LEPROSY

Leprosy is an ancient disease and is a leading cause of permanent physical disability among the
communicable diseases. It is a chronic mildly communicable disease that mainly affects the skin, the
peripheral nerves, the eyes and mucosa of the upper respiratory tract.

Leprosy or Hansen’s disease is one infectious disease whose prospects for control and eradication appear
to be bright. A century ago, the disease was thought to be incurable, and victims suffered not just
deformities but great stigma that made them virtual social outcasts. Now, the WHO reports that not only
is the disease curable but it can actually be eliminated worldwide as a public health problem. The total
number of people in the world who have been cured of leprosy has topped 10 million as of mid-1998.
The global prevalence has been reduced by more than 70 percent and one to two million deformities have
been prevented. These successes were made possible by Multi-Drug Therapy (MDT) – a combination of
three drugs: rifampicin, clofazimine and dapsone – which accordind to WHO had been provided to all
known cases of the disease by the end of 1997. MDT continues to be highly effective in curing leprosy
completely with very low relapse rates of around 0.3 per 1000 cases per year. More importantly, no
resistance to all three drugs together has been detected anywhere in the world in Mycobacterium leprae,
the bacillus that causes the disease.

LEPROSY CONTROL PROGRAM (DOH)

Leprosy has been a public health problem in the Philippines for several decades. The disease is unequally
distributed throughout the country. In 1987, in the provinces of Ilocos Norte and Ilocos Sur, Abra, Sulu,
Palawan, Cebu, La Union, Pangasinan and Metro Manila, the prevalence rate is lower than 0.40/ 1000
population. The National Prevalence Rate as of 1998 was 0.65/1000.

The nationwide implementation of Multi-Drug Therapy (MDT) since 1998 has resulted in the decrease in
the prevalence rate of leprosy. The prevalence rate of the disease declined from 7.2/10000 population in
1986 to 1.2/10000 population in 1997. Since then, the treatment of leprosy has shifted from institutional
care to that of home treatment.

Signs and Symptoms

Early S/S
Change in skin color – either reddish or white
Loss of sensation on the skin lesion
Decrease/ loss of sweating and hair growth over the lesion
Thickened and/or painful nerves
Muscle weakness or paralysis of extremities
Pain and redness of the eyes
Nasal obstruction or bleeding
Ulcers that do not heal
Late S/S
Loss of eyebrows – madarosis
Inability to close eyelids – lagophthalmos
Clawing of fingers and toes
Contractures
Sinking of the nosebridge
Enlargement of the breasts in males or gynecomastia
Chronic Ulcers

Infectious Agent
Mycobacterium leprae, an acid fast, rod-shaped bacillus which can be detected be Slit Skin Smear (SSS)

Method of Transmission
Airborne – inhalation of droplet/spray from coughing and sneezing of untreated leprosy patient
Prolonged skin-to-skin contact

Diagnosis of leprosy is currently based on clinical signs and symptoms especially if there is history of
contact with person with Leprosy (PWL). Only in rare instances is there a need to use laboratory and
other investigations to confirm a diagnosis.

Slit Skin Smear (SSS) examination is an optional procedure. It is done only when clinical diagnosis is
doubtful. The main objective is to prevent misclassification and wrong treatment. A ready referral
facility must be recognized in the conduct of SSS procedures.

Susceptibility
Children especially twelve years and below are more susceptible.

Prevention
Avoidance of prolonged skin-to-skin contact especially with a lepromatous case
Children should avoid close contact with active, untreated leprosy case
BCG vaccination
Good personal Hygiene
Adequate Nutrition
Health Education

Management/ Treatment
Ambulatory chemotherapy through use of Multi-drug therapy
Domiciliary treatment as embodied in R.A. 4073 which advocates home treatment

