bacterial infections .pptx

INTRODUCTION
Bacterial infections are one of the most common dermatological problems
observed in outpatient clinics. These include pyodermas and other bacterial
infections such as tuberculosis, anthrax, leprosy, and various other bacterial
infections.
Natural defenses of skin:
• Intact skin
• Keratin
• Skin sloughing
• Sebum
• Sweat
• Normal skin flora

BACTERIAL FLORA OF NORMAL SKIN
The organisms that characteristically survive and multiply in various ecologic
niches of skin constitute the normal cutaneous flora. The skin possesses
protective mechanisms to limit colonization, and the survival of organisms on
the surface lies in part in the ability of the organisms to resist these
mechanisms. Microbial colonization on the skin adds to the skin’s defence
against potentially pathogenic organisms. Although microbes normally live in
synergy with their hosts, occasionally colonization can result in clinical
infection. An understanding of the composition of this flora and the attributes
of its major elements are important for treating many bacterial infections of
the skin.
The members of the normal flora can be classified as follows:
1.Resident flora
2.Transient flora
3.Temporary residents

NORMAL
FLORA
Resident flora
E.g., Gram positive cocci- Staphylococcus species, Micrococcus
species.
- Gram positive rods- Coryneforms or diphtheroids. - Gram
negative bacilli- Acinetobacter species.
- Anaerobes- Propionibacteria species.
Transient flora
E.g., Streptococcus, Micrococcus, gram negative rods from
gastrointestinal tract, Candida and Cryptococcus.
Temporary residents
E.g., Staphylococcus aureus in the anterior nares and
perineum.

PYODERMA
Pyoderma is defined as ANY PURULENT SKIN DISEASE.
Primary pyoderma
SUPERFICIAL • Follicular: Follicular impetigo, chronic folliculitis of the
legs
• Nonfollicular: Impetigo
DEEP • Follicular: Sycosis barbae, furuncle, carbuncle (with
perifollicular involvement)
• Non-follicular: Ecthyma, cellulitis, erysipelas, paronychia,
necrotizing fasciitis
Secondary pyoderma
SECONDARY FOLLICULITIS:
Acne conglobata
Hidradenitis suppurativa
Dissecting cellulitis of scalp
Acne keloidalis nuchae
Pyoderma vegetans
Infected eczemas
Intertrigo
Infected ulcers (tropical ulcers)
CUTANEOUS INVOLVEMENT IN SYSTEMIC BACTERIAL
DISEASES
For example, in bacteremia and bacterial endocarditis
CLASSIFICATION OF PYODERMA

Primary Pyoderma
• S. aureus and group A β-hemolytic streptococci (S. pyogenes) are the two
organisms most isolated from the lesions in cases of primary pyoderma.
Other gram-positive organisms include nongroup A streptococci (groups B,
C, and G), Streptococcus pneumoniae, coagulase-negative staphylococci
(Staphylococcus epidermidis), and Enterococci.
Patterns changes are noted in the aetiology of primary pyoderma:
• Group A β hemolytic streptococci were the major organism, whereas S.
aureus is the major pathogen in recent years.
• The incidence of pyoderma varies from place to place, and the studies have
shown that bacterial skin infections may account for up to 17% of the clinical
visits.

IMPETIGO
Impetigo is a common, contagious, superficial infection predominantly seen
in pre-school children, hence also called as SCHOOL SORES.
• It is not commonly seen in adults, but its common in people playing closed
contact sports like wrestling and rugby.
It occurs in bullous and non-bullous forms.

NON-BULLOUS IMPETIGO BULLOUS IMPETIGO
CLINICAL FEATURES EARLY LESIONS
Single or multiple 2-4mm
erythematous macules or short-
lived vesicles or pustules.
LATE LESIONS
superficial erosion with typical
HONEY COLOURED crust and rapid
direct extension of infection to
surrounding skin
EARLY LESIONS
small vesicle or superficial bullae
LATE LESIONS
flaccid , transparent bullae which
may rupture.
collarette of scale, no crusting,
little surrounding erythema may be
seen.
EXTENSION Extends peripherally without
central clearing
Extends peripherally with central
clearing (IMPETIGO CIRCINATA)
DISTRIBUTION Face usually around mouth& nose,
extremities
Face, trunk, Buttocks, perineum,
axillae, extremities

NON-BULLOUS IMPETIGO BULLOUS IMPETIGO
ASSOCIATION Mild lymphadenopathy No systemic symptoms,
associated with weakness, fever,
diarrhea
PATHOLOGY Small neutrophilic vesiculo-
pustules in epidermis
Spongiosis
Upper dermis-lymphocytes and
neutrophils
Gram positive cocci+
Cleavage of upper epidermis at
granular layer
Acantholysis+,
few inflammatory cells
Upper dermis- neutrophils
Gram positive cocci+
COURSE Benign, self limited
Resolves in 2 weeks
Resolves in 3-6 weeks
COMPLICATIONS Post streptococcal
glomerulonephritis
SSSS (staphylococcal scalded
skin syndrome)
Complications of impetigo include osteomyelitis, septic arthritis, pneumonia,
septicaemia, and glomerulonephritis. Cellulitis has also been reported to
develop in nearly 10% of patients, usually with non-bullous variant.
Lymphangitis, suppurative lymphadenitis, guttate psoriasis, and scarlet fever
are rare sequelae. Streptococcal strains of M groups 2, 49, 53, 55–57, and 60
induce post-streptococcal glomerulonephritis associated with impetigo.
• A latent period of 18– 21 days following impetigo to the development of
glomerulonephritis is typical, unlike a 10-day latent period following
pharyngitis.

Impetigo
Localized skin
involvement
Wash skin, remove crust,
use disinfectants
Apply topical antibiotic
twice daily to infected skin
for 1 week
Extensive skin involvement,
bullous disease and/or
lymphadenopathy
Treat as for localized skin
involvement plus systemic
antibiotics (ﬂucloxacillin,
cloxacillin
• Topical antibiotic twice daily for 5–7 days, mupirocin, fusidic acid,
retapamulin and 2% clindamycin cream
TREATMENT

ECTHYMA
Ecthyma is a pyogenic infection, deeper variant of impetigo having a similar
aetiology, adherent crusts beneath which ulceration occurs. Poor hygiene,
malnutrition, and repeated trauma are some of the predisposing factors. It
may also be noted in immunocompromised states such as diabetes,
neutropenia (chemotherapy-induced), and HIV infection.
• Age: Extremes of age
• Causative organisms: Group A Streptococcus such as S. pyogenes,
Pseudomonas aeruginosa and Staphylococcus aureus.
• Pathology: The infection and inflammation is much deeper in ecthyma than
in impetigo
• There is loss of the epidermis and dermis leading to ulceration and lesions
heal with scarring.

CLINICAL FEATURES
• Small bullae or pustules on an erythematous base are soon surmounted by a
thick choclate coloured adherent crust of dried exudate and an indurated
base with surrounding rim of erythema.
• The crust is thicker than in impetigo and is removed with difficulty, giving a
purulent, punched out ulcer
• Lesions are few, new lesions develop by autoinoculation
• Mc sites: Buttocks, thighs and legs
DIFFERENTIAL DIAGNOSIS
• Pyoderma gangrenosum.
• Ecthyma gangrenosum.
• Tick bites.

TREATMENT
Depends on the extent and severity of infection. Any underlying disease or
skin infection such as scabies or dermatitis should also be treated.
• Soaking crusted areas
Soak a clean cloth in a mixture of half a cup of white vinegar in a litre of
tepid water. Apply the compress to moist areas for about ten minutes
several times a day. Gently wipe off the crusts.
• A topical antibiotic ointment such as fusidic acid or >mupirocin is often
prescribed for localised ecthyma. A topical antiseptic such as
povidone iodine, superoxidised solution, antibacterial Manuka honey or
hydrogen peroxide cream may be used instead. Apply it at least three times
a day to the affected areas and surrounding skin. The treatment should be
applied after removing crusts. Look carefully for new lesions to treat.
Continue for several days after healing.
• Oral antibiotics are recommended if the infection is extensive or proving
slow to respond to topical antibiotics. The antibiotic of choice is a penicillin,
usually dicloxacillin or flucloxacillin, which are active against
both Streptococcus pyogenes and Staphylococcus aureus. The duration of
treatment varies; several weeks of therapy may be necessary to completely
resolve ecthyma.
• Improving hygiene

FOLLICULITIS
Infection process involving the hair follicle is known as folliculitis.
CAUSATIVE AGENTS
most infections are due to coagulase- positive staphylococcus organisms, in
the immunocompromised patients, the normally colonizing organisms may
become pathogenic (e.g., folliculitis caused by Micrococcus, Pityrosporum,
and Demo-dex organisms).
• gram-negative folliculitis caused by Klebsiella, Enterobacter, and Proteus
species may occur in long-term antibiotic-treated acne vulgaris patients as a
superinfection.
• Hot tub folliculitis due to Pseudomonas aeruginosa can also occur after
exposure to a poorly chlorinated hot tub or whirlpool.

Predisposing
factors
occlusion
Hyperhydration
of skin
Use of topical
steroids
DM
AD
Shaving,
plucking of hair,
waxing
HOT AND
HUMID
WEATHER
CLINICAL FEATURES
Depending on depth of follicular
involvement:
1.Superficial Folliculitis(IMPETIGO OF
BOCKHART)
• Small pustules(1-4mm) or crusted
papules on an erythematous base,
usually clustered and heal without
scarring. It is a superficial infection of
the follicular ostium with S. aureus. It
occurs on the scalp and sometimes on
the extremities. The lesions are seen
as follicular pustules with a rim of
erythema. The lesions heal without
scarring within 7–10 days but may
become chronic and recurrent. In HIV-
infected individuals, it may be severe
and is associated with pruritus
2.Deep Folliculitis (SYCOSIS BARBAE)
• Large erythematous papules, often
with a central pustule and plaques
studded with pustules and crusts.

MOST COMMON SITES
• face(beard area)
• Scalp
• Chest
• Back
• Axillae
• buttocks
DIAGNOSIS
• Clinical
• Gram staining and bacterial cultures to identify the causative organisms in
severe, recurrent or treatment-resistant cases
• Gram staining
• Acne vulgaris
• Rosacea
• Chloracne
• Pseudo-folliculitis barbae
• Keratosis pilaris

GRAM-NEGATIVE FOLLICULITIS
1.Post acne antibiotic treatment
2.In patients with long-term antibiotic therapy for acne vulgaris, pustular
lesions commonly aggravate on the facial “T” zones.
3.Hot tub folliculitis
4.Multiple disseminated pustular lesions on an inflammatory base are seen
on the trunk, buttocks, legs, and arms.
• Mild constitutional symptoms such as fever and malaise may be associated.
• It is a self- limiting disease, which resolves within 7–10 days.
immunocompromised patients may develop ecthyma gangrenosum.

