Cutaneous Infections
Dr. Sitwat Ahmed Fareed
Consultant Dermatologist
United Medical and Dental College and Patel Hospital
INFECTIONS
● BACTERIAL:-
● 1.Impetigo Contagiosa
● 2.Staphylococcal Scalded Skin Syndrome
● 3.Scarlet fever
● 4.Erysipelas
● 5.Cellulitis
● 6.Ecthyma
● 7.Folliculitis
● 8.Furuncle & Carbuncle
● 9.Necrotising Fasciitis
● MYCOBACTERIAL
● 1. Tuberculosis
● 2. Leprosy
● IMPETIGO:
Contagious, superficial, pyogenic infection
` of skin.
1.NON BULLOUS ( post streptococcal or staph)
Frequent, worldwide outbreaks more in school going
children, overcrowding, hygiene, Scabies. Crusted
honeycolored dirty scar
2. BULLOUS ( staphyloccal)
Sporadic (by localized exfoliative toxin of Staph.Aureus)
Split below granular layer. Clean thin no scar.
No systemic involvement usually.
Diagnosis
swabs for culture, biopsy
Management; self healing, cleansers, Topical (Mupirocin,
fusidic acid)
Systemic antibiotics ( flucloxacillin, coamoxiclav)
● ERYSIPELAS
.Strep hemolyticus
.Skin and subcutaneous tissue
.Prodrome
.Morphology
1.Sharply demarcated red unilateral
● CELLULITIS
.Loose connective tissue
.Raised hot tender red
.More diffuse not well demarcated
.Bullae, suppuration and necrosis
● ECTHYMA
.Hard dried exudate
.Ulcer Scarring
.Buttocks, thighs and legs
● FOLLICULITIS
superficial inflammation of hair follicle. So no scaring
Diagnosis; staph. Aureus , pseudomonas, pityrosporum
etc. may be sterile due to trauma, friction, chemicals.
Management: Maybe self healing
Topical: mupirocin, fusidic acid
Systemic: flucloxacillin, clindamycin
● Necrotizing fasciitis is a term that describes a disease condition of
rapidly spreading infection, usually located in fascial planes of
connective tissue that results in tissue necrosis (dead and/or
damaged tissue).
● Fascial planes are bands of connective tissue that surround
muscles, nerves, and blood vessels.
● Fascial planes can bind structures together as well as allow body
structures to slide over each other effectively.
● The disease occurs infrequently, but it can occur in almost any area
of the body.
● Although many cases have been caused by group A beta-hemolytic
streptococci (Streptococcus pyogenes), most investigators now
agree that many different bacterial genera and species, either alone
or together (polymicrobial infections), can cause this disease.
Occasionally, mycotic (fungal) species cause necrotizing fasciitis.
● Furuncle (boil or abscess)
Acute necrotic hair follicle infections with staph aureus.
May not be centered on hair follicle. Deep, so may scar.
Occur in adolescence. Above begins as pustule then
inflammatory nodule, then necrotic, then scar.
Can cluster as contiguous follicles to form a Carbuncle.
● Carbuncle
Predisposed by Diabetes, malnutrition, cardiac failure,
obesity, prolonged steroid use, or generalized dermatosis.
Clinical: dome shaped, acutely tender, 3-10 cm, then
suppuration, pus discharge from multiple orifices, necrosis
of skin, yellow slough. Usually, on back of neck and
shoulder. Systemic symptoms present. Results in scarring.
Swabs for culture
Management: incision and drainage
Oral flucloxacillin
Hansen’s
Disease
Dr Sitwat Ahmed
United Medical and Dental
College
Jesus healing the 10 lepers shunned by society
Recognized in ancient China, Egypt & India . It has left
behind a terrifying image , of disfigurement, mutilation
&rejection from society
Mother Teresa established
119 leprosy centers in India
Treated 150,000 lepers
DR Ruth Fau , founder
MALC
Game Plan
● Epidemiology
● Transmission & Immunology
● Clinical features &Differentials
● Treatment
● Lepra Reactions
● Post Test
Etiology
● Chronic granulomatous infection caused by M.
leprae
● Acid fast , slow growing bacillus; obligate Discovered by
Gerhard Hansen in
intracellular 1873
● Affects skin , nerves , URT mucosa & eyes
Causes progressive damage if untreated
Global
Epidemiology
● Elimination of leprosy as a public health problem achieved in
2000 globally
● The prevalence has dropped by 99%
● Total cases at the end of 2015 --- 176 176 cases (0.2 cases /
(
10 000 people) 5.2 million cases in
1985)
● New cases at the end of 2015---- 211 973 (2.9 new cases /
100 000 people) 21% drop from 2005.
● TODAY LEPROSY IS A FOCALIZED INFECTION LIMITED TO “HOT SPOTS ”.
● 95% OF LEPROSY CASES FOUND IN 14 COUNTRIES
● INDIA BEARS 60% OF THE GLOBAL CASE LOAD.