WHO classification of Leprosy which is the basis of the modern management or Mult-Drug Therapy:
Paucibacillary (tuberculoid and indeterminate)
Non-infectious types
Duration of treatment: 6-9 months
Multibacillary (lepromatous and borderline)
Infectious types
Duration of treatment: 24-30 months
Types of fungal skin infections
Some common fungal skin infections are listed below.
Dermatophyte infections
Most basic fungal skin infections are caused by dermatophytes - types of fungi that cause skin, nail and
hair infections. They are very common, affecting between one and two in 10 people at some point in their
lives.Dermatophyte infections include the following.
Athlete's foot (Tinea pedis and Tinea manuum)
Around 25 in 100 adults have athlete's foot at some time in their lives. It's caused by a combination of
fungi andbacteria, causing your skin to become itchy, dry, scaly and red, especially between your toes.
Sometimes it causesblisters and cracked skin. You often pick up athlete's foot from contaminated skin
scales in swimming pools, showersand saunas. If you don't wash your hands after touching a
contaminated area, it can spread to your hands where it'sknown as Tinea manuum. It mostly affects the
creases on your palms and sides of your fingers.
Nail infections
Onychomycosis is the name for any fungal nail infection. Tinea unguium (ringworm of your nails) is a
commoninfection. Your nails become malformed, thickened and crumbly. Not all nails affected like this
are caused by fungalinfections, but it's a common cause. Toenail infections are commonly linked with
athlete's foot. Your fingernails canbe affected too.
Ringworm of the groin (Tinea cruris)
This is often called 'jock itch' because it occurs in sportspeople and is common among young men. It
causes an itchy,red rash in your groin and the surrounding area and is usually seen in men who have been
sweating a lot. Often youwill also have athlete's foot, and scratching your feet, followed by your groin
may spread the infection.
Ringworm on the body (Tinea corporis)
This often affects exposed areas of your body, such as your abdomen (tummy) or your limbs, causing red
raised or flat patches and rings that can merge, grow and spread. The rings are scaly at the edge with clear
skin at the centre.The patches spread out from the centre. Ringworm can be caught from domestic
animals.
Ringworm of the scalp (Tinea capitis)
This usually affects young children, especially those living in urban areas and who are of African-
Caribbean origin. Itspreads from person to person, causing hair loss and inflammation of the affected
area. You can be infected by thisfungus without developing any symptoms, but become a carrier,
spreading the infection to others, sometimes for years.
Yeast infections
Other fungal skin infections are caused by yeast infections. Yeast infections include the following.
Intertrigo
 Intertrigo is a yeast infection of skin folds caused by the fungus Candida albicans, which lives on your
skin and inyour digestive system. It affects areas where skin touches skin, such as your armpits, groin,
and under heavy breastsor fat folds, where the environment is warm and moist. It can cause itching,
soreness, spots and scales, creating awhite-yellow curd over the infected area.
Pityriasis versicolor
This yeast infection causes dark patches to form on pale or untanned skin and light patches on tanned or
darker skin. Another name for this condition is Tinea versicolor (versicolor means 'of various colours').
Teenagers and youngadults are most often affected in the UK.
Thrush (Candida albicans)
The fungus Candida albicans usually lives in harmony with us and rarely causes problems. However, in
certain

Fungal skin infections

Ringworm of the groin (Tinea cruris)

DEFINITION
Tinea cruris is a dermatophyte infection of the groin.

SYNONYMS
Jock itch
Ringworm

EPIDEMIOLOGY & DEMOGRAPHICS

• Most common during the summer
• Men are affected more frequently than women

PHYSICAL FINDINGS & CLINICAL PRESENTATION

• Erythematous plaques have a half-moon shape and a scaling border.
• The acute inflammation tends to move down the inner thigh and usually spares the
scrotum; in severe cases the fungus may spread onto the buttocks.
• Itching may be severe.
• Red papules and pustules may be present.
• An important diagnostic sign is the advancing well-defined border with a tendency
toward central clearing

ETIOLOGY
 • Dermatophytes of the genera Trichophyton, Epidermophyton, and Microsporum. T.
rubrum and E. floccosum are the most common causes.
• Transmission from direct contact (e.g., infected persons, animals). The patient's feet
should be evaluated as a source of infection because tinea cruris is often associated with tinea pedis.

WORKUP
Diagnosis is based on clinical presentation and demonstration of hyphae microscopically using potassium
hydroxide.

LABORATORY TESTS
• Microscopic examination
• Cultures are generally not necessary

TREATMENT

NONPHARMACOLOGIC THERAPY
• Keep infected area clean and dry.
• Use of boxer shorts is preferred to regular underwear.
ACUTE GENERAL Rx
• Drying powders (e.g., Miconazole nitrate [Zeasorb AF]) may be useful in patients with
excessive perspiration.
• Various topical antifungal agents are available: miconazole (Lotrimin), terbinafine
(Lamisil), sulconazole nitrate (Exelderm), betamethasone dipropionate/clotrimazole (Lotrisone).
• Oral antifungal therapy is generally reserved for cases unresponsive to topical agents.
Effective medications are itraconazole (Sporonax) 100 mg/day for 2-4 wk, ketoconazole (Nizoral) 200 mg
qd, fluconazole (Diflucan) 200 mg qd, and terbinafine (Lamisil) 250 mg qd

Tinea Capitis

DEFINITION
Tinea capitis is a dermatophyte infection of the scalp.

SYNONYMS
Ringworm of the scalp, ringworm of the head, gray patch tinea capitis, black dot tinea capitis, tinea
tonsurans, superficial mycosis, dermatophytosis, kerion

EPIDEMIOLOGY & DEMOGRAPHICS

Most common dermatophytosis of childhood, primarily affecting children between 3 and 7 years of age.
About 3%-8% of American children are affected, and 34% of household contacts are asymptomatic
carriers. Adult and geriatric populations are less frequently affected, possibly due to the fungistatic effect
of the sebum found in older persons. African American children are particularly susceptible, possibly due
to increased coiling of hair shafts. In urban populations, large family size, low socioeconomic status, and
crowded living conditions may contribute to an increased incidence of tinea capitis. The predominant
etiologic agent of tinea capitis in the United States and in Western Europe has changed from
Microsporum audouinii (gray patch) to Trichophyton tonsurans (black dot) in the past 50 years.

