Bacterial skin infection

• The population of micrococaceae per square cm of

the skin has been estimated as;
600 for hands
60 for forearms
300 for scapular region
500000 to 10,00,000 in the axilla.
• Total anaerobic organism is about
1.46 X 10.6 for the scalp
2.41 X 10.6 for the axilla
 NORMAL SKIN FLORA
CLASS ORGANISM LOCATION ON BODY
AEROBIC COCCI • Staph Epidermidis All body sites, especially
• Staph Hominis intertriginous
• Staph Luteus,
Micrococcus
AEROBIC CORYNEFORM • Corynebacterium Intertriginous
minutissimum
• Corynebacterium xerosis
ANAEROBIC CORYNEFORM • Propionibacterium Sebaceous glands and
acnes follciles
• P.avidum
• P.Granulosum

GRAM NEGATIVE • Acenitobacter sp Intertriginous

YEAST • Pityrosporum ovale Skin rich in sebaceous
• orbiculare glands ( scalp, upper
chest and back)
• Staph aureus: not a resident flora but may be
found in
– Nares: 30%
– Perineum: 20%
– Axillae & toe web : 10%
– Atopic skin: 90%
 Diseases caused by Staph aureus
• 1. Direct • 2. Dry infection
– Impetigo • 3. Toxins
– Ecthyma – Bullous impetigo
– Sup. Folliculitis – SSSS
– Sycosis vulgaris – TSS
– Furuncle – Staph scarlatina
– Carbuncle • 4.Botyromycosis
– Abscess
• 5. Pyoderma vegetans
– Pyomyositis
 PYODERMAS
• purulent skin disease
PYODERMAS
PRIMARY SECONDARY

SUPERFICIAL DEEP

FOLLICULAR NON NON

FOLLICULAR
FOLLICULAR
FOLLICULAR

• SYCOSIS
• FOLLICULAR • ECTHYMA
BARBAE
IMPETIGO • CELLULITIS
• FURUNCLE • ERYSIPELAS
• CHRONIC IMPETIGO • PARONYCHIA
FOLLICULITIS OF • NECROTIZING
• CARBUNCLE
LEG FASCITIS
 SECONDARY
PYODERMAS

SECONDARY FOLLICULITIS- acne conglobata

hidradenitis suppurativa
dissecting cellulitis of scalp
acne keloidalis
pyoderma vegetans
infected eczemas
intertrigo
infected ulcers
CUTANEOUS INVOLVEMENT IN SYSTEMIC BACTERIAL DISEASES:
in bacteremia & bacterial endocarditis
 PRIMARY PYODERMAS
• Staph aureus (major)
• Streptococcus pyogenes
• Other groups of strep
• Pneumococci
• CoNS
• enterococci
 IMPETIGO
• Highly contagious superficial pyoderma
• In pre school and young school age children (school sores)
• Over crowding, poor hygiene, existing skin disease
(scabies), in healthy subjects also
• Summer months
• Staph > strep
• Incubation period :1-3 days (strep)
4-10 days (staph)
• M=F
2 types: bullous & non bullous impetigo

NON BULLOUS IMPETIGO

• More common (70%)
• Vesicle/pustules----
------ honey colored
crusted plaque
• Heal without scarring
• Staph aureus > strep pyogenes
 Clinical features
• Thin walled vesicle on an erythematous base

• Vesicles ruptures rapidly

• Exuding serum dries : yellowish brown crusts

(thicker & dirtier in strep form)

Irregular peripheral extension occurs without central

clearing, multiple lesions may coalase

Crust dries & seperates to leave erythema , that fades

without scarring
• Sites involved: face (esp around nose & mouth
limbs
• Scalp affected in tinea capitis
• Lesions can be anywhere in children with
atopic eczema / scabies
• Mucous membarne involvement is rare
• Spontaneous resolutiuon in 2-3 weeks
• Prolonged course underlying
 BULLOUS IMPETIGO
Staph aureus : phage group 2 type 71
• Painless flaccid bullae and moist erosions with surrounding
erythema
• Bullae spread peripherally with central clearing ( impetigo circinata)
• Organism can be cultures from the blister fluid
• Pathophysiology:
Exfoliative toxin (epidermolytic toxin ) in the blister fluid--------
trypsin like serine protease----- cleave desmoglein 1
ET A & B acts as superantigen --------stimulate B & T cells to
proliferate
• Localisation of epidermal splitting in bullous
impetigo

