Bacterial Infections

Impetigo
Folliculitis
Erysipelas
Cellulitis
Leprosy
Normal microbial flora
 The term "normal microbial flora" denotes the
population of microorganisms that inhabit the skin and
mucous membranes of healthy normal persons.

 The skin and mucous membranes always harbor a

variety of microorganisms that can be arranged into
two groups:

(1) The resident flora consists of relatively fixed types of

microorganisms regularly found in a given area at a given
age;
 if disturbed, it promptly reestablishes itself.
(2) The transient flora consists of nonpathogenic or
potentially pathogenic microorganisms that inhabit the
skin or mucous membranes for hours, days, or weeks;

it is derived from the environment

does not produce disease
does not establish itself permanently on the surface
generally of little significance so long as the normal resident
flora remains intact.
However, if the resident flora is disturbed, transient
microorganisms may colonize, proliferate, and produce
disease.
Bacterial infection of the skin
(pyodermas)
 Cutaneous bacterial infections are
caused by resident or transient bacteria
in the epidermis and mucosa.
 Infections with pyogenic (pus forming)
bacteria
 Usually Staphylococcus aureus and/or
Streptococci (usually Group A β
haemolytic Streptococci - GABS)
 Con’t

Factors in development of bacterial skin

infection
1) The portal of entry
2) The host defences
3) The pathogenic properties of the
organism
 Con’t

Classification
1. Primary infections
2. Secondary infections
 Con’t

1. Primary infections
Infections that are produced by
the invasion of normal skin by a
single species of pathogenic
bacteria
 Con’t

2. Secondary infections
 Infections afterthe integrity of the
skin has been broken, or the local
immune system is altered by the
primary skin condition
AD, scabies, tinea, …
 May show mixture of organisms
IMPETIGO
 Impetigo is a contagious superficial (stratum
corneum) pyogenic infection of the skin.
 Bacterial producing toxins that cause blisters
and crusts.
 Neglected or untreated impetigo can extend
to the dermis, resulting in ecthyma
 When it becomes ecthyma, which may heal
forming a scar.
 Con’t

 Impetigo presents as either a primary

pyodermal of intact skin or a
secondary infection
 Laboratory - Gram stain, Culture
 Two main clinical forms are
recognized:
1. Non-bullous impetigo
2. Bullous impetigo.
1. Nonbullous Impetigo
 70 % of cases of impetigo
 Affects both children and adults
 Caused by Group A Streptococcus, S.
aureus or both.
 Spread occurs from nasal carriers to
skin or from skin to skin
 Pruritus or soreness
 Con’t
 The face (especially around the nares)
commonly affected.
 The initial lesion begins as small
erythema, followed by multiple vesicle
or pustule that quickly evolves into a
honey-colored crusted plaque.
 The crusts are thick and firmly adherent;
they discharge pus when pressured
 Con’t

 Constitutional symptoms are absent

 Regional lymphadenopathy is present
in patients with prolonged untreated
infection.
 Extension of infections and PSGN are
possible complications.
 Most cases will respond to treatment
and heal with out scaring.
 Systemic antibiotics to prevent PSGN.
2. Bullous Impetigo
Less common form of impetigo
Mainly affects newborns and
infants
Caused by S. aureus
Exfoliative toxins types A and B
are responsible for the clinical
pictures.
 Con’t

 Rapidly progressing flaccid bullae,

usually arising from grossly normal
skin and initially contain clear yellow
fluid that subsequently becomes dark
yellow and turbid.
 Light brown to golden-yellow crusts is
formed later.
 Con’t
 Complication – SSSS, Cellulitis,
lymphangitis, and bacteremia with
resultant osteomyelitis, septic
arthritis, pneumonitis, and septicemia
 SUMMARY
Xcis Bullous Impetigo
Non bullous Impetigo