PHYSICAL FINDINGS & CLINICAL PRESENTATION

• Triad of scalp scaling, alopecia, and cervical adenopathy.
• Primary lesions including plaques, papules, pustules, or nodules on the scalp (usually
occipital region).
• Secondary lesions include scales, alopecia, erythema, exudates, and edema.
• Two distinctly different forms:
○ Gray patch—lesions are scaly and well demarcated. The hairs within the patch break off a
few millimeters above the scalp. One or several lesions may be present; sometimes the lesions join to
form a larger ones.
○ Black dot—early lesions with erythema and scaling patch are easily overlooked until
areas of alopecia develop. Hairs within the patches break at the surface of the scalp, leaving behind a
pattern of swollen black dots.

• Scalp pruritus may be present.

• Fever, pain, and lymphadenopathy (commonly post cervical) with inflammatory lesions.
• Hair loss is usually reversible.
• Kerion: inflamed, exudative, pustular, boggy, tender nodules exhibiting marked edema
and hair loss seen in severe tinea capitis. Caused by immune response to the fungus. May lead to some
scarring.
• Favus: production of scutula (hair matted together with dermatophyte hyphae and keratin
debris), characterized by yellow cup-shaped crusts around hair shafts. A fetid odor may be present.

ETIOLOGY
Most commonly caused by the Trichophyton (80% of the cases in the United States) or Microsporum
genera. Most common causative species for black dot tinea capitis is T. tonsurans and for gray patch tinea
capitis are M. andouinii and M. canis. Transmission occurs via infected persons or asymptomatic carriers,
fallen infected hairs, animal vectors, and fomites. M. audouinii is commonly spread by dogs and cats.
Infectious fungal particles may remain viable for many months.

WORKUP
• KOH testing of hair shaft extracted from the lesion, not the scale, as the T. tonsurans
spores attach to or reside inside hair shafts and will rarely be found in the scales.
• Wood's ultraviolet light fluoresce blue-green on hair shafts for Microsporum infections
but will fail to identify T. tonsurans.
• Fungal culture of hairs and scales on fungal medium such as Sabouraud's agar may be
used to confirm the diagnosis, especially if uncertain.

TREATMENT
• Griseofulvin—gold standard FDA approved treatment with excellent long-term safety
profile. Micronized and ultramicronized preparations are absorbed better, and side effects are infrequent,
especially when administered with fatty meals. Periodic monitoring of hematologic, liver, and renal
function may be indicated, especially in prolonged treatment over 8 weeks.
○ Children: 10-25 mg/kg/d orally (to a maximum of 0.5-1.0 gram per day) for at least 4-8
weeks (recommended until hair regrowth occurs—usually after 6-8 weeks, or 2 weeks beyond cure to
prevent relapse)
○ Adults: 250 mg orally bid or 500 mg qd (or tid for a few cases of black dot type) for 4-12
weeks

• New alternative treatments—oral terbinafine, itraconazole, or fluconazole are comparable

in efficacy and safety to griseofulvin, with shorter treatment and better patient compliance. Monitoring of
CBC, LFTs, and renal function monthly may be indicated.
• The adjuvant use of antifungal shampoos is recommended for all patients and household
contacts. Shampoo like selenium sulfide 2.5% used for 5 minutes or ketoconazole shampoo used 2 to 3
times/week can help prevent infection or eradicate asymptomatic carrier state by inhibiting fungal growth.
• Severe inflammatory kerion can be managed with additional prednisone 1 mg/kg/day and
erythromycin.

Tinea Corporis

DEFINITION
Tinea corporis is a dermatophyte fungal infection caused by the genera Trichophyton or Microsporum.

SYNONYMS
Ringworm
Body ringworm
Tinea circinata

EPIDEMIOLOGY & DEMOGRAPHICS

• The disease is more common in warm climates.
• There is no predominant age or sex.

PHYSICAL FINDINGS & CLINICAL PRESENTATION

• Typically appears as single or multiple annular lesions with an advancing scaly border;
the margin is slightly raised, reddened, and may be pustular.
• The central area becomes hypopigmented and less scaly as the active border progresses
outward
• The trunk and legs are primarily involved.
• Pruritus is variable.
• It is important to remember that recent topical corticosteroid use can significantly alter
the appearance of the lesions.

ETIOLOGY
Trichophyton rubrum is the most common pathogen.
WORKUP
Diagnosis is usually made on clinical grounds. It can be confirmed by direct visualization under the
microscope of a small fragment of the scale using wet mount preparation and potassium hydroxide
solution; dermatophytes appear as translucent branching filaments (hyphae) with lines of separation
appearing at irregular intervals.

LABORATORY TESTS
• Microscopic examination of hyphae
• Mycotic culture is usually not necessary
• Biopsy is indicated only when the diagnosis is uncertain and the patient has failed to
respond to treatment

TREATMENT

NONPHARMACOLOGIC THERAPY
Affected areas should be kept clean and dry.

