Bacterial Infection

Bacterial infections
Dr. Raed Abu Serriya
Dr. Raed Abu Serriya 1

Bacterial Infections
◦ Impetigo
◦ Ecthyma
◦ Folliculitis
◦ Furunculosis
◦ Erysipelas/ Cellulitis
◦ Paronychia
◦ Angular chelitis
◦ Sycosis vulgaris
◦ erythrasma
◦ Tuberculosis of the skin
◦ Leprosy
Impetigo
3
Impetigo
 An acute highly contagious gram-positive
bacterial infection of the superficial layers
of the epidermis.
 Occurs in all ages, but children younger
than 6 years have a higher incidence of
impetigo than adults
 Most common bacterial skin infection

Impetigo
Encouraging factors
 Hot humid weather

 Crowded living conditions
 Poor personal hygiene
 Unhygienic work environment

Forms of Impetigo
 2 forms
◦ nonbullous impetigo
◦ bullous impetigo

Nonbullous impetigo
 Impetigo Contagiosa
 Crusted Impetigo

Nonbullous Impetigo
 Etiology:
◦ β-haemolytic strains of Streptococci, S
aureus, or a mixture of both organisms.
◦ Usually in the face especially around the

mouth and nose
◦ Thin-walled vesicles on erythematous base,

which rupture so rapidly that it is rarly seen

Nonbullous Impetigo
 Diffirential diagnosis:
◦ Varicella
◦ Herpes simplex
◦ Tinea corporis

Nonbullous Impetigo
Treatment:
 For severe cases systemic antibiotics
(such as flucloxacillin, erythromycin,
penicillin or cefalexin) are needed
 For minor cases the removal of crusts by

compressing them and application of a
topical antibiotic such as neomycin, fusidic
acid , mupirocin or bacitracin will suffice

Nonbullous Impetigo
 Complications
◦ 2–5% of cases of impetigo are associated with the

development of acute glomerulonephritis
◦ Treatment does not reduce risk of development

Bullous Impetigo
 Bullous impetigo begins as a rapid onset of
blisters that enlarge and rupture.
 Casued by Staphylococcci
 most common in neonates and infants
 Trunk is the most common site

Bullous Impetigo
 Treatment:
Topical antibiotics
Systemic antibiotics (e.g. dicloxacillin, cephalexin

or erythromycin)

Staphylococcal scalded skin syndrome

Ecthyma
 A deeper form of pyogenic infection (
known as negleted impetigo or ulcerative
dermatitis)
 Mainly caused by sterptococci
 Most common on lower extremities

Predisposing Factors
 Trauma
 Poor Hygiene
 Not treated impetigo

 After an incubation period of few days, it
begins with sudden onset of fever, rigors
and malaise.
 The skin shows redness, hotness, swelling
and pain

Treatment
 Appropriate antibacterial therapy for at
least 10 days
 Treatment of the offending factor

Erysipelas
 Acute, superficial cellulitis with infection and

inflammation in the dermis and upper
subcutaneous tissue involving the superficial
dermal lymphatics

Cellulitis
This inflammation of the skin occurs at

a deeper level than erysipelas

Erysipelas and Cellulitis
erysipelas cellulitis
organism Strept. Strept.

Staph.
Haemophylus influenzae
Tisue affected Superficial (dermis and upper Deep (subcut. Tissue)
subcut. Tissue)
Clinical picture Acute sever systemic symptoms Fever and mailaise may
(fever,malaise,shivering) be present
morphology Erythematous lesion with well Erythematous lesion with

defined border ill- defined border
Bullae are common Necrosis may be present

Erysipelas Cellulitis
 Causes
◦ Streptococcus 80% of cases
◦ Staphylococcus aureus has been
implicated in cases of recurrent
erysipelas secondary to
lymphedema

 Portals of entry
◦ local factors, such as venous
insufficiency, stasis ulcerations,
inflammatory dermatoses,
Fungal infections, insect bites,
and surgical incisions

 In all age groups, but the peak
incidence in patients aged 60-80
years
 More severe infections may
exhibit numerous vesicles and
bullae along with petechiae and
even frank necrosis

Cellulitis

Therapy I
 Elevation and rest of the affected limb are
recommended to reduce local swelling
and inflammation
 Complete rest
 Saline wet dressings

Therapy II
 Antipyretics
 Systemic antibiotics:
◦ Penicillin
◦ Cephalosporin
◦ Dicloxacillin.
◦ At least 10 days

Prophylaxis
(at least 6 months)
◦ if three relapses within a few
years
◦ benzathine penicillin 1.2 – 1.5
mega units im. every 4 weeks or
more frequently or
erythromycin 250mg 3xdaily
Complications
 Complications occur in 13-17% of patients

with erysipelas.
 Abscess, gangrene, and thrombophlebitis.
 Recurrent erysipelas may lead to
lymphoedema
 Less common complications (<1%) are
acute glomerulonephritis, endocarditis,
septicemia.