Age affected Children and adults Newborns and infants

Prevalence More common(70%) Less common

Possible etiology Gr. A Strept., S. Aureus or S. Aureus
both

Color of crusts Honey clored Light brown to golden

yellow

Possible complications PSGN, extension SSSS, cellulitis, lymphangitis,

bacteremia (osteomy. Septic
arthritis…)

Treatment 1st topical 1st topical

Systemic to prevent Systemic for severe cases
PSGN
Management of Impetigo

 Local management for small lesions: -

 Removal of crusts
 Drying agent - Gentian violet (GV) paint
0.5% apply BID
 Maintenance of cleanliness
 Topical antibiotics - such as 2% mupirocin,
Gentamycine, Fucidic acid.
 Con’t
 Systemic treatment: if severe, multiple lesions
 For Non bullous impetigo- a single dose of
benzathin penicillin coupled with local care.
▪ Oral Amoxacyllin or Ampicillin can also be
used.
 For Bullous impetigo: - Cloxacillin 500 mg po QID
for 7 to 10 days.
Amoxi+ clavulanic acid, cephalexin
 Con’t

 In cases, with an allergy to penicillin,

erythromycin can be given.
 The underlining skin conditions such
as eczemas, scabies, fungal infection,
or pediculosis should be treated.
ECTHYMA
 A consequence of neglected impetigo
 The dermis is also affected
 characterized by thickly crusted erosions
or ulcerations
 Causes - S. aureus and/or group A
streptococcus, Pseudomonas aeruginos
 Poor hygiene and neglect are key
elements in pathogenesis
 Con’t
 Most commonly occur on the lower
extremities
 Children, neglected elderly patients or
individuals with diabetes mellitus are
specially predisposed.
 The ulcer has a “punched out” appearance
with dirty grayish-yellow crust, indurated
red margin
Adult with ecthyma before Immediately crust removed
crust removed
One month later Two months later
 Con’t

Management
 Systemic antibiotics covering the
etiologic agents with local wound care
and correction of underlying conditions
is the treatment
 The lesions heal slowly with scaring.
 Serious complications may occur
FOLLICULITIS
 It is an infection of the hair follicles.
 It occurs on hair bearing areas of the
skin.
 Application of greasy substance such
as Vaseline is a predisposition.
 The most common etiologic agent is
staphylococcus aureus. However, fungi
and virus can also cause it.
 Con’t
 Presents as small fragile dome-shaped
pustule occurs at the infundibulum of
a hair follicle
 Often on the scalps of children and in
the beard area, axillae, extremities,
and buttocks of adults
Folliculitis Infection at the
mouth of a hair follicle.
See a pustule with a hair
coming out of the centre
 Furuncle/ Carbuncle
 Furuncle and carbuncle are common in
obese, diabetic patients and
immunosuppressive conditions.