• d/t local production of toxin

(in SSSS: toxin is disseminated
haemetogenously)
 Clinical features
• Bullae are less rapidly ruptured
• Becomes larger (1-2 cm )
• Persist for 2-3 days
• Contents: clear----cloudy
• Thin , flat brownish crusts formed
• Central clearing and peripheral extension gives rise to circinate pattern
• Face is often affected
• Lesion occurs nywhere , may be widely & irregularly distributed
• Favours sites of existing skin disease (miliaria, trivial injuries)
• Buccal mucous membrane may be involved
• Regional adenitis is rare
 Histopathology
• Subcorneal blister with occasional
acantholytic cells
• Blister cavity : neutrophils
• Upper dermis: mixed perivascular
inflammatory inflitrates of neutrophils and
lymphocytes
 DD
• Immuno bullous diseases
• Localised SSSS
• Contact dermatitits( irritant / allergic)
• Herpes simplex infections
• Self limiting
• Resolves within days to weeks

• Spread to other close contacts

• Relapse is frequent with individual with
underlying skin diseases & staphylococcal
carriers
 complications
• Osteomyelitis
• Septic arthritis
• Pneumonia
• septicemia
• Glomerulonephritis
• Lymphangitis
• Suppurative lymphadenitis
• Guttate psoriasis
• Scarlet fever
• Streptococcal strains : M group 2,49,53,55-57,
60

post streptococcal glomerulonephritis

18-21 days latent period
(10 days latent period following pharyngitis)
 investigations
• Culture and sensitivity
 Treatment
• Topical: fusidic acid / mupirocin
disinfectants
Topical Ratapamulin is a relatively new
antibiotic
• If more extensive involvement, LNE
Systemic therapy is indicated:
flucloxacillin/ cloxacillin (first line)
erythromycin / clarithromycin (second line)
tetracyclines (third line)
 ECTHYMA
• Formation of adherent crusts beneath which ulceration occurs.
• Age group: extremes of ages
• Causative organism :
Streo. Pyogenes, Pseudomonas aeruginosa, staph
aureus
• Predisposing factors:
Damaged skin
immunocompromised
( HIV ,neutropenia)
Diabetes
outbreaks in military camps
Moist,humid enviornment
over crowding
• Pathology: infection and inflammation are deeper
ulceration -----heals with scarring
• Clinical features:
small bullae / pustules on an erythematous
base
crusting , increases in size
with an indurated base
crust is thicker ,
only removed with difficulty
purulent irregular ulcer
Sites: buttocks, leg, thighs
Few in number------------Autoinnoculation
• DD:- Pyoderma gangrenosum
Ecthyma gangrenosum
Tick bites
• Course: heals after a few weeks with scarring
• Investigations :
Gram stain
culture and sensitivity
 Management
• Improved hygiene, nutrition
• Treatment of scabies, underlying disease
• Antibiotics : should cover
strep pyogenes, staph aureus,
pseudomonas
• crust removed after soaking with disinfectant
• Topical: Fusidic acid/ Mupirocin
Sulconazole / miconazole cleared the
lesion in a wk
Oral antibiotics: given for 1-2 wks
if staph is suspected-----erythromycin,
clindamycin
doxycycline
if ecthyma gangrenosum: piperacillin, gentamycin, amikacin
ciprofloxacin, ofloxacin
 CELLULITIS & ERYSIPELAS
CELLULITIS ERYSIPELAS
• Acute / sub acute/ chronic • Infection of dermis and
inflammation of loose upper sub cutaneous tissue
connective tissue • Well demarcated
• Ill defined eythematous edematous browny
indurated plaque indurated plaque with
• Lower extremities elevated border
• Face and scalp
a) Erysipelas:
• Erysipelas is an acute bacterial infection of
the skin and subcutaneous tissues caused by
beta-hemolytic Streptococci.
• The commonest sites involved are the face
and extremities
• Prodromal symptoms
High fever, chills, headache, vomiting, andjoint pain.