Folliculitis
 Aninflammation of the hair follicles

caused by infection (coagulase-
positive staphylococci).

Folliculitis
 Supeficial folliculitis
◦ folliculitis
 Deep Folliculitis
◦ Furunculosis
◦ Carbuncle
◦ Coalesced boil , nearby each other ,
with multiple openings and skin
between them shows necrosis.
Folliculitis
 Predisposing risk factors :

◦ Friction
◦ Hyperhidrosis
◦ Occlusion
◦ Shaving, Epilation

Folliculitis
Other predisposing risk factors
◦ Preexisting dermatitis
◦ Reduced host resistance, such as patients
with diabetes mellitus or immunologic
disorders
◦ Staphylococcal nasal carriers
◦ Skin injuries, abrasions, surgical wounds,
and draining abscesses
◦ Skin occluded for topical corticosteroid
therapy

Folliculitis

Folliculitis
 The primary lesion in folliculitis is a

papule or pustule with a central hair.
Typical body sites affected are the face,

scalp, thighs, axilla, and inguinal area
 Deep folliculitis inflames the entire

follicular structure and tends to be more
symptomatic.

Furuncle

Furunculosis

Therapy
◦ Wash with antibacterial soaps to prevent or
control mild cases of folliculitis.
◦ Topical antibiotics may be used.
◦ Systemic antibiotics with coverage of S aureus
often are needed, since S aureus is the most
common pathogen.This organism often is
penicillin resistant; therefore, dicloxacillin or a
cephalosporin is the first choice

Paronychia
 Infalamation of the nail fold
◦ Acute
◦ chronic
◦ Caused mainly by staphylococci

and streptococci

Clinical picture
 Acute form:
◦ Bacterial
◦ Mainly children
◦ digit is red, swollen, and painful
◦ pus formation by drainage
◦ Treatment with systemic and
topical antibiotics
Angular chelitis
 common skin condition affecting the

corners of your mouth.
 Painful ,cracked sors .
 saliva collects at the corners and causes
dryness, over time the dry skin may crack
open .
sometimes bacteria or fungi get into the
crack which can cause inflammation or
infection.
Sycosis vulgaris
 Pyogenic infection of the wole hair
follicles.
 Organism staph. aureus
 Males after puberty
 Chronic with remission and relapses
 N.B Tenia barbae

erythrasma
 Superficial mild chronic infection of the
skin.
 Corynebacterium minutissimum
 Predisposing factors :
obesity, Diabetes, Hyperhedrosis,
increase humidity

 Chronic form
◦ Mainly adult women
◦ Represents irritant- or allergic contact
dermatitis
◦ Secondary infections by candida or bacteria
◦ Redness, edema and absence of the cuticle
◦ Onycholysis by matrix damage
◦ Treatment
 Avoidance of water and chemical exposure
 Combined topical

Mycobacterial Infections
 Themost impportant
mycobacterial infections are
Tuberculosis and Leprosy

Cutaneous tubeculosis
A chronic granulomatous disease
caused by Mycobacterium
tuberculosis, Mycobacterium
bovis or BCG (bacillus Calmette-
Guerin)

Route of infection
 Exogenousby inoculation
 Endogenous

Mode of infection
 Inhalationof droplets expelled
from patients
 Direct inoculation of the
organism into the skin

Classification of cutaneous tuberculosis
 Exogenous
1. Primary tuberculosis complex
2. Warty tuberculosis (Tuberculosis verrucosa cutis)
3. Some lupus vulgaris
 Endogenous
1. Scrofuloderma
2. Orificial tuberculosis
3. Some lupus vulgaris
4. Metastatic tuberculous abscess (tuberculosis
gumma)
5. Acute miliary tuberculosis

