SKIN DISEASES

1. NAME: MUSHTAQ AHMED
ROLL NO: 525
TOPIC ASSIGNED: 3 SKIN DISEASES AND THEIR TREATMENT
SUBMITTED TO:SIR KHEZAR HAYAT
1) LEPROSY:
INTRODUCTION:
Leprosy is also known as Hansen's disease, after the scientist who discovered M. leprae in 1873.Leprosy is an
infectious disease that causes severe, disfiguring skin sores and nerve damage in the arms and legs. The disease has
been around since ancient times. Outbreaks of leprosy have affected, and panicked, people on every continent. The
oldest civilizations of China, Egypt, and India feared leprosy was an incurable, mutilating, and contagious disease.
However, leprosy is actually not contagious. You can catch it only if you come into close and repeated contact with nose
and mouth droplets from someone with untreated leprosy. Children are more likely to get leprosy than adults.
Today, about 180,000 people worldwide are infected with leprosy, according to the World Health Organization,
most of them in Africa and Asia. About 200 people are diagnosed with leprosy in the U.S. every year, mostly in
the South, California, Hawaii, and some U.S. territories
Cause OF Leprosy:
A slow-growing type of bacteria called Mycobacterium leprae.
Symptoms of Leprosy:
 Leprosy primarily affects the skin and the nerves outside the brain and spinal cord, called the
peripheral nerves.
 It may also affect the eyes and the thin tissue lining the inside of the nose.
The main symptom of leprosy is
 Disfiguring skin sores, lumps, or bumps that do not go away after several weeks. The skin sores are
pale-colored.
Nerve damage can lead to:
 Loss of feeling in the arms and legs and Muscle weakness

2. INCUBATION PERIOD: It takes about 3 to 5 years for symptoms to appear after coming into contact with the leprosy-
causing bacteria. Some people do not develop symptoms until 20 years later. The time between contact with the bacteria
and the appearance of symptoms is called the incubation period. Leprosy's long incubation period makes it very difficult
for doctors to determine when and where a person with leprosy got infected.
TYPES of Leprosy:
Leprosy is defined by the number and type of skin sores you have.
 Tuberculoid: A mild, less severe form of leprosy. People with this type have only one or a few patches of flat,
pale-colored skin (paucibacillary leprosy). The affected area of skin may feel numb because of nerve damage
underneath. Tuberculoid leprosy is less contagious than other forms.
 Lepromatous: A more severe form of the disease. It has widespread skin bumps and rashes (multibacillary
leprosy), numbness, and muscle weakness. The nose, kidneys, and male reproductive organs may also be
affected. It is more contagious than tuberculoid leprosy.
 Borderline. People with this type of leprosy have symptoms of both the tuberculoid and lepromatous forms.
Leprosy Diagnosis:
 skin biopsy
Leprosy Complications:
Complications of leprosy include:
 Blindness or glaucoma.
 Disfiguration of the face (including permanent swelling, bumps, and lumps).
 Erectile dysfunction and infertility in men.
 Kidney failure.
 Muscle weakness that leads to claw-like hands or an inability to flex the feet.
 Permanent damage to the inside of the nose, which can lead to nosebleeds and a chronic, stuffy nose.
 Permanent damage to the nerves outside the brain and spinal cord, including those in the arms, legs, and
feet.
TREATMENT:
In response to the increased incidence of dapsone resistance, the WHO introduced a multidrug regimen in
1981 that includes rifampicin, dapsone, and clofazimine. Some clinical studies have also shown that certain
quinolones, minocycline, and azithromycin have activity against M leprae. The WHO recently recommended
single-dose treatment with rifampin, minocycline, or ofloxacin in patients with paucibacillary leprosy who have

3. a single skin lesion. However, the WHO still recommends the use of the long-term multidrug regimens
whenever possible because they have been found to be more efficacious.
US regimens emphasize the use of rifampin, which is the most bactericidal drug used to treat leprosy. Although
a single dose of 600 mg once monthly (the WHO standard) is considered bactericidal, treatment plans in the
United States may include doses of 600 mg/day.
Multidrug Therapy Plan Recommended by the WHO:
Type of
Leprosy
Daily, Self-
Administered
Monthly Supervised
Months of
Treatment
Paucibacillary Dapsone 100 mg Rifampicin 600 mg 6-12
Multibacillary Dapsone 100 mg,
Clofazimine 50 mg
Rifampicin 600 mg,
Clofazimine 300 mg (WHO); 200 mg
(NHDP)
24
Pediatric Dapsone 2 mg/kg,
Clofazimine 1 mg/kg
Rifampicin 10 mg/kg,
Clofazimine 6 mg/kg
Same as in adults
 Paucibacillary leprosy
should be treated for 6-12 months with dapsone 100 mg/day unsupervised plus rifampin 600 mg/month
supervised.
This regimen should be followed by treatment with dapsone as monotherapy for 3 years in patients with
tuberculoid leprosy or 5 years in patients with borderline lepromatous leprosy.
 Multibacillary leprosy
should be treated for 24 months with dapsone 100 mg/day
clofazimine 50 mg/day unsupervised, and rifampin 600 mg plus clofazimine 300 mg/month supervised.

