Scabies

Human scabies is an intensely pruritic skin infestation caused by the host-

specific mite Sarcoptes scabiei hominis. Approximately 300 million cases of
scabies (see the image below) are reported worldwide each year.

Signs and symptoms

Burrows are a pathognomonic sign and represent the intraepidermal tunnel created
by the moving female mite. They appear as serpiginous, grayish, threadlike
elevations in the superficial epidermis, ranging from 2-10 mm long. High-yield
locations for burrows include the following:
Webbed spaces of the fingers
Flexor surfaces of the wrists
Elbows
Axillae
Belt line
Feet
Scrotum (men)
Areolae (women)
In geriatric patients, scabies demonstrates a propensity for the back, often appearing
as excoriations. In infants and small children, burrows are commonly located on the
palms and soles.
ne- to 3-mm erythematous papules and vesicles are seen in typical distributions in
adults. The vesicles are discrete lesions filled with clear fluid, although the fluid may
appear cloudy if the vesicle is more than a few days old.
Nodular scabies
Nodules occur in 7-10% of patients with scabies, particularly young children. In
neonates unable to scratch, pinkish brown nodules ranging in size from 2-20 mm in
diameter may develop.
Crusted scabies
In crusted scabies, lesions are often hyperkeratotic and crusted and cover large
areas. Marked scaling is common, and pruritus may be minimal or absent. Nail
dystrophy and scalp lesions may be prominent. The hands and arms are the usual
locations for lesions, but all sites are vulnerable.
Secondary lesions
These lesions result from scratching, secondary infection, and/or the hosts immune
response against the scabies mites and their products. Characteristic findings
include the following [1, 2, 3] :
Excoriations
Widespread eczematous dermatitis
Honey-colored crusting
Postinflammatory hyperpigmentation
Erythroderma
Prurigo nodules
Frank pyoderma
Diagnosis

The diagnosis of scabies can often be made clinically in patients with a pruritic rash
and characteristic linear burrows. The diagnosis is confirmed by light microscopic
identification of mites, larvae, ova, or scybala (feces) in skin scrapings.
In rare cases, mites are identified in biopsy specimens obtained to rule out other
dermatoses. Characteristic histopathology in the absence of actual mites also may
suggest the diagnosis of scabies.
Clinically inapparent infection can be detected by amplification of Sarcoptes DNA in
epidermal scale by polymerase chain reaction (PCR) assay. [4] In addition, elevated
immunoglobulin E (IgE) titers and eosinophilia may be demonstrated in some
patients with scabies.

Whenever possible, the diagnosis of scabies should be confirmed by identifying

the mite or mite eggs or fecal matter (scybala). This can be done by carefully
removing the mite from the end of its burrow using the tip of a needle or by
obtaining a skin scraping to examine under a microscope for mites, eggs, or mite
fecal matter (scybala). However, a person can still be infested even if mites,
eggs, or fecal matter cannot be found; fewer then 10-15 mites may be present on
an infested person who is otherwise healthy.

Management

Scabies treatment includes administration of a scabicidal agent (eg, permethrin,

lindane, or ivermectin), as well as an appropriate antimicrobial agent if a secondary
infection has developed.
Pruritus may be partially alleviated with an oral antihistamine, such as hydroxyzine
hydrochloride (Atarax), diphenhydramine hydrochloride (Benadryl), or
cyproheptadine hydrochloride (Periactin). In rare cases, prednisone may be used to
treat severe pruritus.
Because of their heavy mite burden, patients with crusted scabies may require
repeated applications of topical scabicides or treatment that simultaneously uses oral
ivermectin and a topical agent, such as permethrin.

Pathophysiology
Mode of transmission

Transmission of scabies is predominantly through direct skin-to-skin

contact, and for this reason scabies has been considered a sexually
transmitted disease. The mite does not penetrate deeper than the
superficial layer of the epidermis, the stratum corneum.
A person infested with mites can spread scabies even if he/she is
asymptomatic. [6]There may be a prolonged interval (up to 10 wk) between
the primary infection, when the patient becomes contagious, and the onset
of clinical manifestations. [7]Scabies is less frequently transmitted by indirect
contact through fomites such as infested bedding or clothing. However, the
greater the number of parasites on a person, as in crusted scabies, the
more likely that indirect contact will transmit the disease.
The S scabiei hominis mite that infects humans is female and is large
enough (0.3-0.4 mm long) to be seen with the naked eye. (The male is
about half this size.) The mite has 4 pairs of legs and crawls at a rate of 2.5
cm/min; it is unable to fly or jump.[8] Although its life cycle occurs completely
on the host, the mite is able to live on bedding, clothes, or other surfaces at
room temperature for 2-3 days, while remaining capable of infestation and
burrowing. At temperatures below 20C, S scabiei are immobile, although
they can survive such temperatures for extended periods. (See the image
below.)
Classic scabies

