Marcia Ramos-e-Silva, MD, PhD

Nurimar Conceição Fernandes, MD, PhD

Associate Professor of Dermatology - Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

Overview
Cutaneous diseases are a major health problem in all underdeveloped and developing regions; it is an established fact that they receive much less attention when affecting women than men. It is also undoubted that the effects of illnesses in general, including parasitic and tropical, are different in men and women.1,2 Parasitic diseases are most prevalent among populations with little personal hygiene and deprived of basic sanitation (unavailability of potable water, inadequate disposal of human waste, lack of latrines) and good nutritional status. Other predisposing factors, such as decreased immune protection to infectious agents, low level of education, and other situations included in the overall framework of a low socio-economic level, are also features in many developing countries.3 Characteristically, populations exposed to these factors are the ones in which women are often underprivileged.1,2

Parasitic and tropical diseases
Parasitic diseases are widespread throughout the World and, although almost any infection-causing organism can be a parasite, only Protozoa, Helminthes and Arthropods are considered cause of parasitic diseases from the clinical point of view.3 These illnesses are also closely linked to warm and humid climates, and most of them are therefore considered tropical and subtropical diseases.4,5 The factors that mostly influence the onset of tropical dermatoses, according to Canizares & Harman,6 are climatic, ecological, human, cultural and socio-economical. Because of them these diseases are called dermatoses of the poor, of the developing and underdeveloped countries; and also dermatoses of malnutrition, illiteracy, sun radiation, humidity and insect bites.

Gender inequalities in the Third World
There has been a general lack of awareness of the effects of gender and sex on the distribution and consequences of diseases. The term "gender" encompasses the sociocultural aspects of the differences between the behavior of men and women, while the term "sex" relates to physiological attributes, such as influence of female hormones, menarche, pregnancy and menopause.1 Besides the obvious sex differences, gender inequalities of health in Third World Countries exist and health hazards are present at every stage of a woman's life cycle. Health issues which pose the greatest hardship to women in these countries include reproductive problems, excess female mortality in childhood, violence against girls and women, occupational and environmental hazards, and cervical and breast cancer.7 Gender, as well as sex differences, affects people's risk and responses to tropical diseases, and the determinants and consequences include economic, social and personal dimensions.8

In countries where tropical diseases are endemic although both men and women suffer from poverty and deprivation, there is now substantial evidence that women are particularly disadvantaged due to societal factors. Exposure to disease, intensity of infection, duration of illness, care during illness, access to and utilization of health care services, and finally the impact of illness on family life are all influenced by the significantly lower and subordinate social status of women in many countries. All these factors make them economically dependent on men worsening their secondary role in the social group.1,9

Feminization of poverty
The global change in the traditional social structure has led to an increase in women serving as heads of households.10 The number of aging partnerless women is increasing,11 and treatment of dermatoses, including tropical, during pregnancy is a difficult situation.2 The rising number of women living in poverty, many of whom are mothers, poses a social and political dilemma for the 21st century.11 Literate women are usually the first members in a household to apply their knowledge and skills to raise the levels of sanitation, nutrition, and education; thus contributing to upgrade the general living standards of their homes.1 The fact that households where women are the heads also tend to be poorer makes them more vulnerable to the effects of tropical diseases that are "diseases of poverty". This phenomenon has been identified as the "feminization of poverty", a situation in which women make up the majority of the poor.12 Tropical diseases have huge economic consequences, and although the economic effects of illness on women have not really been studied, there is the fact that when the women in a household falls sick, it has repercussions not only for her as an individual but for the entire group.1 Women have mainly domestic roles in developing countries, which require them to remain indoors.13 On the other hand and besides the fact that the home is the setting where many vector-borne diseases are transmitted,14 extensive clothing often worn by women in these situations protects them from insect bites.13,15 Effects of nutritional status in tropical diseases have not been formally investigated but it was observed that among the urban poor in India male children and adults receive the most nutritious foods.16 It is also known that anemic adolescent girls are, for example, at greater risk of morbidity from parasitic and other infections.1 Another very important point related to women's health is that the professionals frequently give little credibility to their experiences of symptoms, as they tend to attribute women's illness to psychiatric problems, and treat them inappropriately. This leads to a loss of confidence in their own perceptions of illness and health17 explaining women's preference to consult non professional healers, as they usually provide better understandable explanations.1