ACUTE GENERAL Rx
• Various creams are effective; the application area should include normal skin about 2 cm
beyond the affected area:
1. Miconazole 2% cream (Monistat-Derm) applied bid for 2 wk
2. Clotrimazole 1% cream (Mycelex) applied and gently massaged into the affected areas
and surrounding areas bid for up to 4 wk
3. Naftifine 1% cream (Naftin) applied qd
4. Econazole 1% (Spectazole) applied qd

• Systemic therapy is reserved for severe cases and is usually given up to 4 wk; commonly
used agents:
1. Ketoconazole (Nizoral), 200 mg qd
2. Fluconazole (Diflucan), 200 mg qd
3. Terbinafine (Lamisil), 250 mg qd

BACTERIAL INFECTIONS

Impetigo
DEFINITION
impetigo is a superficial skin infection generally secondary to Staphylococcus aureus and/or
Streptococcus spp.
Common presentations are bullous impetigo (generally secondary to staphylococcal disease) and
nonbullous impetigo (secondary to streptococcal infection and possible staphylococcal infection); the
bullous form is caused by an epidermolytic toxin produced at the site of infection.

SYNONYMS
impetigo vulgaris
Pyoderma

EPIDEMIOLOGY & DEMOGRAPHICS

• Bullous impetigo is most common in infants and children. The nonbullous form is most
common in children ages 2 to 5 yr with poor hygiene in warm climates.
• The overall incidence of acute nephritis with impetigo varies between 2% and 5%.

PHYSICAL FINDINGS & CLINICAL PRESENTATION

• Multiple lesions with golden yellow crusts and weeping areas often found on the skin
around the nose, mouth, and limbs (nonbullous impetigo) ( Fig. 1-136 ).
• Presence of vesicles that enlarge rapidly to form bullae with contents that vary from clear
to cloudy; there is subsequent collapse of the center of the bullae; the peripheral areas may retain fluid,
and a honey-colored crust may appear in the center; as the lesions enlarge and become contiguous with
the others, a scaling border replaces the fluid-filled rim (bullous impetigo); there is minimal erythema
surrounding the lesions.
• Regional lymphadenopathy is most common with nonbullous impetigo.
• Constitutional symptoms are generally absent.

ETIOLOGY
• S. aureus coagulase positive is the dominant microorganism.
• S. pyogenes (group A β-hemolytic streptococci): M-T serotypes of this organism
associated with acute nephritis are 2, 49, 55, 57, and 60.

WORKUP
Diagnosis is clinical.

LABORATORY TESTS
• Generally not necessary
• Gram stain and C&S to confirm the diagnosis when the clinical presentation is unclear
• Sedimentation rate parallel to activity of the disease
• Increased anti-DNAse B and antihyaluronidase
• Urinalysis revealing hematuria with erythrocyte casts and proteinuria in patients with
acute nephritis (most frequently occurring in children between 2 and 4 yr of age in the southern part of the
U.S.)
TREATMENT
NONPHARMACOLOGIC THERAPY
Remove crusts by soaking with wet cloth compresses (crusts block the penetration of antibacterial
creams).
GENERAL Rx
• Application of 2% mupirocin ointment (Bactroban) tid for 10 days to the affected area or
until all lesions have cleared.
• Oral antibiotics are used in severe cases: commonly used agents are dicloxacillin 250 mg
qid for 7 to 10 days, cephalexin 250 mg qid for 7 to 10 days, or azithromycin 500 mg on day 1, 250 mg
on days 2 through 5, erythromycin 250 mg qid.
• impetigo can be prevented by prompt application of mupirocin or triple antibiotic
ointment (bacitracin, Polysporin, and neomycin) to sites of skin trauma.
• Patients who are carriers of S. aureus in their nares should be treated with mupirocin
ointment applied to their nares bid for 5 days.
• Fingernails should be kept short, and patients should be advised not to scratch any lesions
to avoid spread of infection.

Cellulitis
DEFINITION
Cellulitis is a superficial inflammatory condition of the skin. It is characterized by erythema, warmth, and
tenderness of the area involved.

SYNONYMS
Erysipelas (cellulitis generally secondary to group A β-hemolytic streptococci)

EPIDEMIOLOGY & DEMOGRAPHICS

• Occurs most frequently in diabetics, immunocompromised hosts, and patients with
venous and lymphatic compromise.
• Frequently found near skin breaks (trauma, surgical wounds, ulcerations, tinea
infections). Edema, animal or human bites, subadjacent osteomyelitis, and bacteremia are potential
sources of cellulitis.

PHYSICAL FINDINGS & CLINICAL PRESENTATION

Variable with the causative organism
• Erysipelas: superficial-spreading, warm, erythematous lesion distinguished by its
indurated and elevated margin; lymphatic involvement and vesicle formation are common.
• Staphylococcal cellulitis: area involved is erythematous, hot, and swollen; differentiated
from erysipelas by nonelevated, poorly demarcated margin; local tenderness and regional adenopathy are
common; up to 85% of cases occur on the legs and feet.
• H. influenzae cellulitis: area involved is a blue-red/purple-red color; occurs mainly in
children; generally involves the face in children and the neck or upper chest in adults.
 • Vibrio vulnificus: larger hemorrhagic bullae, cellulitis, lymphadenitis, myositis; often
found in critically ill patients in septic shock.