4. Corticosteroids have been used to treat nerve damage associated with leprosy, Prednisolone is believed to minimize
pain and acute inflammation. The recommended initial dose is prednisolone 40 mg daily.
 increasing resistance in patients treated for leprosy have been reported in Southeast Asia .The drug most
commonly found to be resistant is dapsone.
 References:
 (Leprosy Treatment & Management Author: Darvin Scott Smith, MD, MSc, DTM&H; Chief Editor:
Michael Stuart Bronze, MD Author Darvin Scott Smith, MD, MSc, DTM&H Adjunct Associate
Clinical Professor, Department of Microbiology and Immunology, Stanford University School of
Medicine; Chief of Infectious Diseases and Geographic Medicine, Department of Internal Medicine,
Kaiser Redwood City Hospital
 BASIC AND CLINICAL PHARMACOLOGY VIA BERTRAM G.KATZUNG (11TH
EDITION), DRUGS
USED IN LEPROSYPAGE NO: 831.
 Treatment of leprosy (http://apps.who.int/medicinedocs/en/d/Jh2988e/)
Surgical Care IN PATIENTS WITH LEPROSY:
 A)Surgical treatment:
The goals of surgical treatment in patients with leprosy are to prevent further deterioration, to improve motor function,
and, to improve sensation.
Preoperative requirements: First, a full sensory and motor appraisal with functional and occupational assessment must
be completed to determine the extent of damage. Additionally, patients must have completed the multidrug therapy and
should have negative skin smear results. The patient should not use steroids a few months before surgery. Stiffness of
hands and feet should be minimized with preoperative therapy.
B) Neural surgery:
 Attempts to restore autonomic function and sensation are rarely undertaken. Nerve grafts may be of some benefit in
patients with localized lesions.
C) Reconstruction and functional restoration:
In leprosy management, the goal of most surgical procedures is to remedy motor paralysis due to primary nerve
Contractures of the hand, such as the thumb web contracture, can be repaired with Z-plasty, and joint stability can be
improved with tenodesis.
D) Amputation is a last resort and is reserved for cases of extremely diseased tissue.
E) Cosmetic surgery: After the disease is controlled medically, the following cosmetic procedures may also be
considered:
 Nasal reconstruction
 Removal of excess skin
 Replacement of eyebrows using transplants of scalp hair
 Removal of breast tissue formation due to gynecomastia.
2) ACNE VULGARIS:
Signs and symptoms:
Acne vulgaris is characterized by noninflammatory, open or closed comedones and by inflammatory papules, pustules,
and nodules. Acne vulgaris typically affects the areas of skin with the densest population of sebaceous follicles (eg, face,
upper chest, back).

5. Local symptoms of acne vulgaris may include pain, tenderness, or erythema.
Systemic symptoms are most often absent in acne vulgaris. Severe acne with associated systemic signs and symptoms,
such as fever, is referred to as acne fulminans.
Severe acne, characterized by multiple comedones, without the presence of systemic symptoms, is known as acne
conglobata. This severe form of acne frequently heals with disfiguring scars. Additionally, acne vulgaris may have a
psychological impact on any patient, regardless of the severity or the grade of the disease
CLINICAL FEATURES OF ACNE VULGARIS:
Superficial lesions:
 Open and closed comedones (blackheads and whiteheads)
 Papules (small, tender red bumps)
 Pustules (white or yellow "squeezable" spots)
Deeper lesions:
 Nodules (large painful red lumps)
 Pseudocysts (cyst-like fluctuant swellings)
Secondary lesions:
 Excoriations (picked or scratched spots)
 Erythematous macules (red marks from recently healed spots, best seen in in fair skin)
 Pigmented macules (dark marks from old spots, mostly affecting those with dark skin)
 Scars or various types
Individual acne lesions usually last less than 2 weeks but the deeper papules and nodules may persist for
months. Many acne patients also have oily skin (seborrhoea).
Diagnosis: Examination in patients with acne vulgaris includes the following features:
 Comedonal acne:
Presence of open and closed comedones but usually no inflammatory papules or nodules
 Mild acne:
Presence of comedones and a few papulopustules
 Moderate acne:
Presence of comedones, inflammatory papules, and pustules; a greater number of lesions are present than in milder
inflammatory acne Nodulocystic acne: Presence of comedones, inflammatory lesions, and large nodules greater than 5
mm in diameter; scarring is often evident.
Laboratory tests:
Acne vulgaris is a clinical diagnosis. However, laboratory testing may be indicated in the following situations:
 Female patients with dysmenorrhea or hirsutism: Consider a hormonal evaluation with levels of total and/or free
testosterone, dehydroepiandrosterone sulfate, luteinizing hormone, and follicle-stimulating hormone
 Culture skin lesions to rule out gram-negative folliculitis

