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Bacterial cutaneous infection
TONY SCARIA 2010
KMC
Erysipelas
• a/c inflammation of lymphatics
• Grp A beta haemolytic streptococcus pyogenes
• Malar area of face & lower extremities
• Regional lymphadenopathy +
• Recurrent erysipelas 2* to lymphedema
• Staphylococcus aureus
Skin trauma
Inoculation of bacteria
Fiery red , indurated tense shiny
plaque with raised sharply
demarcated advancing margins
Erysipiliod  caused by eryspilothrix acquired
from fish bone
Milian’s ear sign in erysipelas  can involve
ear lobule but not in case of cellulitis
ERYSIPELAS CELLULITIS
CAUSATIVE AGENT GROUP A BETA HEMOLYTIC
STREPTOCOCCUS
STRAPH & STREPT
BORDERS SHARP DIFFUSE
LYMPHANGITIS MORE COMMON LESS COMMON
TOXICITY LESS MORE
Scarlet fever
• Grp A beta haemolytic
streptococci
• Pyogenic exotoxin A,B,C
• Most common in children 2-
10 years usually following
streptococcal pharyngitis
Pastia’s lines in scarlet fever
• Accentuation of linear erythema in
skin folds
Impetigo
Bullous
•Staph aureus
Non bullous
•Impetigo
contagiosum
•Streptococcus >>
staph
•Most common
Impetigo contagiosum(non bullous)
• Grp A beta haemolytic streptococci
>> staph aureus
• Mc infection in Preschool /young
children
• Face,especially around mouth and
nose
• Thin walled blisters on erythematous
base rupture immediately  honey
coloured crust
• Lesions spread with out central clearing
• Lymphadenopathy
• Complications
• Scarlet fever, erysiplelas, cellulitis,post
streptococcal GN
Gloden yellow honey
coloured crust
Bullous impetigo
• Coagulase positive group II S
aureus
• Neonates and infants
• Face and other parts of body
• Thick walled persistent blisters on
bland skin rupture
slowlyvarnish like crust
• Lesions heal in centre to form
annular patches
• Complications
• Ssss ,pemphigus
neonatorum,cellulitis,lymphangitis
• Rx
• FUSIDIC ACID
• MUPIROCIN
• RETAPAMULIN
• SYSTEMIC
• DICLOXACILLIN
• ERYTHROMYCIN
• CEPHALOSPORIN
Complications
• PSGN
• SSSS
• SCARLET FEVER
Ecthyma
• Vesicle or vesicopustule
• Deep infection of skin d/t Gp A streptococci
• Which involves extra follicular portion (i.e hair follicles spared)
• Post streptococcal GN can develop
• Involves LL
• MC : buttocks , thigh and legs
• STAPH + STREPTECTHYMA
PYOGENICUM
• PSEUDOMONAS AERUGINOSAECTHYMA
GANGRENOSUM
• PARAPOX VIRUS
• ZOONOSES FROM SHEEP & GOAT
ECTHYMA
CONTAGIOSUM
Ecthyma gangrenosum
• Skin manifestation of Ps aeruginosa bacteremia
• In critically ill immunocompromised neutropenic patients
• Lesions
• Haemorrhage necrosis surrounding erythema
• In gluteal or perineal region
• Early lesion to necrosis in 12 hrs
• Rx
• Antipseudomonal Ab
Sycosis barbae
• Staph aureus infection of beard deep
infection of hair follicles
Sycosis nuchae
• Deep infection of hair follicle caused by staph aureus  scarring 
acne keloid nuchalis
CORYNEBACTERIUM INFECTION
• PITTED KERATOLYSIS
• CAUSED BY
• CORYNEBACTERIUM
DERMATOPHILUS
CONGOLENSIS
• MICROCOCCUS
• MULTIPLE SHALLOW PIT
ON PALM & SOLES
• IN PATIENTS WITH
HYPERHIDROSIS
DISHWASHERS
CORYNEBACTERIUM INFECTION
• TRICHOMYCOSIS AXILLARIS
• AFFECT AXILLARY HAIR
• YELLOWISH NODULES 
UNDIGESTED KERATIN
Erythrasma
• c/c superficial infection of skin with
mild patches in axillae , groins ,toes and
ankles
• Well demarcated brown red macular
patches
• Corynebacterium minutussimum
• Lipophilic G +ve aerobic di
• Produces porphyrin's coral red
fluresecence
• Doc : erythromycin ,clarithromycin
coral red fluresecence
Leprosy / hansens disease
Mycobacterium leprae
Cardinal signs of leprosy
• Hypopigmented or erythematous skin lesions with definite loss of
sensation
• Involvement of peripheral nerves  definite thickening
• Skin smear  AFB
M leprae
• Less acid fast than M tuberculae (hence 5 % H2SO4 or 1% HCl is used)
• Obligate intracellular bacillus
• Can remain viable 1- 7 days
• pRopagation is limited to armadillo,mouse foot pad,nude mice
• Generation time 12-13 days
• First bacillus to be associated with human disease
• Modifies fite stain
• In tissue sections
• Portal of entry  skin and respiratory tract
• Chief mode of exit  nasal mucosa of untreated LL patients
• Modes of transmiision
• Droplets >>contact>breast milk>transplacental>insect vectors