In classic scabies infection, typically 10-15 mites (range, 3-50) live on the
host. [8]Little evidence of infection exists during the first month (range, 2-6 wk), but
after 4 weeks and with subsequent infections, a delayed type IV hypersensitivity
reaction to the mites, eggs, and scybala (feces) occurs. The time required to induce
immunity in primary infestations probably accounts for the 4-week asymptomatic
latent period. With reinfestation, the sensitized individual may develop a rapid
reaction (within hours). The resultant skin eruption and its associated intense pruritus
are the hallmarks of classic scabies. (See the images below.)
An immunologic study analyzing the cellular infiltrate types and patterns in scabies
lesions concluded that T4-cell dominance is the cause of persistent itching, while an
increase in T8 cells reduces pruritus. [9]
Crusted scabies

Crusted, or Norwegian, scabies (so named because the first description was from
Norway in the mid-1800s) is a distinctive and highly contagious form of the disease.
In this variant, hundreds to millions of mites infest the host individual, who is usually
immunocompromised, elderly, or physically or mentally disabled and impaired.
(Assessment of immune function may be indicated in individuals presenting with
crusted scabies.) [10, 11] Some data suggest a higher incidence of autoimmune
diseases in patients with scabies. [12]
Crusted scabies can be easily confused with severe dermatitis or psoriasis because
widespread, crusted lesions appear with thick, hyperkeratotic scales over the
elbows, knees, palms, and soles. The diagnosis of crusted scabies should be
considered when suspected dermatitis or suspected psoriasis does not respond to
usual treatments. (See the images below.) [2]
Serum immunoglobulin E (IgE) and IgG levels are extremely high in patients with
crusted scabies, yet the immune reaction does not seem to be protective. Cell-
mediated immunity in classic scabies demonstrates T4-cell predominance in the
dermal infiltrate, while one study suggests a T8-cell predominance in crusted
scabies.
Certain patient populations are susceptible to crusted scabies. These include
patients with primary immunodeficiency disorders or a compromised ability to mount
an immune response secondary to drug therapy. A modified host response may be a
key factor in patients with malnutrition. Motor nerve impairments result in the inability
to scratch in response to the pruritus, thus disabling the utility of scratching to
remove mites and destroy burrows. Rare cases have been described in which
immunocompetent patients have developed the crusted variant without clear
explanation.
Risk factors

Prevalence rates for scabies are higher in children and sexually active individuals
than in other persons. Patients with poor sensory perception due to entities such as
leprosy and persons with immunocompromise due to conditions such as status
posttransplantation, human immunodeficiency virus (HIV) disease, and old age are
at particular risk for the crusted variant.
A 2009 study conducted in an impoverished rural community in Brazil identified the
following major risk factors for scabies in that community] :
Young age
Presence of many children in the household
Illiteracy
Low family income
Poor housing
Sharing clothes and towels
Irregular use of showers

Cutaneus
Cutaneous larva migrans (CLM) is the most common tropically acquired
dermatosis whose earliest description dates back more than 100 years.
Cutaneous larva migrans manifests as an erythematous, serpiginous,
pruritic, cutaneous eruption caused by accidental percutaneous penetration
and subsequent migration of larvae of various nematode parasites.
Cutaneous larva migrans is most commonly found in tropical and
subtropical geographic areas and the southwestern United States. It has
become an endemic in the Caribbean, Central America, South America,
Southeast Asia, and Africa. However, the ease and the increasing
incidence of foreign travel by the world's population have no longer
confined cutaneous larva migrans to these areas.

Pathophysiology
In cutaneous larva migrans (CLM), the life cycle of the parasites begins
when eggs are passed from animal feces into warm, moist, sandy soil,
where the larvae hatch. They initially feed on soil bacteria and molt twice
before the infective third stage. By using their proteases, larvae penetrate
through follicles, fissures, or intact skin of the new host. After penetrating
the stratum corneum, the larvae shed their natural cuticle. Usually, they
begin migration within a few days.
In their natural animal hosts, the larvae of cutaneous larva migrans are able
to penetrate into the dermis and are transported via the lymphatic and
venous systems to the lungs. They break through into the alveoli and
migrate to the trachea, where they are swallowed. In the intestine they
mature sexually, and the cycle begins again as their eggs are excreted.
Humans are accidental hosts, and the larvae lack the collagenase needed
to penetrate the basement membrane and invade the dermis. Therefore,
cutaneous larva migrans remains limited to the skin when humans are
infected.
The pruritic symptoms occur secondary to an immune response to both the
larvae and their products.
Epidemiology
Frequency

Cutaneous larva migrans is rated second to pinworm among helminth

infections in developed countries. Prevalence is high in regions of warm
climate, where individuals may be more inclined to walk barefoot (eg,
beaches, lower socioeconomic communities) and come in contact with
animal feces.
Age

Cutaneous larva migrans can affect persons of all ages because it depends on
exposure, but it tends to be seen in children more commonly than in adults.
Prognosis
The prognosis for cutaneous larva migrans is excellent. Cutaneous larva
migrans is a self-limiting disease. Humans are accidental, dead-end hosts,
with the larva dying and the lesions resolving within 4-8 weeks, as long as
1 year in rare cases.