ETIOLOGY
• Group A β-hemolytic streptococci (may follow a streptococcal infection of the upper
respiratory tract)
• Staphylococcal cellulitis
• H. influenzae
• Vibrio vulnificus: higher incidence in patients with liver disease (75%) and in
immunocompromised hosts (corticosteroid use, diabetes mellitus, leukemia, renal failure)
• Erysipelothrix rhusiopathiae: common in people handling poultry, fish, or meat
• Aeromonas hydrophila: generally occurring in contaminated open wound in fresh water
• Fungi (Cryptococcus neoformans): immunocompromised granulopenic patients
• Gram-negative rods (Serratia, Enterobacter, Proteus, Pseudomonas):
immunocompromised or granulopenic patients

LABORATORY TESTS
• Gram stain and culture (aerobic and anaerobic)
1. Aspirated material from:
a. Advancing edge of cellulitis
b. Any vesicles
2. Swab of any drainage material
3. Punch biopsy (in selected patients)

• Blood cultures in hospitalized patients, in patients who have cellulitis superimposed on

lymphedema, in patients with buccal or periorbital cellulitis, and in patients suspected of having a salt-
water or fresh-water source of infection. Bacteremia is uncommon in cellulitis (positive blood cultures in
only 4% of patients)
• ALOS titer (in suspected streptococcal disease)
Despite the previous measures, the cause of cellulitis remains unidentified in most patients.

IMAGING STUDIES
CT or MRI in patients with suspected necrotizing fasciitis (deep-seated infection of the subcutaneous
tissue that results in the progressive destruction of fascia and fat).

TREATMENT
NONPHARMACOLOGIC THERAPY
Immobilization and elevation of the involved limb. Cool sterile saline dressings to remove purulence from
any open lesion. Support stockings in patients with peripheral edema.
ACUTE GENERAL Rx
Erysipelas
• PO: dicloxacillin 500 mg PO q6h
• IV: cefazolin 1 g q6-8h or nafcillin 1.0 or 1.5 g IV q4-6h
Nnote: Use erythromycin, clindamycin, or vancomycin in patients allergic to penicillin.
Staphylococcus cellulitis
• PO: dicloxacillin 250 to 500 mg qid
• IV: nafcillin, 1 to 2 g q4-6h
• Cephalosporins (cephalothin, cephalexin, cephradine) also provide adequate
antistaphylococcal coverage except for MRSA
• Use vancomycin 1.0-2.0 g IV qd or linezolid 0.6 g IV q12h in patients allergic to
penicillin or cephalosporins and in patients with methicillin-resistant S. aureus (MRSA). Daptomycin
(Cubicin), a cyclic lipopeptide can be used as an alternative to vancomycin for complicated skin and skin
structure infections. Usual dose is 4 mg/kg IV given over 30 min every 24 hr
H. influenzae cellulitis
• PO: cefixime or cefuroxime
• IV: cefuroxime or ceftriaxone
Vibrio vulnificus
• Doxycycline 100 mg IV or PO bid +/- third-generation cephalosporin. Ciprofloxacin is an
alternative antibiotic
• IV support and admission into ICU (mortality rate >50% in septic shock)
Erysipelothrix
• Penicillin
Aeromonas hydrophila
• Aminoglycosides
• Chloramphenicol
• Complicated skin and skin structure infections in hospitalized patients can be treated with
daptomycin (cubicin) 4 mg/kg IV every 24 hr

Erysipelas

DEFINITION
Erysipelas is a type of cellulitis caused by infection of the superficial layers of the skin and cutaneous
lymphatics. Erysipelas is characterized by redness, induration, and a sharply demarcated, raised border.

SYNONYMS
St. Anthony's fire

EPIDEMIOLOGY & DEMOGRAPHICS

PREDOMINANT AGE: Occurs most often in the young or old

RISK FACTORS: Patients with impaired lymphatic or venous drainage (mastectomy, saphenous vein
harvesting), and immunocompromised patients

RECURRENCE RATE: Relatively common

PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Distinctive red, warm, tender skin lesion with induration and a sharply defined,
advancing, raised border is present ( Fig. 1-90 ).
• Most common sites are lower extremities or face.
• Systemic signs of infection (fever) are often present.
• Vesicles or bullae may develop.
• After several days, lesions may appear ecchymotic.
• After 7 to 10 days desquamation of affected area may occur.

ETIOLOGY
• Usually group A β-hemolytic streptococci
• Less often group B, C, or G streptococci
• Rarely Staphylococcus aureus

COMPLICATIONS
• Abscess
• Necrotizing fasciitis
• Thrombophlebitis
• Gangrene
• Metastatic infection

WORKUP
History, physical examination, and laboratory evaluation

LABORATORY TESTS
Diagnosis is usually made by characteristic clinical setting and appearance.
• CBC and WBC often elevated
• Blood cultures positive in 5% of patients
• Gram stain and culture of any drainage from skin lesions
• Culture of aspirated fluid from leading edge of skin lesion has low yield

IMAGING STUDIES
• Duplex ultrasound for patients suspected of having DVT
• CT scan or MRI for patients with suspected necrotizing fasciitis

TREATMENT
NONPHARMACOLOGIC THERAPY
• Elevation of the affected limb
• Warm compresses
ACUTE GENERAL Rx
Typical erysipelas of extremity in nondiabetic patient:
• PO: penicillin V 250 mg to 500 mg qid
• IV: penicillin G (aqueous) 1 to 2 million units q6h
NOTE: Use erythromycin or cephalosporin in patients allergic to penicillin.
Facial erysipelas (include coverage for Staphylococcus aureus):
• PO dicloxacillin 500 mg q6h
• IV nafcillin or oxacillin 2 g q4h
VIRAL SKIN INFECTIONS

Warts

DEFINITION
Warts are benign epidermal neoplasms caused by human papillomavirus (HPV).