• Schwaan cells are first cell to be involved in leprosy
Leprosy
• Grows better in cooler places
• Skin
• PNS
• URT
• Eyes
• Testis
• Spares warmer areas of axilla groin scalp midline back ovaries lung &
CNS
• The Ridley Jopling classification
• Indeterminate
• Tuberculoid
• Borderline:
• borderline-tuberculoid,
• borderline-borderline,
• borderline-lepromatous
• Lepromatous
Indian classification (by indian leprosy
association)
Most common type in india is
tuberculoid (TT)
WHO Classification  treatment
Paucibacillary
• 1-5 lesion
• No nerve or only one nerve
• Skin smears –ve at all sites
Multibacillary
• > 5 lesions
• > 1 nerve irrespective of skin
lesions
• Skin smears + at all sites
• Pure neuritic (indian classification)
• Asymmetric nerve involvement with no skin lesion and usually of tuberculoid
origin
• Painless trophic ulcers
In neuritic type skin biopsy is negative
Indeterminate
leprosy
tuberculoid
leprosy TT
Borderline
tuberculoid
Borderline
lepromatous
Lepromatous
leprosy
Peripheral
neuritic
Vague solitary
assymetrical
Usually single
raised lesion with
well defined &
partly ill defined
borders & numb
when touched
Inverted saucer
shaped lesion or
punched out
Small
erythematous
patches &
macules
Number Solitary Solitary Satellite lesions Many Innumerable
AFB Nil Nil Nil / scanty + +
Nerve Local nerve
thickened
Local nerve
thickened
Symmetrical
nerve thickened
Symmetrical
Nerve thickening
is a late feature
Sensory loss Definite sensory
loss
Definite sensory
loss
Less definite
sensory loss on
patches
Late glove &
stocking
anesthesia
h/p Epitheliod
granuloma in
dermis reaching
up to ddermis
Absent ghrenz
zone
Many epitheliod
granuloma in
dermis
Ghrenz zone +
Diffe
Ghrenz zone +
Onion peel
perineurium
Diffuse
infiltration with
foamy
macrophages 
virchows lepra
cells
Ghrenz zone +
Diagnosis
• Skin smears
• 7 in number
• 4 from skin lesion
• 2 from ear lobes
• 1 from nasal swb
• Nerve biopsy is taken from sural nerve
• Bacilli are absent in lungs , ovaries and CNS
• Most common cranial nerve to get involve is VII
• Goll & burdech tract  proprioception
• Not involved in leprosy
• Other organs involved in leprosy are
• Eyes
• Iritis
• Corneal beading
• Testes
• Muscles
• Myopathy , wasting
Mouse foot pad culture
• Detect drug resistance
• Evaluating potency of antileprosy treatment
• Detecting viability of bacilli during Rx
Histamine test
• Very reliable method to detect at an early stage
• Peripheral N damage d/t leprosy  flare response is lost if peripheral N is
damaged
Morphological index response to Rx/drug
resistance/ disease activity/
• Percentage of solid staining bacilli in a stained smear to total no of
bacilli
Live bacilli  solid stained
Dead bacilli Fragmented
Bacteriological index  density of bacilli in
stained smear
Downgrading reaction
• In untreated patients and in 3rd trimester of pregnancy
• Clinically mimic reversal reaction
Lepromin test  to detect CMI / Test for prognosis
Early or Fernandez reaction
• after 48 hours of injection
• Erythema & induration >10 mm
is +ve
• Delayed hypersensitivity
reaction to soluble constituents
Late or Mitsuda reaction
• After 3 weeks
• Nodule > 5 mm is +ve
• indicates CMI to bacillary
component of Ag of lepra bacilli
Mitsuda lepromin / Dharmendra lepromin antigen intradermally
Lepromatous leprosy
• CMI ↓↓
• lepromin test negative
• Bacillary load ↑↑
• Temperature and pain lost first >>
Hypoaesthesia is a late sign
• Ulnar N most common >>low median
>posterior tibial>
• Radial N is involved last  serious
• Acral,distal,symmetric anaesthesia
common
• M.leprae PGL-1(phenolic glycolipid)
ab +
Lepromatous leprosy
b/l symmetrical multiple lesions
Lion with out teeth
• Leonine facies
• Atrophy of anterior nasal spine  collapse of nose
• Alveolar resorption Loosening of teeth
• Loss of eye brow
Lepromatous leprosy
• Clear sub epidermal free grenz zone
• Virchow or lepra cells
• Foamy macrophages laden with acid
fast bacilli
• Intracellular bacilli in spheroidal
masses (globi)
• Epitheliod and giant cells are not seen
(absence of CMI)
Globi in LL/ AFB forming spherical cluster
Lucio phenomenon
• Characterised by arteritis and
ulcers on legs is limited to
patients with diffuse non
nodular lepromatous leprosy