CHRONIC FOLLICULITIS OF THE LEGS
(DERMATITIS CRURIS PUSTULOSA ET
ATROPHICANS, NIGERIAN SHIN
DISEASE)
It is a chronic and recurrent bacterial infection caused by S. aureus. It has
been reported from West Africa and various parts of India.
It is commonly seen in adult males.
Clinically characterized by symmetrical follicular pustules on the anterior
surface of the legs and may extend to thighs also.
It is a recalcitrant condition and heals with atrophic scarring.
Certain systemic abnormalities such as hypergammaglobulinemia and low
complement levels have been reported in many cases.

GRADE CLINICAL FEATURES HISTOPATHOLOGY
GRADE1 Only follicular pustules seen, a few of them
show perifollicular erythema
• Hyperkeratosis
• Parakeratosis
• Follicular plugging +/-
GRADE 2 Follicular pustules predominate with a
significant number of infiltrated papules
around broken hairs. Papules showed
excoriation marks, crusting, or peripheral rim
of white scales. Palpating hand could feel a
wiry roughness due to the broken or
irregular hairs. Alopecia may be observed,
but not marked
• Hyperkeratosis
• parakeratosis
• follicular plugging present
• neutrophilic abscess in the stratum
corneum
• irregular and board-based (rete pegs
fused)
• acanthosis
• perivascular and perifollicular
inflammatory infiltrate composed of
lymphocytes and plasma cells
• no dermal oedema
GRADE 3 Infiltrated scaly papules predominate with a
few scattered pustules at the periphery,
marked alopecia, shininess, and atrophy
• Hyperkeratosis
• church spires papillomatosis
• irregular and broad-based acanthosis
• perivascular, and perifollicular
GRADE 4 Near-complete alopecia, skin appears
atrophic, shiny, and scaly. Pustules are not
seen. A few discrete scaly papules are
observed at the periphery.
• Hyperkeratosis
• irregular acanthosis
• blunting of rete pegs
• perifollicular, and perivascular

GRADE 3 DERMATITIS CURUIS PUSTOLSA ET ATROPHICANS SHOWING MARKED ALOPECIA,
DRYNESS, PAPULES, AND SCATTERED PUSTULES
Reproduced under Open Access charter from: Saranya TM, Sasidharanpillai S, Govindan A.
Histopathology features in dermatitis cruris pustulosa et atrophicans: A case series.
Available from: https://dx.doi.org/10.25259/JSSTD_35_2020
Journal of Skin and Sexually Transmitted Diseases (https://jsstd.org)
JOURNAL OF SKIN AND SEXUALLY TRANSMITTED DISEASES

A. Biopsy from a patient with dermatitis
curuis pustolsa et atrophicans
showing inflammatory infiltrate
around sweat duct, blood vessels, and
hair follicle. Infiltrate extending into
the epidermis with intercellular
edema (H and E, ×100)
B. biopsy from a pustule of dermatitis
showing neutrophilic abscess in
stratum corneum (H and E, ×200)
C. biopsy from dermatitis curuis pustolsa
et atrophicans showing broad-based
acanthosis in some areas (arrow) and
rete pegs beginning to fuse (arrow
head) with each other in other areas
(H and E, ×100)
D. biopsy from a papule of dermatitis
showing hyperkeratosis and church
spire papillomatosis (left arrow) (H
and E, ×100); inset: Another focus
from the same section showing
irregular and broad-based acanthosis
(right arrow, H and E, ×100).
JOURNAL OF SKIN AND SEXUALLY TRANSMITTED DISEASES

SYCOSIS BARBAE
(SYCOSIS VULGARIS, BARBER’S ITCH)
It is derived from the Greek word “Sykosis” meaning fig-like.
• This condition is usually seen in young males.
• Clinically, it is characterized by an erythematous follicular
papule or pustule centered by a hair. These may remain
discrete or may coalesce to form a raised plaque studded
with pustules.
• When similar lesions occur on the nape of the neck, it is
called “sycosis nuchae”. A variant of deep folliculitis
associated with the destruction of the hair follicles and
atrophic scarring is known as “lupoid sycosis”.

FURUNCLE(BOIL)
Furuncle is a deep infection of the hair follicle including the perifollicular
region in the dermis and subcutaneous tissue, occur only in hair-bearing skin
and caused by S.aureus.
CLINICAL FEATURES
It presents as a small, deep seated, tender, follicular inflammatory nodule,
soon becoming pustular and then necrotic
• The necrotic core discharges pus from the follicular opening and heals with
scarring.
SITES
• Face
• Neck
• Axillae
• Buttocks
• Thighs
• Perineum

HISTOPATHOLOGY
Biopsy specimens reveal a dense neutrophilic infiltrate in the subcutaneous
tissue.
• Furuncles are characterized by an acute, suppurative reaction involving the
follicle below the infundibulum, as well as perifollicular necrosis with
fibrinoid debris.
• Ruptured epidermoid or pilar cyst
• Hidradenitis suppurativa
• Cystic acne
TREATMENT
• Simple furuncles- warm compresses may promote maturation, drainage,
and resolution.
• Larger or deeper fluctuant lesions -incision and drainage and Systemic
antibiotic therapy is recommended.

CARBUNCLE
A carbuncle is a deep infection of a group of contiguous follicles with S.
aureus, accompanied by intense inflammatory changes in the surrounding
and underlying connective tissues, including the subcutaneous fat.
• Carbuncles tend to be larger than abscesses/boils as they represent a cluster
of coalescing boils connected under the skin surface.
• More commonly seen in patients along with diabetes, malnutrition, cardiac
failure, drug addiction or severe generalized dermatoses, obesity and during
prolonged steroid therapy.
• Age : Predominantly in middle or old age.
• Sex : Males > females
• Causative organism: Staphylococcus aureus.

CLINICAL FEATURES
• It starts as smooth, dome‐shaped and acutely tender nodule which
increases in size 3-10cm over few days
• Suppuration begins after 5–7 days, pus is discharged from the multiple
follicular orifices giving a sieve like appearance
• Necrosis of the intervening skin leaves a yellow slough surmounting a
crateriform nodule.
• In some cases, the necrosis develops more acutely without a preliminary
follicular discharge, and the entire central core of the lesion is shed, to leave
a deep ulcer with a purulent floor and associated with fever and other
constitutional symptoms.
SITES
• back of the neck
• Shoulders
• Hips
• thighs
Lesions usually heal with scarring

TREATMENT
•Incision and drainage or saucerization
under local anesthetic is required to
remove pus and necrotic tissue and
expedite healing.
•Systemic and topical antibiotics.
MANAGEMENT
Topical treatment:
• Used locally, without any regional
lymphadenopathy and absence of
systemic symptoms.
Commonly used are:
2% mupirocin, 2% fusidic acid used
three times daily for 10 days.
MRSA is suspected, 1%silver
sulphadiazine cream, newer agents
like topical retapamulin and
indolmycin is used

Systemic treatment:
• For methicillin sensitive infections:
• Penicillinase resistant penicillin's(DOC)- Ex: Cloxacillin, Oxacillin, Dicloxacillin, Nafcillin,
Methicillin
• Beta lactamase inhibitors- Amoxicillin and clavulanic acid
• Macrolides –Ex: erythromycin, clarithromycin
• Cephalosporins- first generation: cephalexin, cefadroxil
second generation: cefprozil, cefuroxime
third generation: cefixime, ceftriaxone
cefamycins: cefoxitin, cefotetan
• Tetracyclines- doxycycline, minocycline
• Quinolones- ciprofloxacin, levofloxacin, moxifloxacin
If MRSA is suspected:
• Vancomycin- DOC
• Others: linezolid, daptomycin, quinpristin-daflopristin, sulfmethoxazole and trimethoprim,
clindamycin, tigecycline
• Newer drugs: Oritavancin, Dalbavancin , tedizolid
Eradication of carriers (S.aureus): in case of recurrent infections
• Topical mupirocin in nasal vestibule twice daily for 5 days/month for 3 consecutive months
• Methods to decolonize the skin (e.g. axillae, perineum/ groin, submammary area) include
topical mupirocin, washes containing chlorhexidine or triclosan

ERYSIPELAS
Erysipelas, or also known as St. Anthony’s fire is a superficial variant of
cellulitis caused primarily by group A streptococci that affects the dermis with
prominent lymphatic involvement; in contrast, classic cellulitis is centered in
the deep dermis and subcutaneous tissues
• Erysipelas is usually a disease of the very young, the aged, the debilitated,
and those with lymphedema or chronic cutaneous ulcers.
ETIOLOGY
Erysipelas lesions usually begin as a bright red plaque. It spreads rapidly and
may manifest as well-demarcated, erythematous, oedematous, and brawny
indurated plaques, which are warm to touch. Superficial bulla often develops
in the lesion as tissue oedema lifts the superficial skin layers.
• It is usually caused by group A streptococci.
• Groups G, B, C, and D streptococci are occasionally implicated.
S. aureus, Pneumococcus spp., Klebsiella pneumoniae, Yersinia
enterocolitica, and Haemophilus influenzae type b can also cause an
erysipelas like infection.

CLINICAL FEATURES
Erysipelas classically affects the face; the lower extremity is the most
common location.
• After an incubation period of 2 to 5 days, there is an abrupt onset of fever,
chills, malaise, and nausea.
• A few hours to a day later, a sharply marginated erythematous plaque with a
ridge-like border develops which progressively enlarges.
• It is clearly demarcated from the surrounding skin , hot, tense, and
indurated with non-pitting edema.
• The affected area is painful to palpation and may burn.
• Regional lymphadenopathy is usually present, with or without lymphangitis.
• Pustules, vesicles, bullae, and small areas of hemorrhagic necrosis may also
form
• When the infection resolves, desquamation and post-inflammatory
pigmentary changes may ensue.

HISTOPATHOLOGY
Biopsy specimens reveal diffuse edema and a neutrophilic infiltrate in the dermis. Dilation of the
lymphatics, foci of suppurative necrosis, and dermal–epidermal separation are often seen.
• other forms of cellulitis
• soft tissue infections (erysipeloid, necrotizing fasciitis)
• inflammatory causes of pseudo-cellulitis
TREATMENT
• A 10- to 14-day course of penicillin is the treatment of choice for erysipelas caused by streptococci.
• Macrolides (erythromycin) may be used in penicillin-allergic patients
Erysipelas may recur in patients with abnormal local circulation (e.g. lymphedema), and penicillin
prophylaxis is occasionally required

CELLULITIS
Cellulitis is an infection of the deep dermis and subcutaneous tissue that
manifests as areas of erythema, swelling, warmth, and tenderness. Fever with
chills and malaise are often present in cellulitis.
Lymphangitis, streaks of erythema extending from the lesion, is common and
lymph nodes are frequently enlarged and tender.
When S. aureus is the responsible pathogen, superficial pustules and vesicles
may eventually result in exfoliation
ETIOPATHOGENESIS
• Cellulitis in immunocompetent adults is most often caused by group A
streptococci or S. aureus, and the latter organism is the most frequent in
children.
• A mixture of Gram-positive cocci and Gram-negative aerobes and anaerobes
is often implicated in cellulitis surrounding diabetic and decubitus ulcer
• Bacteria typically gain access to the dermis via a break in the skin barrier in
immunocompetent individuals, but a bloodborne route is common in
immunocompromised patients.

