2. • Skin is the largest organ in the body with surface area of up to 18,000 sq cms and having
15% of body weight. Its functions are—protective barrier to deeper tissues from infections,
chemicals, other agents like heat, solar rays, etc; thermoregulation; fluid, electrolyte, acid
and base balance maintenance;
perception.
3. HISTORY AND PHYSICAL EXAMINATION
Although many skin disorders are easily recognized by simple
inspection, the history and physical examination are often necessary
for accurate assessment.
The entire body surface, all mucous membranes, conjunctiva, hair,
and nails should always be examined thoroughly under adequate
illumination
The color, turgor, texture, temperature, and moisture of the skin and
the growth, texture, caliber, and luster of the hair and nails should be
noted.
Skin lesions should be palpated, inspected, and classified on the bases
of morphology, size, color, texture, firmness, configuration, location,
and distribution.
4. • One must also decide whether the changes are those of the primary lesion
itself or whether the clinical pattern has been altered by a secondary factor
such as infection, trauma, or therapy.
Primary lesions are classified as macules, papules, patches, plaques, nodules,
tumors, vesicles, bullae, pustules, wheals, and cysts
Primary lesions may change into secondary lesions, or secondary lesions may
develop over time where no primary lesion existed. Primary lesions are usually
more helpful for diagnostic purposes than secondary lesions
Secondary lesions include scales, ulcers, erosions, excoriations, fissures,
crusts, and scars
If the diagnosis is not clear after a thorough examination, one or more
diagnostic procedures may be indicated and culture should be performed in
treatment-resistant cases
5. Types of Skin lesions
Erythema A patch of redness caused by capillary
dilatation or hyperaemia
Macula A small circumscribe flat area of altered skin
color
Papule A small (<5mm) solid elevated skin lesion
Plaque A large (> 5mm) solid elevated skin lesion
Nodule A circumscribe elevated solid skin lesion
Vesicle A small (<5mm) fluid-filled elevated skin
lesion
Bulla A large (>5mm) fluid-filled elevated skin
lesion
Pustule A small (<5mm) pus containing elevated skin
lesion
6. Wheal A transient skin lesion consisting of an elevated pale centre with a
surrounding flare of erythema. It is characteristic of urticaria and
can be produced by the release of histamine in the dermis.
Scale A sheet of adherent corneocytes in the process of being shed
Crust Dried exudate consisting of a mixure of serum and scale,
sometimes with erythrocytes and leucocytes.
Ulcer A discontinuity in the skin surface involving the complete loss
epidermis
Erosion A superficial ulcer
Excoriation A scratch mark
Lichenification A patch of plaque in which the epidermis appears to be thickened
and the normal skin creases are more prominent
Scar A patch or plaque in which the skin surface has lost the normal
surface crease, contour and skin appendages.
7. Nice Questions
For a good Diagnosis:
1. When and where and how did it begging?
2. Has it changed and if so how?
3. Does it come and go?
4. Is it itchy, painful or tender?
5. Does anyone else in the family have a similar lesion?
6. Does anything make it better or worse?
7. How is their general health, are they otherwise well and thriving?
9. Cutaneous Bacterial Infections
1) Impetigo ( contagious) is the most common skin infection in children
throughout the world. There are 2 classic forms of impetigo: nonbullous and
bullous
Etiolog: Staphylococcus aureus mostly but also group A beta-hemolytic
streptococci . Staphylococci generally spread from the nose to normal skin and
then infect the skin.
Risk factor ; are insect bites, abrasions, lacerations, chickenpox, scabies
pediculosis, and burns.
S. aureus strains that produce exfoliative toxins that blister the superficial
epidermis by hydrolyzing human desmoglein 1, resulting in a subcorneal vesicle
Sign and symtoms, superficial pustules, blisters which become oozing, Erosions
with yellow crusts as it spreads, Itching, common localisation is the face.
constitutional symptoms are generally absent.
11. • The DDx viruses (herpes simplex, varicella-zoster), fungi (tinea corporis,
kerion), arthropod bites, and parasitic infestations (scabies, pediculosis
capitis), all of which may become impetiginized.
complications of either nonbullous or bullous impetigo include osteomyelitis,
septic arthritis, Cellulitis, pneumonia, and septicemia. Positive blood culture
results are very rare in otherwise healthy children with localized lesions.