There are some parasitic and tropical dermatoses that have undoubted differences in their characteristics, frequency and/or importance when affecting women as compared to men. Among them, seven diseases will be discussed in more detail, especially in their relationship to women. Leprosy shows a higher tendency to develop reactions in women although less frequent in this group. In tuberculosis, erythema induratum tends to occur in young women; while tinea nigra and tinea capitis, when in adults, affect women rather than men. Scabies is more observed in young women and children, in whom frequently shows eczematization; and schistosomiasis may lead to complications in pregnancy, among many other important features in women.

LEPROSY (REACTIONS)

Leprosy is expected to remain a public health problem for at least the next decade. Considerable differences exist in the registered incidence rates between the two sexes. Case detection rates are higher among men but it is assumed that risk and prevalence of infection among women is underestimated.18 Women seem to have greater resistance to clinical leprosy and, therefore, lower incidence and less severe clinical forms, apparently associated with levels of estrogen and other female hormones; nevertheless, the effects on women are far more devastating, a phenomenon Kaur attributes to cultural reasons - what she calls women's "greater socioeconomic vulnerability".1,11 Reversal reactions are more common among women and pregnant women have a higher risk of relapse, neuritis and erythema nodosum leprosum.19 Economic dependence on men and shame make women hide the disease which becomes worse, while confinement to home and activities such as washing and cooking with anaesthetic hands exacerbate the disease and put women at risk.11

Synonym: Hansen's disease

Clinical description
Leprosy reactions are acute emergencies in the course of human infection by Mycobacterium leprae. Two types of reaction are differentiated: type 1 (reversal reaction) and type 2 (erythema nodosum leprosum) (Figures 1,2,3,4).

A patient is diagnosed as having a reversal reaction (type 1) when the following clinical signs are present: redness, swelling and sometimes tenderness of lesions; neuritis (swelling, pain, tenderness, paresthesia or nerve function impairment); edema of hands, feet or face, occasionally fever. Type 2 reaction is characterized by multiple, small, tender nodules with or without ulceration on the arms and legs; neuritis; fever, edema, iritis, arthritis. Their etiologies are unknown and their pathogenesis poorly understood. Several studies indicate that type 1 is associated with activation of the cellular immune system but the stimulus is not known. Type 2 is generally considered to be an immune complex phenomenon.18,19

First appearance of leprosy, reactivation of the disease and relapse are likely to occur particularly in the third trimester of pregnancy or immediately after delivery. Leprosy reactions increase during pregnancy, occuring in 32% of the women with active leprosy under treatment.20 Erythema nodosum leprosum is prevalent in the first trimester with a second peak in the third trimester to fifteen months postpartum.21,22,23 During lactation erythema nodosum leprosum more commonly affects nerves and has a higher tendency to be more severe, even necrotic.23

Histopathology
In reversal downgrading reaction, dermal edema on skin histology is a common feature. Positive characteristics for a reversal upgrading reaction are increased numbers of large Langhans' giant cells, formation of discrete granulomas, fibrinoid necrosis of granulomas and reduction in the expected number of acid fast bacilli.24

Erythema nodosum leprosum is characterized by influx of polymorphs though in the late stage lymphocytes predominate. Vasculitis affecting arterioles or venules is a significant feature. The reaction is often present in the deep dermis or subcutis.

Laboratory studies
Smears of scraping from skin lesions stained for acid-fast bacilli is the standard technique used to estimate the number of Mycobacterium leprae.

Laboratory finding may include anemia, leukocytosis, neutrophilia, elevated sedimentation rate and proteinuria.

Differential diagnosis
Principal criteria for the clinical diagnosis of leprosy are: loss of sensation in clinically suspected skin lesions, and thickening of peripheral nerves with loss of sensation in the corresponding skin area. Skin smears demonstrate acid fast bacilli. Histopathological diagnosis is based on cellular infiltration of nerve branches and on the presence of intracellular acid fast bacilli.