CLINICAL FEATURES
• Cellulitis is often preceded by systemic symptoms such as fever, chills, and
malaise.
• The affected area displays all four of the cardinal signs of inflammation.
• The borders are usually ill-defined and non-palpable.
• In severe infections, vesicles, bullae, pustules or necrotic tissue may be
present
• Ascending lymphangitis and regional lymph node involvement may occur.
• There may be abscess formation and purpura.
• In children, cellulitis most often affects the head and neck, whereas in adults
it tends to involve the extremities.

• Perianal cellulitis caused by S. pyogenes presents in young children as
perianal erythema, which may be associated with painful defecation and
blood-tinged stool. Perianal cellulitis may be a trigger for guttate psoriasis.
• H. influenzae, a gram-negative rod, causes facial cellulitis in children 3
months to 4 years of age characterized by violaceous, indurated plaques.
Meningitis is a feared complication. The advent of the H. influenzae vaccine
has dramatically reduced the incidence of this form of cellulitis.
• Tinea pedis, eczemas, ulcers, trauma, burns, diabetes mellitus, and
malnutrition may be associated with cellulitis.

HISTOPATHOLOGY
• A mild or moderate inflammatory infiltrate composed of lymphocytes and
neutrophils can be seen throughout the dermis, often extending into the
subcutaneous fat.
• Additional findings include edema, which occasionally leads to subepidermal
bullae, and dilation of lymphatics and small blood vessels.
DIFFERENTIAL DIAGNOSIS OF LOWER EXTREMITY CELLULITIS
• DVT
• Eczema or dermatitis due to stasis, contact factors
• Superficial thrombophlebitis
• Lipo-dermatosclerosis
• Other forms of panniculitis
• Drug eruptions
• Radiation damage following radiotherapy
• Inflammatory breast cancer (carcinoma erysipeloides).

TREATMENT
Treatment is typically targeted against group A streptococci and S. aureus.
• For uncomplicated cases, a 10-day course of an oral antibiotic that covers
these organisms
• Hospitalization and parenteral antibiotics may be necessary for patients
who are seriously ill, have facial involvement, or fail to respond to oral
therapy.
• If MRSA is suspected, when there is cellulitis in association with an abscess,
agents such as clindamycin, TMP-SMX or doxycycline should be used
• Diabetic or decubitus ulcers complicated by cellulitis require broad-
spectrum coverage, such as piperacillin/tazobactam or, in penicillin-allergic
patients, metronidazole plus ciprofloxacin.
• Adjunctive measures include immobilization and elevation of an affected
extremity and the application of wet dressings to areas with bullae or
exudate.

ERYSIPELAS CELLULITIS
Caused by strep.pyogenes Caused by strep pyogenes and rarely staph.aureus
Involves upper subcutaneous tissue and lymphatic
vessels
Involves deeper subcutaneous tissue
History of antecedent throat infection Intertrigo or deep fissures for portal of entry
Common site include face, bridge of nose, and
cheeks
Commonest site is legs
Well defined margins are seen Indistinct margins seen
Vesicles or bullae formation is seen Bullae formation is severe
self-limiting If left untreated necrosis sets in

NECROTIZING FASCIITIS
Necrotising fasciitis is a very serious bacterial infection of the soft
tissue and fascia. The bacteria multiply and release toxins and enzymes that
result in thrombosis in the blood vessels which result in the destruction of
the soft tissues and fascia.
The main types of necrotising fasciitis are:
1.Type I (polymicrobial: more than one bacteria involved)
2.Type II (due to haemolytic group A streptococcus, and/or staphylococci
including methicillin-resistant strains/MRSA)
3.Type III (gas gangrene: clostridium species)
4.Other: marine organisms (vibrio species, Aeromonas hydrophila, considered
Type III in some reports) and fungal infections (candida and zygomycetes,
type IV in some reports).

An opening in the skin that allows bacteria to enter the body. This may occur
following minor injury (small cut, graze, pinprick, injection), or a large wound
due to trauma or surgery (laparoscopy, sclerotherapy, endoscopic-gastrostomy,
thoracostomy, Caesarean section, hysterectomy).
Sometimes no point of entry can be found.
• Cervicofacial necrotising fasciitis can follow mandibular fracture or dental
infection.
• Direct contact with a person who is carrying the bacteria.
• Particularly invasive strains of bacteria like streptococci that evade the immune
system and produce a toxin called cysteine protease SpeB, which dissolves
tissue.
In children, type II necrotising fasciitis may complicate chicken pox.
Other causes of necrotising fasciitis in children include omphalitis, necrotising
enterocolitis, and urachal anomalies.

RISKS FOR NECROTISING FASCIITIS
• Aspirin and NSAIDS
• Advanced age
• Diabetes mellitus
• Immune suppression
• Obesity
• Drug abuse
• Severe chronic illness
• Malignancy.
PTHOPHYSIOLOGY
The infection starts in the superficial fascia. Enzymes and proteins released by the
responsible micro-organisms cause necrosis of fascial layers.
• Horizontal spread of infection may not be clinically apparent on the skin surface and hence
diagnosis may be delayed. The infection then spreads vertically up into the skin and down into
deeper structures. Thrombosis occludes the arteries and veins leading to ischaemia and
necrosis of the tissues.
Streptococci produce:
• M proteins, which initiate an inflammatory response with the release of
numerous cytokines (IL-1, IL-6, TNFα)
• Exotoxins, which destroy neutrophils allowing bacterial growth and destroying tissues.
• Aerobic and anaerobic bacteria produce hydrogen, nitrogen, and hydrogen sulfide gases that
destroy hyaluronic acid enabling the spread of infection.

CLINICAL SYMPTOMS
Signs and symptoms vary between individuals but often some or all the following
are present.
INITIAL SYMPTOMS
• The most common site of infection is the lower leg. Necrotising fasciitis may also
affect upper limb, perineum, buttocks, trunk, head and neck.
• Symptoms appear usually within 24 hours of a minor injury.
• Pain is often very severe at presentation and worsens over time.
• There may be flu-like symptoms, such as nausea, fever, diarrhoea, dizziness and
general malaise.
• Intense thirst develops as the body becomes dehydrated.

CLINICAL FEATURES AFTER 3 TO 4 DAYS
• The affected area starts to swell and may show a purplish rash
• Large dark marks form that turn into blisters filled with dark fluid
• The wound starts to die, and area becomes necrosed
• Oedema is common
• A fine crackling sensation under the skin (crepitus) is due to gas in the
tissues
• Severe pain continues until necrosis/gangrene
destroys peripheral nerves when the pain subsides
By about days 4–5, the patient is very ill with dangerously low blood
pressure and high temperature. The infection has spread into the
bloodstream and the body goes into toxic shock. The patient may have
altered levels of consciousness.
Metastatic abscesses can develop in liver, lung, spleen, brain, pericardium,
and rarely, in the skin.

AREA OF
TENDERNESS
,ERYTHEMA,
WARMTH AND
SWELLING
(UNRESPONSIV
E TO
ANTIBIOTICS)
TENSE AND
SHINY SKIN
SKIN COLOUR
CHANGING
FROM RED
AND PURPLE
TO
CHARACTERISTI
C GRAY BLUE IN
ILL DEFINED
PATCHES
WITHIN 36 HRS
HEMORRHAGIC
BULLAE
FORMATION
NECROSIS OF
FAT AND
FASCIA
PRODUCING
THIN WATERY
MALODOROUS
FLUID
ANESTHESIA
OVER THE
AREA
Subcutaneous tissue may feel woody (hard) on palpation
Pt. becomes extremely toxic, fever with chills, malaise, tachycardia, shock.

DIAGNOSIS
A thorough history and clinical examination are crucial in arriving at the diagnosis of
necrotising fasciitis. Special care should be taken when examining immunocompromised
patients, as the presentation of symptoms/signs may be atypical.
• Clostridial and streptococcal infections because of traumatic or surgical wound
usually manifest quickly compared to necrotising fasciitis due to other organisms.
• A positive finger test is highly pathognomic for necrotising fasciitis.
(A 2–cm vertical incision is made in the affected skin and an index finger is pushed into
the tissue. The test is positive if the finger passes through the subcutaneous tissue
without resistance)
• There is poor adherence of tissue to the fascia on incising the site.
• Necrotic tissue/pus oozes out of the fascial planes.
• Dishwater-coloured fluid seeps out of the skin.
• Typically, necrotising fasciitis does not bleed.
LABORATORY SCREENING INVESTIGATIONS
• White blood cell (WBC) count > 15.4 x 109/L
• Serum sodium < 135 mmol/L
• Raised C-Reactive Protein (CRP) (> 16 mg/dL)
• Raised creatinine kinase (CK) level (> 600 U/L)
• Urea > 18 mg/dL.

• Blood culture, deep tissue biopsy and Gram stain help in identifying the
culprit organism(s) and guide the choice of antibiotic. If Staphylococcus
aureus is detected, MRSA sensitivity test should be done. Blood cultures are
usually negative for clostridial species.
• Fungal culture should be performed in immunocompromised and trauma
patients.
LABORATORY RISK INDICATOR FOR NECROTISING FASCIITIS
The Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC) is a tool that aids
in distinguishing necrotising fasciitis from other tissue infections based on six
parameters. A score of ≥ 6 favours necrotising fasciitis. This test is not appropriate
for all cases and is not completely reliable.
PARAMETERS FOR LRINEC
• CRP (mg/dL) ≥15: 4 points
• WBC count (109/L): <15: 0 points, 15–25: 1 point, >25: 2 points
• Haemoglobin (g/L): >135: 0 points, 110–135: 1 point, <110: 2 points
• Serum sodium (mmol/L) <135: 2 points
• Creatinine (umol/L) >141: 2 points
• Glucose (mmol/L) >10: 1 point

HISTOPATHOLOGY
• Gangrene of subcutaneous tissues followed by coagulation necrosis
• Fibrinoid necrosis in media of vessels passing through destroyed fascia.
• Infiltration of neutrophils, mononuclear cells and bacteria in upper layer of
dermis.