SYNONYMS
Verruca vulgaris (common warts)
Verruca plana (flat warts)
Condyloma acuminatum (venereal warts)
Verruca plantaris (plantar warts)
Mosaic warts (cluster of many warts)

EPIDEMIOLOGY & DEMOGRAPHICS

• Common warts occur most frequently in children and young adults.
• Anogenital warts are most common in young, sexually active patients. Genital warts are
the most common viral STD in the U.S., with up to 24 million Americans carrying the virus that causes
them.
• Common warts are longer lasting and more frequent in immunocompromised patients
(e.g., lymphoma, AIDS, immunosuppressive drugs).
• Plantar warts occur most frequently at points of maximal pressure (over the heads of the
metatarsal bones or on the heels).
PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Common warts have an initial appearance of a flesh-colored papule with a rough surface;
they subsequently develop a hyperkeratotic appearance with black dots on the surface (thrombosed
capillaries); they may be single or multiple and are most common on the hands.
• Warts obscure normal skin lines (important diagnostic feature). Cylindrical projections
from the wart may become fused, forming a mosaic pattern.
• Flat warts generally are pink or light yellow, slightly elevated, and often found on the
forehead, back of hands, mouth, and beard area; they often occur in lines corresponding to trauma (e.g., a
scratch); are often misdiagnosed (particularly when present on the face) and inappropriately treated with
topical corticosteroids.
• Filiform warts have a fingerlike appearance with various projections; they are generally
found near the mouth, beard, or periorbital and paranasal regions.
• Plantar warts are slightly raised and have a roughened surface; they may cause pain when
walking; as they involute, small hemorrhages (caused by thrombosed capillaries) may be noted.
• Genital warts are generally pale pink with several projections and a broad base. They
may coalesce in the perineal area to form masses with a cauliflower-like appearance.
 • Genital warts on the cervical epithelium can produce subclinical changes that may be
noted on Pap smear or colposcopy.

ETIOLOGY
• Human papillomavirus (HPV) infection; >60 types of viral DNA have been identified.
Transmission of warts is by direct contact.
• Genital warts are usually caused by HPV types 6 or 11.

WORKUP
• Diagnosis is generally based on clinical findings.
• Suspect lesions should be biopsied.

LABORATORY TESTS
Colposcopy with biopsy of patients with cervical squamous cell changes

TREATMENT

NONPHARMACOLOGIC THERAPY
• Importance of use of condoms to reduce transmission of genital warts should be
emphasized.
• Watchful waiting is an acceptable option in the treatment of warts, because many warts
will disappear without intervention over time.
• Plantar warts that are not painful do not need treatment.

GENERAL Rx
• Common warts:
1. Application of topical salicylic acid 17% (e.g., Duofilm). Soak area for 5 min in warm
water and dry. Apply thin layer once or twice daily for up to 12 wk, avoiding normal skin. Bandage.
2. Liquid nitrogen, electrocautery are also common methods of removal.
3. Blunt dissection can be used in large lesions or resistant lesions.
4. Duct tape occlusion is also effective for treating common warts. It is cut to cover warts
and left in place for 6 days. It is removed after 6 days and the warts are soaked in water and then filed
with pumice stones. New tape is applied 12 hr later. This treatment can be repeated until warts resolve.

• Filiform warts: surgical removal is necessary.

• Flat warts: generally more difficult to treat.
1. Tretinoin cream applied at hs over the involved area for several weeks may be effective
2. Application of liquid nitrogen
3. Electrocautery
4. 5-Fluorouracil cream (Efudex 5%) applied once or twice a day for 3-5 wk is also
effective. Persistent hyperpigmentation may occur following Efudex use

• Plantar warts:
 1. Salicylic acid therapy (e.g., Occlusal-HP). Soak wart in warm water for 5 min, remove
loose tissue, dry. Apply to area, allow to dry, reapply. Use once or twice daily; maximum 12 wk. Use of
40% salicylic acid plasters (Mediplast) is also a safe, nonscarring treatment; it is particularly useful in
treating mosaic warts covering a large area.
2. Blunt dissection is also a fast and effective treatment modality.
3. Laser therapy can be used for plantar warts and recurrent warts; however, it leaves open
wounds that require 4-6 wk to fill with granulation tissue.
4. Interlesional bleomycin is also effective but generally used when all other treatments fail.