• Mexico and carribean only
Histoid leprosy
• Type of LL
• Shiny cutaneous and subcutaneous
nodules
• Caused by drug resistant lepra bacilli
• In b/w skin appears normal
Tuberculoid leprosy (most common type of
leprosy in INDIA and Africa
• CMI ↑↑
• Lepromin +ve
• Bacillary load ↓↓
• Skin lesions anaesthetic early
• One or few sharply defined
annular asymmetric macules or
plaques with a tendency towards
central clearing , elevated border
Tuberculoid leprosy histopathology
• Noncaseating granuloma with
epitheliod and giant cells
Grenz zone involved in TL
Indeterminate leprosy
• Bacteriologically negative
• One or two vague hypopigmented macules
• Definite sensory impairement
Borderline Tuberculoid
• SATellite lesions
• Nerve Abscess (mainly ulnar nerve abscess)
• Rx with I & D
• SANTA BanTa
SATellite lesions
Borderline leprosy (BL)
• Inverted saucer shaped ulcers
• All kinds of bizzare lesions in single
patient distributed asymmetrically
• Epitheliod cells +
Treatment
• Chaulmoogra oil
• First effective antileprosy Rx
• Form Myanmar
• MDT is used since 1982
• Not C/I in HIV infected patients and is safe in pregnancy
• Rifampicin  highly bactericidal and most effective against M leprae
• Dapsone is bacteriostatic
Blister packets for MDT
Regimen Duration Surveillance
Paucibacillary • Rifampicin 600mg
once a month (under
supervision)
• Dapsone 100mg (daily
self administered)
6 months 2 years
Multibacillary • rifampicin 600mg once
a month
• Clofazimine 300mg
once a monthor
Clofazimine 50 mg
daily
• Dapsone 100mg daily
self administered
12 months 5 years
Treatment of single lesion leprosy
• ROM regimen
• Rmp
• Ofloxacin
• Minocycline
• ROM -6 (Monthly for 6 months) - Paucibacillary
• ROM -12 (Monthly for 12 months) – Multibacillary
Dapsone
• Bacterostatic
• Metabolized by acetylation
Uses
• Dermatitis
herpetiformis
• Actinomycetoma
• Rhinosporidiosis
• P. jiroveci
s/e
• Hemolytic anemia (mc)
• Methaemoglobinemia
• Hypermelanosis
• Hepatitis
• Agranulocytosis
• IMN like syndrome
• Peripheral neuropathy
Clofazimine
• Dye with bacteriostatic action
• Interfering with template function
• Antiinflammatory action
• Used in lepra reaction
• s/e
• Discolouration of skin & body secretions
• Icthyosis of skin
Lepra reactions
Type 1 (reversal)
• Borderline type of leprosy (BT,BB,BL)
• In 1st month or yr after Rx initiation
• Sudden increase in effective CMI in
reponse to rapid killing of bacilli
• Type IV
• a/c tenderness and swelling at the site
of skin or nerve lesion
• a/c neuritis  wrist drop
• Rx
• Mild  NSAIDS
• Severe  high dose glucocorticoid
Type 2 (erythema nodosum leprosum)
• In lepromatoum leprosy and also in BL
• With in 2 years of RX
• d/t activation of t helper cells
• Type III HS (arthus reaction)
• Tender inflamed subcutaneous nodules
• Rx
• Glucocorticoids
• Thalidomide (DOC)
• Cloazimine
• Aspirin
Type 1 reaction (down grade & reversal ) Type 2 reaction(erythema nodosum leprosum)
Borderline leprosy (BB BT BL) Lepromatous leprosy
Type IV hypersensitivity Type III reaction
• Before initiation of antileprotic Rx  downgrade
• After initiation of antileprotic Rx reversal
• Follows institution of antileprotic treatment
signs of inflammation in previously involved macule
papule or placque
Neuritis  ulnar nerve is most commonly involved
Crops of resh painful erythematous papules or
nodules
No systemic features Systemic features fever joint pain hepatitis
• TNF α PLAYS IMPORTANT ROLE IN TYPE 2
Rx
• Glucocorticoid along with continuation of
antileprotic drugs
• NO ROLE FOR THALIDOMIDE
Rx
• MILD  NSAID
• SEVERE  GLUCOCORTICOIDS IF IT FAILS
THALIDOMIDE 200-300MG
Erythema nodosum leprosum
• Thalidomide  DOC
Dapsone
• Bacteriostatic
• 1-2 mg/kg
• Half life >24 hours
• s/e
• Hemolutic anemia
• Methaemoglobinemia
• c./I
• Hb <7
• G6PD deficiency
clofazimine
• Dye with leprostatic and anti inflammatory property
• s/e
• Reddish brown discolourarion of exposed parts
• Hair and body secretions
• Dry & itchy skin
New drugs
• Rifapentine
• Most effective
Staphylococcal scalded skin syndrome
• Newborns and children
• vary from localized blister formation to exfoliation of much of the skin
surface
• constitutional symptoms, including fever, lethargy, and irritability with poor feeding.