Classification of cutaneous tuberculosis
 Tuberculides
1.Lichen scrofuloderm
2.Papulonecrotic tuberculides
3.Erythema induratum of Bazin

Primary tuberculosis complex
 Previously uninfected
 Typically occurs in a wound
 Lesion develops 2–4 weeks after inoculation
 Presents as a firm, painless, red-brown
papule with ‘apple jelly’ translucence on
diascopy that may
ulcerate or crust
 Associated with regional lymphadenopathy
 It usually heals spontaneously in 3-12
months
Tuberculosis verrucosa cutis
 Previously infected
 Presents with large verrucous papule
or
plaque at the site of re-inoculation
 Due to strong immunity and
hypersensitivity
against M. tuberculosis

Scrofuloderma
 Caused by direct extension of the organism
to the skin overlying an infected lymph
node
or bone
 Occurs in persons with low immunity
 Lesions are most common over the cervical
lymph nodes
 May ulcerate or form draining sinuses
 Heals with characteristic cord-like scar

Tuberculosis cutis orificialis
 Autoinoculation of the mucous membranes

Occurs at the mouth, nose, anus, urinary
meatus or genitalia from infected secretions
or visceral involvement
 Presents as painful punched-out ulcers with
undermined edges
 Indicates failing resistance to disease

Lupus vulgaris
 The most common form
 Chronic, very slowly progressive cutaneous
form
 Associated with strong immunity to M.
tuberculosis
 Presents with atrophic red-brown plaques
on the head and neck in ~90% of cases
 Lesions can ulcerate and cause destruction
of underlying structure, ectropion or
eclabium
Lupus vulgaris

Metastatic tuberculosis
(Tuberculosis gumma)
 Occurs in patients with internal
tuberculosis and decreased immunity
 Presents with ulcerated nodules and
sinuses
 Most commonly on extremities

Miliary tuberculosis of the skin
 Presents with generalized macules, papules,
pustules, nodules or purpura associated with
fulminant pulmonary or meningeal
involvement
 Systemically ill with poor prognosis
 Occurs in persons with low immunity

Tuberculids
 Cutaneous reaction related to an
immunologic response to the organism ;
associated with an underlying focus of
distant infection with hematogenous
spread
 The skin presents no clinically active
lesion

Lichen scrofulosorum
 Occurs in children and young adults

Presents with asymptomatic clusters of
lichenoid papules and discoid plaques on
the trunk
 Resolves spontaneously and can recur
 Associated with infection of the bone or
lymph
nodes

Papulonecrotic tuberculid
 Most commonly seen in children
 Presents with successive crops of dusky-
red
papules with or without central necrosis
on
the extensor extremities which heal
spontaneously with varioliform scars
 Typically have infected lymph nodes

Erythema induratum of Bazin
 Typically seen in girls and young women

 Presents with ulcerated nodules on the
posterior calves with underlying
panniculitis
and vasculitis
 Increasing prevalence during cold wether

Diagnosis
 Positive tuberculin test with PPD
 Histopathology
 Culture of tissue
 Polymerase chain reaction for M.
tuberculosis DNA in tissue

Treatment
 Isoniazid (10–15 mg/kg per day) and rifampin

(10–20 mg/kg per day) for 9 months
Pyrazinamide, ethambutol or streptomycin is
added for the initial 2 months of therapy if drug
resistance is a consideration (Hispanic or Asian
population), or if the duration of therapy is
limited to 6 months

Leprosy
 Chronic granulomatous infection of the
skin, nasal mucosa, nerves and eyes
72
Mode of transmission
 Droplet infection
 Contact through the skin
 From lepromatous mother to her fetus
 From the placenta and even milk of
lepromatous leprosy mothers
73
Pathogenesis
 Infection caused by Mycobacterium leprae
 Low infectivity (Incubation period ~5 years)
 Transmission is not fully known although
droplet infection via an upper respiratory route
is suspected
 Genetic predisposition may play a role in
disease development
 Animal reservoirs: armadillos and monkeys
74
Pathogenesis
 By defect of macrophage-monocyte
series and T-helper lymphocytes survive
M.leprae and replicate inside the
macrophage and Schwann cell of non-
myelinated nerves
75
Disease classification
 Tuberculoid leprosy
 Borderline tuberculoid leprosy
 Borderline borderline leprosy
 Borderline lepromatous leprosy
 Lepromatous leprosy
76
Tuberculoid leprosy
 <3 skin lesions which are anesthetic and
anhidrotic
 Highest immune resistance and reactivity
 Organisms are not identified in tissues
(paucibacillary)
 Nerve involvement
 Strong positive reaction to the lepromin
skin test
77
Borderline tuberculoid leprosy
 Few (3–10) skin lesions
 May have enlarged nerves with mild
motor impairment
78
Borderline borderline leprosy
 Indeterminate type
 Multiple asymmetric annular plaques
 Host resistance is unstable
 Organisms may be identified
79
Borderline lepromatous leprosy
 Skin lesions are symmetrical and