• Skin manifestations
*The infection is usually predisposed by trauma to the skin.

*The lesion has sharply demarcated erythema which is

bright red & hot with bullae formation.

*Relapsing erysipelas damages the lymphatics and may lead

to permanent lymphoedema.
 cellulitis
• is acute bacterial infection of the skin and subcutaneous
tissue most often caused by streptococci or staphylococci

• Symptoms and signs: pain, rapidly spreading erythema, and

edema; fever may occur, and regional lymph nodes may
enlarge
•
• Risk factors include skin abnormalities (trauma, ulceration,
fungal infection, other skin barrier compromise due to
preexisting skin disease), which are common in patients with
chronic venous insufficiency or lymphedema.
• The skin is hot, red, and edematous, often
with surface appearance resembling the skin
of an orange (peau d'orange). The borders are
usually indistinct.
• Petechiae are common
• Cellulitis may mimic deep venous thrombosis
cellulitis
 Treatment
• First line :
flucloxacillin 500 mg Qid
clarithromycin 500mg BD
If more severe infection :
clindamycin 600mg 8 hourly IV
If strep infection: penicillin is the treatment of choice
Benzyl penicilin 600-1200mg 6 hourly in more severe
cases for 5 days
 FOLLICULITIS
• Infection of hair follicle
• Causative oraganism
Staph aureus
Micrococcus,
pityriosporum, ( immunoscompromised)
demodex species

klebsiella
enterobacter long term antibiotic
proteus treated acne vulgaris
Pseudomonas aeuroginosa: “Hot tub folliculitis”
• Superficial folliculitis :
1. Acute superficial folliculitis
( Bokharts impetigo)
2. Chronic folliculitis of the leg
3. Gram negative folliculitis
i. Post acne treatment
ii. Hot tub folliculitis
• Deep folliculitis
1. Sycosis barbae
2.furuncle
3. carbuncle
• Superficial pustular folliculitis
(follicular impetigo of Bokhart)
infection of ostia of hair follicle
dome shaped pustules at the orifice of the
follicle
•Caused by staph
aureus and affects
mainly extremities and
scalp.

•Topical steroids are a

common predisposing
factor.
 Treatment
• Hand washing is the single most important
behavioral modification in the prevention of
spread
• First line:
• cleanse the affected area once daily with an
antiseptic wash
• Avoid heavy occlusive ointment
• Topical antibiotics twice daily to the affected area
(fucidin/ mupirocin/ clindamycin 2%)
• Second line:
flucloxacillin, cloxacillin, cephalexin, clindamycin

• Third line :
tetracycline, erythromycin
Daily application of 6.25% aluminium chloride
hexahydrate in completely anhydrous ethyl alcohol
was reported to be very effective in chronic
folliculitis of unspecified origin (except scalp )
 Sycosis barbae
• :
subacute or chronic pyogenic infection of whole
depth of follicle
If the follicles are destroyed with clinically
evident scarring, the term lupoid sycosis or
ulerythema sycosiforme is applied.

Folliculitis decalvans : in the scalp

• Occur in males after puberty
• Staph aureus
• DD: pseudofolliculitis caused by ingrown hairs
tinea barbae
 Treatment
• First line:
topical therapy with antibiotics plus steroid
combination preparations
Consider letting beard grow
• Second line:
systemic antibiotics
oral retinoids
• Third line:
Laser hair removal
photodynamic therapy
 FURUNCLE
• Acute , infection of whole length of hair follicule along with peri
follicular area involvement
• Staph aureus
• Predisposing factors :
Malnutrition
Diabetes
immunosuppression
HIV
• lesions: tender erythematous follicular nodule----becomes
pustular and necrotic---heals after discharge of a necrotic core
with permanent scarring
 Carbuncle
• Deep infection of group of contiguous follicles
accompanied by intense inflammatory changes in
the surrounding and underlying connective tissue
including subcutaneous fat.
• Cluster of coalasing boils is connected to each
other under the skin
• Staph aureus
• Back of the neck, shoulder , hips and thighs
• Usually solitary
 Treatment
• Incision and drainage
or saucerization under local anaesthesia
• Flucloxacillin or any penicillinase resistant
antibiotic
 Necrotizing subcutaneous infection

• Necrotizing Fascitis:
 Usually occurs in diabetics and those with aterial insufficiency.
 Causative org.- strept pyogenes. Staph aureus and gram negative rods may
also be involved.
 Excessive collagenase production leads to dissolution of connective tissue.
 CLINICAL FEATURES- org gain entry at site of trauma… then there is diffuse
swelling limb… with appearnece of clear bulla which rapidly turns violaceous.
This rapidly progresses to frank gangrene and myonecrosis with shock and
organ failure.
 Very painful with high mortality.
 FOURNIER’S GANGRENE- variant occuring on the scrotum.
 Apart from antibiotic treatment, extensive surgical debridement is essential.
 SSSS
• Staphylococcal scalded skin syndrome
• Exfoliative dermatosis
• Children(<6yrs) , neonates
• Localised form: in older children and adults
• Associated diseases: renal failure
malignanacy, immunosuppresion, alcohol
abuse
• Trivial infection of skin-------------ET produced
against DG1-----------seperation of keratinocyte
(intraepidermal) btn granular and spinous layer
• Cell necrosis doesnot occur (unlike TEN)
• Bullous impetigo/ SSSS
• ET-B>ET-A
• Staph aureus all strains can cause SSSS
• CA-MRSA causes SSSS in Neonates
• Presentation: localised staph infection--------fever,
irritability and skin tenderness-------------widespread
erythematous skin eruptions ( flexures)----------
progressed to blister formation and nikolsky
positive----------painful erosions-------heal within 7-14
days
• Clinical variant: Localised SSSS
more in the flexures, axillae , groins , limb flexures
Healing of the localised form leaves wrinkled
desquamating skin with hyperpigmentation
• DD: TEN
no necrosis of cells
HPE:split in granular layer
Tzank : Number of epithelial cells with large nuclei
with no inflammatory cells
in TEN: few epthelial cells and many inflammatory
cells
Course of disease:
genrealised form: settles within few weeks
Localised form: may be prolonged with relapses
• Investigations:
Swabs & cultures from blister fluid : no growth
of organism
( isolated from original septic site)
• Typing of S. aureus
• PCR of toxin production
• Blood cultures: +ve (adults) rare in children
• ESR: may be elevated
• Management:
• Parenteral penicillinase resistant antibiotics:
Flucloxacillin
clindamycin ( either alone or in comb with
Rifampicin or tetracycline
tigecycline
daptomycin
If MRSA is suspected: Vancomycin or Tobramycin
• Mortality Rate :
children: 4 %
adult: 60%
 TOXIC SHOCK SYNDROME
• Serious life threatening disease
• Fever, acute erythema -desquamation, circulatory
shock, multisystem disease
• Toxins elaborated by : Staph aureus or strep pyogenes
• Super-absorbant tampons in 1970s
(15%death rate)
Incidence: rare, 1-17/100000 tampon users/annum
Age: MC in extremes of ages & in menstruating women (15-
40 yrs)
Mc in females
• Associated diseases:
Recent chicken pox infection,
cellulitis, necrotising fasciitis,Diabetes
HIV, malignancy, alcohol misuse.
Pathophysiology:
Toxic shock syndrome toxin 1
(staph enterotoxin F/ pyrogenic enterotoxin C)
Is the main bacterial mediator of the disease
• HPE: non specific features
perivascular lymphocytic infiltrate
dermal oedema
if blistering: sub epidermal
Presentation:
Acute onset fever , rash
vomiting diarrhoea followed by liver, kidney, muscle, CNS
involvement
Circulatory shock is rapid (Doesn’t not respond to IVF
management)----rapid onset
Acute renal impairment
Multiorgan failure
(GIT, renal, hepatic, CNS, muscular, hematological, mucous membrane)
Atleast 3 systems should be involved
Rash: wide spread macular erythema/ scarlantiniform/ papulopustular
• Oedema of hands and feets
• Generalised mucous membrane erythema:
conjunctiva
esophagus, vaginal bladder mucosa may ulcerate
Thromocytopenia : retiform pattern purpura at
the peripheries
Desquamation is highly characteristic
(10-21 days after onset,
confined to fingertips/ palmar or plantar/
generalised)
Reversible patchy alopecia/ telogen effluvium
Transverse ridging/ partial loss of nail
 DD
• Septic shock & other infections
• Kawaski disease
prolonged fever
cardiac involvement
generalised LNE
absence of peripheral shock

• Clostridium sordellii infection ( high mortality)

• Disease course
recover in 3 weeks if intense care is given
with prompt use of appropriate IV antibiotics
Mortality rate : 7%
 investigations
• Clinical Dx
• Blood cultures
• Microbiological swabs from wounds, vagina of
menstruating or postpartum women
• Routine investigation shows: raised creatinine
that precedes refractory hypotension
 Management
• First line
• IV clindamycin ( 600-900 mg TDS)
• Benzyl penicillin (2.4 -4.8g daily in 4divided
doses )
• Antibiotics continued 1-2 wks
• Second line
• For severe cases: IV Ig
• (initial 2g/kg, then 0.4g/kg for 4 days)
 BLISTERING DISTAL DACTYLITIS
• Group Beta hemolytic streptococci
• Distal phalanx
• 2-16 years of age
• Multiple bullae over volar aspects of hands and fingers
• Nail bed also may be involved
• Recurrent case is associated with ingrown toe nails
• DD:
Herpetic whitlow
bullous impetigo
pompholyx eczema
Investigation:
organism is cultured from blistering fluid
Treatment:
Flucloxacillin /cloxacillin (B lactamase resistant antibiotics)
Skin diseases related to coryneform bacteria

• 1. AV – propionibacterium acnes &

granulosum
• 2. Erythrasma- C. minutissimum
• 3. Trichomycosis axillaris
• 4. Pitted keratolysis
 ERYTHRASMA
• Chronic superficial skin infection caused by C. minutissimum.
• C/F
– 1. Classical form
• 2nd MC form
• Well defined, scaly, pink-brown spreading patches at flexures, groin,
intergluteal, axillae
– 2. Toe web infection
• MC form
• Scaling, fissuring & maceration
– 3. generalised form
• Least common
• Patches as in classical form at trunk & extremities
• Diagnosis : Wood’s lamp examination- coral red
flurescence

• Treatment
– 1. systemic : Erythromycin 250mg qid * 1week
single dose of 1g clarithromycin
– 2. Topical : antifungals and antibiotics
clotrimazole & miconazole
(for 2 weeks)
 Trichomycosis axillaris
• Bacterial infection of axillary hair by corynebacterium tenuis
characterised by presence of yellow, red or black concretions
on hair shaft.

• C/F : 1. Concretions surrounding hair shaft

2. Sweat is coloured ( stains clothes) & malodourus
(yellow (mc), black, red)
Treatment:
Use of an effective antiperspirant such as Aluminium chloride is
effective
 Pitted keratolysis
• Superficial skin infection caused by Corynebacterium

• C/F : 1. minute superficial pits & erosions usually on the

sole with minimum inflammation
2. Malodour
3. Hyperhidrosis
Treatment: Topical antifungal, antibiotics and
antiperspirant.
Treatment of hyperhidrosis usually brings the disease
under control (Botulinum toxin)
 ANTHRAX
• Zoonotic infection
• Humans: accidental host
• Caused by: Bacillus anthracis
gram positive nonmotile brick shaped organism
3 clinical forms
1. Cutaneous athrax (diract contact)
2. Wool sorters disease (inhalational anthrax)
3. Gastrointestinal anthrax
• Cutaneous anthrax( malignant pustules)

• Pruritic painless papules (within 10 days of inoculation)

