polo ralph laure Epidermal parasitic skin diseases

golf polos Epidermal parasitic skin diseases

Epidermal parasitic skin diseases (EPSD) occur worldwide and have been known since ancient times. Despite the considerable burden caused by EPSD, this category of parasitic diseases has been widely neglected by the scientific community and health care providers. This is illustrated by the fact that in the recent edition of The Communicable disease control handbook, a reference manual for public health interventions, only one EPSD (scabies) is mentioned.1 EPSD fulfil the criteria defined by Ehrenberg Ault (2005) for neglected diseases of neglected populations, but are not listed on national or international agendas concerning disease control priorities.2,3 This probably explains why efforts to control EPSD at the community level have very rarely been undertaken.4

Six EPSD are of particular importance: scabies, pediculosis (head lice, body lice and pubic lice infestation), tungiasis (sand flea disease) and hookworm related cutaneous larva migrans (HrCLM). They are either prevalent in resource poor settings or are associated with important morbidity. In this paper we focus on these diseases, summarize the existing knowledge on the epidemiology and the morbidity in resource poor settings and focus on the interactions between EPSD and poverty.

We use the term “underprivileged population” to designate a typical resource poor setting in low income countries, in contrast to the socioeconomic characteristics of affluent communities in high income countries. The expressions “hot climate country” and “cold climate country” are used when we refer to climatic restrictions on the occurrence of EPSD.

Searches of PubMed and LILACS using keywords “parasitic skin disease”, “scabies”, “pediculosis”, “tungiasis”, “cutaneous larva migrans” and their synonyms were used as a source of references. Searches were made without time limitations. Articles in English, French, Portuguese and Spanish were reviewed and analysed where quantitative data were provided, the study design was sound and the study had been performed in a resource poor setting in a low income country. Of 95 articles identified by these criteria, 50 were selected and cited in the reference list.

The six major EPSD differ considerably in their biological and epidemiological characteristics and life cycles (Table1). Scabies is caused by a mite (Sarcoptes scabiei), pediculosis by lice, tungiasis by sand fleas (Tunga penetrans) and HrCLM by nematode larvae. Although HrCLM and tungiasis are self limiting diseases, the parasites may persist for months and can cause long lasting sequels. S. scabiei and lice propagate continuously and cause persisting symptoms if the infestation remains untreated.5

Table 1. Biological and epidemiological characteristics of the six major EPSDhtml, 7kb

In EPSD, host parasite interactions are restricted to the stratum corneum, the upper layer of the epidermis, which is where the ectoparasites complete their life cycles, in part or entirely. In other parasitic skin diseases, such as leishmaniasis, loiasis or onchocerciasis, other layers of the dermis are also affected. Whereas S. scabiei and lice accomplish their life cycle within or on top of the epidermis, T. penetrans needs the host only for the production of eggs and completes its other developmental stages off host. In contrast, animal hookworm larvae that have penetrated into the epidermis find themselves at a biological impasse and cannot develop further.

Scabies, pediculosis capitis and pediculosis pubis occur worldwide but pediculosis corporis is restricted to cold climate countries and is virtually absent in the tropics (Table1). HrCLM is very rare in industrialized parts of the world but is ubiquitously present in developing countries.6 Tungiasis is geographically restricted to the Caribbean, sub Saharan Africa and South America.7

Except in epidemic circumstances, data on EPSD are not recorded so there is no reliable information available on global disease occurrence, changes in incidence over time, and spatial distribution in endemic areas. Hengge et al.8 suggested that 300 million cases of scabies exist worldwide, with many more individuals being at risk at any point in time. several billion people globally. As tungiasis and HrCLM are climatically and spatially restricted, the number of people at risk is lower, although still sufficient to merit attention.