6. Management:
Treatment of acne vulgaris should be directed toward the known pathogenic factors including
 follicular hyperproliferation,
 excess sebum,
 Propionibacterium acne vulgaris:
 inflammation.
Appropriate treatment: isbased on the grade and severity of the acne.
 Retinoid-like agents: ( topical tretinoin, adapalene, tazarotene, isotretinoin)
 Antibiotics: ( tetracycline, minocycline, doxycycline, trimethoprim/sulfamethoxazole,
clindamycin, topical clindamycin, topical erythromycin, daptomycin)
 Selective aldosterone antagonists ( spironolactone)
 Estrogen/progestin combination oral contraceptive pills: ( ethinyl estradiol, drospirenone, and
levomefolate; ethinyl estradiol and norethindrone; ethinyl estradiol and norgestimate; ethinyl
estradiol and drospirenone)
 Acne products ( erythromycin and benzoyl peroxide, clindamycin and tretinoin, clindamycin and
benzoyl peroxide, azelaic acid, benzoyl peroxide)
When a topical or systemic antibiotic is used, it should be used in conjunction with benzoyl
peroxide or topical retinoid to reduce the emergence of resistance.
References:
1. Lehmann HL, Robinson KA, Andrews JS, Holloway V, Goddman SN. Acne therapy: a
methodological review. J. Am. Acad. Dermatol. 47, 231-240 (2002)
2. Current Measures for the Evaluation of Acne Severity – Medscape Dermatology Expert Review
3. Tan JK, Jones E, Allen E, Pripotnev S, Raza A, Wolfe B. Evaluation of essential clinical components
and features of current acne global grading scales. J Am Acad Dermatol. 2013 Nov;69(5):754-61.

7. 3) SCABIES:
INTRODUCTION:
Scabies is an ectoparasitic infestation of the skin caused by the human itch mite, Sarcoptes scabiei.
A) GENERAL INFORMATION :
BIOLOGY OF THE SCABIES MITE:
Infestation begins when one or several pregnant female mites are transferred from the skin of an infested person to the
skin of an uninfested person.
After transfer from the skin of an infested person, adult female mite travels on the skin surface at the rate of about 1 inch
per minute seeking a burrow site. After finding a suitable location,she burrows into superficial layers of the skin, forming a
slightly elevated narrow tunnel where she deposits 2 to 3 eggs daily during her 4 to 6 week life span.
The eggs progress through larval and nymphal stages to form adults in 10 to 17 days.
The adults migrate to the skin surface and mate. The males die quickly and the females penetrate the skin and repeat
the cycle. The mite requires human skin to complete its life cycle and is unable to survive off the host at room
temperature for more than 3 to 4 days.
B) CLINICAL PRESENTATION:
Scabies infestations are generally categorized as typical or atypical (crusted, keratotic or
Norwegian).
1)Patients with typical (conventional) scabies:
usually have only 10 to 15 live adult female mites on the body at any given time. Intense pruritis, usually worse at night,
and a papular rash with or without burrows occur. The rash and pruritis result from an immune-mediated delayed
hypersensitivity reaction to the mite, its eggs, and fecal material. Areas of the body commonly involved are wrists, finger
webs, antecubital fossae, anterior axillary folds, breasts, waistline, lower abdomen, genitals, and buttocks.The scalp and
face are rarely involved in adults, but may be observed in young children with scabies
2. Atypical Scabies:
When diagnosis and treatment are delayed, scabies can have an unusual or atypical presentation, involving heavy
infestation with hundreds to thousands of mites. When extensive hyperkeratotic skin lesions with crusting and scaling
develop, the infestation is called crusted scabies or hyperkeratotic (formerly “Norwegian”) scabies. Crusted scabies is
highly contagious because
thousands of mites are imbedded in the thick crusts and easily shed in scales and flakes from affected skin. Crusted
scabies is commonly misdiagnosed by dermatologists, and patients with crusted scabies may develop symptoms of
typical scabies in as little as a few days.