------vesicle that ulcerate with a cental black
escharsurrounded by a ring of vesicle
• Regional lymphadenopathy present
• DD: milkers nodules
orf
• Investigation:
demonstration of bacilli in gram stain from the ulcer
• Treatment:
• Crytalline penicillin 12-24 million units in divided doses
• Alternative drugs:
ciprofloxacin
erythromycin
tetracycline
chloramphenicol
• Supportive corticosteroid therapy may be required in
case of extensive oedema
 BACILLARY ANGIOMATOSIS
• A/k/a epitheliod angiomatosis
• Friable angiomatous papules and nodules
• Caused by Bartonella hensae & bartonella quintana
• Reservoirs are cats &humans
• Adults (any age can be affected)
• AIDS / severe immunosuppression
• Skin lesion is follwed by symptomatic blood dissemination
of organism
• Bacteria enters RBCs a
• Stimulate angiogenesis ion the vascular endothelium
• Lesion appear solitary/ in crops
• Any site (mucosal surfaces also)
• Local LNE in common
• HPE:
lobular proliferation of small blood vessels
that contain swollen endothelial cells.
Contain granular material consist of clumps of
bacteria , seen with Warthin Starry stain
• DD:
kaposi sarcoma
pyogenic granuloma
cutaneous lymphomas
Complications:
bacillary peliosis (cyst like inflammatory structures
develop in internbal organs like liver
(endothelial cells lining these spaces contain large
number of organisms)
• Investigations:
HPE is characteristics: granular structures
containing bacilli seen with warthin starry stain
Cultures not done
PCR
Management
Doxycycline or erythromycin given (>8 weeks)
Relapses are common
MISCELLANEOUS
 BOTRYOMYCOSIS
• Actinophytosis
• Bacterial pseudomycosis

• Chronic granulomatous reaction to bacterial infection

• MC caused by staph aureus
• and rarely pseudomonas
• MC over the extremities, peri anal region
• Single or multiple abscesses of skin or sub cutaneous
tissue-----breaks down to form multiple discharging
sinuses
 DD
• Mycetoma
• Furunculosis
• Actinomycosis
 Investigations
HPE: presence of small clusters of micro
organism on biopsy
Methanamine silver stains is used to identify the
organsm (gram stain is ineffective)
Mixed inflammatory response seen in the
surrounding tissue
Microbiological Culture
 Treatment
Flucloxacillin or erythromycin
 ACTINOMYCETE INFECTION
• Actinomycis & Nocardiosis are the two
important infection
• Higher bacteria
• Uncommon infection
• Actinomyces: produce large granules
• Nocardia : partially acid fast
• Both form branching filaments
 ACTINOMYCOSIS
• Chronic spreading suppurative and granulomatous disease
• Actinomyces israelli
• Draining sinuses are formed ----sulphur granules are
discharged
• A/k/a lumpy jaw (cattle)
• Common in rural tropical areas and in agricultural workers
• Poorer dental hygiene
• Occur at any age (rare before 10 years)
• Males> females
• Pathogenic actinomyces are normal
inhabitants of the human mouth.
• Hence actinomycosis is endogenously
acquired
• Differs from mycetoma in being caused by
endogenous and anaerobic agents and having
no tendency to be confined to the extremities
• Trauma: site of entry
• Dental extraction: actinomycosis of jaw
•
• Pathology:
small abscesses / pus filled sinus tracts--------
organism forms granular colonies in the surrounding
tissue-------------delicate myceluial filaments radiates
(club shaped filaments /ray fungus)--------------
surrounded by inflammatory infiltrates……..breaks
down to form multiple fistulaes discharging pus
containing sulphur granules.
• Sulphur granules are lobulated masses of
intertwining filaments
 Causative organism
• Actinomyces israelii
• A.bovis
• A. naeslundii, A. meyeri, A. neuii,
• Arachnia propionica
• Bifidobacterium eriksonni
 Clinical variants
• Cervicofacial actinomycosis (MC)
• Thoracic actinomycosis
• Abdominal actinomycosis
• Primary cutaneous actinomycosis
• Pelvic actinomycosis
 DD
• Tuberculosis
• Syphilitic gummata
• osteomyelitis
 investigations
• HPE
• Cultures:
cultures of A.israelli appear after anerobic
incubation at 37 degC for 2-4 days on enriched
media (brain- heart infusion glucose agar) as white
glistening colonies
• Demonstartion of granules:
sulphur granules 1-2mm
Crushed and examined under microscope
• Sensitive to antibiotics against gram positive organism
• Therapy of choice:
long term penicillins
10-12 million penicillin per day in 2 divided dosesfor 30 -45
days
Followed by wide surgical excision of the infected tissue
and then 2-5 million units of penicillin given IM daily for
12-18 months (in severe case)
Or
5 million units of Penicillin V orally
 Second line
• Tetracycline derivatives
• Erythromycin
• Chloramphenicol
• imipenem
 NOCARDIOSIS
• Acute to chronic suppurative disease
• Caused by aerobic actinomycete Nocardia
• Primary infection is usually pulmonary
• Hematogenous spread to other organs
• CNS is frequently attacked
• Primary cutaneous Nocardiosis
& Mycetoma due to Nocardia spp
• Opportunistic pathogen
• Cause disease in people with
progressive chronic disease,
HIV/AIDS,
biologicals such as Anti TNF antibodies,
solid organ transplant recepient
Cushing syndrome
Diabetes
Cortocosteroids
• Causative organism :
N. asteroides : primary cutaneous nocardiosis
N. brasiliensis: actinomycetoma ( entry via a wound)
• In systemic nocardiosis, symptoms resemble
that of pulm. Tuberculosis
• Involvement of brain and meninges in 30%
cases
• Skin 30% cases
• Involvement of skin and S/C tissue produces
solitary or multiple abscesses which may
involve muscles and bones
 Investigations
• Pus / sputum smears:
stained by- gram stain , methanamine silver stain, acid fast
stain
Narrow branching hyphae which is only parially acid fast
• Treatment:
Co-trimoxazole
Alternatives: ampicillin
minocycline
Amikacin,
cefotaxime
linezolid
 DERMATOSES POSSIBLY
ATTRIBUTABLE TO BACTERIA
 Chancriform pyoderma
• Uncommon condition
• Children
• Necrotising reaction to a strain of staphylococcus aureus, by
minor trauma
• C/F: sharply marginated solitary ulcer ,sometimes exceeding size
more than 1 cm
• With an indurated base , bright red areola
• Regional LNE +
• DD: epithelioma, primary syphilis
primary tuberculosis, swimming pool granuloma
Management: antibiotics
 PYODERMA VEGETANS
• Uncertain etiology
• Epithelial hyperplasia & chronic granulomatous change
with eosinophils (in pustular form)
• A/K/A dermatitis vegetans
• Staph or strep usually isolated
• Lesions failed to respond to antibiotics alone
• Underlying conditions:
alcoholism, lymphoma,, ulcerative colitis
severe psoriatic arthritis
Response to heavy bacterial colonisation or epidermal
invasion in a person with defective immunity
Pustular variety: pyodermite vegetante of hallopeau
• Develop at any site
• Flexures more involved
• Hyperplastic plaque----- break down to form
erosion----------central clearing
• Oral invlovement: white plaques and pustules
• Lesion may heal sponatneously