numerous
 Nerve involvement is not prominent
80
Lepromatous leprosy
 Diffuse skin infiltration with characteristic

leonine facies and loss of the eyebrows
 No host resistance or reactivity
 Organisms are numerous (multibacillary)
 No reaction to lepromin skin test
81
Diagnosis
 Slit skin smears stained with Ziehl–

Neelsen reveals organisms
 Organisms cannot be cultured in vitro
 Histopathology
82
Treatment
 Dapsone (1 mg/kg per day) for 1 year in all

types
 Rifampin (10 mg/kg per day) should be added
for 6 months in cases of tuberculoid, borderline
tuberculoid or indeterminate disease
 Clofazimine (1 mg/kg per day) should be added

for 2 years in cases of borderline,
borderline lepromatous and lepromatous
disease
83
 Type I reaction (downgrading or reversal
reaction that represents an enhanced cell-
mediated response to M. leprae)
and type II reactions (erythemanodosum
leprosum due to circulating
immunecomplexes with potential
multisystem involvement) are treated
with systemic corticosteroids

85
86
Thanks

Bacterial Infection

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Bacterial Infection

Uploaded by

Copyright:

Available Formats

Bacterial infections

Dr. Raed Abu Serriya

Dr. Raed Abu Serriya 1

Dr. Raed Abu Serriya 4

 Hot humid weather

Dr. Raed Abu Serriya 5

Dr. Raed Abu Serriya 6

Dr. Raed Abu Serriya 7

◦ Usually in the face especially around the

◦ Thin-walled vesicles on erythematous base,

Dr. Raed Abu Serriya 8

Dr. Raed Abu Serriya 9

 For minor cases the removal of crusts by

Dr. Raed Abu Serriya 10

◦ 2–5% of cases of impetigo are associated with the

◦ Treatment does not reduce risk of development

Dr. Raed Abu Serriya 11

 most common in neonates and infants

 Trunk is the most common site

Dr. Raed Abu Serriya 12

Systemic antibiotics (e.g. dicloxacillin, cephalexin

Dr. Raed Abu Serriya 16

Dr. Raed Abu Serriya 17

 Mainly caused by sterptococci

 Most common on lower extremities

Dr. Raed Abu Serriya 18

Dr. Raed Abu Serriya 19

Dr. Raed Abu Serriya 20

Dr. Raed Abu Serriya 21

 Acute, superficial cellulitis with infection and

Dr. Raed Abu Serriya 22

This inflammation of the skin occurs at

Dr. Raed Abu Serriya 23

organism Strept. Strept.

morphology Erythematous lesion with well Erythematous lesion with

Dr. Raed Abu Serriya 24

Dr. Raed Abu Serriya 25

Dr. Raed Abu Serriya 26

Dr. Raed Abu Serriya 27

Dr. Raed Abu Serriya 28

Dr. Raed Abu Serriya 32

Dr. Raed Abu Serriya 33

 Complications occur in 13-17% of patients

Dr. Raed Abu Serriya 35

 Aninflammation of the hair follicles

Dr. Raed Abu Serriya 36

 Predisposing risk factors :

Dr. Raed Abu Serriya 38

Dr. Raed Abu Serriya 39

Dr. Raed Abu Serriya 40

 The primary lesion in folliculitis is a

Typical body sites affected are the face,

 Deep folliculitis inflames the entire

Dr. Raed Abu Serriya 41

Dr. Raed Abu Serriya 42

Dr. Raed Abu Serriya 43

Dr. Raed Abu Serriya 45

◦ Caused mainly by staphylococci

Dr. Raed Abu Serriya 46

 common skin condition affecting the

 N.B Tenia barbae

Dr. Raed Abu Serriya 49