8. C. EPIDEMIOLOGY OF SCABIES:
1. Transmission:
Transfer of the mite is usually from one person to another by direct skin-to skin contact. Mites may also be transmitted
via clothing, bed linen or other fomites.
2. Incubation Period:
In a previously unexposed healthy individual, the interval between exposure and the onset of itching is usually 4-6
weeks.
3. Period of Communicability:Since the scabies mite is an ectoparasite, an exposed individual is potentially
immediately infectious to others, even in the absence of symptoms. Cases are communicable from the time of
infestation until mites and eggs are destroyed by treatment.
D. DIAGNOSIS:
Definitive diagnosis requires microscopic identification of the mite and/or its eggs or fecal pellets on specimens collected
by skin scraping, biopsy or other means.
MANAGEMENT OF SYMPTOMATIC CASES:
Often the first indications of a scabies outbreak are complaints of itching and rash. Properly performed skin
scrapings will almost always be positive in persons with crusted scabies but are generally negative in cases of
typical scabies, even when performed by experienced operators.
TREATMENT:
Patient Being
Treated
Treatment
Options
Dose How To Treat How Long is
Treatment
Typical Scabies Treatment A
5% permethrin cream
(Elimite, Acticin)
Adult dose –
30-60 grams tube can
treat two adults
Massage cream into
skin from under chin
to soles of feet
Attention to hairline,
neck, temple in
geriatric patients.
One treatment usually
sufficient
May repeat if needed
7 days after 1st
treatment.
Treatment B
Ivermectin (Mectizan
or Stromectol )
oral antiparasitic
Used for patients who
have failed treatment
with or cannot tolerate
topical treatment
200 mcg/kg Given orally to treat
suspect/confirmed
cases of
scabies
Single dose; 2nd dose
may be necessary to
eliminate infection
Atypical Scabies Treatment A
5% permethrin cream
(Elimite, Acticin)
Adult dose – 30
grams
Massage cream into
skin from under chin
to soles of
feet
Apply once, 2nd
application 12 hrs
later
May repeat if needed
7 days after 1st round
of treatment
Treatment B
5% permethrin cream
(Elimite, Acticin)
10% crotamiton lotion
Adult dose – 30
grams
Enough lotion to
cover skin chin to
feet
Apply permethrin
once as above and
again 12 hrs later
on day 1 and day 7
Apply crotamiton as
One week long
treatment sufficient;
reassess 7 days after
treatment completed

9. above on days 2-6
Treatment C
5% permethrin cream
(Elimite, Acticin)
Ivermectin (Mectizan
or Stromectol ) oral
antiparasitic
Adult dose – 30
grams
200 mcg/kg
Apply permethrin
once as above and
again 12 hrs later
Single oral dose
One treatment;
reassess 14 days
after
treatment
Benzyl benzoate
Benzyl benzoate (25%) is the secondline treatmentfor typical scabies.It isavailable as an emulsionand should
be appliedtopicallyfrom the neck down. Benzyle benzoate isregisteredfor use on all people butis not
recommendedforyoung children(< 6 months).Benzyl benzoate shouldbe appliedtopically to dry skin from the neck
down. Benzyl benzoate shouldbe lefton the skinfor a full 24 hours. The initial treatment should be followedbya
secondtreatment one weeklater to kill any miteshatched from survivingeggs.
E. Treatment Failures
1. Treatment failures can result from:
a. Inadequate application of scabicide;
b. Infected, crusted, or keratotic lesions with insufficient penetration of scabicide;
c. Reinfestation from untreated contacts;
d. Resistance of mites to scabicide.
References:
 Sargent SJ. Ectoparasites. In Mayhall CG (ed): Hospital Epidemiology and Infection
Control,3rd edition Edition. Baltimore: Williams & Wilkins 2004:755-757.
 Schultz MW, Gomez M, Hansen RC, et al. Comparative study of 5% permethrin cream
and 1% lindane lotion for the treatment of scabies. Arch Dermatol1990; 126:167-170.
 Green MS. Epidemiology of scabies. Epidemiologic Reviews 1989; 11:126-150.
 Lettau LA. Nosocomial transmission and infection control aspects of parasitic and
Ectoparasitic diseases Part III. Ectoparasites/summary and conclusions. Infect Control
Hosp Epidemiol 1991; 12:179-185.
 www.ausgoal.gov.au/creative-commons Department for Health and Ageing, Government of South Australia.
All rights reserved. ISBN: 978-1-74243-3 FIS: 12110.2-1 Printed July 2012.