Oxford Health Education Unit 2 Ibarra, J. (1989) Health at Schaal 4, 147-151

H. Bradshaw

Yellow Fever in 1987 The years 1986-1987 were bad ones for yellow fever, with reports from W H O I of several explosive outbreaks in West Africa and an increase of sporadic endemic cases notified from South America(Table I). Yellow fever is a viral infection, originating in wild animals, that zoonotically infects man. Virus particles are only present in the blood, and thus available to the mosquito vectors for six to nine days, after which periodic bouts of fever are accompanied by the vomiting of blood. Mortality in adults is high (see Table I). Once of widespread importance, yellow fever is now confined to tropical regions of Africa and South America but the epidemiological picture varies depending on the region involved. The main vectors are Aedes spp, with Ae. aegypti being the main species implicated in urban epidemics, and anthropophilic sylvan mosquitoes like Ae. simpsoni, Ae. africanus and Haemogogus spp being implicated in sporadic cases originating from the sylvatic nidus. There has been a gradual increase in the number of cases reported from South America, from 50 in 1983 to 235 in 1987, 70% of which were from Peru. In Peru the number of sporadic cases reported in 1987 was the greatest since 1965 and stems from an increasing number of people emigrating from the high-

lands and becoming involved in agricultural activities in forest regions. Most cases were in males older than 15 years. In Africa the pattern of yellow fever was quite different from South America and was on an epidemic scale (Fig. I ). For instance near Bamako, Mali, 305 cases were notified though it is suspected that the actual number of cases is five times greater. Most of the patients were less than 15 years of age, reflecting the time since the last mass immunization campaign in 1969. As in the South American cases most of the patients were male. Interestingly, the main vector involved in this epidemic was Ae. furcifer, an anthropophilic wild mosquito, although specimens of Ae. aegypti captured in the capital Bamako, were found positive, confirming the potential for an urban epidemic. A campaign to vaccinate all people at risk in the region reached 84% of the target population (three million

Table I. Numbers of casesand deathsdue to yellow fever, notified to WHO, 1986-1987 1986 1987 Cases Deaths Cases Deaths Africa 3291 S. America 159

623 131

2063 235

892 21 I

people) and as a consequence this epidemic died out in November 1987. The statistics were even more alarming for Nigeria, for during 1986/1987 it was estimated that yellow fever affected 30 000 people, killing 10 000 of them. Mass vaccination campaigns have only reached 28% of the population at risk although this has meant immunizing 17 million people. Encouragingly, one million doses were produced by the Nigerian Federal Production Laboratory at Yaba. The recent increase in cases of yellow fever can be linked to rapid demographic and environmental changes, including (I) increasing growth and density of human populations, (2) uncontrolled urbanization, (3) migration of susceptible populations into enzootic areas, (4) deforestation, and (5) the occurrence of high densities ofAe. aegypti. In 1927, yellow fever was thought to have been completely eradicated but this opinion was obviously premature and it is still a problem that cannot be ignored as epidemics can flare up extremely quickly, as seen in the events of 1986/1987. W H O are stressing the importance of intensifying yellow fever control in the medium to long term. This means vector control, especially for Ae. aegypti, as well as mass immunization. The simplest solution that has been I~) 1989,ElsevierSciencePublishersLtd,(UK)0165~S147/89/$02.00