• Exfoliative toxin of staph aureus
• Nikolsky's sign +ve
• The skin is usually fragile and often tender, with thin-walled, fluid-filled bullae.
Gentle pressure results in rupture of the lesions, leaving denuded underlying skin
• The mucous membranes are usually spared.
• Significant amounts of fluid can be lost in more extensive cases.Illness
usually follows localized infection at one of a number of possible sites. SSSS
is much less common among adults but can follow infections caused by
exfoliative toxin–producing strain
SSSS
• Most severe form
• Ritters d/s in new born
• TEN in older people
• Milder and most form of SSSS
• Pemphigus neonatorum (neonatorum)
• Bullus impetigo(children & adults)
SSSS
• STERILE BULLAE (as it is caused by toxin)
• Potato chip peeling
Tubercular infections of skin
PAUCI BACILLARY
• LUPUS VULGARIS
• TUBERCULOUS VERRUCA
CUTIS
MULTIBACILLARY
• SCROFULODERMA
• TUBERCULOUS CHANCRE
• TUBERCULOUS GUMMA
TUBERCULID(ANAPHYLATIC)
• LICHEN SCROFULOSUM
• BASINS DS
• NODULAR TUBERCLE
Lupus vulgaris
• Mc form of skin TB
• Females >>males
• Seen in previously infected /sensitized
patients
• a/w underlying active TB in lung or LN
• More common in head and neck
• Red brown plaques
• Apple jelly nodule on diascopy
• Scarring & SCC can develop
• Lupus vorax
• Cartilage of nose and ears is progreesively
destroyed
CENTRAL SCARRING &
PERIPHERAL EXTENSION
Lupus vulgaris  mc skin tb in ADULTS
• Single erythematous annular plaque slowly increase in size over
decades central scarring
• Match stick test is positive
• For demonstrating apple jelly nodules
• Gentle pressure applied it penetrates and on with drawal a drop of blood appears
Scrofuloderma
• Mc in children
• Skin TB extension from
underlyingtuberculous focus
• Infected LN ,muscles or bones
Buruli ulcer
• Mycobacterium ulcerans
• Penetrating skin trauma c/c painless  heals spontaneously
• c/c lymphoedema and disfiguring scarring
Tuberculids
• Symmetric generalised exanthems in skin of tuberculous patients
• Hypersensitivity reactions to tubercle bacillus
• Strongly +ve mantoux test
• Tuberculous involvement of ( usually inactive ) of visera or LN
• Absence of M tuberlosis bacilli in tissue by culture or smear
• Satisfactory therapeutic response of skin lesions to ATT
• 3 entities are accepted as tuberculids /definite/true tuberculid
• Papulonecrotic tuberculid
• Lichen scrofulosum
• Erythema induratum (bazins d/s)
• Facultative tuberculoids
• Erythema nodosum
• Erythema induratum
• Non tubeculids
• Lichenoid tuberculid
• Rosacea like tuberculid
• Lupus miliaris disseminates faciei
Swimming pool or fish tank granuloma
• M .marinum
• After contact with tropical fish
tank/swimming pool/salt water fish
• At the site of trauma  A small violet
nodule lymphangitic spread in a
sporotrichiod fashion
Tuberculous chancre
• Skin TB in person with no previous
infection and immunity
• Usually in children  follows injury
• Firm non healing shallow
• Undermined ulcer with a
granulomatous base a/w painless
regional lymphadenopathy
Tuberculosis verucca cutis
• Anatomist wart/post mortem
wart/prosecutors wart
• In previously infected individuals
with high degree of immunity
• Handling of infected
sputum/material MC seen on
hands and legs
• no regional lymphadenopathy
ERYTHEMA INDURATUM
• PAINFUL NODULES OVER BACK OR SIDES OF LEGS OF YOUNG WOMEN

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Bacterial cutaneous infection DERMATOLOGY REVISION NOTES

  • 2. Erysipelas • a/c inflammation of lymphatics • Grp A beta haemolytic streptococcus pyogenes • Malar area of face & lower extremities • Regional lymphadenopathy + • Recurrent erysipelas 2* to lymphedema • Staphylococcus aureus Skin trauma Inoculation of bacteria Fiery red , indurated tense shiny plaque with raised sharply demarcated advancing margins Erysipiliod  caused by eryspilothrix acquired from fish bone
  • 3.
  • 4. Milian’s ear sign in erysipelas  can involve ear lobule but not in case of cellulitis
  • 5. ERYSIPELAS CELLULITIS CAUSATIVE AGENT GROUP A BETA HEMOLYTIC STREPTOCOCCUS STRAPH & STREPT BORDERS SHARP DIFFUSE LYMPHANGITIS MORE COMMON LESS COMMON TOXICITY LESS MORE
  • 6. Scarlet fever • Grp A beta haemolytic streptococci • Pyogenic exotoxin A,B,C • Most common in children 2- 10 years usually following streptococcal pharyngitis
  • 7.
  • 8.
  • 9. Pastia’s lines in scarlet fever • Accentuation of linear erythema in skin folds
  • 10.
  • 13. Impetigo contagiosum(non bullous) • Grp A beta haemolytic streptococci >> staph aureus • Mc infection in Preschool /young children • Face,especially around mouth and nose • Thin walled blisters on erythematous base rupture immediately  honey coloured crust • Lesions spread with out central clearing • Lymphadenopathy • Complications • Scarlet fever, erysiplelas, cellulitis,post streptococcal GN Gloden yellow honey coloured crust
  • 14. Bullous impetigo • Coagulase positive group II S aureus • Neonates and infants • Face and other parts of body • Thick walled persistent blisters on bland skin rupture slowlyvarnish like crust • Lesions heal in centre to form annular patches • Complications • Ssss ,pemphigus neonatorum,cellulitis,lymphangitis
  • 15.
  • 16. • Rx • FUSIDIC ACID • MUPIROCIN • RETAPAMULIN • SYSTEMIC • DICLOXACILLIN • ERYTHROMYCIN • CEPHALOSPORIN
  • 18. Ecthyma • Vesicle or vesicopustule • Deep infection of skin d/t Gp A streptococci • Which involves extra follicular portion (i.e hair follicles spared) • Post streptococcal GN can develop • Involves LL • MC : buttocks , thigh and legs
  • 19. • STAPH + STREPTECTHYMA PYOGENICUM • PSEUDOMONAS AERUGINOSAECTHYMA GANGRENOSUM • PARAPOX VIRUS • ZOONOSES FROM SHEEP & GOAT ECTHYMA CONTAGIOSUM
  • 20. Ecthyma gangrenosum • Skin manifestation of Ps aeruginosa bacteremia • In critically ill immunocompromised neutropenic patients • Lesions • Haemorrhage necrosis surrounding erythema • In gluteal or perineal region • Early lesion to necrosis in 12 hrs • Rx • Antipseudomonal Ab
  • 21. Sycosis barbae • Staph aureus infection of beard deep infection of hair follicles
  • 22. Sycosis nuchae • Deep infection of hair follicle caused by staph aureus  scarring  acne keloid nuchalis
  • 23. CORYNEBACTERIUM INFECTION • PITTED KERATOLYSIS • CAUSED BY • CORYNEBACTERIUM DERMATOPHILUS CONGOLENSIS • MICROCOCCUS • MULTIPLE SHALLOW PIT ON PALM & SOLES • IN PATIENTS WITH HYPERHIDROSIS DISHWASHERS
  • 24. CORYNEBACTERIUM INFECTION • TRICHOMYCOSIS AXILLARIS • AFFECT AXILLARY HAIR • YELLOWISH NODULES  UNDIGESTED KERATIN
  • 25. Erythrasma • c/c superficial infection of skin with mild patches in axillae , groins ,toes and ankles • Well demarcated brown red macular patches • Corynebacterium minutussimum • Lipophilic G +ve aerobic di • Produces porphyrin's coral red fluresecence • Doc : erythromycin ,clarithromycin coral red fluresecence
  • 26. Leprosy / hansens disease Mycobacterium leprae
  • 27. Cardinal signs of leprosy • Hypopigmented or erythematous skin lesions with definite loss of sensation • Involvement of peripheral nerves  definite thickening • Skin smear  AFB
  • 28. M leprae • Less acid fast than M tuberculae (hence 5 % H2SO4 or 1% HCl is used) • Obligate intracellular bacillus • Can remain viable 1- 7 days • pRopagation is limited to armadillo,mouse foot pad,nude mice • Generation time 12-13 days • First bacillus to be associated with human disease • Modifies fite stain • In tissue sections • Portal of entry  skin and respiratory tract • Chief mode of exit  nasal mucosa of untreated LL patients • Modes of transmiision • Droplets >>contact>breast milk>transplacental>insect vectors
  • 29. • Schwaan cells are first cell to be involved in leprosy
  • 30. Leprosy • Grows better in cooler places • Skin • PNS • URT • Eyes • Testis • Spares warmer areas of axilla groin scalp midline back ovaries lung & CNS
  • 31.
  • 32. • The Ridley Jopling classification • Indeterminate • Tuberculoid • Borderline: • borderline-tuberculoid, • borderline-borderline, • borderline-lepromatous • Lepromatous
  • 33. Indian classification (by indian leprosy association) Most common type in india is tuberculoid (TT)
  • 34. WHO Classification  treatment Paucibacillary • 1-5 lesion • No nerve or only one nerve • Skin smears –ve at all sites Multibacillary • > 5 lesions • > 1 nerve irrespective of skin lesions • Skin smears + at all sites
  • 35.
  • 36. • Pure neuritic (indian classification) • Asymmetric nerve involvement with no skin lesion and usually of tuberculoid origin • Painless trophic ulcers In neuritic type skin biopsy is negative
  • 37.
  • 38.
  • 39. Indeterminate leprosy tuberculoid leprosy TT Borderline tuberculoid Borderline lepromatous Lepromatous leprosy Peripheral neuritic Vague solitary assymetrical Usually single raised lesion with well defined & partly ill defined borders & numb when touched Inverted saucer shaped lesion or punched out Small erythematous patches & macules Number Solitary Solitary Satellite lesions Many Innumerable AFB Nil Nil Nil / scanty + + Nerve Local nerve thickened Local nerve thickened Symmetrical nerve thickened Symmetrical Nerve thickening is a late feature Sensory loss Definite sensory loss Definite sensory loss Less definite sensory loss on patches Late glove & stocking anesthesia h/p Epitheliod granuloma in dermis reaching up to ddermis Absent ghrenz zone Many epitheliod granuloma in dermis Ghrenz zone + Diffe Ghrenz zone + Onion peel perineurium Diffuse infiltration with foamy macrophages  virchows lepra cells Ghrenz zone +
  • 40. Diagnosis • Skin smears • 7 in number • 4 from skin lesion • 2 from ear lobes • 1 from nasal swb • Nerve biopsy is taken from sural nerve
  • 41. • Bacilli are absent in lungs , ovaries and CNS • Most common cranial nerve to get involve is VII • Goll & burdech tract  proprioception • Not involved in leprosy • Other organs involved in leprosy are • Eyes • Iritis • Corneal beading • Testes • Muscles • Myopathy , wasting
  • 42. Mouse foot pad culture • Detect drug resistance • Evaluating potency of antileprosy treatment • Detecting viability of bacilli during Rx
  • 43. Histamine test • Very reliable method to detect at an early stage • Peripheral N damage d/t leprosy  flare response is lost if peripheral N is damaged
  • 44. Morphological index response to Rx/drug resistance/ disease activity/ • Percentage of solid staining bacilli in a stained smear to total no of bacilli Live bacilli  solid stained Dead bacilli Fragmented
  • 45. Bacteriological index  density of bacilli in stained smear
  • 46. Downgrading reaction • In untreated patients and in 3rd trimester of pregnancy • Clinically mimic reversal reaction
  • 47. Lepromin test  to detect CMI / Test for prognosis Early or Fernandez reaction • after 48 hours of injection • Erythema & induration >10 mm is +ve • Delayed hypersensitivity reaction to soluble constituents Late or Mitsuda reaction • After 3 weeks • Nodule > 5 mm is +ve • indicates CMI to bacillary component of Ag of lepra bacilli Mitsuda lepromin / Dharmendra lepromin antigen intradermally
  • 48. Lepromatous leprosy • CMI ↓↓ • lepromin test negative • Bacillary load ↑↑ • Temperature and pain lost first >> Hypoaesthesia is a late sign • Ulnar N most common >>low median >posterior tibial> • Radial N is involved last  serious • Acral,distal,symmetric anaesthesia common • M.leprae PGL-1(phenolic glycolipid) ab +
  • 50. Lion with out teeth • Leonine facies • Atrophy of anterior nasal spine  collapse of nose • Alveolar resorption Loosening of teeth • Loss of eye brow
  • 51. Lepromatous leprosy • Clear sub epidermal free grenz zone • Virchow or lepra cells • Foamy macrophages laden with acid fast bacilli • Intracellular bacilli in spheroidal masses (globi) • Epitheliod and giant cells are not seen (absence of CMI)
  • 52.
  • 53. Globi in LL/ AFB forming spherical cluster
  • 54. Lucio phenomenon • Characterised by arteritis and ulcers on legs is limited to patients with diffuse non nodular lepromatous leprosy • Mexico and carribean only
  • 55. Histoid leprosy • Type of LL • Shiny cutaneous and subcutaneous nodules • Caused by drug resistant lepra bacilli • In b/w skin appears normal
  • 56. Tuberculoid leprosy (most common type of leprosy in INDIA and Africa • CMI ↑↑ • Lepromin +ve • Bacillary load ↓↓ • Skin lesions anaesthetic early • One or few sharply defined annular asymmetric macules or plaques with a tendency towards central clearing , elevated border
  • 57. Tuberculoid leprosy histopathology • Noncaseating granuloma with epitheliod and giant cells
  • 59. Indeterminate leprosy • Bacteriologically negative • One or two vague hypopigmented macules • Definite sensory impairement
  • 60. Borderline Tuberculoid • SATellite lesions • Nerve Abscess (mainly ulnar nerve abscess) • Rx with I & D • SANTA BanTa SATellite lesions
  • 61. Borderline leprosy (BL) • Inverted saucer shaped ulcers • All kinds of bizzare lesions in single patient distributed asymmetrically • Epitheliod cells +
  • 62. Treatment • Chaulmoogra oil • First effective antileprosy Rx • Form Myanmar • MDT is used since 1982 • Not C/I in HIV infected patients and is safe in pregnancy • Rifampicin  highly bactericidal and most effective against M leprae • Dapsone is bacteriostatic
  • 64. Regimen Duration Surveillance Paucibacillary • Rifampicin 600mg once a month (under supervision) • Dapsone 100mg (daily self administered) 6 months 2 years Multibacillary • rifampicin 600mg once a month • Clofazimine 300mg once a monthor Clofazimine 50 mg daily • Dapsone 100mg daily self administered 12 months 5 years
  • 65. Treatment of single lesion leprosy • ROM regimen • Rmp • Ofloxacin • Minocycline • ROM -6 (Monthly for 6 months) - Paucibacillary • ROM -12 (Monthly for 12 months) – Multibacillary
  • 66. Dapsone • Bacterostatic • Metabolized by acetylation Uses • Dermatitis herpetiformis • Actinomycetoma • Rhinosporidiosis • P. jiroveci s/e • Hemolytic anemia (mc) • Methaemoglobinemia • Hypermelanosis • Hepatitis • Agranulocytosis • IMN like syndrome • Peripheral neuropathy
  • 67. Clofazimine • Dye with bacteriostatic action • Interfering with template function • Antiinflammatory action • Used in lepra reaction • s/e • Discolouration of skin & body secretions • Icthyosis of skin
  • 68. Lepra reactions Type 1 (reversal) • Borderline type of leprosy (BT,BB,BL) • In 1st month or yr after Rx initiation • Sudden increase in effective CMI in reponse to rapid killing of bacilli • Type IV • a/c tenderness and swelling at the site of skin or nerve lesion • a/c neuritis  wrist drop • Rx • Mild  NSAIDS • Severe  high dose glucocorticoid Type 2 (erythema nodosum leprosum) • In lepromatoum leprosy and also in BL • With in 2 years of RX • d/t activation of t helper cells • Type III HS (arthus reaction) • Tender inflamed subcutaneous nodules • Rx • Glucocorticoids • Thalidomide (DOC) • Cloazimine • Aspirin
  • 69. Type 1 reaction (down grade & reversal ) Type 2 reaction(erythema nodosum leprosum) Borderline leprosy (BB BT BL) Lepromatous leprosy Type IV hypersensitivity Type III reaction • Before initiation of antileprotic Rx  downgrade • After initiation of antileprotic Rx reversal • Follows institution of antileprotic treatment signs of inflammation in previously involved macule papule or placque Neuritis  ulnar nerve is most commonly involved Crops of resh painful erythematous papules or nodules No systemic features Systemic features fever joint pain hepatitis • TNF α PLAYS IMPORTANT ROLE IN TYPE 2 Rx • Glucocorticoid along with continuation of antileprotic drugs • NO ROLE FOR THALIDOMIDE Rx • MILD  NSAID • SEVERE  GLUCOCORTICOIDS IF IT FAILS THALIDOMIDE 200-300MG
  • 70. Erythema nodosum leprosum • Thalidomide  DOC