• Genital warts:
1. Can be effectively treated with 20% podophyllin resin in compound tincture of benzoin
applied with a cotton tip applicator by the treating physician and allowed to air dry. The treatment can be
repeated weekly if necessary.
2. Podofilox (Condylox 0.5% gel) is now available for application by the patient. Local
adverse effects include pain, burning, and inflammation at the site.
3. Cryosurgery with liquid nitrogen delivered with a probe or as a spray is effective for
treating smaller genital warts.
4. Carbon dioxide laser can also be used for treating primary or recurrent genital warts (cure
rate >90%).
5. Imiquimod (Aldara) cream, 5% is a patient-applied immune response modifier effective
in the treatment of external genital and perianal warts (complete clearing of genital warts in >70% of
females and >30% of males in 4-16 wk). Sexual contact should be avoided while the cream is on the skin.
It is applied three times/wk before normal sleeping hours and is left on the skin for 6-10 hr.

• Application of trichloroacetic acid (TCA) or bichloracetic acid (BCA) 80%-90% is also

effective for external genital warts. A small amount should be applied only to warts and allowed to dry, at
which time a white “frosting” develops. This treatment can be repeated weekly if necessary.

Molluscum Contagiosum

DEFINITION
Viral infection characterized by discrete skin lesions with central umbilication

EPIDEMIOLOGY & DEMOGRAPHICS

• Molluscum contagiosum spreads by autoinoculation, scratching, or touching a lesion.
• It usually occurs in young children. It is also common in sexually active adults and
patients with HIV infection.
• Incubation period varies between 4 and 8 wk.
• Spontaneous resolution in immunocompetent patients can occur after several months.

PHYSICAL FINDINGS & CLINICAL PRESENTATION

 • The individual lesion appears initially as a flesh-colored, firm, smooth-surfaced papule
with subsequent central umbilication. Lesions are frequently grouped. The size of each lesion generally
varies from 2 to 6 mm in diameter.
• Typical distribution in children involves the face, extremities, and trunk. Mucous
membranes are spared.
• Distribution in adults generally involves pubic and genital areas.
• Erythema and scaling at the periphery of the lesions may be present as a result of
scratching or hypersensitivity reaction.
• Lesions are not present on the palms and soles.

ETIOLOGY
Viral infection of epithelial cells caused by a pox virus

DIAGNOSIS
Diagnosis is usually established by the clinical appearance of the lesions (distribution and central
umbilication). A magnifying lens can be used to observe the central umbilication. If necessary, the
diagnosis can be confirmed by removing a typical lesion with a curette and examining the content on a
slide after adding potassium hydroxide and gentle heating. Staining with toluidine blue will identify viral
inclusions.

WORKUP
Careful examination of the papules

LABORATORY TESTS
Generally not indicated in children. STD screening for other sexually transmitted diseases is
recommended in all cases of genital molluscum contagiosum.
TREATMENT

NONPHARMACOLOGIC THERAPY
Prevention of autoinoculation by scratching or touching lesions

GENERAL THERAPY
• Therapy is individualized depending on number of lesions, immune status, and patient's
age and preference.
• Observation for spontaneous resolution is reasonable in patients with few, small, not
irritated, and not-spreading lesions. Genital lesions should be treated in all sexually active patients.
• Curettage following pretreatment of the area with combination prilocaine 2.5% with
lidocaine 2.5% cream (EMLA) for anesthesia is useful for treatment of few lesions. Curettage should be
avoided in cosmetically sensitive areas because scarring may develop.
• Treatments with liquid nitrogen therapy in combination with curettage are effective in
older patients who do not object to some discomfort.
• Application of cantharidin 0.7% to individual lesions covered with clear tape will result
in blistering over 24 hr and possible clearing without scarring. This medication should be avoided on
facial lesions.
 • Other treatment measures include use of tretinoin 0.025% gel or 0.1% cream at hs, daily
use of salicylic acid (Occlusal) at hs, and use of laser therapy.
• Trichloroacetic acid peel generally repeated every 2 wk for several weeks is useful in
immunocompromised patients with extensive lesions.

Herpes Simplex

DEFINITION
Herpes simplex is a viral infection caused by the herpes simplex virus (HSV); HSV-1 is associated
primarily with oral infections, whereas HSV-2 causes mainly genital infections; however, each type can
infect any site; following the primary infection, the virus enters the nerve endings in the skin directly
below the lesions and ascends to the dorsal root ganglia where it remains in a latent stage until it is
reactivated.

EPIDEMIOLOGY & DEMOGRAPHICS

• More than 85% of adults have serologic evidence of HSV-1 infection. The seroprevalence
of adults with HSV-2 in the United States is 25%; however, only about 20% of these persons recall having
symptoms of HSV infection.
• Most cases of eye or digital herpetic infections are caused by HSV-1.
• Frequency of recurrence of HSV-2 genital herpes is higher than HSV-1 oral labial
infection.
• The frequency of recurrence is lowest for oral labial HSV-2 infections.
• The incidence of complications from herpes simplex (e.g., herpes encephalitis) is highest
in immunocompromised hosts.

PHYSICAL FINDINGS & CLINICAL PRESENTATION

PRIMARY INFECTION:
• Symptoms occur from 3 to 7 days after contact (respiratory droplets, direct contact).
• Constitutional symptoms include low-grade fever, headache and myalgias, regional
lymphadenopathy, and localized pain.
• Pain, burning, itching, and tingling last several hours.
• Grouped vesicles ( Fig. 1-119 ) usually with surrounding erythema appear and generally
ulcerate or crust within 48 hr.
• The vesicles are uniform in size (differentiating it from herpes zoster vesicles, which vary
in size).
• During the acute eruption the patient is uncomfortable; involvement of lips and inside of
mouth may make it unpleasant for the patient to eat; urinary retention may complicate involvement of the
genital area.
• Lesions generally last from 2 to 6 wk and heal without scarring.