• Infection with nephritogenic strains of GABHS may result in acute
poststreptococcal glomerulonephritis
Systemic Treatment:
• Cephalexin, 25-50 mg/kg/day in two divided doses for 7-10 days
• OR erythromycin: 25-50 mg/kg/24 hours divided in 4 doses for 7-10 days.
Local Treatment:
• Dress or bathe affected areas with potassium permanganate, betadine
solution or saline. When the lesion is dry to apply antibiotic cream.
12. Staphylococcal scalded skin syndrome
• Is caused by the release of two exotoxins (epidermolytic toxins A and B)
from phage group 2 staphylococci, particularly strains 71 and 55. The
epidermolytic toxins produce the split by binding to and cleaving
desmoglein I.
• Occurs mostly in children younger than 5 years, particularly neonates
(newborn babies).
• Lack of specific immunity to the toxins and an immature renal clearance
system (toxins are primarily cleared from the body through the kidneys)
make neonates the most at risk.
• Foci of infection include the nasopharynx and, less commonly, the
umbilicus, urinary tract and blood. The clinical manifestations of
staphylococcal scalded skin syndrome are mediated by hematogenous
spread
13. Staphylococcal scalded skin syndrome
signs and symptoms
• fever
• Irritability
• Characteristics of the skin lesion include:
1- fluid-filled blisters (bullae) in the armpits, groin and body orifices such as
the nose and ears.
2- other parts of the body including the arms, legs and trunk. In newborns,
lesions are often found in the diaper area or around the umbilical cord.
3- Top layer of skin begins peeling off in sheets, leaving exposed a moist, red
and tender area. epidermis may separate in response to gentle shear force
(Nikolsky sign)
DDx: epidermolytic hyperkeratosis, pemphigus, drug eruption, erythema
multiforme, and drug-induced toxic epidermal necrolysis. Toxic epidermal
necrolysis
14. Staphylococcal scalded skin syndrome
Management
• Paracetamol when necessary for fever and pain.
• Maintaining fluid and electrolyte intake.
• Skin care (the skin is often very fragile). The skin should be gently moistened and
cleansed. Application of an emollient provides lubrication and decreases discomfort.
Topical antibiotics are unnecessary.
• Recovery is usually rapid, but complications such as excessive fluid loss, electrolyte
imbalance, faulty temperature regulation, pneumonia, septicemia, and cellulitis may
cause increased morbidity.
• Antibiotic
1. Cloxacillin, Clindamycin should be added to inhibit bacterial protein (toxin)
synthesis. semisynthetic penicillinase-resistant penicillin, should be prescribed,
because the staphylococci are usually penicillin resistant OR
2. Gentamycin
3. Cephalosporin 2dn generation
17. FOLLICULITIS
• superficial infection of the hair follicle, is most often caused by S. aureus
The lesions are discrete, dome-shaped pustules with an erythematous base, located
at the ostium of the pilosebaceous canals. Hair growth is unimpaired
Favored sites include the scalp, buttocks, and extremities.
RISK FACTOR
• Poor hygiene, maceration, drainage from wounds and abscesses, and shaving of the
legs, Folliculitis can also occur as a result of tar therapy or occlusive wraps. The moist
environment encourages bacterial proliferation
FOLLICULITIS KELOIDALIS NUCHAE: It may start after the neck is shaved. It is a
common condition in African males. usually caused by staphylococci.
Clinic Characteristic:
• Keloidal scars are produced in the deeper cutaneous tissue.
• New papules and pustules occur at the rims of the keloid.
• The course is very chronic.
DDX: Candida follicular papules and pustules
19. FOLLICULITIS MANAGEMENT
Systemic Treatment for 21 days: (severe cases )
• Cloxacillin: 50-100 mg/kg/24 hours divided in 4 doses for 7 days.
• Erythromycin: 25-50 mg/kg/24 hours divided in 4 doses for 7 days.
• Cephalexin: 50-100 mg/kg/24 hours divided in 4 doses for 7 days. In severe
lesion admition and IV treatment.
Local Treatment:(usually the only one needed for mild cases)
• Dress or bathe with potassium permanganate solution or betadine or
chlorhexidine. When the lesion is dry to apply antibiotic cream.