The major differential diagnosis of type 2 reaction (erythema nodosum leprosum) is erythema nodosum. It is a nodular painful syndrome which results from a hypersensitivity reaction to various possible antigenic stimulus. The painful nodules vary in number and may come together into plaques; they are red violet color, brilliant and located on the tibial crest, feet, knees, internal surface of the thighs, buttocks and sometimes forearms. In the regressive stage they resemble contusions and heal without scarring. These lesions never ulcerate. A septal panniculitis is the histologic feature.25

Treatment
Pregnancy and lactation do not contraindicate standard multiple drug therapy with dapsone, rifampicin and clofazimine. These drugs should be continued without interruption during the episodes of leprosy reactions.

The reversal reaction must be treated daily with 60mg of prednisone; the control of the reaction allows the prednisone to be decreased and discontinued over a period of two months.

Erythema nodosum leprosum is suppressed by thalidomide, the treatment of choice, in a dosage of 100mg three times daily. After controlling the reaction it can be tapered (100mg weekly) to a maintenance dosage or complete withdraw.18 In fertile women this drug is contraindicated. Women of childbearing age are treated with prednisone.19,24

Conclusion
Type 1 reactions occur with significant greater frequency in women. In pregnancy the immunological response is suppressed. Leprosy reactions are triggered off by pregnancy: type 1 occurs in postpartum while type 2 peaks in late pregnancy. Both types continue into lactation.

TUBERCULOSIS OF THE SKIN

Mycobacterium tuberculosis is the predominant cause of cutaneous tuberculosis but M. bovis, sometimes called M. tuberculosis (var. bovis), may also infect the skin. It is classified as primary inoculation tuberculosis, reinfection tuberculosis and tuberculids. Erythema induratum is a chronic nodular eruption that usually occurs on the lower legs of young women. The disease has been recently classified as nodular vasculitis and represents a multifactorial syndrome of lobular panniculitis. The term erythema induratum should be reserved for those cases with tuberculosis etiology while today the term nodular vasculitis is used to describe the disease in association or not with tuberculosis.26

Synonym: Nodular vasculitis (erythema induratum)

Clinical description
Recurrent crops of small, tender, erythematous, violaceous nodules that at times coalesce to form a tender plaque with or without ulceration. Most lesions affect both shins and calves and persist for several weeks; they tend to heal with scarring (Figure 5). The association with tuberculosis at an extracutaneous site (kidneys, lymph nodes, lungs and endometrium) has been described in 55,9% of patients in previous large studies.27 More recently mycobacterial DNA was detected on lesion biopsy specimens of erythema induratum using the polymerase chain reaction (PCR).28

Histopathology
Lobular panniculitis with varying combinations of primary vasculitis, granulomatous inflammation, septal fibrosis and caseation necrosis. Acid-fast bacilli are rarely found in stained sections.

Laboratory study
Strongly positive tuberculin test is usually present in patients with erythema induratum.

Differential diagnosis
The following clinical features distinguish erythema induratum from erythema nodosum: a chronic recurrent course; skin lesions that involve shins and calves are concentrated on the lower third of the leg; skin nodules heal with ulcerations or depressed scars.

Treatment
The drugs currently employed in chemotherapy of tuberculosis are rifampicin, pyrazinamide and isoniazid (Table 1). Response to treatment is quite variable. A good therapeutic response supports the diagnosis of tuberculosis as a cause.29

Pregnant women with tuberculosis have not a different course or prognosis. Rifampicin, pyrazinamide and isoniazid are used during pregnancy with enough safety. Pyrodoxine should be used (40 - 50mg daily) to avoid convulsions on the newborn.29

Table 1: Schedule for tuberculosis

Conclusion
Erythema induratum is believed to represent a tuberculid. This term is applied to any group of eruption that arises in response to an internal focus of tuberculosis and is regarded as a hypersensitivity reaction to Mycobacterium tuberculosis. Response to treatment is quite variable, relapses are common and even periods of improvement and worsening frequently occur during the antituberculosis therapy.

The diagnosis should be made on the following presumptive criteria:29
1. granuloma with caseation necrosis or
2. granuloma without caseation necrosis and positive tuberculin test or
3. established tuberculosis at another site;
4. clinical improvement after eight weeks of exclusive antituberculosis therapy.

