After mating, the male dies, and the female penetrates the epidermis, digging furrows to lay eggs and feces.

In four to six weeks, females can release 40–50 eggs. After hatching, the hexapod larvae leave the furrows. The number of adult mites in an infected individual is estimated at 12 parasites.

Pruritus is the main symptom of scabies, being more intense at night. In most cases, this symptom begins insidiously, progressively intensifying. It can affect almost the entire body; the face is rarely affected.

The characteristic lesion is linear, serpiginous, and raised, measuring a few millimeters; at one end, a papular-vesicular lesion may be observed, described by some authors as a “black spot.” These lesions are most often observed on the lateral surfaces of the fingers, palmar regions, hands, wrists, and feet.

Scalp scabies is not common in adults; however, it may accompany or resemble seborrheic dermatitis.

Left untreated, erythematous papular lesions appear in the armpits, breasts, penis, buttocks, interdigital spaces, waist, and feet.

Long-term patients may present papular-nodular reddish-brown lesions, mainly located on the genitalia, armpits, trunk, and elbows. These lesions are very itchy and their regression is slow, even after proper treatment. These manifestations are called nodular scabies (Fig. 1). It had been assumed that there was no mite in these lesions. However, recent studies have demonstrated the presence of S. scabiei.3,4 In children, nodular scabies may simulate mastocytosis.5

Figure 1.

Nodular scabies – intense pruritus and erythematous papular nodular lesions.

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In newborns and young children, the face and scalp may be affected, and cervical polymicroadenopathy may be observed. Eczema or hive lesions may hinder the diagnosis, especially in infants.6

In the elderly, the skin reaction to the presence of the mite may be less pronounced and cause atypical conditions. Dorsal injuries may be mistaken for senile pruritus. Vesicobullous lesions, which are clinically and histologically similar to bullous pemphigoid, have been reported in patients older than 6 years without debilitating disease.

Crusted scabies, also known as Norwegian scabies, is a clinical variety of scabies that occurs due to mite hyperinfestation; over one million parasites can be found in this condition. Currently, it is observed primarily in immunosuppressed patients, those under chemoterapy, those with malignant neoplasms, and transplant recipients. The frequency of this clinical form has increased in HIV-positive patients.7,8 Australian aborigines and carriers of the HTLV1 virus are also relatively frequently affected.9 Clinically, it is characterized by hyperkeratotic, crusted lesions with cutaneous fissures and thickened and dystrophic nails (Fig. 2). Secondary infections may be observed in these patients. In the vast majority of cases, the pruritus is very intense. The differential diagnosis is mainly made with Darier's disease and psoriasis.

Figure 2.

Crusted scabies. Intense, constant pruritus and generalized erythematous, squamous lesions. HTLV+ patient. Personl archive: Dr. Paulo Roberto Machado.

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Differential diagnosis is made with most pruritic conditions, such as atopic dermatitis, drug rash, papular urticaria, insect bites, and pyoderma.

Direct examination of the lesions should always be done, especially in atypical cases. Two drops of mineral oil are placed on the lesions, which are then scarified with a scalpel blade or curette, removing the furrow ceiling, which is placed on a glass slide. It is then examined under the microscope at 10× and 40× magnification. The mite, eggs, and/or feces may be observed. A few drops of 30% potassium hydroxide can be placed on the collected material prior to microscope observation.

PCR may be useful in clinically atypical cases.10

Dermoscopy can also be used to find the parasite (Fig. 3).11 Epiluminescence microscopy is another recommended method for mite visualization;12 confocal microscopy and optical coherence tomography may also be used.13

Figure 3.

Sarcoptes scabiei. Dermoscopy. At the lower end, a “hang glider”-shaped dark spot, corresponding to the anterior segment of the mite.

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In the treatment of scabies, it is important that all household residents are treated, in order to avoid reinfestation.

Permethrin: a synthetic, effective, and non-toxic pyrethroid is available as a 5% cream or lotion. It can be used in children, adults, pregnant women, and nursing mothers.

