SCABIES

By SABESH S
Pharm D 3rd year
01 INTRODUCTION
INTRODUCTION
Scabies is a contagious skin condition caused by the mite Sarcoptes scabiei
which burrows into the skin and causes severe itching. Scabies is transmitted by
direct skin-to-skin contact or indirectly by contact with contaminated material
(fomites). This condition is often challenging to diagnose as many patients may
have only subtle symptoms. However, other patients may present with the
classic history of exposure, severe pruritis that is worse at night, and reference
to other individuals with similar symptoms.
INTRODUCTION
Itch is relentless, especially at night. Skin-to-skin contact transmits the
infectious organism therefore, family members and skin contact relationships
create the highest risk. Scabies was declared a neglected skin disease by the
World Health Organization (WHO) in 2009 and is a significant health concern
in many developing countries. Infested individuals require identification and
prompt treatment because a misdiagnosis can lead to outbreaks, morbidity, and
an increased economic burden.
02 EPIDEMIOLOGY
 EPIDEMIOLOGY
 The estimated worldwide prevalence of scabies is 300 million infected
individuals each year. It is a significant health concern in many developing
countries and was declared a neglected skin disease by the World Health
Organization in 2009.
 Scabies is highly prevalent in the following geographic regions: Africa,
South America, Australia, and Southeast Asia. The high prevalence
correlates with poverty, poor nutritional status, homelessness, and
inadequate hygiene.
EPIDEMIOLOGY
 EPIDEMIOLOGY
 It is more common among children and young adults. Cases in these countries
are associated with significant morbidity due to complications and secondary
infections. These may include abscesses, lymphadenopathy, and post-
streptococcal glomerulonephritis.
 Scabies outbreaks in industrialized countries may occur sporadically or as
institutional outbreaks in schools, nursing homes, long-term acute care (LTAC)
facilities, hospitals, prisons, retirement homes, and areas of overcrowding
 EPIDEMIOLOGY
 Scabies occurs more commonly in fall and winter months in these countries.
Prevalence rates for scabies in developing nations are higher than those in
industrialized countries.
 Age-related demographics
The World Health Organization reports a prevalence rate of 5-10% in
children in resource-poor tropical countries.
In a 2009 retrospective study of 30,078 children in India, scabies was
found to be the second most common skin disease in all age groups of
children and the third most common skin disease in infants.
In parts of Bangladesh, the number of children with scabies exceeds
the number with diarrheal and respiratory diseases combined.
03 ETIOLOGY
 ETIOLOGY
The mite that causes scabies is Sarcoptes scabiei var. Hominis. It is an arthropod belonging to the order
Acarina. It belongs to the class Arachnida, order Astigmata, and family Sarcoptidae.
Clinically, it presents in three forms: classic, nodular, or a contagious crusted variant also called
Norwegian scabies.
Sarcoptes scabiei resides in the dermal and epidermal layers of humans as well as animals. Scabies
occurs worldwide and is a common skin condition. The infestation begins with the female mite
burrowing within the stratum corneum of its host where it lays its eggs. It later develops into larvae,
nymphs, and adults
 RISK FACTORS
 Direct contact: skin-to-skin contact with a person with scabies, which can be quite brief (such as
through holding hands or sexual contact).
 Fomites: indirect contact through bedding, clothes, or towels, although this is far less common than
direct contact.
 Living conditions: poverty and overcrowding are key risk factors. This includes institutional care
facilities, such as residential aged care homes, hospitals, and prisons.
 Environment: transmission is more common in warm, tropical, humid environments.
 Immunosuppression: HIV infection or immunosuppressive medication increases the risk of
infection with scabies and may also lead to more severe and persistent infection
0 PATHOPHSIOLOGY
4
 PATHOPHSIOLOGY
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. 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. Scabies is less frequently transmitted by
indirect contact through fomites such as infested bedding or clothing.
 Mite life cycle
1. The female S scabiei var hominis mite lays 60-90 eggs in her 30-day lifespan, although less
than 10% of the eggs result in mature mites. Eggs incubate and hatch in 3-4 days (90% of the
hatched mites die)
2. Larvae (3 pairs of legs) migrate to the skin surface and burrow into the intact stratum
corneum to make short burrows, called molting pouches (3-4 days)
3. Larvae molt into nymphs (4 pairs of legs), which molt once into larger nymphs before
becoming adults
4. Mating takes place once, and the female is fertile for the rest of her life; the male dies soon
after mating
5. The female makes a serpentine burrow using proteolytic enzymes to dissolve the stratum
corneum of the epidermis, laying eggs in the process; she continues to lengthen her burrow
and lay eggs for the rest of her life, surviving 1-2 months
6. Transmission of impregnated females from person-to-person occurs through direct or indirect
skin contact
 THREE FORMS