TINEA NIGRA

Tinea nigra is a superficial and benign infection of the stratum corneum caused by Exophiala werneckii. The fungus occurs in soil, vegetation and humus. More recently Stenella araguata was also isolated as a causative agent. The infection occurs by traumatic inoculation of the agent into the skin. Women under 20 years of age are more susceptible especially those who are hyperhydrotic.30

Synonyms: Keratomycosis nigricans palmaris, cladosporiosis epidermica, microsporiasis nigra.

Clinical description
Brown or black non-scaly macules with circular border on the palmar surfaces (Figure 6).

Histopathology
The stratum corneum contains dark-colored fungal element composed of septated, branching hyphae and budding cells. Biopsy of tinea nigra is not necessary for diagnosis.31

Laboratory study
Skin scrapings of the affected area on a slide in one or two drops of 10% KOH solution show light brown to dark green, branched septated hyphae, 1.5 - 3.0 mm in diameter. Skin scales are inoculated into Sabouraud dextrose agar and kept at room temperature. In one to two weeks typical black yeast colonies are formed.30

Differential diagnosis
The pigmented lesions simulate nevus and melanoma but these lesions uncommonly have a palmar location. Melanoma and nevi are elevated or indurated.31 Contact dermatitis and post-inflammatory melanosis are disclosed by history and course.

Treatment
Keratolytic agents such as Whitfield's ointment, tincture of iodine, 2% salicylic acid or 3% sulphur are effective. The main topical imidazoles currently available (clotrimazole, miconazole, econazole, ketoconazole, isoconazole, tioconazole) applied twice daily for three weeks are equally effective and safe during pregnancy.32

Conclusion
Tinea nigra is a fungal infection that causes little discomfort to the patient. The primary clinical importance is that a correct diagnosis in the differentiation of pigmented lesions may avoid unnecessary biopsy or surgical intervention.

TINEA CAPITIS

Tinea capitis is a dermatophyte infection of the scalp, eyebrows and eyelashes caused by species of Microsporum and Trichophyton.

It is primarily a disease of children. Infections may be seen in adults when almost invariably women rather than men are affected. All the dermatophytes usually responsible for scalp ringworm in children can cause tinea capitis also in the elderly: M. canis, T. violaceum, T. mentagrophytes, T. tonsurans.

Favus is a distinctive form of scalp ringworm caused by T. schönleinii. The infection may also be seen in an adult woman, provoking severe scarring alopecia.33,34,35,36,37

Synonyms: scalp ringworm, dermatophytosis

Clinical description
Tinea capitis presents with several different clinical aspects. Infected hairs often break at scalp level in anthropophilic Trichophyton infections (black dot). In Trichophyton tonsurans infection the clinical presentation is often characterized by chronic scaling and alopecia without inflammation.38 When T. violaceum is isolated the following types are observed: gray patch, black dot, seborrheic, pustular inflammatory, kerion and favus.39 When M. canis is isolated gray patch, seborrheic, pustular inflammatory and kerion are observed (Figure 7).

Histopathology
Hyphae are confined to hair; in kerion celsi, a dense dermal infiltrate of lymphocytes, plasma cells, neutrophils and eosinophils. In folliculitis there are fungal remnants in the follicles and perifollicular inflammation.40

Laboratory study
Broken, altered or discolored hairs should be plucked and placed in a drop of 10-20% KOH, covered with a coverslip; the material on the slide may be better distributed by applying pressure to the coverslip. Clinical specimens are inoculated into Sabouraud dextrose agar and cultures are incubated for at least 15 days.

Differential diagnosis
Alopecia areata has the characteristic exclamation mark: hairs which are narrower at the base than the top, and usually shows a flat non-desquamative surface. Seborrheic dermatitis or psoriasis may also be confused and, in this case, it is necessary to search for lesions on the trunk or in the nails.40

Treatment
Oral therapy is usually given for scalp disease. The usual dose of griseofulvin for an adult is between 500-1000mg daily, with food.

The main alternative is ketoconazole; it is more active than griseofulvin in scalp ringworm caused by T. tonsurans. It is given in a dose of 200mg daily.

The therapy has to be continued for 6-12 weeks until clinical and mycological cure. The other alternatives are itraconazole (100mg daily) for six weeks and oral fluconazole (50mg daily) for 20 days.