It should be applied over the entire body, from neck to toe. In children, it should also be applied to the scalp and retroauricular ridges. The drug should be applied at nighttime, for two consecutive nights. On the third day, in the morning, all bedding should be removed and washed.

Precipitated sulfur: recommended at concentrations of 5–10% in petroleum jelly. It does not cause side effects. It can be used in children, pregnant women, and nursing mothers. It should be applied on the entire body for four consecutive nights, and removed during the day.

Ivermectin: used systemically. It is a semi-synthetic macrocyclic lactone suitable for adults and children over 5 years. The dose prescribed is 200μg/kg, given as a single dose, which may be repeated after seven days. For immunosuppressed patients, two doses should be used at a one-week interval. It is the gold standard in the treatment of crusted scabies, in which it is associated with topical keratolytics, such as 5% salicylated petroleum jelly.

Ivermectin may also be used topically, at 1%, in propylene glycol or as a lotion. It should be applied on the entire body and the application should be repeated after one week.14

New medications are currently being investigated. The use of Tinospora cordifolia lotion showed similar efficacy to permethrin, with no side effects in treatment.15 Moxidectin is another promising medication whose efficacy and safety have already been demonstrated.16

Potent topical corticosteroids, two to three times daily, are used in the treatment of nodular scabies. Occlusion or triamcinolone infiltration (3–4mg/mL) can also be used.17 Topical pimecrolimus and tacrolimus have been used in cases of corticosteroid resistance, with good results.18 In resistant cases, obeying the legal restrictions, oral thalidomide at a dose of 100mg daily may be used.

It is caused by Tunga penetrans, the smallest of fleas; it measures on average 1mm, and lives in dry and sandy places, especially in rural areas, in pig pens and corrals. The main hosts of these hematophagous fleas are pigs and humans. After feeding, the male leaves the host; the fertilized female penetrates the skin, introducing its head and chest into the epidermis, leaving out the respiratory stigmas and the egg-laying orifice.33 The eggs develop and the abdomen dilates, showing a yellowish nodule with a blackened spot in the center (Fig. 5A). There is pruritus and eventually pain. They are usually observed in the nail folds of the toes, interdigital spaces, and plantar regions.34–36 When many nearby lesions occur, they resemble a honeycomb (Fig. 5B and C). Secondary infections may occur, and the lesions serve as a gateway to other diseases.37 After the eggs are fully developed, the flea begins to expel them within two weeks; subsequently, the female dies.

Figure 5.

(A) Tungiasis – typical aspect. Isolated lesion. Note a pustule, in regression, with central crusted area. (B, C) Tungiasis. Multiple lesions, isolated and confluent.

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The flea is removed with a needle, and an antiseptic is applied to the wound. In generalized cases, oral thiabendazole 25mg/kg is used for ten days.38

Prophylaxis consists of wearing shoes.

Recent studies have shown that low viscosity dimethicone (NYDA) applied for seven days is effective and safe.39

All cimicids (bed bugs) are blood-sucking parasites of birds and mammals. Two thirds of the species are bat parasites. The genus Cimex, with the species lectularius and hemiptera, is a human parasite. Commonly known as bed bugs, these insects have nocturnal habits and live in the cracks and holes of furniture and mattresses. At night, especially at dawn, they bite humans. During the meal they inject saliva, which contains an anticoagulant and anesthetic.

These bites are most commonly observed on the face, neck, arms, and hands. They cause hives and pruritic lesions (Fig. 6), often in linear arrangement. Distant sensitization injuries may occur, including bullous lesions.40,41

Figure 6.

Bedbug dermatitis. Multiple, characteristic linear erythematous papular lesions located in the abdomen.

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Bed bugs share important traits with triatomine insects, but it is unclear whether these similarities include the ability to transmit Trypanosoma cruzi, which causes Chagas disease.