 Both furuncle and carbuncle are caused

by S. aureus.
 Con’t

 A furuncle or boil is an acute, deep-

seated, red, hot, tender nodule or
abscess that evolves around the hair
follicle.
 Solitary or multiple
 Hard, tender, red folliculocentric nodule
 Undergoes abscess formation 
Ruptures
 Con’t
 A carbuncle is a more extensive,
deeper infection comprised of
communicating abscesses usually
arising in several adjacent hair
follicles.
 develops when multiple, closely set
furuncles coalesce.
 Fever and malaise are often present
 Con’t
Management
 Avoid greasy applications on the skin.
 Topical antibiotic - Mupiricine
 Systemic antibiotics: - Cloxacillin or
erythromycin is choices of treatment.
 Severe infections (Presence of systemic
symptoms) - maximal antibiotic dosage by the
parenteral route
 For deep abscesses (furuncle and carbuncle)
incision and drainage is mandatory.
ERYSEPELAS
 Erysipelas is a bacterial infection of the
dermis and upper subcutaneous tissue
 Most commonly due to group A
streptococcus, less commonly caused
by group B, C, G or by S. aureus.
 Diabetes mellitus is a known
predisposing factor apart from barrier
and other host factors
 Con’t
 Characterized by - Painful, bright-red,
edematous indurated plaque with an
advancing raised border, sharply
demarcated from the surrounding
normal skin is seen on examination
 Face or a lower extremity
 Treatment and Prognosis is the same as
in cellulitis
CELLULITIS
 Cellulitis is bacterial infection of dermis and
subcutaneous tissue
 S. aureus and group A streptococci are by far
the most common etiologic agents
 In young children, Hemophilus influenza type
B should be considered as a possible etiology
for cellulites especially of the face (facial
cellulitis)
 In many cases there is a history of an
antecedent lesion
 Con’t
 Patients experience erythema, local pain, and
tenderness and variable degrees of systemic
symptoms
 Indurated, tender and hot, vaguely
demarcated lesion with swelling of the
affected limb is evident.
 looks erysipelas but lack of distinct margins
deeper edema, surface bulla/necrosis
 Regional lymph nodes may be involved.
 Con’t
Complications
 Without effective Tx complications are
common - fasciitis, myositis, subcutaneous
abscesses, and septicemia.
 Pretibial cellulitis can result in osteomyelitis
from contiguous spread.
 Post streptococcal glomerulonephritis can
occur in some cases.
 If Lymphangitis is not treated properly, it can
lead to lymphoedema.
 Con’t
Management
 Treat the fever and pain and elevate the
affected part.
 Systemic treatment with appropriate
antibiotics
 Crystalline penicillin or procaine penicillin is the first
line therapy and
 oral Ampicillin or Amoxicillin may be used for mild
infection
 The antibiotics should be continued for 10- 14 days.
 Con’t

 Admission and parentral antibiotics

are indicated in infants and severely ill
adults.
 Follow up:
 Response to the antibiotic
 For proper timing of surgical intervention.
Leprosy (Hansen’s disease)
 Is a chronic mycobacterial infectious
disease caused by mycobacterium leprae
 Primarily affects the skin & nerves, but
also eyes and other different organ
 A disabling, deforming and stigmatizing
disease
 Early diagnosis & prompt treatment
 Con’t

 Earliest description -
from India In 1870,
Armauer Hansen –
identifies M. leprae
 It is confined to
humans, armadillos
 Etiology
 Mycobacterium leprae
 Non-cultivable
 Gram +ve
 Non-motile
 Aerobic
 Obligate Interacellular
 Acid fast bacilli
 Grows best in cooler areas of the
body; skin, peripheral nerves,
anterior chamber of the eye,
testes.
 Its unique trisaccharide binds to
 Con’t
 Don’t grow on artificial
media
 Foot pad of mice,
armadillos
 Humans – primary
reservoir
 Animal reservoir
 armadillos
 monkeys
 chimpanzee
Epidemiology
 A disease of the developing world
 India has 2/3 of the world’s leprosy
burden
 M ‫׃‬F 2:1
 The age group mainly - is b/n 15-45yrs
 young /2nd or 3rd decade/
 Long Incubation period
 For tuberculoid - 20 years or longer
For lepromatous -up to 5 years
Transmission
 Not fully understood
 Nasal discharges from the highly
infectious individuals are believed to be
the main source
 Only lepromatous leprosy cases are
known to be infectious
 Entry is through the respiratory route
 Entry of bacilli via the skin is less likely
possibility
Pathogenesis
 M. leprae- lives within cells /macrophages,
Schwann cell
 Requires a temperature of ~ 27-33ºC
 For disease susceptibility- genetic &
environmental factors
 Inhaled M. leprae multiply
 Has brief bacteremic phase before binding
to macrophages or Schwann cells
 Con’t

 Proper recognition of
M. leprae by APC
→Activation of
Macrophage →
phagocytosis of M.
leprae
 Con’t