Nodular scabies
hypersensitivity
reaction to the female
Classic scabies
mite.
mites on an individual
that range between 10 Crusted scabies
to 15 organisms
patients who are
immunocompromised
 CLASSIC SCABIES
• The classic form of scabies may have a population of mites on an individual
that range between 10 to 15 organisms. It typically takes ten minutes of skin-to-
skin contact for mites to transmit to another human host, in cases of classic
scabies.

• Transmission of the disease can also occur by fomite transmission via clothing
or bed sheets. This presentation of scabies often manifests with hyperkeratotic
plaques that can be diffuse or localized to the palms, soles, and under
fingernails.

• 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
 NODULAR FORM
The nodular form of scabies is a variant of the classic form. This form
presents with erythematous nodules with a predilection towards the axilla
and groin. The nodules are pruritic and considered to be a
hypersensitivity reaction to the female mite.

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.
 NORWEGIAN SCABIES
• The crusted variant, Norwegian scabies, can have up into millions of mites on a single individual. Crusted
scabies occurs in patients who are immunocompromised due to immunosuppressive therapy, diabetes, human
immunodeficiency virus (HIV), or older age.

• This high density requires only short contact with patients and contaminated materials for infection to occur.
The immunological condition of the host and the extent of spread usually determines the number of infesting
mites.

• 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.

• 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.
CRUSTED
SCABIES
0 CLINICAL
PRESENTATION
5
 HISTORY
Patient history can reliably suggest the presence of scabies. Lesion distribution and intractable pruritus that is
worse at night, as well as scabies symptoms in close contacts (including multiple family members), should
immediately rank scabies at the top of the clinical differential diagnosis.

Lesion distribution differs in adults and children. Adults manifest lesions primarily on the following parts of the
body:
• Flexor aspects of the wrists
• Interdigital web spaces of the hands
• Dorsal feet
• Axillae
• Elbows
• Waist
• Buttocks
• Genitalia
 HISTORY
Pruritic papules and vesicles on the scrotum and penis in men and areolae in women are highly characteristic.

Infants and young children may develop lesions diffusely, but unlike in adults, lesions are common on the face,
scalp, neck, palms, and soles.

All cutaneous sites are susceptible in immunocompromised and elderly patients, who often have a history of a
widespread, pruritic, eczematous eruption.

Signs and symptoms of pruritus tend to crescendo progressively over 2-3 weeks before compelling the patient to
seek medical attention. (However, debilitated or immunocompromised patients may not have the urge to
scratch.)

Scabies appears to occur in clusters. If there is an outbreak in the community, consider scabies in an individual
presenting with rash and itching.
 PHYSICAL
EXAMINATION
• Clinical findings include primary and secondary lesions.
• Primary lesions are the first manifestation of the infestation and typically include small papules, vesicles,
and burrows.
• Secondary lesions are the result of rubbing and scratching, and they may be the only clinical manifestation
of the disease.

PRIMARY SCABIES LESIONS

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)
 PHYSICAL
EXAMINATION
Classic scabies typically has a distribution involving the axillae, elbow
flexures, wrists and hands, and genital area. This is commonly known as the
circle of Hebra.