Pregnancy and lactation contraindicate these mentioned drugs.41

Conclusion
Tinea capitis is frequent in adult females especially during the fifth decade. Most patients reported in the literature are menopausal or post menopausal women. Poor physiological defense in the elderly, probably due to the qualitative and quantitative differences of the sebum could explain its higher frequency in mature women.

SCABIES

Overview
Human scabies is caused by obligatory parasite mites of the species Sarcoptes scabiei var. hominis. This agent was discovered, in 1687, by Giovan Bonomo, whose findings raised great controversies and discussions at that time.42 Its incidence throughout the world shows cyclical fluctuations, not yet fully understood. It is often assumed that allergic sensitivity to the mite or its products plays an important role in determining the development of lesions other than burrows and in producing pruritus.

Sarcoptes scabiei var. hominis is transmitted from person to person by body contact, particularly among family members and bed partners, although also fomite spread can occur since mites can survive for 2 to 3 days in bedding, clothing, and house dust.44

Synonym: itch, mange

Clinical description
Among the skin lesions of scabies, only the burrows and vesicles are directly associated with the presence of the mite. Other lesions are the result of allergic sensitivity, scratching or secondary infection. Burrows occur most frequently on the anterior aspects of the wrists, the ulnar border of the hand and between the fingers. The points of the elbows, the anterior axillary fold, the skin around the nipples and the natal cleft are other sites often involved. In children burrows are often found on the palms; in infants under the age of two both palms and soles are often infested, presenting vesicular lesions, and eczema may be widespread and severe.43

In adult males 85% of subjects carry mites on the hands and wrists and 63% of the vigorous feeders may be recovered from this area. The elbows, feet and ankles, and penis and scrotum each carry mites in 30-40% of subjects. Male genitalia must be examined when there is suspicion of scabies because over 30% of infested men have penile lesions.45 The distribution in adult women is similar but the palms are more often colonized, and the region of the nipple often involved. Eczematous changes may follow scratching, and are particularly characteristic on the breasts of young women, with burrows near the nipple.46 (Figures 8,9)

The onset of pruritus is usually first noticed two weeks or longer after infestation, but earlier in subsequent infestations.43 Type IV hypersensitivity reaction to the mites and their products begins around the first month after the infestation and results in a papular or eczematous eruption in the involved sites. At this time itching, the most obvious manifestation of scabies is usually intensely severe and most prominent at night or after a hot bath.43,44

In the form called crusted or Norwegian scabies a thickened horny layer hosts an enormous number of mites. The presence of huge numbers of mites is possible either because of the host's very poor hygienic conditions or by altered immune response allowing the mite to multiply. In general crusted scabies is a disease of the mentally retarded, debilitated or immunosupressed patients.44 Men and women are equally affected; it is rare among children and elderly population; and there is no racial predilection. It is essential for clinicians to be familiar with this form of scabies because of its highly contagious nature and unusual clinical signs, which may be easily overlooked.47,48

Histopathology
The histological appearance of the inflammatory lesions has been regarded as non-specific, but even in the many cases in which they show no mites or ova in the tunnels of the horny layer that would seal the diagnosis, the combination of spongiosis and vesicles in malpighian layer with a dermal infiltrate should certainly suggest scabies.

Laboratory studies
Presence of mites, eggs or fragment of eggshells under the optical microscope in material removed from burrows confirms the diagnosis. The mites are whitish, hemispherical mites; the male measures about 0.2 X 0.15mm while the female 0.4 X 0.3mm. The turtle-shaped fertilized females excavates a sloping burrow, through the stratum corneum and the granular and malpighian layers, extending it by cytolysis by 2mm each day, mainly during the night, and depositing two or three eggs to a total of 10-50, during her lifetime of 4-5 weeks, and then dying in the burrow.43,49 The six-legged larvae emerge from the eggs after 3 or 4 days, wander to the skin surface and form shallow pockets in the horn of the original or a new host; they reach maturity about 14-17 days after the eggs were laid. Copulation occurs in the pocket and the female excavates her burrow, whilst the male soon dies.43,44

Differential diagnosis
There are various pruritic disorders that may resemble scabies and in tropical areas it must be differentiated mainly from insect bites, pediculosis, and papular urticaria.