• Poorly responds to antibiotics

• Corticosteriods appear to produce improvement
THANK YOU
• Superficial infection caused by Corynebacterium Minutissimum is called as:
a. Erysipelas
b. Cellulitis
c. Carbuncle
d. Erythrasma

• Penicillins are used as drug of choice in treatment of:

a. Folliculitis
b. Erysipelas
c. Pseudofolliculitis
d. furuncle
• Which of the following is true :
a. In Furuncle, site of infection is deeper than folliculitis
b. In folliculitis, curving of hair leads to inflamm rxn
c. Erysipelas is deeper than cellulitis
d. None of the above is true

• Inflamm around hair appendages is common pathogenesis in:

a. Folliculitis
b. Furuncle
c. None of the above
d. Both of the above
• Deeper structures are involved in:
a. Erysipelas
b. Cellulitis
c. Both of above
d. None of above

• Infections caused by coryneforms are all except:

a. Impetigo
b. Trichomycosis axillaris
c. Pitted keratolysis
d. Erythrasma
• Common causes of hidradenitis suppurativa are:
a. Staph aureus
b. Anaerobes
c. Strept. Pyogenes
d. Both a and b.

• Superficial folliculitis is:

a. Sycosis barbae
b. Bockhart impetigo
c. Sycosis nuchae
d. Both a and c
• A diabetic middle aged female presented with a tender erythematous
swelling with multiple pus discharging points over right thigh, most probable
dagnosis is:
a. Carbuncle
b. Furuncle
c. Folliculitis
d. Perifolliculitis