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, as in the image below. In immunocompromised
patients, bullous lesions may be observed.

One- 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.

Unlike adults, children commonly present with facial and neck involvement. In
very young children and infants, a widespread, eczematous eruption primarily
on the trunk is common, as in the image below. In addition, infants may have 1-
to 3-mm papules, vesicles, and pustules on the palms and soles.
 PHYSICAL
EXAMINATION
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, as demonstrated in the images below. Mites are
rarely found within the nodules.

Crusted scabies
Crusted scabies, previously referred to as Norwegian scabies, manifests with
marked thickening and crusting of the skin. Lesions are often hyperkeratotic
and crusted and cover large areas. Marked scaling is common, and pruritus may
be minimal or absent. Nail dystrophy (subungual hyperkeratosis) and scalp
lesions may be present.

The hands and arms are the usual locations for lesions, but all sites are
vulnerable. Mites can number in the thousands to millions in this form of
scabies.
 PHYSICAL
EXAMINATION
Secondary scabies lesions

These lesions result from scratching, secondary infection, and/or the host’s
immune response against the scabies mites and their products. Characteristic
findings include the following :

Excoriations
Widespread eczema
Honey-colored crusting
Postinflammatory hyperpigmentation
Erythroderma
Prurigo nodules
Frank pyoderma
0 DIAGNOSIS
6
 DIFFERENTIAL
DIAGNOSIS Differential Diagnoses
nodular scabies: • Acropustulosis of Infancy
• Urticaria pigmentosa (in
• Allergic Contact Dermatitis
young child)
• Lymphoma • Asteatotic Eczema
• Atopic Dermatitis
crusted scabies:
• Seborrheic dermatitis • Bedbug Bites
• Langerhans cell histiocytosis
• Psoriasis • Chickenpox
• Eczema • Dermatitis Artefacta
• Ichthyosis
• Erythroderma • Dermatitis Herpetiformis
• Irritant Contact Dermatitis
• Pediatric Atopic Dermatitis
 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 IgE titers and eosinophilia may be
demonstrated in some patients with scabies.
 DIAGNOSIS
Locating Mite Burrows

• Burrow ink test

A burrow can be located by rubbing a washable felt-tip marker across the suspected site and removing
the ink with an alcohol wipe. When a burrow is present, the ink penetrates the stratum corneum and
delineates the site. This technique is particularly useful in children and in individuals with very few
burrows.

• Tetracycline
Topical tetracycline solution is an alternative to the burrow ink test.

Skin Scraping
Definitive testing relies on the identification of mites or their eggs, eggshell fragments, or scybala.
Scraping 15 or more burrows often produces only 1 or 2 eggs or mites, except in a case of crusted
scabies, in which many mites will be present.
 DIAGNOSIS
Crusted scabies
Add 10% potassium hydroxide to the skin scraping. This
dissolves excess keratin and permits adequate microscopic
examination.

Adhesive Tape Test

Strips of tape are applied to areas suspected of being
burrows and then rapidly pulled off. These are then applied
to microscope slides and examined.
Histologic Findings

1. The histologic features of scabies are distinctive enough to suggest the diagnosis, although they are common
to a variety of arthropod reactions. If a burrow is excised, mites, larvae, ova, and feces may be identified
within the stratum corneum.
2. A superficial and deep dermal infiltrate composed of lymphocytes, histiocytes, mast cells, and eosinophils is
characteristic.
 Scabies mite in the stratum corneum

DIAGNOSIS
Spongiosis and vesicle formation with exocytosis of eosinophils
and occasional neutrophils are present, as in the image below.
Biopsy of older lesions is nondiagnostic, demonstrating only
excoriation and scale crusts.

Crusted scabies
Crusted scabies demonstrates massive hyperkeratosis of the
stratum corneum, with innumerable mites in all stages of
development. The dermis shows a superficial and deep, chronic
inflammatory infiltrate with admixed interstitial eosinophils.

