After reading this note you will be able to recognise, classify and initiate appropriate investigation and management of common skin and soft‑tissue infections seen in Kenyan hospitals. Always verify drug choices, doses and local protocols against the Kenya Ministry of Health guidelines and your hospital formulary.
Definition
Skin and soft‑tissue infections (SSTIs) are a spectrum of bacterial, fungal or parasitic conditions that involve the epidermis, dermis, subcutaneous tissue, fascia, muscle or associated structures, ranging from superficial cellulitis to necrotising fasciitis.
Anatomy and physiology you need
| Layer | Relevant features for infection |
|---|---|
| Epidermis | Keratinised barrier; breach (trauma, ulcer) allows entry |
| Dermis | Rich vascular supply – rapid spread of organisms & inflammatory cells |
| Subcutaneous fat | Loose connective tissue – favours cellulitis, abscess formation |
| Superficial fascia (Camper) | Plane for spread of cellulitis; barrier to deeper structures |
| Deep fascia (Scarpa) | Tight, low‑vascular plane – when breached → necrotising fasciitis |
| Muscle | Highly vascular; infection usually secondary to spread from fascia |
Understanding these layers helps localise the infection clinically and predicts the route of spread.
Causes and risk factors
| Agent / Condition | Typical presentation | Kenyan risk factors |
|---|---|---|
| Staphylococcus aureus (incl. MRSA) | Purulent cellulitis, abscess, impetigo | Skin trauma, community‑acquired MRSA, HIV |
| Streptococcus pyogenes (Group A) | Non‑purulent cellulitis, erysipelas | Crowded living conditions, lymphatic obstruction |
| Gram‑negative bacilli (e.g., Pseudomonas) | Wet ulcers, diabetic foot infections | Chronic wounds, burns, immunosuppression |
| Anaerobes (e.g., Bacteroides) | Deep tissue/necrotising infections | Poor hygiene, necrotic tissue, diabetic foot |
| Fungi (Candida, dermatophytes) | Intertriginous erythema, chronic ulceration | Diabetes, HIV, prolonged antibiotics |
| Parasites (Leishmania) | Ulcerating lesions | Rural exposure, malnutrition |
| HIV infection | Extensive, atypical presentations, opportunistic pathogens | Low CD4 count |
| Tuberculosis (cutaneous TB) | Lupus vulgaris, scrofuloderma | Co‑existing pulmonary TB |
| Malaria (severe) | Secondary bacterial SSTI due to immunomodulation | High parasitaemia, splenomegaly |
| Sickle cell disease | Leg ulcers, osteomyelitis | Vaso‑occlusive crises, poor perfusion |
| Rheumatic diseases (e.g., lupus) | Vasculitic skin lesions prone to infection | Immunosuppressive therapy |
| Trauma, animal bites, burns | Direct inoculation | Agricultural work, road traffic injuries |
Pathophysiology
- Break in skin barrier → entry of microorganisms
- Colonisation & multiplication → local inflammatory response
- Release of bacterial toxins & enzymes → tissue damage, edema
- Spread along fascial planes (if deep fascia breached) → rapid expansion, necrosis
- Host immune response (neutrophils, cytokines) → pus formation, systemic signs (fever, tachycardia)
- Compromise of microcirculation → hypoxia, further bacterial proliferation → possible septic shock
Arrows illustrate progression: breach → colonisation → toxin release → fascial spread → immune response → microcirculatory failure.
Clinical features
| Aspect | Key questions / findings | Why it matters |
|---|---|---|
| Onset | Sudden vs gradual; time since first sign | Rapid onset suggests cellulitis, necrotizing infection; gradual points to chronic ulcer or deep‑seated abscess |
| Pain | Intensity, progression, pain out of proportion to appearance | Severe, disproportionate pain is a red flag for necrotizing fasciitis or deep tissue involvement |
| Systemic symptoms | Fever, chills, rigors, malaise, headache, nausea, vomiting | Presence indicates systemic inflammatory response; helps grade severity and need for inpatient care |
| Local signs | Erythema, warmth, swelling, tenderness, induration, bullae, necrosis, purulent discharge, foul odor | Erythema & warmth = cellulitis; fluctuance = abscess; bullae/necrosis = severe infection or toxin‑mediated disease |
| Progression | How fast the lesion is expanding (cm/hr) | Fast spread (>2 cm in 24 h) suggests aggressive infection (e.g., necrotizing fasciitis) |
| Trauma / breach | Recent cuts, insect bites, surgical wounds, pressure sores, animal bites | Provides portal of entry; certain organisms are linked to specific portals (e.g., