Common Bacterial Infections

By:-

Dr. Naif Al-Shahrani

Salman bin Abdazziz University

Normal skin flora NORMAL SKIN FLORA

Class Organisms Location on body

Aerobic cocci Staphylococcus aureus*, S. saprophyticus, S. epidermidis† , Micrococcus luteus, M. roseus, M. varians

All body sites, especially

intertriginous areas

Aerobic coryneform Corynebacterium minutissimum, C. lipophilicus, C. xerosis, C. jeikeium, Brevibacterium epidermidis

Intertriginous areas (e.g. axillae, groin, toe webs)

Anaerobic coryneform bacteria

Propionibacterium acnes, P. granulosum, P. avidum

Sebaceous glands and follicles

Gram-negative bacteria Acinetobacter spp. Axillae, perineum, antecubital fossa

Yeast Malassezia furfur Skin rich in sebaceous glands (e.g. scalp)

Impetigo

• It is the most common bacterial infection in children

• Highly contagious, spreading rapidly via direct person-to-person contact

• The primary pathogen is S.aureus and, less commonly, Streptococcus pyogenes

• Non Bullous : usually at site of trauma

• Bullous: (considered a localized form of SSSS)

Impetigo

• Predisposing factors include

– warm temperature, high humidity,

– poor hygiene

– atopic diathesis

– skin trauma (chickenpox, insect bite, abrasion, laceration, burn)

– S. aureus colonization

Treatment

• local wound care

– Cleansing

– removal of crusts

– wet dressings

• For healthy patients with a few, isolated superficial lesions and no systemic symptoms:

– mupirocin 2% ointment or fusidic acid equally effective to oral antibiotics

Folliculitis

• Folliculitis: infection localized to the hair follicle

• Furuncle: entire follicle and surrounding tissue are involved

• Carbuncle : multiple furuncles grouped together

• S. aureus is the most common infectious cause of folliculitis

• Gram-ve folliculitis A.V. treated with long courses of oral antibiotics

Folliculitis

• Factors predisposing – occlusion

– maceration and hyperhydration with hot and humid weather,

– shaving, plucking or waxing hair

– topical corticosteroids

– diabetes mellitus

– atopic dermatitis.

– Obesity

– Immunodeficiency

– Poor hygiene

Folliculitis

• Site: face, chest, back, axillae or buttocks

• Superficial folliculitis (Bockhart'simpetigo) are small, 1–4 mm pustules or crusted papules on an erythematous base

• Gram stain and bacterial cultures in recurrent or treatment-resistant cases

Folliculitis treatment

• Localized:– antibacterial washes – bacitracin or mupirocin 2% may also be used for 7-10

days

• Widespread or recurrent:– appropriate β-lactam antibiotics, macrolides or

clindamycin

• Chronic S. aureus carriage • mupirocin 2% ointment applied twice daily to the nares,

axillae/groin and/or submammary area for 5 days MONTHLY.

Furuncles, Carbuncles

• S. aureus is the most common causative organism

• Furuncles usually begin as a hard, tender, red nodule that enlarges and becomes painful and fluctuant; rupture results in decreased pain, Systemic symptoms are usually absent

Furuncles, Carbuncles

• Carbuncles are collections of furuncles that extend deep into the subcutaneous tissue.

• The surface usually displays multiple draining sinus tracts and occasionally ulcerates.

• They usually occur in areas with thicker skin (e.g. nape of neck, back, thigh)

• Systemic symptoms are usually present.

• Carbuncles are slow to heal scar formation

Treatment

• Simple furuncles: – warm compresses may promote maturation, drainage and

resolution of symptoms

• Fluctuant lesions – incision and drainage

• Systemic antibiotics should be used in four instances: – (1) furuncles around the nose, within the nares or in the

external auditory canal– (2) large and recurrent lesions– (3) lesions with surrounding cellulitis– (4) lesions not responding to local care

MRSA(methicillin resistance)

• Furunculosis is the most frequently reported manifestation of community acquired MRSA

• MRSA can manifest as :– abscesses or frank cellulitis

– impetigo, bullous impetigo, scalded skin syndrome, nodules or pustules

– bacteremia, septic shock and a toxic shock-like syndrome

Treatment MRSA

• Emperical treatment with Vancomycin is indicated in :

– patients with severe, life-threatening infection

– in patients with a history of MRSA colonization

– in intravenous drug users

Blistering Distal Dactylitis

• Children aged 2-16 years

• Presents as a localized infection of the volar fat pad of a finger or a toe

• Blister formation and involvement of the nail fold or more proximal portion of the digit

• Darkening of the surrounding skin before blister formation

Blistering Distal Dactylitis

• Group A β-hemolytic Streptococcus, S. aureusand, rarely, S. epiermidis are the responsible organisms

DDx:• Herpetic whitlow • Thermal or chemical burn• Acute paronychia• Bullous impetigo (vesicles more superficial)• Frictional bullae

Blistering Distal Dactylitis

Treatment

• Incision and drainage

plus

• a 10-day course of an oral antistaphylococcalantibiotic (e.g. cephalexin) can prevent development of new sites of infection as well as local extension.

Ecthyma

• Considered as : ulcerated form of non-bullous impetigo like lesion

• Due to either a primary infection with Str. pyogenes or streptococcal superinfectionof a pre-existing ulceration

Staphylococcal Scalded Skin Syndrome

• Staphylococcal toxin-mediated infections includes:

– SSSS

– Bullous impetigo

– Toxic shock syndrome

• Exfoliative toxins (ETs) ETA and ETB are serine proteases with a very high specificity for human desmoglein 1 (DG-1)

Staphylococcal Scalded Skin Syndrome

• Increased frequency of staphylococcal scalded skin syndrome in children younger than 5 years due to :

– Absence of antibodies specific for exotoxins

– Immature renal function in this age group may impair clearance

– The relative quantity of DG-1 in the skin differs with age

SSSS clinical features

• Severe tenderness of the skin

• Erythema

• Flaccid bullae within the superficial epidermis.

• In 1-2 days, the bullae are sloughed moist skin and areas of thin, varnish-like crust.

SSSS clinical features

• The flexural areas are the first to exfoliate.

• Scaling and desquamation continue for 3-5 days

• Re-epithelialization in 10-14 days, without scarring

• The Nikolsky sign is positive.

• The mortality rate is 3% for children, over 50% in adults, and almost 100% in adults with underlying disease

SSSS work up

• Cultures taken from intact bullae are negative

• Blood cultures are almost always negative in children, but may be positive in adults

• The leukocyte count may be elevated or normal

• Electrolytes and renal function should be followed closely in severe cases

• PCR serum test for the toxin is available.• BIOPSY

SSSS treatment

• Localized disease :– Oral treatment with a β-lactamase-resistant

antibiotic e.g.dicloxacillin, cloxacillin, for a minimum of 1 week

– Emollient

– Isolation

– treatment of S. aureus carriers

• Extensive, generalized forms of SSSS – hospitalization and parental antibiotics.

Toxic Shock Syndrome

• It is a multisystem disease caused by an exotoxin produced by S. aureus.

• Dermatologic manifestations are more extensive and predictable in staphylococcal TSS than in streptococcal TSS.

Toxic Shock Syndrome

• Sudden onset of high fever with myalgias, vomiting, diarrhea, headache and pharyngitis

– Diffuse macular erythroderma > scarlatiniform eruption with flexural accentuation

• Erythema and edema, then Delayed desquamation of palms and soles

• Hyperemia of conjunctiva and mucous membranes

• Strawberry tongue

• After recovery, Beau's lines, telogen effluvium may occur

Streptococcal Toxic Shock Syndrome

• Rapidly progressive, often fatal illness

• Toxins act as superantigens and can cause stimulation of T cells By binding to the class II MHC of APC

• Most common initial symptom is severe local pain in an extremity

• Mortality 30 to 60%

• Severe complications of streptococcal TSS include renal failure, DIC , and adult RDS

Scarlet Fever

• Between 1 and 10 years of age

• >10 years antibodies prevent rash but not the sore throat

• Caused by toxins types A, B and C by group A streptococci

• Lead to a delayed-type hypersensitivity reaction

Clinical features

• Rash appears 12–48 hours after the fever.

• The rash starts as erythema of the neck, chest and axillae, and behind the ears.

• After 4-6 hours, the remainder of the body is involved

• spares the face , but cheeks may have flushing

Clinical features

• Complications of scarlet fever include – Otitis– Mastoiditis– Sinusitis– Pneumonia– Myocarditis– Meningitis– Arthritis– Hepatitis– Acute glomerulonephritis– Rheumatic fever

Treatment

• penicillin is the drug of choice (10-14-day course)

• Antibiotic treatment as long as 10 days after the onset of symptoms will prevent the development of rheumatic fever.

• Erythromycin can be used in penicillin-allergic patients.

Erysipelas

• It is an infection of the dermis with significant lymphatic involvement

• Caused by infection with:– group A streptococci and less often by

– S. aureus,

– Pneumococcus species,

– Klebsiella pneumoniae,

– Yersinia enterocolitica,

– Haemophilus influenzae type

Clinical features Erysipelas

• Abrupt onset (clearly demarcated erythematous plaque) hot, tense, tender and indurated with non-pitting edema

• The lower extremity is the most common location

.

• When the infection resolves, desquamation and postinflammatory pigmentary changes may occur

Treatment Erysipelas

• The treatment of choice is 10-14-day course of penicillin

• Erythromycin in penicillin-allergic patients

• Hospital admission and I.V or I.M. antibiotics for children and debilitated patients.

• prophylaxis with daily penicillin for Recurrent erysipelas

Cellulitis

• Cellulitis is an infection of the deep dermis and subcutaneous tissue

• most commonly Str. pyogenes and S. aureus

• In childhood S. aureus >>>> H. influenzae

• Diabetic ulcers and decubitus ulcers ( Gram+vecocci and Gram-ve and anaerobes)

• immunocompetent via break in the skin barrier

• immunocompromised bloodborne route is most common

Cellulitis clinical features

• Systemic symptoms: fever, chills and malaise.

• 4 cardinal signs of inflammation: rubor (erythema), calor (warmth), dolor (pain), and tumor (swelling).

• The lesion usually has ill-defined, non-palpable borders. In severe infections, vesicles, bullae

• Pustules ,necrotic tissue, ascending lymphangitisand regional lymph node involvement may occur.

Cellulitis clinical features

• Children head and neck region

• Adults extremities

• I.V. drug abusers the upper extremities

• Complications include – acute glomerulonephritis (streptococci)

– Lymphadenitis

– subacute bacterial endocarditis.

– Damage to lymphatic recurrent cellulitis

Necrotising Fasciitis

• is essentially a ‘severe inflammation of the muscle sheath that leads to necrosis of the subcutaneous tissue and adjacent fascia, that is difficult to diagnose early and difficult to manage effectively.

Risk factors for NF

• >50 years of age

• Diabetes mellitus

• Peripheral vascular disease

• Intravenous drug use

• Alcoholism

• Immunosuppression

• Obesity

Clinical diagnosis of NF

• Hx:– minor trauma

– insect or human bites

– recent surgery

– skin infection or ulcers

– injection sites and

– illicit intravenous drug usage

• Many cases, however, remain idiopathic

Clinical diagnosis of NF

• Severe pain precedes skin changes by 24 to 48 h in >97.8% of patients

• Mild erythema, cellulitis or swelling overlying the affected area.

• tender area >> smooth, swollen area of skin with distinct margins progressing to dusky blue/purple, ‘bruising’ violaceous plaques, and finally full thickness necrosis with haemorrhagic bullae

Radiology

• MRI are probably the best radiological adjunctive investigation.