● SOME AREAS SHOW VERY HIGH NOTIFICATION RATES FOR NEW CASES
AND WITNESS INTENSE TRANSMISSION
Situation in Pakistan
New Cases of Pakistan World Comments
leprosy n (%) (%)
Total new cases 446
New 332 (74%) 60.2% indicates presence of
multibacillary advanced cases and disease
cases burden
No. of children 31 (7%) 8.9% indicates continued
transmission in the communities
No. of women 215 (48%) 38.8% indicates a fair access to
leprosy services for women
New cases with 85 (19%) 6.7% indicates delayed
grade-2 detection ;physician
disabilities
Relapses 14 misdiagnosis contributes
Indicates treatment failure
Cases among 143 (32%) Indicates importance of contact
house hold screening
contacts
WHO Global Leprosy Update, 2015
1
case
Annual leprosy 79
report of 2015 (18%)
(MALC)
Total cases: 446
5 cases
89
cases
(20%)
16
256
cases
(57%).
132
(52%)
Break up of Leprosy cases in
Pakistan
Total leprosy cases
446
Major Referral Hospitals in Pakistan:
1-Marie Adelaide Leprosy Centre in
Karachi
2- Rawalpindi Leprosy Hospital
Leprosy control Units :
● Total 170 in no
● Housed in DHQ hospitals
● Staffed by paramedics trained at MALC
● Dx patients of leprosy.
● Do contact screening & defaulter tracing
● Provide standard MDT free of cost .
● Patients with complications are referred to the main referral hospitals.
Transmission
and
immunology
Transmission
M Leprae survivea in warm humid
environments for 16 d & 46 days in
moist soil
Natural reservoirs .
I.P 2-5 yrs.
Symptoms can
take 20 yrs to
develop
CLASSIFICATION
Important for:
- For appropriate treatment.
-To predict risk of complications & lepra reactions
-Prognosis
Two systems :
A-The Ridley– Jopling system :
uses clinical ,histopathological features and the bacteriological
index. : 1-Tuberculoid
2- Borderline Tuberculoid
3- Borderline
4- Borderline Leprematous
5- Leprematous
B-WHO classification :
based on the number of skin lesions . Paucibacillary &
Multibacillary
Immunology of Different types of
Leprosy
● Intracellular pathogen , recognized by our innate immunity.
● Macrophages recognize and present antigen .The immunological
response mounted by the host dictates the clinical phenotype .
● The polar forms conform to an immunological paradigm:
- Tuberculoid Leprosy: high CMI , Th1 type immune response, granuloma
formation.
- Lepromatous leprosy : low CMI ,a humoral Th2 response ,bacterial
dissemination with no granuloma formation
● The borderline forms is immunologically dynamic &movement between
the 2 poles occurs.
● These immunological shifts underlie “ lepra reactions”
1-5 skin lesions 6 or more skin lesions
Clinical
Features
I.P 2-10 yrs
The age-old stigma associated with the disease remains an obstacle
to self-reporting and early treatment
Peripheral Nerve
involvement
● Affects all sensory,
motor and autonomic
function .
● Nerve enlargement due
to granulomatous
inflammation (caseous
necrosis occurs )
● Nerve pain
misdiagnosed as joint pain
● May present as a
painless burn or ulcer .
Indeterminate Leprosy
Earliest & transitory stage
One or two vague hypopigmented
macules with definite sensory
impairment
Tuberculoid Leprosy
● Single or few lesions with well-
defined edges
● Asymmetrical
● SSS-ve
● Scaly, dry, hairless and anaesthetic
● good prognosis
● lesions often self-heal.
● Damage to peripheral nerves is
limited
--
Borderline Tuberculoid: Borderline Leprematous:
More numerous skin Numerous , hypoaesthetic
patches than TT patches
Still asymmetrical Almost symmetrical
Well defined, large SSS+ve
Satellite lesions
SSS-ve
Leprematous Leprosy:
● Disfiguring
● Skin changes - Poorly defined , symmetrically distributed
● hypopigmented / erythematous macules,fleshy papules & nodules
● Nasal mucosa affected- sensation of nasal stuffiness &epistaxis
● Dermal nerve destruction leads to a glove & stocking neuropathy
● Peripheral oedema of the legs and ankles due to increased stasis .
● Peripheral nerves involved late
saddle
The skin deformity
thickens ‘leonine due to
facies septal
Eye lash and eye perforation
brow loss
Pure neuritic leprosy (PNL)
affects peripheral nerve trunks in the absence of cutaneous
signs.
Complications of Leprosy
Laryngeal involvement, was life threatening before effective chemotherapy
was available
● Cause of blindness in
3.2% of affectees
● Through nerve damage
and by direct bacillary
invasion of eye itself leads
to :
1-lagophthalmos
2- corneal ulceration
3- acute or chronic
iridocyclitis
4- secondary cataract
Differential
s
Ptyriasis alba Ptyriasis Vitiligo
versicolor
Erythema Multiforme
Cutaneous TB Sarcoidosis
Granuloma annulare Dermatophyte infection
Differentials in nerve conditions :
Hereditary sensory motor neuropathy type III
Charcot Marie Tooth Disease
Refsum’s disease
Amyloidosis .