TREATMENT
• Extensive surgical debridement (fasciotomy) is the mainstay of effective treatment.
• Empiric therapy should be initiated with broad-spectrum coverage against streptococci,
staphylococci (including MRSA), Gram-negative bacilli and anaerobes – e.g. vancomycin,
linezolid, or daptomycin combined with piperacillin/ tazobactam or carbapenem.
• In penicillin allergy, empiric therapy with ciprofloxacin plus metronidazole or clindamycin can
be used
• Supplemental oxygen, fluids, and medicines may be needed to raise blood pressure.
• Hyperbaric oxygen and intravenous immunoglobulin may also be considered.
• When the acute infection has subsided, the wound should be closed with skin grafting if
required. Vacuum-assisted wound closing devices may be useful to heal a persistent ulcer.
OUTCOME
Prompt diagnosis and treatment are essential to reduce the risk of death and disfigurement
from necrotising fasciitis.
• If diagnosed and treated early, most patients will survive necrotising fasciitis with minimal
scarring. If there is significant tissue loss, later skin grafting will be necessary and in some
patients amputation of limbs is required to prevent death.
• Up to 25% of patients will die from necrotising fasciitis, due to complications such
as renal failure and septicaemia(blood poisoning) and multiorgan failure.

STREPTOCOCCAL INTERTRIGO
Intertrigo caused by group A streptococci is an under-recognized entity that
usually affects infants and young children. Infants are particularly vulnerable
due to irritation and friction in moist, deep skin folds of the neck, axillae,
antecubital and popliteal fossae, and inguinal region.
CLINICAL FEATURES
• Sharply demarcated, intensely erythematous patches or thin plaques in an
intertriginous site, often accompanied by a foul odor.
• In contrast to intertriginous candidiasis, satellite lesions are uncommon.
• In genetically predisposed children, cutaneous streptococcal infection may
trigger psoriasis.
• Bacterial culture can confirm the diagnosis
• simple intertrigo: barrier creams and other measures to reduce friction and
minimize moisture.
A 10-day course of oral penicillin or amoxicillin is effective.

BLISTERING DISTAL DACTYLITIS
Blistering distal dactylitis is a localized infection of the volar fat pad of a finger
or a toe caused by Group A Streptococcus spp. or S. aureus and most seen in
children aged 2–16 years.
CLINICAL FEATURES
• Darkening of the skin is often observed for several days to a week before
blister formation
• Tense blisters on an erythematous base containing thin seropurulent fluid
on the distal phalanx, usually of a finger, and typically on the palmar pad,
may extend sometimes to the nail folds, proximal part of the palmar skin
• Herpetic whitlow
• Bullous impetigo
• Pompholyx eczema.

TREATMENT
• Drainage of intact bullae
• β‐ lactamase‐resistant
antibiotics (flucloxacillin,
dicloxacillin, cloxacillin,
temocillin) for 10 days
• Topical therapy(mupirocin)
with wet dressings

PARONYCHIA
It is the infection of the lateral and/or of the proximal nail folds.
PREDISPOSING FACTORS
• Nail biting, thumb-sucking
• Diabetes mellitus
• Overzealous manicuring with unsterile instruments
• Ingrown toe nail
• linjury from a splinter or thorn
• Manicure procedures
It can be: Acute or Chronic

ACUTE PARONYCHIA:
• Caused by S.aureus , GroupA beta-hemolytic streptococci
• Characterized by acute onset of pain and erythema of proximal and/ or lateral
nail fold with subsequent development of a superficial abscess
TREATMENT
• Without abscess: topical + systemic antibiotics + NSAIDS
• With abscess: Incision and drainage

BOTRYOMYCOSIS
Also called as Granular bacteriosis, Bacterial pseudo-mycosis.
• Botryomycosis was named for its characteristic groups of granules that
resemble grapes.
• It is a rare, chronic, purulent and granulomatous bacterial infection that
primarily affects the skin and is most often caused by S. aureus.
CLINICAL FEATURES
• It presents as cutaneous and subcutaneous nodules, ulcers, or verrucous
plaques.
• Multiple sinuses and fistulas may discharge purulent fluid or yellow granules
composed of bacterial masses.
• Most patients have localized involvement of an extremity following trauma.
• The lesions may be pruritic or tender, and they may affect the underlying
muscle or bone.

DIAGNOSIS
• When botryomycosis is suspected, both bacterial and fungal cultures should be
obtained and a skin biopsy performed for histopathologic examination as well as
culture.
• Microscopic examination (fresh mount or 20% KOH) shows coarsely lobulated
granules with club-like projections.
• Gram staining of crushed granules usually displays masses of staphylococci.
• Mycetoma
• Actinomycosis
• Ruptured epidermoid cyst
• staphylococcal abscess
• Tuberculosis, and
• Dimorphic fungal or atypical mycobacterial infections.
TREATMENT
It is treated surgically with debridement or excision in conjunction with antibiotic
therapy.

ERYTHRASMA
Erythrasma is caused by Corynebacterium minutissimum.
Favoured sites of infection are:
• Inguinal
• Intergluteal
• Interdigital
• Axillary
• Sub-mammary areas.
It is more common in obese, elderly, and diabetic patients especially in moist climates.
Clinically, it is characterized by well circumscribed red-brown plaques that are usually
asymptomatic. Mixed infections with dermatophytes and Candida species can also occur
Differential diagnosis
• Sebo-psoriasis
• Dermatophytosis
• pityriasis versicolor
• candidiasis.

Pityriasis versicolor predominantly occurs on the upper trunk, and
although it is difficult to differentiate erythrasma of the toe clefts from
tinea pedis or candida infection, coral red fluorescence under Wood’s light
is diagnostic.
Since many patients have both tinea pedis and erythrasma, mycological
examination of scales is important. Flexural psoriasis also needs to be
excluded.
Wood’s lamp examination reveals coral-red fluorescence due to the
presence of porphyrin production by the bacteria. Since the organism is
bacterial, KOH preparations only rarely demonstrate it in the scales. Gram
stain preparations are preferable and show gram-positive rod-like
organisms, filamentous and coccoid forms. Culture is rarely required,
except as a research procedure.

TRICHOBACTERIOSIS (TRICHOMYCOSIS)
This is an asymptomatic bacterial disorder affecting the hair shafts on the skin
folds, primarily of the axillary hair. Pubic hair may also be affected. Like
erythrasma, this disease is also more prevalent in warm and moist
environment.
ETIOLOGY
Disturbances in apocrine sweat production and bacterial proliferation are
crucial for the development of trichomycosis. Corynebacterium tenuis is the
pathogenic agent. According to the current taxonomic position, most agents
are denoted as Corynebacterium species.
CLINICAL FEATURES
It can exhibit three different clinical presentations. The most common clinical
variant is trichomycosis flava (yellow), while rubra (red) and nigra (black)
variants occur much less frequently. It consists of a bacterial biofilm that
encases the hair shaft.

INVESTIGATIONS
• Wood’s lamp reveals a pale yellowish fluorescence. Direct examination of
infected hair can be seen as concretions or bacterial masses consisting of
coccoid and diphtheroid shapes measuring between 0.5 and 1 μm, and could
be seen adhered to the hair, which rules out most mycoses that affect the hair
(tinea and piedra)
TREATMENT
• Treatment strategies include topical erythromycin, clindamycin, and imidazole
derivatives.
• Benzoyl peroxide has also proven to be effective in treating and preventing
Trichobacteriosis. Clipping or shaving axillary hair and the use of antiperspirant
products such as aluminum chloride prevent recurrences.

Polarized dermoscopy image revealing waxy and yellowish adherent
nodules and concretions along the entire length of the hair of the axilla

PITTED KERATOLYSIS
Pitted keratolysis is a skin infection of the feet that was initially described by
Castellani in 1910.
ETIOLOGY
• It is thought to be caused by Dermatophilus congolensis, Kytococcus
sedentarius (formerly Micrococcus species), Actinomyces keratolytica,
Streptomyces, and Corynebacterium species.
• The warm, moist, and occlusive environment favours these organisms.

CLINICAL FEATURES
Pitted keratolysis manifests as discrete pits or crater like lesions on the
plantar surfaces. These punched lesions congregate on the thicker, pressure-
bearing areas of the feet (heel, balls of feet, and toepads).
• The craters range from 1–7 mm in diameter and are similar in depth. Some
pits have a brownish colour that may give feet a dirty appearance. The
adjacent pits may coalesce to form larger craters. Hyperhidrosis may be
associated with this disease and the pits become more prominent when
water soaked.
The feet of a patient who has pitted keratolysis is typically malodorous
providing a distinct clue to the correct diagnosis.

• Plantar warts
• Taenia pedis
• Punctate nevus syndrome
• Arsenic keratosis
TREATMENT
Systemic and/or topical erythromycin is the treatment of choice for pitted
keratolysis.
• Other options include topical imidazole derivatives.
• Sweat control, topical keratolytic agents, and hygiene measures also help in
preventing the recurrences.

ERYSIPELOID
Erysipeloid is an acute infection of traumatized skin occurring most frequently
in fishermen, butchers, and housewives handling raw fish, poultry, and meat
products.
• This is also named as Rosenbach’s disease or pseudo-erysipelas.
ETIOLOGY
Erysipeloid is caused by gram-positive bacillus Erysipelothrix rhusiopathiae.
CLINICAL FEATURES
Human infections may be of three clinical varieties:
1.Localized cutaneous
2.Diffuse cutaneous
3.Generalized

• The most common localized cutaneous infection clinically
presents with polygonal plaques on the finger or hand, violet or
purple-red in colour, warm and tender, and have well-defined
raised margins.
• As the lesion advances centrifugally, the central region clears
with desquamation. When fingers are involved, the swelling may
be severe (whale finger/seal finger). The incubation period varies
from 1–7 days after inoculation.
• A diffuse cutaneous form has been described, which involves
multiple areas of the body.
• In the systemic form, the constitutional symptoms occur,
cutaneous lesions may be seen, and clinical involvement may
include septicaemia, endocarditis, cerebral abscess, arthritis, and
empyema.

INVESTIGATIONS
• The organism can be seen using gram stain of the serous discharge. The
organism grows slowly in media enriched with blood and incubated in an
atmosphere containing 5–10% CO2.
• The histopathological examination reveals dilatation of the blood vessels in the
papillary and subpapillary areas and perivascular inflammatory infiltrate
consisting of neutrophils and lymphocytes.
TREATMENT
• Penicillin and cephalosporins are the first-line choices for the treatment. A 7
day course is appropriate and clinical improvement usually occurs 2–3 days
after the beginning of the treatment.
• Patients allergic to penicillin may be treated with a combination
of erythromycin and rifampicin.

PERIANAL STREPTOCOCCAL
CELLULITIS/DERMATITIS
• The name is inappropriate for this superficial infection as it lacks fever and other
systemic symptoms, although surface swabs yield GAS in all cases.
• Most patients are children aged between 6 months and 10 years, with with a male
predominance (4:1) but occasional adult cases are seen.
• It's associated with guttate psoriasis and vulvovaginitis (females).
• Fraction of the patients were found to harbour streptococcus pyogenes in the throat,
usually of the same strain, and sometimes there is a recent history of pharyngitis or
impetigo in a family member. In some reported cases, there had been symptoms for
many weeks or months suggesting that chronic infection may occur.
CAUSATIVE ORGANISMS
• Streptococcus pyogenes is the main organism responsible but occasionally
staphylococcus aureus has been reported to cause a similar clinical appearance with
satellite pustules at the periphery.