The distribution of EPSD is irregular, and incidence and prevalence vary in relation to area and population studied. A study in a resource poor community in urban Bangladesh, for example, showed that virtually all children aged less than 6years developed scabies within a period of 12 months.9 In a rural village in the United Republic of Tanzania, the overall prevalence was 6%, in rural and urban Brazil 8 10%, and in rural India 13%.10 12 In Egyptian children, the prevalence was estimated to be 5% but in Australian Aboriginal communities the prevalence in this age group approached 50%.13,14 Of 5 9 year olds children living in a displacement camp in Sierra Leone, 86% were found to be infested with S. In contrast, in Germany the incidence was estimated at 1500 per 10000 children per year.16

During peak transmission, the prevalence of tungiasis in children living in resource poor rural and urban communities in Brazil and Nigeria reached more than 60%.7,17 In contrast, in high income communities in these same countries, tungiasis is restricted to single cases that typically occur when people visit local beaches.18 The situation is similar for HrCLM, with prevalence in children as high as 15% during the rainy season and an incidence of 1.840 cases per 10000 individuals per year.19

EPSD usually show considerable seasonal variation of disease occurrence (Table1).20 23 In the tropics, the cyclical changes are particularly evident in tungiasis and HrCLM; prevalence of tungiasis is highest in the dry season and of HrCLM in the rainy season.19,20

The factors responsible for the high burden of EPSD in resource poor communities are complex and have not been clarified. It has been suggested that crowding, sharing of beds, frequent population movements, poor hygiene, lack of access to health care, inadequate treatment, malnutrition and social attitudes contribute to the high burden of scabies in these settings.24 It is difficult to disentangle the relative importance of economic, environmental and behavioural factors, since they frequently coexist.25 There is, however, circumstantial evidence that extreme poverty and its economic and social consequences play a pivotal role (Fig.1).9,25

Fig. 1. Typical setting in a resource poor neighbourhood in north eastern Brazil in which EPSD are prevalent and the exposure risk for tungiasis and cutaneous larva migrans is high

Tungiasis is a paradigmatic example for this complex web of causation. Sand flea disease is a zoonosis affecting a broad spectrum of animals, with pigs, dogs, cats and rats as the principal reservoirs. In resource poor settings, stray dogs and cats are common and organic waste frequently litters the soil. Rats are attracted if garbage is not collected, sewage not disposed of properly and food stored inadequately. The risk for infestation is high if feet are not protected by shoes and socks, either because people cannot afford them or if wearing shoes is not part of local custom.26,27 In resource poor rural and indigenous populations in the hinterland of Brazil, the transmission of T. penetrans occurred almost exclusively indoors.7 Dwellings in these settings typically do not possess a solid floor, or the ground is covered with rough concrete or broken tiles with many crevices, thus providing an ideal habitat for the off host development of T. penetrans. In an urban environment it spreads in slums, where roads and paths are not paved, waste litters the area and yards consist of sand or mud.

Atypical paths of transmission in resource poor settings are another epidemiological characteristic of EPSD. When laundry is dried on the ground, instead of using clothes lines, there is a high risk of contamination from dog and cat faeces containing hookworm larvae. In resource poor settings, the high frequency of lesions of HrCLM on the upper part of the body, including the face, probably reflects this particular type of transmission.28

Another epidemiological peculiarity in poor settings is the observation that deficient sanitation is a significant risk factor for scabies.9 So far, it seems that scabies is not influenced by hygienic practices or the availability of water, since the prevalence of scabies is very high in the Kuna Indians in Panama and among children in the Solomon Islands, where individuals take frequent baths and where careful daily personal hygiene is traditional.29,30 We suggest that deficient sanitation is a characteristic of poor households and that poor hygiene does not by itself increase the odds of acquiring scabies. In children living in a poor urban neighbourhood in north eastern Brazil, the infestation rate depended significantly on the income of the household: the lower the family’s income, the more head lice episodes a child experienced per unit of time. In high income countries, children of all socioeconomic groups are at similar risk for infestation with Pediculus humanus var. capitis.16A peculiar epidemiological characteristic of EPSD is the concomitant presence of several ectoparasites on the same individual. In a fishing community in Brazil, for instance, 9% of the inhabitants were simultaneously infested with two or more ectoparasites.33 Not surprisingly, individuals with EPSD also tend to be co infected with intestinal helminths.33

Although the morbidity associated with EPSD is significant, a systematic assessment of the severity of the burden is still lacking. Engels Savioli34 suggested that EPSD may represent a considerable subjective burden, although disability adjusted life years (DALYS) have not yet been calculated.