Diagnosi
s
Diagnosis
Presence of skin lesions with definite sensory loss or thickened
peripheral nerves is highly suggestive
Rarely nerve biopsy may be needed to confirm the dx -
performed on a purely sensory nerve (e.g. radial cutaneous or
sural nerve).
Interpretation of the Bacteriological Index
Treatment
History of Anti Leprosy Treatment
First anti leprosy
drug –1940s
Resistance
encountere
d in 1960s
Rifampicin and clofazimin were
discovered-1960s
● MDT Introduced in the mid-1980s
● Provided free of costworld wide by WHO since
1995
MDT
● Provides a simple & effective cure
before disability developes
● Patients are non-infectious within 72 h
of rx
● Most national programmes report cure
rates >90%..
● So far no resistance has developed
● Relapse rates : 0 - 2.5% in PB & 0 - 7.7%
in MB .
● 90% of relapses occurr when BI >4.
● Leprosy should be treated by a specialist
● Patients with MB disease, nerve
impairment should be followed for 2 years
after cure
12
Supervised Unsupervised
Single lesion paucibacillary :
Rifampicin 600+ Ofloxacin 400+ Minocycline as a single
dose
Second LineDrugs: minocycline, clarithromycin,
moxifloxacin , ethionamide
Clofazimine Side effects :
-Clofazimine crystals may be deposited in tissues— can cause enteropathy
-Icthiosis
-Red-brown skin and conjunctival discolouration and darkening of involved
skin
Dapsone Side effects :
Haemolysis especially in G6PD
deficiency
Cytopenias
Severe hypersensitivity syndrome
Counselling a patient with leprosy
Leprosy is not:
● Hereditory
● A curse of God
● Due to past sins
● Dependant on caste or class
● Doesnot always lead to deformity
● Is 100% curable
● A completely normal social life should be
encouraged
Preventing Disabilities:
Secondary damage to
neuropathic areas must be
prevented.
Advise on protective
footwear.
Teach self-examination and
early trauma recognition .
Lepra
Reactions
Erythema Nodosum Leprosum:
● Fever & crops of new, painful, erythematous
nodules appearing during rx
● Affect face & extensor surfaces
● Due to Ag-Ab complex deposition
● Can be recurrent or chronic
● Systemic symptoms common- uveitis,
neuritis, arthritis, dactylitis, lympadenitis and
orchitis
● Seen in patients with high bacillary load
and extensive skin lesions (BL -10%, LL—50%)
● T/M: Prednisone 60-80mg/d or
Thalidomide 100-400mg /d
Type -1 Lepra Reaction
Seen in BT, BB & BL during rx
● Systemic symptoms rare
● Oedema of the hands, feet and
face can also be a feature
● Recurrent
The pre existing skin lesions
become acutely inflamed ,
oedematous and may
ulcerate.
Acute neuritis requiring nerve
decompression
Rx of Type -1 Lepra Reaction
● High dose steroids
● MDT should be continued during a reaction
Leprosy in a pregnant female
● ENL reactions occur throughout pregnancy and lactation
● Type 1 reactions common in parturition when CMI is restored
● Onset of nerve damage early
Leprosy in HIV
● HIV doesnot inc .susceptibility to M. leprae or alter its clinical picture
● M. leprae unlike M.TB doesnot accelerate immune function decline
● The response to MDT is unaffected.
● Reactions may occur with increased frequency- esp type 1 reaction
● Latent leprosy infections may be unmasked as IRIS following ARV
Recap
● Leprosy is an infectious but curable infection caused by
M leprae
● It has been eliminated globally but pockets of high
endemicity remain
● It is transmitted after close contact with a leper
● Leprematous leprosy is the most severe disfiguring form
● MDT provides a simple cure for all types of leprosy.
● There can be paradoxical worsening during treatment due
to lepra reactions
● There is a need to increase expertise and number of
skilled leprosy staff, to reduce deformities
● There should be no discrimination of a leprosy patient
Pictures –coutesy
MALC
Identify leprosy type.
loss of sensation, loss of
sweating and loss of hair
inside the lesion
Tuberculoid Leprosy
Identify leprosy type.
bilateral loss of
eyebrows
Leprematous Leprosy
Identify leprosy type
Borderline Tuberculoid
Leprosy
Identify leprosy type
bilateral loss of eyebrows
Leprematous
Leprosy
Signs ?
has facial nerve damage and also loss of eye
lashes.
Signs?
wasting of rt. hand muscles, due to ulnar nerve damage. Claw hand
indicates both ulnar, median involvement.
Signs
?
dressing due to an anesthetic foot ulcer. Foot drop is due to
common peroneal nerve involvement.
A case of borderline leprosy . Started on MDT . Developed painful
swelling in pre existing skin lesions .What does it signify ?
Type 1 reversal reaction
Patient of borderline leprematous leprosy who
was started on MDT and developed new skin
lesions, high fever, arthralgia,
lymphadenopathy, orchitis . Reason ?
An ENL reaction. .
Thankyou