CLINICAL FEATURES
• Perianal soreness or irritation, pain on defecation and sometimes secondary faecal
retention are typical presenting symptoms. The affected skin is bright red and may be
fissured. The genital skin may also be additionally affected
• Diaper dermatitis
• Seborrheic dermatitis
• Kawasaki disease
• IBD
• Scarlet fever
• Candidiasis/candida intertrigo
• Sexual abuse
• Pinworms
• Flexural psoriasis
INVESTIGATIONS
• Perianal swab for microbiology.
MANAGEMENT
• 7-day course of cefuroxime is more effective than a 10-day course of penicillin in the
treatment of perianal streptococcal disease
• Reoccurrence in some patients respond to erythromycin and topical mupirocin for 10–14
days.
• A 2‐week course of oral antibiotic treatment is usually recommended.

Perianal streptococcal dermatitis and
vulvovaginitis

STREPTOCOCCAL VULVOVAGINITIS
vaginal infection with GAS mainly affecting prepubescent girls.
• Mainly affects prepubescent girls but women may also be affected, and perianal
infection occasionally coexists.
Personal or family member with a cutaneous or respiratory infection with GAS.
• In older women, sexual contact with an infected person.
CAUSATIVE ORGANISMS
• Streptococcus pyogenes accounts for 10% of cases of vulvovaginitis in prepubertal
girls.
• Other bacterial causes of vulvovaginitis in prepubertal girls include Escherichia coli,
Enterococcus faecalis, Haemophilus influenzae, Proteus mirabilis and Staphylococcus
aureus which cannot be distinguished clinically.

CLINICAL FEATURES
• The usual complains are irritation or soreness in the vaginal area with
associated pain on passing urine. The skin is erythematous with or
without purulent/watery or yellow vaginal discharge or dysuria.
• Candida infections
• STI
MANAGEMENT
• The symptoms usually settle with appropriate systemic antibiotics;
however, recurrence may be problematic
• The infection responds to oral penicillin or erythromycin. Some report
rapid cure with vaginal clindamycin 2% cream.
• some evidence suggest that there may be concomitant streptococci
and Candida in women therefore treatment with antibiotics plus
fluconazole may be indicated

Phase contrast microscopy from vulvo-vaginal swab

TRICHOMYCOSIS AXILLARIS
The name trichomycosis is a misnomer as it is bacterial infection in origin.
• Trichomycosis axillaris is a superficial bacterial infection of underarm hair.
The disease is characterised by yellow, black or red granular nodules or
concretions that stick to the hair shaft. It can also affect pubic hair (when it
is called trichomycosis pubis).
• It forms adherent granular nodule, yellow, black or red, on the hair shaft.
• It occurs in males and females of all races in temperate and tropical climates
but is more common in males than females.
CONTRIBUTING FACTORS
• Humidity and warmth
• Crowded conditions
• Poor hygiene
• hyperhidrosis
• Obesity

CLINICAL FEATURES
• Trichomycosis axillaris is symptomless and often ignored.
Signs include:
• Sweaty, smelly armpits
• 1–2 mm yellow, red or black concretions encircling the hair shaft, which
make the hair appear beaded or thicker. Yellow concretions are the most
common, whilst red and black are found in tropical climates
• Sweat is also discoloured yellow, red or black, and may stain clothing
• Hair loss is rare and is due to bacteria invading and destroying the hair shaft.
The corynebacterial triad is the occurrence of erythrasma, trichomycosis
axillaris, and pitted keratolysis in a single individual.

DIAGNOSIS
• Trichomycosis axillaris is mostly diagnosed by its clinical appearance.
• Wood lamp examination shows pale-yellow fluorescence.
• Potassium hydroxide preparation and Gram staining can identify the bacteria.
• The condition may resemble pubic lice (pediculosis) and Trichosporon
aselie infections.
MANAGEMENT AND PREVENTION
• The fastest way to get rid of trichomycosis axillaris is to clip or shave the affected
area
• Effective topical antibacterial preparations
include clindamycin, erythromycin and fusidic acid.
• Clotrimazole powder is also curative.
• Recurrences of trichomycosis axillaris are prevented by keeping the
underarm dry and clean.
• Antiperspirants with aluminium chloride reduce sweating
• Antiseptics such as benzoyl peroxide gel or wash reduce bacterial colonisation

MELIOIDOSIS
• Melioidosis is an uncommon tropical disease caused by the bacterium
Burkholderia pseudomallei (formerly Pseudomonas pseudomallei and Malleomyces
pseudomallei).
• Melioidosis is endemic in South-East Asia and northern Australia, and cases also
occur in the South Pacific, Africa, India, the Middle East, and Central and South
America. It may be isolated from soil and water in low‐lying rice growing regions.
• Though it is a systemic infection which can result in the development of skin lesions
such as abscesses, it has the potential to produce fatal disease and is considered a
potential biological warfare agent because it is highly infectious, especially
by inhalation.
Melioidosis is also called Whitmore disease, Vietnamese time bomb, Night cliff
gardener's disease, morphia injector’s septicaemia, and paddy-field disease.

CLINICAL FEATURES
• The disease may run an acute, subacute or chronic course.
• The acute form with fever, prostration, gastroenteritis and pneumonia may be fatal
within 2–4 days, but acute pulmonary infection due to B. pseudomallei is the
commonest clinical manifestation of the illness. Septicaemia may complicate
pneumonitis or appear without localizing signs.
• Transmission in humans is thought to follow environmental contamination of a
minor injury. In humans, B. pseudomallei typically causes a severe, glanders‐like
illness, which may be fatal, but serological evidence and retrospective enquiries
suggest that mild febrile illnesses and subclinical infections occur in human subjects
and probably in animals.
• Other rare modes of transmission include inhalation or ingestion with variable
incubation period.
• Many cases are subacute and last from one-to-many weeks. If the initial lesion is
cutaneous, local abscess formation is rapidly followed by lymphangitis,
lymphadenitis and septicaemia; characteristically, multiple abscesses develop,
subcutaneously or in the muscles, lung, liver and spleen which often ulcerate.
• After infection by inhalation, pneumonic symptoms precede the septicaemic stage.
In many cases, however, the clinical picture is variable, with unexplained fever and
disseminated pyogenic lesions.

CLINICAL VARIANTS
Chronic forms may occur:
Pulmonary symptoms and metastatic abscesses are most seen.
In one patient an associated, severe urticaria cleared after treatment with
tetracycline.
Rarely, the infection remains limited to skin and regional lymph nodes, without
systemic symptoms.
• Tuberculosis
• Staphylococcal disease with sepsis
• Invasive klebsiella infection
• Anthrax
• Tularaemia
• Cat scratch disease
• Glanders
• Nocardiosis
• Plague

COMPLICATIONS
Melioidosis can be life-threatening. The risk is increased with more extensive or severe
disease and co-morbidities such as chronic diseases (diabetes, chronic lung disease,
the liver or kidney disease) and immunosuppression.
Complications include:
• Sepsis
• Organ failure
• Pneumothorax
• Cardiac tamponade
• Recurrence of infection.
TREATMENT
• The treatment of choice is ceftazidime, meropenem or imipenem.
• Can be combined with co‐trimoxazole.
• Alternatives include piperacillin and cefotaxime.
• Abscesses require surgical drainage once antibiotic treatment is established.
• Resistance to some antibiotics, including co‐trimoxazole, has been reported in some
endemic areas, and possible antibiotic sensitivities should be determined

GLANDERS
• Glanders is a rare, sporadic disease caused by the bacterium Burkholderia mallei.
(A.K.A Pseudomonas mallei, Actinobacillus mallei, Pfeifferella mallei, Malleomyces
mallei, Corynebacterium mallei, Mycobacterium mallei, and Bacillus mallei)
• Glanders is primarily a disease of horses and can infect other animals. Humans
working closely with infected animals (mostly horses) or tissue from them,
veterinarians, laboratory workers, stable hands, butchers, and abattoir workers are
usually affected.
• There is no accurate figures for incidence but its seen in parts of Africa, Asia, the
middle east, and central and south America.

CLINICAL FEATURES
• B. mallei bacteria are spread through skin abrasions, mucous membranes, or the
inhalation of contaminated dust. Person-to-person transmission is rare.
The incubation period for glanders is around 1–14 days after infection. The clinical
presentation will depend upon the mode of entry, and it is like that of melioidosis.
Symptoms common to all forms include fever, sweating, muscle ache, chest pain, and
headache.
• at the site of inoculation cellulitis sets in which soon breaks down to form an irregular
ulcer with an offensive haemorrhagic purulent discharge.
• If the primary site is cutaneous, the regional lymphatics become swollen and tender,
and dull‐red nodules along their course break down to form abscesses and sinuses.
• If the nasal or oral mucous membrane is the site of inoculation, there is extensive
necrosis and destruction of the septum and palate.
• Few days to weeks later metastatic lesions begin to appear as grouped, dull‐red
papules, pustules or bullae, especially over the joints and face, which is followed by
ulcers that enlarge and coalesce.
Deep subcutaneous abscesses with multiple sinuses may also occur.
Pulmonary infection causes SOB, muscle pain, cough. If left untreated it leads to
septicaemia and death usually occurs within 10 days.
• Chronic infection may lead to abscess formations in the liver, spleen, lung, skin, or
muscles and the symptoms are less severe than those described in acute infection.
Chronic infection is reported to persist for up to 25 years in some cases.

INVESTIGATIONS
The different clinical variants may simulate sporotrichosis, acute pyogenic infections or
gangrenous pyoderma.
• The diagnosis may be suspected on the history of contact with horses, in which, how
ever, the infection may sometimes be clinically inapparent, but must be confirmed
by isolation of the organisms and by serological tests.
• Blood, sputum and site inoculation site swab cultures confirm diagnosis.
• Meliodosis
• Tuberculosis
• Staphylococcal disease with sepsis
• Anthrax
• Tularaemia
Treatment
The treatment of choice is ceftazidime, meropenem or imipenem

RHINOSCLEROMA
It is a chronic slowly progressive potentially fatal infectious and mildly contagious
disease caused by the bacterium Klebsiella pneumoniae rhinoscleromatis (Klebsiella
rhinoscleromatis) that affects the upper and lower airways.
• The disease occurs sporadically almost all over the world and is endemic but rare in
certain countries including Central, East and West Africa, and Central and South
America and the USA. The disease is acquired by direct or indirect contact with the
nasal exudate of an infected person. It is more common in rural areas where social
and hygiene standards are low.