A recent study demonstrated efficient and bidirectional transmission of T. cruzi between hosts and bed bugs. Most bed bugs that fed on infected mice acquired the parasite; most mice were infected after cohabitation with exposed bed bugs. T. cruzi was also transmitted to mice after the feces of infected bedbugs were applied directly to the skin of the host. These findings suggest that bed bugs may be a T.cruzi vector.42

Corticosteroid cream is used for the treatment, and, depending on the pruritus, antihistamines may also be used. Bed bugs must be eradicated with the use of insecticides.

Several reports suggest an increase in the number of cases worldwide, including in Europe and the United States.43,44

Myiasis is characterized by the invasion of Diptera larvae into the skin, mucous membranes, and organs of humans and animals.

Among the various families of Diptera, the flies are noteworthy because, beside other diseases, they cause myiasis.

According to the evolutionary cycle of the Diptera flies, myiasis is classified into primary and secondary.

In patients with primary myiasis, the larvae invade healthy tissues. This variety is called furunculoid myiasis. In the secondary form, known as cavity myiasis, the flies lay their eggs on skin wounds or in the mucosa.45,46

Furunculoid myiasis

It is observed in tropical regions of the American continent, extending from southern Mexico to northern Argentina. The life cycle of D. hominis is unique. After copulation, the female flies and captures a hematophagous Diptera fly. It lays 10–50 eggs in the prey's abdomen, without affecting its ability to fly.47 When it lands on the skin of a human or animal, the eggs hatch and larvae are released into the host through the hair follicles or the insect bite hole. Larva penetration is usually not noticed. At the larva entry site, an erythematous, papulous, pruritic, and painful lesion arises. The papule increases in size, evolving to a furunculoid aspect, with minor ulceration and outflow of serous exudate. In this opening, it is possible to observe the tail of the larva. The larvae feed on hypodermic material for an average of five to 12 weeks. After this period, the larvae leave the host and fall to the ground, becoming a pupa. Between 60 and 80 days, the pupa evolves into a winged insect. The larva can be exposed by pressing the lesion (Fig. 7).47,48

Figure 7.

Furunculoid myiasis. Ulcero-nodular lesion and etiological agent (Dermatobia hominis).

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The larva actively moves, and patients report a “stinging pain” at the site. Eventually, a secondary infection may occur, with abscess, cellulitis, and adenopathy.

When the larva leaves the nodule, the lesion regresses and heals.47,48

The treatment consists of removing the larva, which can be done by compressing the nodule after a small incision into the lesion orifice. Hole obstruction with petroleum jelly, and placement of adhesive tape, preventing the larva from breathing, facilitates its removal. A lay treatment consists of placing heated bacon over the hole of the lesion – to breathe, the larva penetrates the bacon.

The lesions are usually linear, raised, erythematous, and serpiginous (Fig. 8A). Vesicles and even blisters may also appear. The most affected areas are the feet, legs, buttocks; it appears less often in other regions, such as the face, armpits, and penis. One case with oral mucosa lesions was described. Larvae dislocation triggers intense pruritus.59

Figure 8.

(A) Larva migrans. Intense pruritus. Typical serpiginous lesion with linear aspect. (B) Larva migrans. Numerous lesions caused by multiple larvae.

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When eczema and secondary infection occur, diagnosis can be very difficult. In such cases, it is first recommended to use ointments for the allergic condition, and antibiotics, if necessary. This will make the clinical aspect of larva migrans more evident.

When interdigital spaces are affected, maceration may occur. This clinical presentation may be confused with foot dermatophytosis.

Hematological alterations may also occur, with eosinophilia that, in some cases, reaches 30%. In severe infestations (Fig. 8B), the larvae may invade the blood stream and trigger Loeffler's syndrome, characterized by eosinophilic pneumonia associated with blood eosinophilia.60

Depending on the number of lesions and their location, treatment may be topical or systemic. In patients with multiple lesions or involvement of hyperkeratotic areas, such as the palmoplantar regions, systemic treatment is recommended.