Treatment
Several effective scabicides are available and most give very similar results. Two and a half to ten per cent sulphur ointment is still employed, as well as gamma benzene hexachloride (lindane); malathion; benzyl benzoate; permethin; and monosulfiram.43 Oral ivermectin, an apparently safe drug, is now available and particularly useful for crusted scabies.50

Although there are many warnings about the use of scabicides during pregnancy and breastfeeding, understandable in view of concern about potential toxic effects on the fetus, Burns states that there is no documented evidence that any of the available scabicides has been responsible for harmful effects in these situations. There is no data on levels of scabicides in human milk following their use on lactating women but despite all this and even nowadays many dermatologists prefer to use topical sulphur when managing scabies during both pregnancy and lactation.43

Conclusion
This infestation practically shows no difference between in women and men but eczematous changes following scratching are particularly characteristic on the breasts of young women. In relation to scabies in women its treatment during pregnancy and breastfeeding is controversial until now.

SCHISTOSOMIASIS MANSONI

Overview
Schistosomiasis is one of the most important helminthic infections because of its wide geographical distribution and extensive pathological effect.51,52 It is a systemic disease and its causative agents are human trematodes or flukes. These trematodes affect approximately 200 million people worldwide, mainly in the tropical and subtropical latitudes and sometimes entire communities are affected. Most infected persons experience few, if any, signs and symptoms and only a small minority develop significant disease.53

There are three important species of the genus Schistosoma, known as blood flukes, that infect humans. They are: Schistosoma hematobium, S. japonicum and S. mansoni. S. haematobium is prevalent in Egypt, other parts of Africa and the Middle East; and is responsible mostly for urinary tract infections. S. japonicum is found in the Far East and has a predilection for the small intestine. S. mansoni, on the other hand, is confined to the Caribbean islands and the northeastern region of South America extending to the Southeast of Brazil and infects mostly the portal circulation and the mesenteric venules of the large intestine.52 These three species share the same basic life cycle (Figure 10), but are unique in some aspects, such as location of adult worms, number of eggs produced, response to the ova by the host, fate of retained eggs, morphology of parasites, among other features.53

Schistosomiasis has important implications for females. In endemic areas schistosomiasis frequently leads to complications in pregnancy including ectopic pregnancy, premature birth and abortion, as well as placental involvement causing damage to the fetus and newborn. Another consequence of schistosomiasis, particularly S. haematobium, is genital tract involvement, a generalized pelvic disease involving bladder, ureters, rectum and external and internal reproductive organs.54

There are various results in prevalence studies of schistosomiasis. The basic requirement for infestation is the contact with contaminated waters of lakes and rivers, so regional differences depend on the habits of the local population. In most communities men show higher prevalence rates because their activities as farming and fishing, but there are other regions were women have higher rates of infection due to washing utensils and clothes. Religious practices may also have influence as with male Muslims who have activities as ablution and ritual washing several times a day.1

Synonym: bilharziasis

Clinical description
The organs mainly affected in schistosomiasis are the urinary tract by S. haematobium; the small intestine by S. japonicum; and large intestine and liver by S. mansoni.52 Cutaneous schistosomiasis is rare and may occur in all three stages of the disease: initial penetration of the skin by the water-borne, free-living cercaria; during the immune-complex-mediated phase; or in the later stages of infection.55

The initial cutaneous manifestation that may appear in schistosomiasis is called schistosomal dermatitis. It is characterized by pruritus sometimes associated to a papular eruption which begins right after contact with water and penetration of the larva (cercaria) through the skin. It disappears usually in a few hours. The immune-complex-mediated phase begins after four to eight weeks. There may be an urticarial reaction, which is particularly severe in infestation by S. japonicum. Sometimes there is association with malaise, fever, diarrhea, liver and spleen enlargement. Eosinophilia is a frequent feature in this phase. Late cutaneous schistosomiasis is rare and when it occurs it is usually associated with other organs involvement and presence of the parasite in the stool or urine. Perigenital, paragenital or schistosomotic granuloma, especially in women, is its more common form of presentation. Ectopic cutaneous schistosomiasis may also occur.55,56