 → complete bacillary lysis

bacterial processing proceeds

to antigenic peptide levels
 Presentation of proper,
specific & complete M. leprae
antigen →
 Con’t

 Activation of naive T

cells with the

generation of IL-12
→ Th1 response →
strong CMI
 Con’t

 A predominantly Th1 response is seen in

tuberculoid leprosy patient → IL-2, IFN- γ &
TNF-β → maintain inflammation

 Th2 response- in lepromatous patient → IL-4,

IL-5, IL-10 → suppress macrophage activity
strong humoral response /Ig M/
Classification
Ridley and Joplig
1. Tuberculoid Leprosy (TT)
2. Borderline Tuberculoid Leprosy (BT)
3. Mid-Borderline Leprosy (BB)
4. Borderline Lepromatous Leprosy (BL)
5. Lepromatous Leprosy (LL)
 Con’t

 Classification determined by clinical,

immune state & histological changes
 TT & LLp are stable poles
 In all cases of TT & most BT – AFB
cannot be found
WHO Classification
1. Paucibacillary (PB) – bacteriologically
negative cases of:
1. Indeterminate Leprosy
2. Tuberculoid Leprosy
3. Borderline Tuberculoid Leprosy.
2. Multibacillary (MB) – all smear positive cases
1. Mid-Borderline Leprosy
2. Borderline Lepromatous Leprosy
3. Lepromatous Leprosy
 Con’t

 PB leprosy ‫ ׃‬/IL, TT & smear –ve BT/

 Few lesions /< 5 /
 No AFB found

 MB leprosy ‫ ׃‬/smear +ve BT, BB , BL & LL/

 Multiple / ≥ 5/
 One or more AFB
Clinical Features
Indeterminate Leprosy
 Vague slightly hypopigmented or
erythematous lesion on the face, limbs or
buttock
 Nerve function is unimpaired.
 This form of leprosy may resolve
spontaneously, progress to any of the forms
may persist indefinitely.
Tuberculoid Leprosy
 Immunity is strong
 Plaque having annular configuration with
raised and clear-cut edges sloping
towards a flattened and hypopigmented
centre
 Both border is sharply marginated
 Indurated, erythematous, scaly
 Solitary
 The surface is dry, hairless, insensitive
Borderline Tuberculoid Leprosy
 Immunity is strong but insufficient to
self-cure.
 These patients are somewhat unstable:
resistance may increase, upgrading to
TT, or decrease, downgrading to BL
 Plaque, papules, or hypopigmented
macule with little or no scale.
 Annular configuration
 Con’t
 Both borders are sharply demarcated
 Little or no scaling, less erythema, less
induration & less elevation
 may have sharply marginated satellite
papules
 Multiple asymmetric lesions with
sensory loss are the rule.
 Nerves are commonly enlarged (not
more than two nerves)
Borderline Leprosy
 It is the immunologic midpoint, being the
most unstable area, with patients quickly
up- or downgrading to a more stable
granulomatous posture
 Characteristic skin changes are annular
lesions with sharply marginated interior and
exterior margins, large plaques with islands
of clinically normal skin
 Nerve trunk palsies → motor & sensory
deficit
Borderline Lepromatous Leprosy
 Lesions resemble that of LL except they are
not absolutely symmetrical
 Resistance is too low to restrain bacillary
proliferation significantly but is still sufficient
to induce tissue-destructive inflammation,
especially in nerves.
 Bacillary invasion of the nose, larynx, eyes,
and testes is less severe than in LL.
 BL usually downgrades to LL.
Lepromatous Leprosy
 Lack of cell-mediated immunity toward M.
leprae permits unrestricted bacillary
replication and widely disseminated,
multiorgan disease.
 Poorly defined, skin-colored nodules are
the most characteristic lesions
 In diffuse non-nodular LL- enlargement of
ear lobes, widening of the nasal root (sadel
nose) & swelling of the fingers
 Con’t
 Hair loss, commonly on the eyebrows
(maderosis) is evident.
 Any given skin lesion may or may not
be hyposthetic.
 Untreated LL disease is progressive,
but this course may be altered by
reactional states (ENL)
Leprosy Reaction
 Immunologicaly driven distinctive,
tissue destructive, inflammatory
processes that appears suddenly in
any form of leprosy
 A process by which leprosy patients
develop a sudden acute inflammatory
response that produces painful
symptoms with loss of nerve function.
 Con’t
 Precipitating factor
 MDT
 Pregnancy
 Inter current infections
 Vaccination (BCG)
 Two principal types of reactions have been
described.
1. Type-1 (Reversal )
2. Type-2 (ENL)
Type 1 reaction
• Type IV hypersensitivity reaction to
bacillary antigen due to change in the
host immunity either to the
tuberculoid end (Upgrading Reaction)
or towards the lepromatous end
(Downgrading Reaction).
• It occurs in borderline disease
commonly after initiation of
treatment
 Con’t