CLINICAL FEATURES
Three clinical stages have been described:
1. Catarrhal stage: patients initially have non-specific symptoms, such as a runny
nose or blocked nose. As the disease progresses, the nasal discharge may
contain pus and develop a foul odour. Dry crusting of the mucous membranes of
the nose can occur. This stage can last for weeks to months.
2. Granulomatous (also called hypertrophic or proliferative) stage: the mucosal tissue
inside the nose becomes bluish-red, and rubbery nodules (lumps) form. As these
granulomatous swellings grow, they can cause nasal enlargement and deformity.
Symptoms include bleeding noses, nasal obstruction (or obstruction elsewhere in
the respiratory tract), loss of the sense of smell, a hoarse voice, and thickening or
numbing of the soft palate.
3. Sclerotic or fibrotic phase: the granulation tissue is replaced by hardened scars,
which can occasionally result in blocked airways.

HISTOPATHOLOGY
Histopathological picture is pathognomonic. A dense infiltrate is observed consisting
mainly of plasma cells and two types of highly characteristic cells which are Mikulicz
cells and Russell bodies.
[Mikulicz cell is a large round vacuolated histiocyte measuring 100–200 μm in
diameter containing Giemsa or Gram‐positive bacilli (A gran ules) or amorphous
clusters of mucopolysaccharide (B granules) The Russell body or colloid body,
measuring 20–40 μm, is a structure in the cytoplasm of the plasma cells, elliptical in
shape, homogeneous and extremely eosinophilic, and as such stains bright red.]
• Inside the Mikulicz cells, the bacilli are protected from therapeutic products in the
blood, and hence there is a need for long‐term therapy to be active against the
bacteria when they are released.
• The diagnosis is based on the clinical features, especially when the lesions are
advanced or pronounced; the characteristic histopathological picture; the finding of
Frisch bacilli, adequately identified bacteriologically; and complement‐fixation tests
(inconsistent results).

Mikulicz cell
Dense inflammatory
cells composed of
lymphocytes, plasma
cells and few
eosinophils

TREATMENT
• Klebsiella rhinoscleromatis may be sensitive to several antibiotics. It is advisable to
determine the antibiotic sensitivity of each strain and to continue the treatment
until bacteriological cure is obtained.
• First line of treatment is with tetracycline – D.O.C for long‐term treatment, at a dose
of 2 g/day, given in divided doses for 6 months, followed by 1 g/day for a similar
period.
In the case of recurrence, cephalexin, at similar doses and duration.
• Ciprofloxacin, 250–500 mg twice a day, with meticulous nasal lavage with saline
twice a day for 4 weeks, has been advocated.
• Trimethoprim– sulfamethoxazole, 160–800 mg twice a day (based on in vitro
sensitivity studies), and betamethasone sodium phosphate, 4 mg i.m. every 3 weeks
for 6 months, have been used.
• In inactive fibrotic stage stage, surgical treatment may be required to correct severe
structural and functional abnormalities, such as the narrowing of the nasal vestibule,
nasopharyngeal stenosis and laryngeal web formation.
• Nasal endoscopic techniques and CO2 laser have been used for the treatment of
obstructive scars.

BACILLARY ANGIOMATOSIS
Bacillary angiomatosis is an opportunistic cutaneous and systemic bacterial infection
caused by Bartonella quintana and Bartonella henselae, gram
negative intracellular bacteria.
• Cats are the main reservoir for B henselae, and humans for B quintana. Although the
infection may be spread via cat bites and scratches, fleas are the major route of
transmission. B quintana is transmitted by the human body louse (Pediculus
humanus) and fleas. Usually affecting immunocompromised patients.
• Toler et al first described this condition in 1982 in an immunocompromised 32-year-
old man.
• Bacillary angiomatosis is seen predominantly with druginduced immunosuppression,
particularly organ transplant recipients, chronic lymphocytic leukaemia, and those
with HIV/AIDS.
• Healthy individuals, including children, can also contract the infection such as after
major local trauma.

CLINICAL FEATURES
• Skin lesions are usually the first manifestation of bacillary angiomatosis.
• Papules and nodules, range in size from pinpoint to 10cm
• Purple, violaceous, or bright red in colour
• Single lesion or many hundreds
• Any skin or mucosal site can be involved, although rarely the palms and soles
• In HIV, large subcutaneous tumours may form
• Lesions may bleed easily
• Overlying skin surface may become ulcerated or crusted
DIAGNOSIS
• Skin biopsy
• PCR

HISTOPATHOLOGY
Histologically, the lesions of bacillary angiomatosis closely resemble pyogenic granuloma.
Typically, there are ulcerated papules or nodules composed of lobules of highly
vascularised oedematous connective tissue with epithelioid cells and inflammatory infiltrates
including neutrophils and leukocytes.
• There is typically a mixed-cell infiltrate and nuclear dust of degenerated inflammatory cells.
Accompanying this peculiar background are diagnostic clumps of pink-
purplish granular material.
• The microorganisms can be seen as basophilic clumps in the stroma and confirmed on Giemsa
or Warthin-Starry stain
Bacillary angiomatosis should be suspected clinically, particularly in an immunocompromised
patient.

COMPLICATIONS
• The infection can cause blood vessels to grow out of control and form tumour-like
masses in other organs including the brain, bone, gastrointestinal tract, and
respiratory tract with airway obstruction.
• Liver involvement is called 'peliosis hepatis' or 'bacillary peliosis’.
TREATMENT
• Erythromycin 500mg QID
• Doxycycline 100mg bd
• Other antibiotic options include trimethoprim +sulpha-methoxazole, tertacyclines,
rifampicin.
• Antibiotics should be continued for 3-6 months to prevent recurrence.
• Large pus-filled lymph nodes or blisters may need to be drained. Supportive therapy
includes hydration and analgesics for pain and fever. Warm moist compresses to
affected nodes may decrease swelling and tenderness.

TULARAEMIA
Tularemia is also known as rabbit fever or deer fly fever, which is an extremely
virulent, pleomorphic, aerobic, intracellular, gram-negative coccobacillus
Francisella tularensis which is transmitted by ticks and other animals.
• Other animals that can transmit F. tularensis include rabbits, squirrels,
opossums, cats, muskrats, and mosquitoes.
• F. tularensis is mainly found in the Northern hemisphere and has been
reported in North America, Russia, Europe, the Middle East, China, and
Japan.
• Two predominant strains of F. tularensis have been isolated:
1. Type A- causes more severe disease, causing death in up to 5% to 7% of
untreated patients.
2. Type B- generally causes a milder illness, which can occasionally
be symptom-free.0-

CLINICAL FEATURES
• In adults – fever, headache, skin changes, malaise, and enlarged lymph nodes of the
head and neck.
• In children – fever, sore throat, enlarged liver and spleen, fatigue and malaise.
• Various clinical subtypes of tularaemia have been described depending on the mode
of transmission and organ systems involved.
CLINICAL SUBTYPES FEATURES
ULCERO-GLANDULAR
(75-85%)
F. tularensis penetrates the skin through a scratch,
graze, or tick or insect bite. Most common form of
tick-borne tularaemia. Causes a painful skin ulcer,
with enlarged, inflamed nearby lymph nodes,
or nodular lymphangitis (swellings beneath the skin
that track along the course of lymph channels,
swellings may be painful and ulcerate). Lymph nodes
may become fluctuant (soft, fluid-like) and rupture.
GLANDULAR
(5-10%)
Causes enlarged lymph nodes without an ulcer.
OCULO-GLANDULAR
(1-2%)
Due to direct contamination of an eye, e.g. from a
squeezed tick spraying blood directly into the eye.

Other clinical subtypes include:
Typhoidal (most lethal, 5-15%)
Pneumonic (rare)
Oropharyngeal (rare)
Gastrointestinal (rare)
PRIMARY LESION:
• This develops at the point of entry after a 2 to 5 day incubation period. The
lesion is a painful red papule (lump) that slowly enlarges and ulcerates
within a few days. The ulcer has raised, hardened, ragged edges, and a
sensitive base. A discharge may be present, and the ulcer may be covered by
an eschar (scab) and/or be itchy. Over weeks to months the ulcer heals and
is replaced by scar tissue.
• The primary lesion caused by type B tularaemia infection may be less
severe, e.g. crusting, but no ulcer.

SECONDARY LESIONS:
• Secondary lesions (called tularemids) develop in 8% to 20% of cases of tularaemia
and take various forms:
• The most common secondary lesions are papular (small elevated lumps)
or papulovesicular (small elevated lumps and blisters). Occasionally the lesions
are macular (flat discolouration), maculopapular (small discoloured
lumps), vesicular, pustular (pus-filled blister), pimple-like, nodular
(larger, solid papule), or plaque-like (broad, flat lesion). These lesions appear around
11 days after the onset of symptoms and may be widespread, symmetrically
distributed on both sides of the body, and itchy.
• Erythema nodosum occurs in 1% to 13% of cases and appears at the end of the
second week of illness.
• Erythema multiforme occurs in 0.5% to 2.0% of cases and predominantly affects the
trunk and extremities. Erythema nodosum may also be present.
• Less common secondary skin lesions include herpes simplex labialis (cold
sores), urticaria, and lymphangitis (red streaks visible along the path of lymph
channels) and swollen, tender lymph nodes.
• Sweet syndrome has also been reported along with tularaemia.

DIAGNOSIS
• The diagnosis of tularaemia is usually made by serologic testing (detection
of antibodies against F. tularensis in the blood). A rising level of antibodies between
the acute and convalescent stages of disease confirms the diagnosis. Because this
process can take 2 to 4 weeks, treatment may be started based on the patient’s
history and clinical features.
• F. tularensis can be isolated from blood, biopsy samples, or other bodily fluids and
tissues. A specific culture medium is required to grow this organism in the
laboratory. F. tularensis is highly infectious to laboratory staff so
infection control precautions are required.
• Blood tests show disturbed liver function in around half of all patients.
The differential diagnosis of a necrotic skin ulcer includes:
• Anthrax
• deep fungal infections
• atypical mycobacterial infections
• milker’s nodule
• glanders
• plague

TREATMENT
Antibiotics used to treat tularaemia include:
• Streptomycin
• Gentamicin
• Doxycycline
• ciprofloxacin.
Treatment usually lasts 10 to 21 days depending on the stage of illness and
the medication used. Although symptoms may last for several weeks, most
patients completely recover.

LYMES DISEASE
• Lyme disease is an infection caused by Borrelia burgdorferi. Lyme disease can
affect any part of the body, most commonly the skin, central nervous
system, joints, heart, and rarely the eyes and liver.
• Lyme disease is common in parts of the United States (Massachusetts area)
and Europe but is reported from many areas of the world. In New Zealand
and Australia, cases have only been confirmed in people that have recently
travelled from an endemic area.
Lyme disease is also called Lyme borreliosis.
• The principal vector of B. burgdorferi infection is the Ixodes tick, different
species of which predominate in different parts of the world, their
distribution corresponding to that of Lyme disease. Patients usually live
close to, or have visited, woodland areas, where small mammals are
necessary hosts for immature stages in the life cycle of the tick.
• Adult ticks may infest in larger mammals, especially deer.