Albendazole at a dose of 15mg/kg/day for three days is a good therapeutic option. Its use does not prevent breastfeeding, and the fetal risk is category C. The cure rate varies from 77% to 100%.61,62

Ivermectin, at a single dose of 200μg/kg, is also effective. Depending on the evolutioncourse, the same dose may be repeated after seven days.63

When the number of lesions is reduced and located in the glabrous skin, topical treatment with thiabendazole 5% ointment may be indicated.

Carbonic snow or liquid nitrogen are also used.64,65

The etiologic agent of ME/LD, a spirochete, was first isolated by Burgdorfer in 1982 in the intestine of Ixodes dammini ticks.75 This spirochete is now called Borrelia burdorgeri sensu lato. It has been identified in biopsies of skin lesions, blood, cerebrospinal fluid, synovial tissue, myocardium, and eyes of patients with LD.12

In the United States, mice and deer are important reservoirs of this spirochete. Elevated serological titers for Borrelia have been observed in horses, cows, sheep, and cats. In Brazil, wild rodents and other mammals, such as skunks, appear to participate in the epidemiological cycle of LD.76

The main transmitters of the disease are Ixodes ticks. In Europe, Ixodes ricinus is the most prevalent, while in the United States it is the Ixodes dammini, also known as I. scapularis. In Brazil, Ambylomma cajannense is the tick believed to be responsible for the transmission of LD. However, the participation of other tick species is not excluded. The evolutionary forms of ticks most associated with Borrelia transmission are nymphs and adult ticks. Nymph bites are painless, which would explain the fact that many infected patients do not remember being bitten by ticks.77

The cutaneous manifestations of LD are divided into early localized (erythema migrans and lymphocytoma cutis); early disseminated initial (ME and multiple lymphocytomas, which may be accompanied by alterations in other organs); and late (acrodermatitis chronica atrophicans).78

ME is the main early clinical manifestation of LD. Three to 30 days after the tick bite, an enlarged papule or small erythematous plaque appears at the site of inoculation, forming a plaque with discontinuous edges and a clear, cyanotic, and/or scaly center that expands centrifugally and may reach a large diameter (Fig. 9). Rapid progression of lesions, which may reach 20–30cm or more in days or weeks, is common. In most patients, these lesions are asymptomatic. Different clinical features have been described in ME: erysipeloid, erythematous, lichenoid.79 European cases of ME tend to present with a small number of lesions and without a tendency to cutaneous spread.80

Figure 9.

Lyme disease. Plaque presenting centrifugal growth, with erythematous-violet borders, measuring approximately 18cm, located on the posterior surface of the thigh.

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In addition to ME, another important cutaneous manifestation of the early phase of LD is lymphocytoma cutis, also called lymphadenosis benign cutis, which simulates B lymphocytic pseudolymphoma. Clinically, it is characterized by a single lump or erythematous plaque, 1 to 5cm in diameter, usually located on the face, pinna, scrotum, or mammary areola. Lymphocytoma is often associated with infection by B. afzelli and B. garinii.81 In 2007, a case of cutaneous lymphocytoma in association with LD was published in Brazil.82

In this acute phase, systemic manifestations such as asthenia, arthralgia, myalgia, skin rash, adenopathy, splenomegaly and signs of meningeal irritation may also be observed. Early LD lesions may disappear without treatment, and manifestations of the second and third stages may appear months or years after initial infection. The main alterations include articular, cardiac, neurological, ophthalmological, and skin involvement. More rarely, late changes may occur in the presence of ME lesions.83 Among the manifestations of the late, cutaneous phases, acrodermatitis chronica atrophicans (ACA), also known as Pick-Herxheimer disease, is more associated with B. afzelii infection and is generally described in Europe. ACA is more common in adults and may manifest from six months to eight years after the tick bite. Clinically, it initiates with an erythematous plaque, evolving with skin atrophy and very prominent blood vessels, particularly in the lower limbs. The face and trunk may also be affected.84

B. burgdorferi infection has been associated with other dermatological diseases such as plaque scleroderma, lichen sclerosus, atrophoderma of Pasini and Pierini, cutaneous B-cell lymphoma, and granuloma annulare.85 In a study conducted in Manaus in 2009, patients with scleroderma and atrophoderma of Pasini and Pierini were analyzed by immunohistochemistry with anti-B. burgdorferi polyclonal antibody; the presence of spirochete was confirmed in samples from both diseases.86