• In chronic recurrent folliculitis, daily application of a benzoyl peroxide 5%
gel or wash may facilitate resolution
20. SUBCUTANEOUS TISSUE BACTERIAL INFECTIONS
• The key is to identify nonnecrotizing or necrotizing. The former responds to
antibiotic therapy alone, whereas the latter requires prompt surgical removal
of all devitalized tissue in addition to antimicrobial therapy
• Necrotizing soft tissue infections are life-threatening conditions that are
characterized by rapidly advancing local tissue destruction and systemic
toxicity.
• Tissue necrosis distinguishes them from cellulitis. In cellulitis, an
inflammatory infectious process involves subcutaneous tissue but does not
destroy it.
• Necrotizing soft tissue infections characteristically manifest with a lack of
early cutaneous signs relative to the rapidity and degree of destruction of the
subcutaneous tissues
21. CELLULITIS
Cellulitis is an infection of the subcutaneous tissue with inflammation of loose
connective tissue, with limited involvement of the dermis and relative sparing of the
epidermis. It’s most often caused by infection by the skin flora: Group A Strep and
Staph aureus. fungal agents may be involved Pseudomonas aeruginosa in
immunocompromised or have diabetes mellitus
• It usually has a portal of entry (like a scratch, scrape, or puncture wound)
• The presentation of a cellulitis is usually red, hot, tender skin .The lateral margins tend
to be indistinct because the process is deep in the skin, primarily involving the
subcutaneous tissues in addition to the dermis. Regional adenopathy and constitutional
signs and symptoms such as fever, chills, and malaise are uncommon.
• The diagnosis is often clinical – it rarely requires culture or biopsy. If there’s an abscess
(likely to be Staph) it should be drained; culture the pus. But without purulent drainage
there should be no attempt to culture the cellulitis, as what you’ll likely receive is the
polymicrobial sample of the skin. blood cultures allow identification of the causal
organism in about 25% of cases
22. • COMPLICATIONS, include subcutaneous abscess, bacteremia, osteomyelitis,
septic arthritis, thrombophlebitis, endocarditis, and necrotizing fasciitis.
Lymphangitis or glomerulonephritis can also follow infection with S. pyogenes.
• The treatment for cellulitis is affected by one of two scenarios. When the person
isn’t toxic and they walk into clinic without systemic signs of infection, a 1st
generation cephalosporin such as cephalexin /cefotaxime and aminoglycoside
such as gentamicin , or antibiotics that’ll cover community acquired MRSA such
as Clindamycin can be picked
• If improvement is not noted or the disease progresses significantly in the first 24-
48 hr of therapy, parenteral therapy is necessary.
• Once the erythema, warmth, edema, and fever have decreased significantly, a 10-
day course of treatment may be completed on an outpatient basis.
Immobilization and elevation of an affected limb, particularly early in the course
of therapy, may help reduce swelling and pain.
23.
24. ACNE /ACNE VULGARIS/ (PIMPLES)
The initial lesion of acne is a microcomedone, which progresses to a comedone.
A comedone is a dilated epithelium-lined follicular sac filled with lamellated
keratinaceous material, lipid, and bacteria
An open comedone, known as a blackhead, has a patulous pilosebaceous orifice
that permits visualization of the plug. An open comedone becomes inflammatory
less commonly than does a closed comedone or whitehead, which has only a
pinpoint opening.
If the inflammatory reaction is close to the surface, a papule or pustule develops. If
the inflammatory infiltrate develops deeper in the dermis, a nodule forms.
Suppuration and an occasional giant cell reaction to keratin and hair are the cause
of nodulocystic lesions. These are not true cysts but liquefied masses of
inflammatory debris.
25. • The primary pathogenetic alterations in acne are (1) abnormal keratinization
of the follicular epithelium, resulting in impaction of keratinized cells within the
follicular lumen; (2) increased sebaceous gland production of sebum; (3)
proliferation of Cutibacterium acnes (formerly Propionibacterium acnes ) within
the follicle; and (4) inflammation.
26.
27. • With the exception of isotretinoin therapy, no evidence shows that early
treatment alters the course of acne. Acne can be controlled and severe scarring
prevented by judicious maintenance therapy that is continued until the disease
process has abated spontaneously. Initial control takes at least 6-8 wk,
depending on the severity of the acne
• All topical preparations must be used for 6-8 wk before their effectiveness can
be assessed. Manipulation and squeezing of facial lesions only ruptures intact
lesions and provokes a localized inflammatory reaction.