CLINICAL FEATURES
Erythema migrans:
It’s an erythematous expanding patch of skin, is the most typical sign of Lyme
disease and is present in 70–80% of cases. It usually appears 7–14 days (range
3–33 days) after the infected tick bite. It starts at the site of the tick bite as a
red papule or macule that gradually expands. The size of the rash can reach
several dozens of centimetres in diameter. A central spot surrounded by clear
skin that is in turn ringed by an expanding red rash (like a bull's-eye) is the
most typical appearance.
It may also present as a uniform erythematous patch or red patch with
central hardening and blistering. The redness can vary from pink to very
intensive purple.
• Erythema migrans is mostly asymptomatic, but can be itchy, sensitive or
warm if touched. It is rarely painful. Fatigue, chills, headache, low-grade
fever, muscle and joint pain, may occur briefly and then recur if the disease
progresses. Lymph glands near the tick bite may be swollen.
• Erythema migrans disappears spontaneously within 3–4 weeks. If left
untreated the disease may disseminate, affect other organs, and progress to
the next stage.

Acrodermatitis chronica atrophicans (ACA):
• Is the most common skin manifestation of the late stage of lyme
disease. Acrodermatitis chronica atrophicans typically presents as a unilateral violet
discolouration of the extensor parts of the upper or lower limbs, especially
the dorsum of the hand, elbow, instep, ankle, or knee. However, it can appear
anywhere on the body and can be bilateral.
• Aca develops in 2 stages. Initial inflammation is followed
by progressive fibrosis and cutaneous atrophy over months or years.
1. Inflammatory stage: ill-defined reddish discolouration and swelling of the affected
area. The skin may be tender or painful.
2. Atrophic stage: thin skin, loss of adnexal structures such as sweat glands, and hair,
the disappearance of elastic fibres, and dilatation of blood vessels. Skin tears and
ulcerates after minor trauma. The skin is described as tissue paper-like.
Less common features of aca include fibrous papules and plaques, and skin-
coloured nodules.
Other features of late-stage lyme disease in patients with aca include:
• Neurological disorders—the most common
• Rheumatological symptoms
• Cardiovascular disease.

ATROPHIC STAGE
INFLAMMATORY STAGE

STAGE FEATURES
LOCALISED LYME DISEASE
(3–33 DAYS AFTER A TICK BITE)
• Erythema migrans
• 'Flu-like illness with low-grade fever, chills, fatigue and joint pain
• Borelial lymphocytoma – red to blue patch on the earlobe, nipple or
scrotum, (common in children)
EARLY DISSEMINATED LYME DISEASE
(DAYS TO WEEKS AFTER A TICK BITE)
• Multiple eythema migrans, smaller than initial patch
• Early neuroborreliosis
• Facial or Bell palsy – one sided paralysis of the facial muscles
(common in children)
• Aseptic meningitis – fever, severe headaches and neck stiffness
• Polyradiculitis – numbness and pain in arms or legs
• Other cranial nerve palsies, mild encephalitis, peripheral neuritis
• Arthritis – painful and swollen large joints (knee is the most affected
join)
• Carditis – abnormal heart rate
• Rare: uveitis, hepatitis
 Progression is gradual over months to years
LATE LYME DISEASE
(MONTHS TO YEARS AFTER INFECTION)
• Acrodermatitis chronica atrophicans (Europe)
• Chronic Lyme arthritis (chronic severe joint pain and swelling) in one
or more large joints, mostly knee (more common in North America
than in Europe)
• Chronic neurological disorders such as:
Disorientation, confusion, dizziness, lack of concentration, short-
term memory loss
Shooting pain, numbness extending to hands/arms and feet/legs.

DIAGNOSIS
Early diagnosis of Lyme disease is essential. Diagnosis can be made on the presence of
erythema migrans and other symptoms, plus a history of or evidence of a tick bite.
• Antibody titres to B burgdorferi using enzyme-linked immunoassay (ELISA) or
immunofluorescent assay.
• Positive results should be confirmed by Western immunoblot.
• Skin biopsy: histopathology
• Erythema migrans is often non-specific
• Borrelial lymphocytoma
• Acrodermatitis chronica atrophicans
• The organism can be cultured or polymerase chain reaction (PCR) test for the
organism can be done on the skin specimen.
Positive antibodies to B. burgdorferi can be in many cases detected for many years
after the successful treatment.
Tick bites may transmit other infections like tick-born
encephalitis, anaplasmosis and babesiosis.
Co-infections should be considered if symptoms of Lyme disease are severe or
prolonged, in case of high fever, and abnormal blood tests results
(leucopenia, thrombocytopenia, or elevation of liver transaminases).

Treatment
First line:
• Doxycycline 100 mg two or three times daily for 14–21 days
Amoxicillin 500–100 mg three times daily for 14–21 days
Second line:
Cefuroxime 500 mg twice daily for 14–21 days
erythromycin 500 mg four times daily for 14–21 days

SCARLET FEVER
Scarlet fever or scarlatina is a bacterial illness that often presents with a
distinctive rash made up of tiny pink-red spots that cover the whole body. It
affects people who have recently had a sore throat (strep throat) or school
sores caused by strains of the group A streptococcus bacteria.
A toxin released by the streptococcal bacteria causes the rash of scarlet fever.
• It is primarily a disease of children.
EPIDEMIOLOGY AND PATHOGENESIS
Scarlet fever is caused by streptococcal pyrogenic exotoxins (SPEs) types A, B,
and C (also referred to as erythrogenic toxins), which are produced by group A
streptococci and lead to immune activation.
• Mostly seen in age group 1-10 yrs of age
• By the age of 10 years, 80% of the population has anti-SPE antibodies which
prevent development of the eruption.
• Scarlet fever usually follows tonsillitis or pharyngitis.

CLINICAL FEATURES
• It is typically preceded by the sudden onset of a sore throat, headache,
malaise, chills, anorexia, nausea, and high fever.
• In young children-vomiting, abdominal pain, and seizures.
• The eruption begins 12–48 hours later as blanchable erythema on the neck,
chest, and axillae.
• Rash becomes generalized within 12 hours and development of tiny
superimposed papules with a sandpaper-like texture (sunburn with goose
pimples).
• Pastia’s lines (linear petechial streaks) are seen in the axillary, antecubital,
and inguinal areas.
• Cheeks are flushed with circumoral pallor also called Filatov’s mask.
• Throat is red and edematous, developing an exudate after 3–4 days
• Palatal petechiae and tender cervical adenopathy
• Tongue is initially white with bright red papillae, but later becomes beefy
red (strawberry tongue).
• Desquamation occurs after 7–10 days, most prominently on the hands and
feet lasting for 2–6 weeks.

HISTOPATHOLOGY
Engorged capillaries and dilated lymphatics, prominent around hair follicles.
• Dermal edema, perivascular neutrophilic infiltrates and small areas of
hemorrhage.
• Spongiosis and parakeratosis are seen during the desquamative stage.
DIAGNOSIS
• Blood picture: elevated leukocyte count with a left shift, Eosinophilia 10–20%
( 2–3 weeks of convalescence), Hemolytic anemia
• Mild albuminuria and hematuria
• Nasal and/or throat cultures grow group A streptococci.
• Detection of anti-streptolysin O (ASO) and anti-DNase B antibodies can also
be useful in confirming the streptococcal infection.

• Drug eruption
• Viral exanthem
• TSS
• Early SSSS
• Kawasaki disease, and
• Recurrent toxin-mediated perineal erythema.
Infection with arcanobacterium haemolyticum, a gram-positive rod, can
result in pharyngitis and a scarlatiniform exanthem in adolescents and young
adults.

COMPLICATIONS
• Otitis media
• Rheumatic fever
• Pneumonia
• Septicaemia
• Glomerulonephritis
• Osteomyelitis
• Death
TREATMENT
• Penicillin (or amoxicillin) is the drug of choice for10–14-days
• Clinical response: 24–48 hours.
• Antibiotic treatment as long as 10 days after the onset of symptoms will prevent the
development of rheumatic fever.
• In penicillin-allergic patients, a first-generation cephalosporin, clindamycin, or a
macrolides.

STAPHYLOCOCCAL SCALDED SKIN
SYNDROME(SSSS)
Also called as Ritter’s disease which was named after Ritter von Rittershain, who first
recognized Staphylococcal scalded skin syndrome (SSSS) in 1878. it is mainly seen in
premature neonates, infants (due to improper renal excretion of exfoliative toxins)
and children below the age of 5 years and rarely in older children and adults.
• SSSS is a febrile, rapidly evolving, desquamative infectious disease in which the skin
exfoliates in sheets
• Disease of infants and young children, who have decreased renal toxin clearance
(especially neonates) and/or a lack of toxin-neutralizing antibodies.
CAUSATIVE AGENT: Staph. aureus group II phage type 71.
Staphylococci reside in a distant focus, i.e., nasopharynx, conjunctiva, and middle
ear. Injection of the organisms or the toxin, produces exfoliation in neonatal mice
which clinically and histologically resembles that in the human disease.
Rarely, adult cases of SSSS have been reported in association with
immunosuppression or renal failure.

Exfoliative
toxin A(ETA)
and
toxin B(ETB)
are serine
proteases
Bind and
cleave
DESMOGLEIN
1
Splitting of
desmosomes
Disruption of
granular layer
Bulla
formation
PATHOGENESIS
Toxin diffuses from primary focus of infection and disseminates
hematogenously to produce widespread effects.

CLINICAL FEATURES
Prodromal
features:
 Fever,
malaise,
irritability, skin
tenderness.
Erythema and
tenderness(ty
pically over
head and
intertriginous
areas)
flaccid sterile
bullae
formation
wrinkled
appearance of
skin
scaling and
desquamation
with varnish
like crusting.
•Periorificial crusting and radial fissuring.
•Nikolsky sign is positive.
•Scaling and desquamation continue for the next 3–5 days, followed
by re-epithelialization without scarring.