The diagnosis of the disease is based on epidemiological, clinical, and laboratory aspects. Laboratory diagnosis is based on serological tests (detection of specific antibodies) and/or on the finding of the etiological agent. In addition to serology, it is important to conduct histopathological and immunohistochemical tests, culture, and, if available, PCR.87

Detection of IgM or IgG anti-B. burgdorferi antibodies is commonly used for serological diagnosis and epidemiological investigation. Enzyme-linked immunosorbent assay (ELISA) tests are most commonly used; however, they present false-positive results in view of cross-reactions with other diseases, such as collagenoses, leishmaniasis, and syphilis. Thus, in non-endemic areas, for the definitive diagnosis it is necessary to perform a confirmatory exam that demonstrates the presence of the agent.88

Histopathological examination of ME lesions reveals proliferation and dilation of blood vessels associated with a central inflammatory infiltrate consisting of macrophages, mast cells, neutrophils, plasma cells, lymphocytes, and rare eosinophils. A pPCRymphocytic vasculitis may also be observed. In older lesions, atrophy of the epidermis and dermis may occur, as well as decreased dermal inflammatory infiltrate.89

PCR has been used to detect Borrelia nucleic acid sequences, with high specificity. However, the sensitivity of this diagnostic method is variable (20–81%). In 2008, Cerar et al. demonstrated that nested-PCR, using the flagellin gene, presented higher sensitivity than PCR (64.6% vs. 24%). PCR positivity is higher when fragments of cutaneous or synovial membrane lesions are used. It is less sensitive when performed on paraffin blocks, blood, synovial fluid, or cerebrospinal fluid.90

The culture using Barbour, Stroenery, Kelly (BSK) medium or variations thereof presents 100% specificity, but with a relatively low sensitivity. Given the difficulties of the technique and the contamination of the material, the results are positive in approximately 45% of the cases.91

In 2007, through a specific immunohistochemistry test for the detection of Borrelia sp., associated with the floating focus microscopy (FFM) technique, Eisendle et al. obtained results superior to nested-PCR in the identification of Borrelia (96% vs. 45.2%), with similar specificity (99.4% vs. 100%). The FFM consists of examining the slide in several planes simultaneously: horizontal and vertical, advancing and retracting the objective of the microscope, with magnifications of up to 400× under bright illumination. According to the authors, these simultaneous movements facilitate the detection of Borrelia.92 In 2010, using this same technique, Talhari et al. demonstrated, for the first time in Brazil, the presence of Borrelia in ME patients from Manaus, using immunohistochemistry with anti-Borrelia polyclonal antibody, and observation by FFM.93

The treatment of this disease is made according to the stage and clinical manifestation presented. In adult patients with localized LD, including ME cases without specific neurological manifestations, the recommended treatment is doxycycline (100mg, 2× daily), amoxicillin (500mg, 3× daily), or cefuroxime axetil (500mg, 2× daily) for 14 days. For children and patients with doxycycline hypersensitivity, amoxicillin at a dose of 500mg or 50mg/kg/day, 3× daily is used; cefuroxime 500mg or 30mg/kg/day, 2× daily can also be used for the same period. Joint manifestations and cases of atrophic acrodermatitis are treated with the same antibiotics for 28 days. In cases of meningitis and other manifestations of early neurological LD, intravenous (IV) ceftriaxone 2g/day or IV crystalline penicillin G at a dose of 18 to 24 million IU daily for 14 days is recommended. For the treatment of chronic erosive arthritis, sulfasalazine, chloroquine, methotrexate, and corticosteroids are recommended.80,94

Transmission of O. volvulus occurs through the bite of insects of the genus Simulium. These are found in greater abundance near the banks of river banks, hence the name “river blindness.”95 Microfilariae can be transmitted by different species of Simulium. In Brazil, the main species are S. guyanense, S. incrustatum, and S. oyapockense.98