28. FUNGAL INFECTIONS(Dermatophytoses)
Dermatophytoses are caused by a group of closely related filamentous fungi with a
propensity for invading the stratum corneum, hair, and nails. The 3 principal genera
responsible for infections are Trichophyton, Microsporum, and Epidermophyton.
Trichophyton spp. cause lesions of all keratinized tissue, including skin, nails, and hair. T
Trichophyton rubrum is the most common dermatophyte pathogen. Microsporum
spp. principally invade the hair, and the Epidermophyton spp. invade the
intertriginous skin. Dermatophyte infections are designated by the word tinea
followed by the Latin word for the anatomic site of involvement
Transmission may be through direct contact or indirectly by infected animal hair or
clothing. Infected animals are frequently asymptomatic. They infect humans
sporadically, inciting an inflammatory reaction
Epidemiology
Host defense has an important influence on the severity of the infection. Disease tends
to be more severe in individuals with diabetes mellitus, lymphoid malignancies,
immunosuppression, and states with high plasma cortisol levels, such as Cushing
syndrome. Additional local factors that predispose to infection include trauma to the
skin, hydration of the skin with maceration, occlusion, and elevated temperature
29. TINEA CORPORIS: Fungal infection of the skin, most common on the exposed
surfaces of the body, namely the face, arms and shoulders.
Presents in typical round lesions which show scaling at the periphery, or in
concentric rings,
• Multiple, large or widespread lesions may be seen if a patient delays seeking
treatment for a long time or is malnourished or immunosuppressed.
• Itching
Microscopic examination of KOH wet mount preparations
and cultures should always be performed when fungal
infection is considered. Tinea corporis usually does not
fluoresce with a Wood lamp.
DDX: psoriasis, seborrheic dermatitis,
30. TINEA CORPORIS MANAGEMENT
Systemic Treatment: severe or extensive disease
Griseofulvin: 10 –15 mg/kg once daily for 2 to 6 weeks.
Fluconazol: 6-12 mg/kg/ by a week for 2 or 3 week.
Itraconazole has produced excellent results in many cases with a 1- to 2-wk course
of oral therapy
When there is severe itching a mild steroid may be added.
Cetirizine: 5mg/kg/day 2 or 3 time p/ day
Local Treatment Tinea corporis usually responds to treatment with one of the
topical antifungal agents (e.g., imidazoles, terbinafine, naftifine) twice daily for 2-
4 wk
31. TINEA CAPITIS: The fungus has grown into the hair follicle and will not be removed by topical
treatment only
• Severe pustular forms exist with follicular pustules and nodules and often massive purulent
secretion, alopecia (infected hairs become brittle and broken). “black-dot ringworm,”
characterized initially by many small circular patches of alopecia in which hairs are broken off
close to the hair follicle
• Lymphnodes in the neck swell.
• the patient may have fever and headache. There may be bacterial superinfection.
Microscopic examination of a KOH preparation of
infected hair from the active border of a lesion
discloses tiny spores surrounding the hair shaft in
Microsporum infections and chains of spores within
the hair shaft in T. tonsurans infections.
A specific etiologic diagnosis of tinea capitis may be
obtained by planting broken off infected hairs on
Sabouraud medium with reagents to inhibit growth of
other organisms. Such identification may require 2 wk
or more
DDx: seborrheic dermatitis, psoriasis, alopecia areata
32. Systemic Treatment:
.griseofulvin (20 mg/kg/24 hr) is the recommended treatment for all forms of tinea capitis. It
may be necessary for 8-12 wk and should be terminated only after fungal culture results are
negative.
Fluconazol: 6-12 mg/kg/ by a week for 2 or 3 week. Neither itraconazole nor terbinafine is
approved by the U.S. Food and Drug Administration (FDA) for treatment of dermatophyte
infections in the pediatric population
In case of bacterial superinfection: antiseptics and / or antibiotics. Vigorous shampooing with a
2.5% selenium sulfide, zinc pyrithione, or ketoconazole shampoo is helpful. It is not necessary
to shave the scalp
.