The late manifestations are due to the deposition of adult worms and/or of eggs of Schistosoma in the perigenital, genital and extragenital skin of patients. The presence of eggs may also occur without any clinical manifestations, or in unrelated lesions of the skin. There can be papules, nodules, polyps, vegetations, large tumours, ulcerations, sinuses, lymphoedema, elephantiasis and leukoplakia.57 Schistosomal granuloma may be considered a potentially precancerous lesion and in one study two in twenty cases showed malignant transformation.58

Vulval lesions are seen in greater frequency with S. haematobium and are an infrequent manifestation of Schistosomiasis mansoni (Figure 11). The existence of venous anastomoses that communicate the mesenteric system with the pudendum plexus and the venous system of the perineum favors the production of genital lesions, under normal conditions.59

Histopathology
Late cutaneous schistosomiasis is diagnosed by histopathology and its most characteristic feature is the finding of degenerated eggs inside epithelioid cell granulomas. (Figure 12)

Laboratory study
Schistosomiasis is diagnosed most frequently by the presence of characteristic ova in stool or urine, depending on the agent. The difference between the eggs of three species of Schistosoma is the presence and localization of a characteristic spine. Schistosoma haematobium shows an apical spine; S. mansoni, a lateral spine (Figure 12); while S. japonicum has no spine. The adult worm of the three human species of Schistosoma does not replicate within the human host. It can live as long as 33 years, although in endemic areas 2 to 5 years are the usual.60

Differential diagnosis
Cutaneous schistosomiasis, depending on its stage, may mimic an enormous number of skin diseases. From pruritus without lesion, papular and urticarial eruptions, nodules, granulomatous lesions and large tumors, skin lesions of schistosomiasis are, in general, only diagnosed by biopsy and histopathology.

Treatment
Infections due to all three agents of schistosomiasis may be completely cured with the drug praziquantel in a single oral total dose of 40mg/kg or divided into two of 20mg/kg. Metrifonate in a total dose of 22.5-30mg/kg is used for S. haematobium; a single dose of 7.5-10mg/kg is given every other week three times. Oxamniquine is prescribed for S. mansoni in a total of 15-60mg/kg; it may be given all at once or twice a day for two days. Good results are achieved in early infestations, however scar formation do not allow the improvement of late complications such as portal hypertension, liver fibrosis and urethral and/or ureteral stenosis.53,55,56

Conclusion
Schistosomiasis is a tropical parasitic disease with great importance in relation to women because of its pregnancy implications, the possible alterations of fetus and newborn of infected mothers, and to the external and internal reproductive organs alterations, that can be caused even by the intestinal affecting species of Schistosoma.

CONCLUDING REMARKS

There is much evidence that skin disease occurring in women is diagnosed later than in men and there are also many skin conditions that have so far received little investigation into their pathogenesis in women.61 Women's health as an end in itself has rarely been at the forefront of international development programs or national health planning and its attention in developing countries has been motivated largely by other concerns. Women have tended to be seen as the vehicle through which specific goals such as family planning and child survival could be achieved rather than as the primary beneficiaries of development programs.8

If sustainable development is the latest challenge to the international community, then women, more than ever before, should be at the front and center of all action strategies;62 and women's health will only be improved if the skin is included in health policy.61 This is not a matter of social justice, nor a feminist issue; it is simple common sense.62

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Figure 1 - Reversal reaction
Figure 2 - Erythema nodosum leprosum
Figure 3 - Erythema nodosum leprosum during lactation - Courtesy of Tania Cestari, Brazil
Figure 4 - Erythema nodosum leprosum (patient in figure 3) - Courtesy of Tania Cestari, Brazil
Figure 5 - Erythema induratum
Figure 6 - Tinea nigra
Figure 7 - Kerion celsi
Figure 8 - Scabies
Figure 9 - Scabies
Figure 10 - Life cycle of Schistosoma mansoni
Figure 11 - Schistosomiasis mansoni - left labium minora
Figure 12 - Histopathology of Schistosomiasis mansoni (vulval lesion in figure 11): egg of S. mansoni with its lateral spine (HE, 160X)

Table 1 - Schedule for tuberculosis