  • 71. Dapsone • Bacteriostatic • 1-2 mg/kg • Half life >24 hours • s/e • Hemolutic anemia • Methaemoglobinemia • c./I • Hb <7 • G6PD deficiency
  • 72. clofazimine • Dye with leprostatic and anti inflammatory property • s/e • Reddish brown discolourarion of exposed parts • Hair and body secretions • Dry & itchy skin
  • 74. Staphylococcal scalded skin syndrome • Newborns and children • vary from localized blister formation to exfoliation of much of the skin surface • constitutional symptoms, including fever, lethargy, and irritability with poor feeding. • Exfoliative toxin of staph aureus • Nikolsky's sign +ve • The skin is usually fragile and often tender, with thin-walled, fluid-filled bullae. Gentle pressure results in rupture of the lesions, leaving denuded underlying skin • The mucous membranes are usually spared. • Significant amounts of fluid can be lost in more extensive cases.Illness usually follows localized infection at one of a number of possible sites. SSSS is much less common among adults but can follow infections caused by exfoliative toxin–producing strain
  • 75.
  • 76.
  • 77.
  • 78. SSSS • Most severe form • Ritters d/s in new born • TEN in older people • Milder and most form of SSSS • Pemphigus neonatorum (neonatorum) • Bullus impetigo(children & adults)
  • 79.
  • 80. SSSS • STERILE BULLAE (as it is caused by toxin) • Potato chip peeling
  • 82. PAUCI BACILLARY • LUPUS VULGARIS • TUBERCULOUS VERRUCA CUTIS MULTIBACILLARY • SCROFULODERMA • TUBERCULOUS CHANCRE • TUBERCULOUS GUMMA TUBERCULID(ANAPHYLATIC) • LICHEN SCROFULOSUM • BASINS DS • NODULAR TUBERCLE
  • 83. Lupus vulgaris • Mc form of skin TB • Females >>males • Seen in previously infected /sensitized patients • a/w underlying active TB in lung or LN • More common in head and neck • Red brown plaques • Apple jelly nodule on diascopy • Scarring & SCC can develop • Lupus vorax • Cartilage of nose and ears is progreesively destroyed
  • 85. Lupus vulgaris  mc skin tb in ADULTS • Single erythematous annular plaque slowly increase in size over decades central scarring • Match stick test is positive • For demonstrating apple jelly nodules • Gentle pressure applied it penetrates and on with drawal a drop of blood appears
  • 86. Scrofuloderma • Mc in children • Skin TB extension from underlyingtuberculous focus • Infected LN ,muscles or bones
  • 87. Buruli ulcer • Mycobacterium ulcerans • Penetrating skin trauma c/c painless  heals spontaneously • c/c lymphoedema and disfiguring scarring
  • 88. Tuberculids • Symmetric generalised exanthems in skin of tuberculous patients • Hypersensitivity reactions to tubercle bacillus • Strongly +ve mantoux test • Tuberculous involvement of ( usually inactive ) of visera or LN • Absence of M tuberlosis bacilli in tissue by culture or smear • Satisfactory therapeutic response of skin lesions to ATT • 3 entities are accepted as tuberculids /definite/true tuberculid • Papulonecrotic tuberculid • Lichen scrofulosum • Erythema induratum (bazins d/s)
  • 89. • Facultative tuberculoids • Erythema nodosum • Erythema induratum • Non tubeculids • Lichenoid tuberculid • Rosacea like tuberculid • Lupus miliaris disseminates faciei
  • 90. Swimming pool or fish tank granuloma • M .marinum • After contact with tropical fish tank/swimming pool/salt water fish • At the site of trauma  A small violet nodule lymphangitic spread in a sporotrichiod fashion
  • 91. Tuberculous chancre • Skin TB in person with no previous infection and immunity • Usually in children  follows injury • Firm non healing shallow • Undermined ulcer with a granulomatous base a/w painless regional lymphadenopathy
  • 92. Tuberculosis verucca cutis • Anatomist wart/post mortem wart/prosecutors wart • In previously infected individuals with high degree of immunity • Handling of infected sputum/material MC seen on hands and legs • no regional lymphadenopathy
  • 93. ERYTHEMA INDURATUM • PAINFUL NODULES OVER BACK OR SIDES OF LEGS OF YOUNG WOMEN