Local Treatment. Topical therapy alone is
ineffective, but it may be an important adjunct
because it may decrease the shedding of spores so
Imidazole cream or Whitfield’s ointment twice daily
for a minimum of 4 weeks.
33. CANDIDAL INFECTIONS (CANDIDOSIS, CANDIDIASIS, AND MONILIASIS)
The dimorphic yeasts ubiquitous in the environment, but C. albicans usually causes
candidosis in children. This yeast is not part of the indigenous skin flora, but it is a
frequent transient on skin and may colonize the human alimentary tract and the
vagina as a saprophytic organism. elevated temperature and humidity ↑the risk.
Many bacterial species inhibit the growth of C. albicans, and alteration of normal
flora by the use of antibiotics may promote overgrowth of the yeast.
Candidal Diaper Dermatitis
• Candidal diaper dermatitis is a ubiquitous problem in infants and, although
relatively benign, is often frustrating because of its tendency to recur.
Predisposed infants usually carry C. albicans in their intestinal tracts, and the
warm, moist, occluded skin of the diaper area provides an optimal environment
for its growth. A seborrheic, atopic, or primary irritant contact dermatitis usually
provides a portal of entry for the yeast.
34. Candidiasis or thrush
presents on the skin as red macules often with small pustules on their periphery
which break down as the lesion spreads outwards. On the oral and vulvo-vaginal
mucosa redness, superficial erosions and white adherent plaques may be seen.
These can be itchy and painful. When oral lesions extend to the throat and
oesophagus they can cause anorexia. Infection of lips / corners of the mouth also
occurs. Severe mucosal candidiasis is seen often in HIV infection
35. • The differential diagnosis of candidal diaper dermatitis includes other
eruptions of the diaper area that may coexist with candidal infection. For this
reason, it is important to establish a diagnosis by means of KOH preparation or
culture.
Tx
• imidazole cream 2 times daily. The combination of a corticosteroid and an
antifungal agent may be justified if inflammation is severe but may confuse the
situation if the diagnosis is not firmly established. Corticosteroid should not be
continued for more than a few days
• Protection of the diaper area by an application of thick zinc oxide paste overlying
the anticandidal preparation may be helpful. Keep lesional skin dry.
• Paint mucosal or smaller wet lesions with Gentian Violet solution once daily
until healed.
• Nystatin ointment or cream twice daily for skin, nystatin oral suspension (1 ml)
swirled around mouth four times daily until two days after clinical cure for oral
candidiasis, nystatin pessaries nightly for 2 weeks for vaginal candidiasis.
• Oral Nystatin 400 000 IU daily, give 3 time for 10 days.
36. VIRAL SKIN INFECTIONS
Chickenpox or varicella is a primary infection with the varicella-zoster virus. It is
a common, very contagious infection in children.
• After a mild prodrome with sometimes fever and malaise the exanthema
appears suddenly.
37. Varicella-zoster virus (VZV, herpiviridae family)
causes primary, latent, and reactivation infections. very contagious infection in
children
The primary infection is manifested as varicella (chickenpox) and results in
establishment of a lifelong latent infection of sensory ganglionic neurons.
Reactivation of the latent infection causes herpes zoster (shingles).
Reservoir: human mucosa and nerves
Transmission: respiratory droplets
Pathogenesis: VZV enters the respiratory tract → replicates in local lymph
nodes → primary viremia → spleen and liver → secondary viremia → skin
(rash) → latent in the dorsal root ganglia. Reactivation of virus due to stress
or immunocompromise causes vesicular lesions and severe nerve pain.
DX: Varicella and herpes zoster are usually diagnosed primarily by their clinical
appearance. Laboratory evaluation has not been considered necessary for
diagnosis or management. But if needed its PCR on (vesicular fluid, crusts). Severe
varicella was the most common illness confused with smallpox before the
eradication of smallpox
38. Clinical features: After a mild prodrome with sometimes fever and malaise,
pharyngitis, malaise, rhinitis the exanthema appears suddenly.
• Asynchronous rash ie Red macules, papules and shortly there after vesicles,
pustules and crusts develop on the trunk scalp and mucous membranes, less so
on extremities and face.
• The skin lesions of varicella and herpes zoster have identical histopathology,
and infectious VZV is present in both. Varicella elicits humoral and cell-
mediated immunity that is highly protective against symptomatic reinfection.