According to its pathophysiological basis, pathology can be schematically divided into two patterns, namely inflammation related and itch related. In tungiasis, the predominant morbidity is the result of heavy inflammation surrounding the lesions, together with secondary bacterial infection (Fig.2 and Fig.3).35 Superinfection reinforces the inflammatory process. secondary morbidity such as suppuration, ulceration, gangrene, necrosis of surrounding tissue, deformation and loss of nails, resulting in physical disability.7,36 Tungiasis has also been associated with tetanus in non vaccinated individuals. In a study in So Paulo, Brazil, tungiasis was identified as the port of entry for 10% of tetanus cases.37 All heavily infested individuals living in a resource poor neighbourhood in north eastern Brazil showed signs of acute and chronic inflammation: 19% had fissures; 50% presented with ulcers; deformation and/or loss of nails occurred in 69%,36 resulting in walking difficulty in all patients and difficulty in gripping in half of the patients with lesions at the fingers. A broad host of pathogenic microorganisms has been isolated from superinfected lesions, such as Staphylococcus aureus, Streptococcus pyogenes, enterobacteriaceae, Bacillus spp., Enterococcus faecalis, Pseudomonas spp., as well as various anaerobic pathogens.35,38

Fig. 2. Tungiasis associated pathology at the heel

Body lice are vectors of a host of pathogenic bacteria, such as Rickettsia prowazekii (the agent of epidemic typhus), Borrelia recurrentis (the agent of relapsing fever), Bartonella quintana (the agent of trench fever and bacillary angiomatosis) and Yersinia pestis (the agent of plague), and can cause important secondary morbidity through life threatening infections.39 Head lice can transfer Y. pestis during blood sucking.40 Lice can passively carry staphylococci, streptococci, Acinetobacter spp. and Serratia marcescens and transfer them from infected lesions to other areas of the skin.41

Morbidity related to itching (pruritus) is best studied in scabies as it is such a common symptom that patients scratch their lesions almost constantly. Repeated scratching of a lesion causes excoriation and denudation of the skin thus creating portals of entry for pathogenic bacteria. The clinical consequences of secondary bacterial infection, especially with group A streptococci, result in significant, frequently unrecognized illnesses, such as cellulitis, boils, pyomyositis, lymphangitis and generalized lymphadenopathy.42 Streptococci and staphylococci bacteria have been isolated from skin burrows as well as from faecal pellets of the ectoparasite, suggesting that the mites themselves may contribute to the spread of pathogenic bacteria.43 Moreover, secondary infection of scabies lesions with group A streptococci is a major precipitant of post streptococcal glomerulonephritis and possibly also of rheumatic fever.44

The debilitating impact of persistent itch has repeatedly been stressed for a variety of non infectious diseases but remains to be assessed for EPSD. In neurophysiology it is known that chronic itch leads to persistent firing of specialized A and C itch fibres in the skin. As a consequence, pain fibres in the neighbourhood are transformed into itch fibres, eventually leading to a sensitization of spinal neurons. A similar consequence can be anticipated to occur in EPSD. Since the pruritus intensifies at night, disturbance of sleep is to be expected. Recently, alterations of sleep have been confirmed in 84% of patients with HrCLM21 and in 72% patients with scabies.42 Tungiasis has also been shown to cause considerable sleep alterations.38

An aspect of morbidity which has been completely neglected is the psychological impact of EPSD. Since lesions on the skin can be seen by the naked eye, in the case of HrCLM and tungiasis even from a distance, the fact that an individual is infested with ectoparasites does not go unnoticed and can be a source of mental strain and distress. The unhealthy aspect of the skin in EPSD and constant scratching of lesions could influence self esteem and affect the ability to adjust socially. In north eastern Brazil, mothers of children with tungiasis are faced with societal notions linking the presence of this ectoparasitosis to neglect. The resulting stigma discouraged mothers from bringing their children to the health centre.45 If patients with scabies are treated with a topical acaricide, the compound has to be applied to the whole body surface. Unfortunately, acaricides, such as sulfur in petrolatum, have a strong odour and so may reinforce stigmatization.

In resource poor communities in Brazil, the severity of tungiasis was directly related to the economic status of the household in which the affected individuals lived.9,46 A similar observation has been made in individuals with scabies in urban Bangladesh. Morbidity also depends on the duration of disease which means that the longer the infestation progresses, the higher the intensity of clinical signs and symptoms. This is of importance where access to health care is limited, delaying diagnosis and limiting availability of drugs for treatment. Finally, infection with HIV and human T lymphotropic virus type1, frequent in many resource poor communities in the tropics, induces an exceptionally severe form of scabies, namely crusted or “Norwegian” scabies.47
polo ralph laure Epidermal parasitic skin diseases

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Ralph Lauren