HISTOPATHOLOGY
• shows a sharply demarcated zone of cleavage at or below the stratum
granulosum.
• There are usually no inflammatory cells in the bullae.
• The upper dermis also lacks an inflammatory infiltrate, and no organisms
are seen on Gram stain of biopsy specimens.
DIAGNOSIS
• Mostly clinical
• Tzank smear
• Cultures taken from intact bullae are negative,
• Blood cultures are almost always negative in children
• Frozen section- determine the split of the bulla
• Slide latex agglutination, double immuno-diffusion, or enzyme-linked
immunosorbent assay (ELISA) tests can identify the toxins responsible for
SSSS

STAPHYLOCOCC
AL SCALDED SKIN
SYNDROME IN A
CHILD
STAPHYLOCOCCAL
SCALDED SKIN
SYNDROME IN AN ADULT

LOCALIZED STAPHYLOCCOCAL SCALDED SKIN
SYNDROME (SSSS)
LOCALIZED SSSS HEALING WITH WRINKLING
DESQUAMATION AND HYPERPIGMENTATION

• Drug reaction
• Viral exanthem
• Sunburn
• Extensive bullous impetigo
• Toxic shock syndrome
• Graft-versus-host disease
• Pemphigus foliaceus

TREATMENT
SSSS is considered a dermatological emergency which requires
hospitalisation and prompt treatment.
• Intravenous antibiotics:
•First-line: a penicillinase-resistant, anti-staphylococcal antibiotic such
as flucloxacillin.
•Other options include ceftriaxone, clarithromycin (for penicillin-allergy),
cefazolin, nafcillin, or oxacillin.
•Methicillin resistance (MRSA) infection: vancomycin.
If there is a good response, oral antibiotics can be substituted within days.
• Supportive treatments:
1.Pain relief:
Paracetamol with addition of alternative analgesia such as ibuprofen or
oral morphine if required whilst the skin heals.
2.Maintenance of fluid and electrolyte intake:
•Intravenous fluids should be considered in young children and for those
with widespread skin involvement.

3. Skincare:
•Gentle washing of the skin at least once a day
•Application of greasy emollients such as 50:50 white soft paraffin/liquid
paraffin or petroleum jelly to soothe the skin and help with healing.
•Burns dressings if required
Despite its alarming appearance of SSSS, children often make an
excellent recovery with complete healing usually occurring within 5–7
days of starting treatment.

DIFFERENCE BETWEEN STAPHYLOCOCCAL-SCALDED SKIN
SYNDROME (SSSS) AND TOXIC EPIDERMAL NECROLYSIS (TEN)
CHARACTERISTICS SSSS TEN
Aetiology S. aureus group 2 phage 71 Drugs
Age Neonates and infants Adults
Constitutional disturbances Mild Severe
Histopathology Split in subcorneal region Epidermal necrosis
Mucous membranes Usually, lips are involved Severe involvement
Course Short (1–2 weeks) Long (>2 weeks)
Scarring Absent Sometimes occurs
Prognosis Good (mortality 2–3%) Bad (mortality 25–50%)
Treatment Antistaphylococcal antibiotics Stopping offending drug, IV Ig

TOXIC SHOCK SYNDROME (TSS)
Toxic shock syndrome is an uncommon but severe acute multisystem illness due
to exotoxins produced by strains of Staphylococcus aureus or Streptococcus pyogenes.
• TSS is caused by the release of exotoxins from toxigenic strains of the bacteria Staph
aureus and Strep pyogenes in a person that lacks anti-toxin antibodies. These
exotoxins act as superantigens.
• TSS starts from a localised staphylococcal infection which produces the causative
exotoxins.
In the early 1980s when an epidemic occurred, TSS was linked to the prolonged use
of highly absorbent tampons in menstruating women. Toxin-producing strains
of Staph aureus causing toxic shock syndrome were first formally described in 1978.
Prior to this time the syndrome was known as staphylococcal scarlet fever. Both
menstrual and non-menstrual forms of toxic shock syndrome are caused by
these toxins, which release massive amounts of cytokines that produce fever, rash,
low blood pressure, tissue injury, and shock. Strains of Staph aureus producing toxic
shock syndrome toxin-1 (TSST-1) cause almost all the cases of menstrual toxic shock
syndrome. Non-menstrual toxic shock syndrome are caused by strains producing
either TSST-1 or staphylococcal enterotoxin B or C.

Non-menstrual toxic shock syndrome is now the more common form and
may occur as a complication of other localised or systemic infections such as
pneumonia, osteomyelitis, sinusitis, and skin wounds (surgical, traumatic, or
burns).
In 1980’s a disease that showed similar signs and symptoms to toxic shock
syndrome but was caused by exotoxins released by toxin-producing M-
protein strains of Strep pyogenes, was described. This disease although
sometimes also referred to as toxic shock syndrome is more correctly known
as streptococcal toxic shock-like syndrome (STSS).
STSS usually develops from a streptococcal soft-tissue infection such
as bacterial cellulitis, necrotising fasciitis, or pyomyositis. Recent influenza A
infection or chickenpox may predispose to secondary streptococcal
infection.

• Surgical packing and meshes
• Abscesses
• Tampons
• Contraceptive sponges and devices
• Recent childbirth
• Miscarriage
• Abortion
• Foreign bodies, including nasal packing to stop nosebleeds and wound packing after surgery.
• Wound infection after surgery.
PATHOGENESIS
Toxic shock
syndrome
toxin(TSST-1)
(superantigen)
Bind to MHC class
2 molecules of APC
and Vβ region of T
cell receptor in a
non antigen
dependent manner
Massive release of
cytokines and
chemokines
Recent studies show that natural killer T cells ,MAST cells and interleukin 17-A produce memory T cells-
“cytokine storm response to bacterial superantigens”.

CLINICAL FEATURES
Sudden onset of high fever with myalgia, vomiting, diarrhea, headache,
pharyngitis and low blood pressure.
Skin manifestations:
• Diffuse macular erythema or scarlatiniform exanthem starting from trunk
spreading to extremities.
Other features: Hyperemia of conjunctiva, erythema and edema of palms
and soles, strawberry tongue, generalized pitting edema, purpura in a
retiform pattern at the peripheries
Desquamation of hands and feet , beau’s line and nail shedding, telogen
effluvium after recovery.
CONJUCTIVAL
HYPEREMIA
BLOTCHY
ERYTHEMA

INDOLENT BLISTERING ASSOCIATED
WITH TOXIC SHOCK SYNDROME
RETIFORM PURPURA IN TOXIC
SHOCK SYNDROME

CDC CRITERIA FOR TSS AND STSS
CDC case definition for toxic shock syndrome
requires presence of the following 5 clinical
criteria:
1. Fever: temperature =/> 38.9 C
2. Low blood pressure (including fainting or
dizziness on standing)
3. Widespread red flat rash
4. Shedding of skin, especially on palms and
soles, 1–2 weeks after onset of illness
5. Abnormalities in 3 or more of the following
organ systems:
• Gastrointestinal: vomiting or diarrhoea
• Muscular: severe muscle pain
• Hepatic: impaired liver function
• Renal: raised urea or creatinine levels
• Haematologic: bruising due to low
blood platelet count
• Central nervous system: disorientation or
confusion
• Mucous membranes: red eyes, mouth, vagina
CDC case definition for STSS requires isolation of
group A streptococci and hypotension with 2 or
more of the following clinical criteria:
1.Renal impairment: decreased urine output
2.Coagulopathy: bleeding problems
3.Liver problems
4.Rash that may shed, especially on palms and
soles, 1–2 weeks after onset of illness
5.Difficulty breathing
6.Soft tissue necrosis including necrotising
fasciitis, myositis and gangrene

TOXIC SHOCK SYNDROMES
STAPHYLOCOCCAL STREPTOCOCCAL
Typical patient Young (15-35) and healthy Young (20-50) and healthy
Diffuse macular
erythroderma
Very common Less common
Vesicles and bullae Rare Uncommon (5%)
Localized extremity pain Rare Common
Soft tissue infection Rare Common
Hypotension 100% 100%
Renal impairment Common Common
Predisposing factors Surgical packing, surgical
meshes, abscesses,
tampons, contraceptive
sponges
Lacerations, bites, bruises,
varicella infections
Positive blood cultures <15% >50%
Mortality <3% 30-60%

HISTOPATHOLOGY
Biopsy shows infiltration of neutrophils and lymphocytes in superficial dermis
along with epidermal spongiosis and exocytosis.

• Scarlet fever
• Meningococcaemia
• Toxic epidermal necrolysis
• Haemorrhagic shock
• Necrotizing Fasciitis/Gas gangrene
• Drug eruption
• Erythema multiforme

TREATMENT
• First line: Hemodynamic resuscitation
• Broad-spectrum antibiotics should be administered for those with an
unidentified organism, if possible after blood cultures. This include
vancomycin or linezolid given the high prevalence of methicillin-
resistant Staphylococcus aureus (MRSA).
• Clindamycin should also be administered to suppress toxin production.
(Studies have shown improved outcomes when Clindamycin is added to
antibiotic regimens)
• It should not be given alone as it is bacteriostatic, rather than bactericidal.
Initially it’s impossible to tell if the infection is polymicrobial, initial therapy
should also cover gram-negative organisms.
Once the organism is identified, and sensitivities have been determined,
antibiotics should be optimized and narrowed in the spectrum. Penicillin is
the preferred antibiotic for group A strep. For MSSA, clindamycin is
recommended, plus flucloxacillin or a beta-lactamase-resistant penicillin
such as nafcillin. Current recommendations are to treat for 7 to 14 days.

• Vasopressors should be administered for patients with shock refractory to IV
fluids.
• Most current guidelines recommend Norepinephrine as a first option.
• Intravenous immunoglobulin (IVIG), is thought to work by neutralizing the
activity of the toxins produced and can be considered for shock refractory to
fluids and vasopressors. The optimal dosing is not well established, but high
dose at 2 g/kg is acceptable.
There are no randomized controlled trials supporting its use, observational
trials have shown a reduction in mortality with IVIG compared to patients
who only received antibiotics.
A small study from 1984 showed reduced illness severity with steroids, but
there was no improvement in mortality.
Corticosteroids are currently not recommended as adjunctive therapy for
TSS.

OUTCOME
• Toxic shock syndrome is a medical emergency that requires prompt
treatment.
• Early diagnosis and appropriate treatment prevents progression of the
disease and possible complications such as heart problems, acute renal
failure, adult respiratory distress syndrome, and DIC.
• The mortality rate of toxic shock syndrome is approximately 5–15%, and
recurrences have been reported in as many as 30–40% of cases. Mortality
rates of STSS are more than 5 times higher than in toxic shock syndrome.

RECURRENT TOXIN
MEDIATED PERIANAL
ERYTHEMA
• It is mediated by superantigen toxins produced by
strains of staphylococci and streptococci.
• Streptococcal infection of the throat leading to
perineal erythema and subsequent rapid
desquamation resulting from bacterial toxins which
is often recurrent.
• Age :Young children usually under the age of 12
years but adults may occasionally be affected
PATHOGENESIS
• Superantigens produced by streptococci and
staphylococci lead to non‐specific T‐cell activation and
toxin mediated erythema at distant skin sites
CLINICAL FEATURES
• After a sore throat, patients develop an eruption in
the perineal area, rash resembles erysipelas with
macular erythema, which undergo rapid
desquamation.

• Other cutaneous features include erythema of the hands, feet and axillae
Some patients also have a strawberry tongue.
INVESTIGATIONS
• The diagnosis is made on clinical grounds
• Swabs from the perineal area do not grow any specific organisms, but
throat swabs may yield Staphylococcus aureus or Streptococcus pyogenes.
MANAGEMENT
• short course of antibiotics, which covers streptococci and staphylococci.

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