The skin lesions—the hallmark of the infection—include
maculopapules, vesicles, and scabs in various stages of
evolution.
39. complications of varicella,
some of them rare, include acute cerebellar ataxia, encephalitis,
pneumonia, nephritis, nephrotic syndrome, hemolytic-uremic syndrome,
arthritis, myocarditis, pericarditis, pancreatitis, orchitis,
Management of chickenpox
• Oral therapy with acyclovir (20 mg/kg/dose; maximum: 800 mg/dose) given as 4
doses/day for 5 days
• Valacyclovir (20 mg/kg/dose; maximum: 1,000 mg/dose, administered 3 times daily
for 5 days)
• Calamine lotion or phenol-zinc lotion as necessary for itch and drying in.
• Antihistamines
• Give rest Isolate patient if possible.
• In severe superinfection a systemic antibiotic e.g. cloxacillin or erythromycin.
• Immunocompromised patients: if available acyclovir 20-40mg/kg/day, 2 times daily
for 5-10 day
40. HERPES ZOSTER
• is caused by the reactivation of latent VZV. It is not common in childhood and shows
no seasonal variation in incidence. Zoster is not caused by exposure to a patient with
varicella; in fact, exposures to varicella boost the cell mediated immune response to
VZV in individuals with prior infection, decreasing the likelihood of reactivation of
latent virus. The lifetime risk for herpes zoster for individuals with a history of
varicella is at least 30%, with 75% of cases occurring after 45 yr of age.
• Herpes zoster manifests as vesicular lesions clustered within 1 or, less commonly, 2
adjacent dermatomes
• After a short period of itch, tenderness or pain along one or occasionally several
dermatomes on one side of the body papules and plaques appear which quickly
change into blisters. More common in thoracic and cervical region.
• After 1-2 weeks crusts begin to fall off. dissemination and complications are more
common and severe in immunocompromised persons
• An increased risk for herpes zoster early in childhood has been described in children
who acquire infection with VZV in utero or in the 1st yr of life.
41.
42. Herpes Zoster
• Therefore, treatment of uncomplicated herpes zoster in the child with an antiviral
agent may not always be necessary, although some experts would treat with oral
acyclovir (20mg/kg/dose; maximum: 800 mg/dose) to shorten the duration of the
illness., Analgesia(ibuprofen 40mg/kg/day 3 times daily). Aspirin contraindicated due
to association with Reye syndrom
• It is important to start antiviral therapy as soon as possible. Delay beyond 72 hr from
onset of rash limits its effectiveness
• Patients at high risk for disseminated dz (immunocompromised should receive IV
acyclovir (500 mg/m2 or 10 mg/kg every 8 hr). Oral acyclovir, famciclovir, and
valacyclovir are options. Affected eye goes to ophthalmology.
• Prevention
VZV transmission is difficult to prevent, especially from persons with varicella,
because a person with varicella may be contagious for 24-48 hr before the rash is
apparent. Herpes zoster is less infectious than varicella; nonetheless, transmission has
been reported even in the absence of direct contact with the patient. Infection control
practices, including caring for patients with varicella in isolation rooms with filtered air
systems, are essential
43. ARTHROPOD BITES AND INFESTATIONS
1) Scabies. Scabies is caused by burrowing and release of toxic or antigenic substances by the female
mite Sarcoptes scabiei var. hominis. which lives and moves in the skin. transmitted through clothing,
linen, or towels.
Scabies is transmitted only rarely by fomites because the isolated mite dies within 2-3 days.
Pathogenesis: An adult female mite measures approximately 0.4 mm in length After impregnation on the
skin surface, a gravid female exudes a keratolytic substance and burrows into the stratum corneum. She
gradually extends this along the boundary with the stratum granulosum. She deposits 10-25 oval eggs and
numerous brown fecal pellets (scybala) daily.
When egg laying is completed, in 4-5 wk, she dies within the burrow. The eggs hatch in 3-5 days, releasing
larvae that move to the skin surface to molt into nymphs. Maturity is achieved in approximately 2-3 wk.