RECURRENT INFECTION:
 • Generally caused by alteration in the immune system; fatigue, stress, menses, local skin
trauma, and exposure to sunlight are contributing factors.
• The prodromal symptoms (fatigue, burning and tingling of the affected area) last 12 to 24
hr.
• A cluster of lesions generally evolve within 24 hr from a macule to a papule and then
vesicles surrounded by erythema; the vesicles coalesce and subsequently rupture within 4 days, revealing
erosions covered by crusts.
• The crusts are generally shed within 7 to 10 days, revealing a pink surface.
• The most frequent location of the lesions is on the vermilion border of the lips (HSV-1),
the penile shaft or glans penis and the labia (HSV-2), buttocks (seen more frequently in women),
fingertips (herpetic whitlow), and trunk (may be confused with herpes zoster).
• Rapid onset of diffuse cutaneous herpes simplex (eczema herpeticum) may occur in
certain atopic infants and adults. It is a medical emergency, especially in young infants, and should be
promptly treated with acyclovir.
• Herpes encephalitis, meningitis, and ocular herpes can occur in patients with
immunocompromised status and occasionally in normal hosts.

ETIOLOGY
HSV-1 and HSV-2 are both DNA viruses.

WORKUP
Diagnosis is based on clinical presentation. Laboratory evaluation will confirm diagnosis.

LABORATORY TESTS
• Direct immunofluorescent antibody slide tests will provide a rapid diagnosis.
• Viral culture is the most definitive method for diagnosis; results are generally available in
1 or 2 days; the lesions should be sampled during the vesicular or early ulcerative stage; cervical samples
should be taken from the endocervix with a swab.
• Tzanck smear is a readily available test; it will demonstrate multinucleated giant cells.
However, it is not a very sensitive test.
• Pap smear will detect HSV-infected cells in cervical tissue from women without
symptoms.
• Serologic tests for HSV: IgG and IgM serum antibodies. Antibodies to HSV occur in 50%
to 90% of adults. Routine tests do not discriminate between antibodies that are HSV-1 and HSV-2; the
presence of IgM or a fourfold or greater rise in IgG titers indicates a recent infection (convalescent
sample should be drawn 2 to 3 wk after the acute specimen is drawn).

TREATMENT

NONPHARMACOLOGIC THERAPY
Application of topical cool compresses with Burow's solution for 15 min four to six times daily may be
soothing in patients with extensive erosions on the vulva and penis (decrease edema and inflammation,
debridement of crusts and purulent material).
ACUTE GENERAL Rx
• Acyclovir ointment or cream (Zovirax) applied using finger-cot or rubber glove q3-6h
(six times daily) for 7 days may be useful for the first clinical episode of genital herpes. Severe primary
genital infections may be treated with IV acyclovir (5 mg/kg infused at a constant rate over 1 hr q8h for 7
days in patients with normal renal function) or oral acyclovir 200 mg five times daily for 10 days. Topical
acyclovir 5% cream can also be used for herpes labialis; when started at the prodrome or papule stage, it
decreases the duration of an episode by about one-half day.
• Valacyclovir caplets (Valtrex) can also be used for the initial episode of genital herpes (1
g bid for 10 days).
• Valacyclovir 2 g PO q12h for 1 day begun within the first symptoms of herpes labialis
can modestly shorten its duration.
• Penciclovir 1% cream (Denavir) can be used for recurrent herpes labialis on the lips and
face. It should be applied q2h while awake for 4 days. Treatment should be started at the earliest sign or
symptom. Its use decreases healing time of orolabial herpes by about one day.
• Docosanol 10% cream (Abbreva), a long-chain saturated alcohol, inhibits fusion between
the plasma membrane and the viral envelope, blocking viral entry and subsequent replication. It is
available over the counter and, when applied at the first sign of recurrence of herpes labialis, may shorten
the durations of the episode by about 12 hr.

CHRONIC Rx
• Recurrent episodes of genital herpes can be treated with acyclovir. A short course (800
mg tid for 2 days) is effective. Other treatment options include 800 mg PO bid for 3 to 5 days, generally
started during the prodrome or within 2 days of onset of lesions; famciclovir (Famvir) is also useful for
treatment of recurrent genital herpes (dose is 125 mg q12h for 5 days in patients with normal renal
function) started at the first sign of symptoms, or valacyclovir (Valtrex) (dose is 500 mg q12h for 3 days
in patients with normal renal function).
• Acyclovir-resistant mucocutaneous lesions in patients with HIV can be treated with
foscarnet (40 to 60 mg/kg IV q8h in patients with normal renal function); HPMPC has also been reported
to be effective in HSV infections resistant to acyclovir or foscarnet.
• Patients with 6 recurrences of genital herpes/year can be treated with valacyclovir 1 g qd,
acyclovir 400 mg bid, or famciclovir 250 mg bid.