Clinically
 Existing skin lesions become
erythematous or edematous and
may desquamate.
 Edema of face, hands or feet is the
presenting symptom
 Acute neuritis
Type 2 reaction - Erythema Nodosum
Leprosum (ENL)
 Immune complex reaction occuing
in patients with multi-bacillary
disease, LL and BL.
 Occur before, during, or after
chemotherapy.
 Median time of onset is 1 year
after onset of treatment.
 Con’t

Clinically
• Crops of new painful and tender bright-
pink, dermal and subcutaneous nodules
arising in clinically normal skin
• Lesions- targetoid, vesicular, pustular,
ulcerative, or necrotic.
• Involvement of both upper and lower
extremities is the rule.
 Con’t

• Favor the extensor arms and medial

thighs, face
• Systemic symptoms- fever , malaise,
anorexia
• Arthralgias and arthritis are more
common in ENL than – neuritis
• Orchitis/ epididymitis, uveitis & iritis.
Diagnosis
 The diagnosis of leprosy relies
primarily on the typical clinical
features.
A complete history and physical
examination
 Laboratory tests
 Con’t
 Diagnosis is based on the cardinal signs of
leprosy.
 At least one of the following cardinal sign
must be present
1. Anesthetic patch (hypo pigmented patch
with loss of sensation)
2. Nerve enlargement and/or tenderness
3. AFB in slit skin smears examination
(positive acid fast bacilli in slit skin smear
examination)
 Thickened greater auricular nerve

Ulnar Claw hand

Foot drop (right foot)

Complete ulnar & medial claw hand
Slit skin smear
Treatment of Leprosy
Principles
 Stop the infection with chemotherapy
 Prevent and treat reactions and so reduce
the risk of nerve damage
 Educate the patient to cope with existing
nerve damage
 Treat the complications of nerve damage
 Rehabilitate the patient socially and
psychologically.
Chemotherapy (MDT)
 PB Leprosy: (Total duration is 6 months)
 Dapsone 100mg daily unsupervised
 Rifampicin 600mg monthly supervised

 MB Leprosy: (Total duration is 12 months)

 Dapsone 100mg daily unsupervised
 Clofazimine 50mg daily unsupervised
 Rifampicin 600mg monthly supervised
 Clofazimine 300mg monthly supervised
Treatment of Reactions
 Mild Reaction (both type 1&2)
 Analegesics and bed rest
 Severe Type I reaction
 Prednisonlone
▪ 40mg/d for 2 wks
▪ 30mg/d for 2 wks
▪ 20mg/d for 2 wks
▪ 15mg/d for 2 wks
▪ 10mg/s for 2 wks
▪ 5mg/d for 2 wks
 Con’t
 Severe Type 2 reaction
• Thalidomide 400mg/day treatment of
choice.
• Systemic corticosteroids (high-dose
steroids (80-mg daily, tapered down
rapidly)
• ENL frequently recurs, steroid dependency
can easily develop