DDx: chickenpox, viral
exanthems,drug eruptions,
dermatitis herpetiformis,
and folliculitis. Eczematous
lesions may mimic atopic
dermatitis and seborrheic
dermatitis
44. Diagnosis made clinically but is confirmed by microscopic identification of mites
(Fig. 688.6A ), ova, and scybala (see Fig.688.6B ) in epithelial debris. Scrapings
most often test positive when obtained from burrows or fresh papules(Burrows
are virtually pathognomonic for human scabies)
A reliable method is application of a drop of mineral oil on the selected lesion,
scraping of it with a No. 15 blade, and transferring the oil and scrapings to a glass
slide
45. TREATMENT.
The choice for scabies is permethrin 5% cream (Elimite) applied to the entire
body from the neck down, with particular attention to intensely involved areas,
which. The medication is left on the skin for 8-12 hr and should be reapplied in 1
wk for another 8-12 hr period.
Additional therapies include sulfur ointment 5–10%, and crotamiton 10% lotion
or cream
Lindane 1% lotion or cream should only be used as an alternative therapy, given
risk of systemic toxicity.
Single dose ivermectin (200 µg/kg) has also been effective in
immunocompetent patients with improvement (cure) noted in 60% at 2 wk and
89% at 4 wk after treatment.
For severe infestations or in immunocompromised patients, oral
ivermectin 200 µg/kg per dose given orally for 2 doses, 2 wk apart can be used
(off-label use).
46. Pediculosis
Three types of lice are obligate parasites of the human host: body or clothing lice
(Pediculus humanus corporis), head lice (Pediculus humanus capitis), and pubic
or crab lice (Phthirus pubis). Only the body louse serves as a vector of human
disease (typhus, trench fever, relapsing fever)
Body and head lice have similar physical characteristics. They are approximately 2-4 mm
in length. Pubic lice are only 1-2 mm in length and are greater in width than length, giving
them a crablike appearance
Pediculosis corporis is rare in children except under conditions of poor
hygiene, especially in colder climates when the opportunity to change clothes on
a regular basis is lacking. The parasite is transmitted mainly on contaminated
clothing or bedding.
Pediculosis capitis
It is the most common form of lice to affect children, in particular those between
the ages of 3 and 12 yr. Fomites and head-to-head contact are important modes
of transmission. In summer months in many areas of the United States and in the
tropics at all times of the year, shared combs, brushes, or towels have a more
important role in louse transmission.
47. Pathology:
• Female lice live for approximately 1 month and deposit 3-10 eggs daily on the human
host. The ova or nits are glued to hairs or fibers of clothing but not directly on the body.
Once the eggs hatch, the nits remain attached to the hair as empty sacs of chitin.
• Freshly hatched larvae die unless a meal is obtained within 24 hr and every few days
thereafter. Both nymphs and adult lice feed on human blood, injecting their salivary
juices into the host and depositing their fecal matter on the skin.
Symptoms of infestation do not appear immediately but develop as an individual
becomes sensitized. excoriations, erythematous macules and papules, and sometimes
secondary bacterial infection. The hallmark of all types of pediculosis is pruritus.
Secondary pyoderma, after trauma from scratching, may result in matting together of
the hair and cervical and occipital lymphadenopathy. Hair loss does not result from
pediculosis but may accompany the secondary pyoderma.
• Diagnosis. Direct examination of the pubic area, axillae, scalp, and other hair-bearing
surfaces for the organism (louse or nits). A nit cannot be moved along or knocked off
the hair shaft with the fingers. Lice are not always visible, but nits are detectable on
the hairs, most commonly in the occipital region and above the ears, rarely on beard
or pubic hair
48. Treatment
• malathion 0.5% in isopropanol is the treatment of applied to dry hair until hair
and scalp are wet, and left on for 12 hr. A second application, 7-9 days after the
initial treatment may be necessary. This product is flammable, so care should be
taken to avoid open flames. Malathion, like lindane shampoo, is not indicated
for use in neonates and infants; however, additional approved therapies include
spinosad (if >6 mo), benzyl alcohol lotion (if >6 mo), and ivermectin for difficult-
to-treat head lice.
• All household members should be treated at the same time.
Nits can be removed with a fine-toothed comb after application of a damp towel
to the scalp for 30 min. Clothing and bed linens should be laundered in very hot
(>130°F) water and then dried for at least 10 min at the highest setting or dry-
cleaned. Children may return to school after the initial treatment.