Humans are the main hosts of the disease. By stinging an infected human, hematophagous females ingest microfilariae, which after two to three weeks become infective larvae. After a period of six to 12 months, these larvae develop into adult worms; males measure 2–4cm in length and females, 40–50cm. Adult worms, male and female, tend to lodge in interstitial spaces and adipose tissue, forming onchocercomas. They mate in these sites. After mating, females give rise to microfilariae, which migrate to connective tissue, superficial dermis, and the ocular globe. Each female can generate approximately one million microfilariae per year, which live up to 2.5 years. Adult females can live between nine and 16 years.99

In the integument, the most common and early manifestation of onchocerciasis is chronic, constant pruritus that may simulate scabies (Fig. 10A). Areas with abrasions, lichenification, and hyperpigmentation are frequent. This condition is known as lizard skin.100,101

Figure 10.

Onchocerciasis. Intense pruritus, presence of lichenification, exulcerations, and hyperpigmentation. Patient from the Infectious Disease Clinic, Ibadan, Nigeria (personal archive: Prof. Dr. Sinésio Talhari).

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Late depigmentation and acromy secondary to chronic pruritus are frequent, especially in the lower limbs (termed leopard skin). Atrophy may occur in the late stages of the disease, which may be mild (Fig. 10B) or very pronounced, leading to enlargement of the scrotum and inguinal hernia. Inguinal hernias are termed hanging groin (Fig. 11).101,102 In some cases, lesions are limited to a certain skin area, especially on the leg, thigh, and gluteal region. This condition is known as sowda. Onchocercomas are painless, firm, rounded or elongated, and vary in size (0.5–10cm in diameter). These lesions are usually located in the pelvis, lateral surfaces of the chest, and lower limbs in African patients; In the Americas, onchocercomas are mainly seen on the scalp, arms, and chest.100

Figure 11.

A. Onchocerciasis. Presence of atrophy, common in patients with long course. Native Brazilian from the Yanomami tribe (personal archive: Prof. Dr. Sinésio Talhari). B. Onchocerciasis. Observe the classic aspect of the “hanging groin” due to long evolution. There is also scrotum elongation (secondary to cutaneous atrophy), and there are nodules in the iliac crest and left groin – probably onchocercomas. Native Brazilian from the Yanomami tribe (personal archive: Prof. Dr. Sinésio Talhari).

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The main ophthalmic lesions are keratitis, iridocyclitis, cataract, choroidoretinal lesions, post-neuritic optic atrophy, and amaurosis. Amaurosis produced by onchocerciasis is extremely common in Africa, resulting in great socioeconomic losses.95,101

The diagnosis of onchocerciasis is based on the observation of microfilariae or the adult worm through direct examination. The procedure is simple and performed without anesthesia: the skin is pinched between the thumb and forefinger to prevent bleeding during material collection. A superficial fragment of skin is collected. The skin sample obtained is placed in saline solution and divided into small pieces with the aid of two scalpels. Microfilariae detection is done under the microscope without any staining at 40–50× magnification (Fig. 12).101O. volvulus may also be seen by histopathological examination of the skin lesions and ophthalmic examination. The usual techniques of biopsy, 10% formalin fixation, and hematoxylin-eosin staining are employed.101,102 The microfilariae can be identified by slit lamp examination.101,102 Recently, immunological methods have been used to identify specific anti-onchocerca antibodies (ELISA and immunofluorescence) and onchocerca DNA (PCR).103

Figure 12.

Onchocerciasis. Observe two microfilariae (Onchocerca volvulus). Direct examination in saline solution. 40× magnification (personal archive: Prof. Dr. Sinésio Talhari).

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Treatment is primarily oral ivermectin, at a single dose of 150μg/kg, every six months. This is a microfilaricidal drug and does not eliminate adult worms, which remain alive, producing new microfilariae.95 A randomized controlled trial suggests that the use of ivermectin every three months would eliminate more female adult parasites, further reducing O. volvulus transmission.104