Nodular scabies
Nodular scabies reveals a dense, mixed, superficial and deep
dermal inflammatory cell infiltrate. Lymphoid follicles may be
present, and the infiltrate occasionally extends into the
subcutaneous fat.
0 TREATMENT
7
 TREATMENT
Approach Considerations
• Scabies treatment includes administration of a scabicidal agent Neonates and pregnant women should be treated for
(eg, permethrin, lindane, or ivermectin), as well as an scabies only if the benefit exceeds the risk and if the
appropriate antimicrobial agent if a secondary infection has diagnosis is confirmed by a positive skin scraping or
developed. biopsy result.
• Treatment failures are uncommon but do occur. The most Crusted scabies may require several treatments with
common causes of treatment failure include the following: scabicides and sometimes several different medications
Improper application used sequentially. [27] Scabetic nodules may require
Inadequate application intranodular steroid injection.
Reinfestation
Resistance
 TREATMENT
Topical therapies

Permethrin 5% cream is the treatment of choice for scabies, applied to the entire body (excluding the face) and left
on for 8 hours, with treatment repeated in 7 days. Some guidelines do not recommend permethrin for use in children
younger than 2 months of age.

Benzyl benzoate 25% emulsion is used as a second-line treatment in cases of allergy or treatment failure but can
cause skin irritation.

Systemic therapies
Ivermectin is an effective oral scabicide and is the mainstay of systemic treatment of scabies for adults and older
children. It is usually given at a dose of 200µg/kg. may repeat in 14 days if necessary.

Ivermectin is effective but more expensive than permethrin. It can be useful in situations where compliance is difficult
or to contain widespread outbreaks (e.g. in care facilities).
 TREATMENT
Itching may persist for up to a month, even following successful treatment.

Pruritus may be partially alleviated with an oral antihistamine, such as hydroxyzine hydrochloride,
diphenhydramine hydrochloride, or cyproheptadine hydrochloride.

Rarely, individuals with a history of atopy may require a tapered dose of prednisone for the treatment of
severe pruritus. Intranodular injection of dilute corticosteroids may be necessary in cases of nodular
scabies.

Crusted scabies
Patients with crusted scabies or their caregivers should be instructed to remove excess scale in order to allow
penetration of the topical scabicidal agent and decrease the burden of infestation. This can be achieved with warm
water soaks followed by application of a keratolytic agent, such as 5% salicylic acid in petrolatum or Lac-Hydrin
cream.
 COMPLICATIONS

Secondary bacterial infection of scabies rashes is common, due to patients scratching the highly pruritic
rash, most commonly with Streptococcus pyogenes (a group A streptococcus) or Staphylococcal aureus.

It is important to recognise and treat secondary infections early with appropriate antibiotics, because of
the risk of sequelae from group A streptococcus including glomerulonephritis and rheumatic fever.

Due to the underlying social determinants of health, many patients who are at highest risk of scabies are
also at risk of these significant post-infectious sequelae
 PATIENT EDUCATION
All household members and close personal contacts older than 2 months and not pregnant should be
treated for scabies, even if they have no symptoms or signs of infestation. (Pets do not require
treatment.)

Detailed directions regarding treatment and environmental control measures should be provided
verbally and in writing.

Instruct patients to launder clothing, bed linens, and towels used within the last week in hot water (60°C
or higher) and to machine dry them, the day after treatment is initiated and again in 1 week.

Items that cannot be washed may be professionally dry cleaned or sealed in plastic bags for 1 week.
REFERENCES
1. Scabies Rachel L. Murray; Jonathan
S. Crane. Scabies - StatPearls - NCBI
Bookshelf (nih.gov)

2. Scabies Treatment & Management:

Approach Considerations,
Pharmacologic Therapy, Prevention
(medscape.com)

3. Scabies | Symptoms, Signs,

Management | Geeky Medics
THANK
YOU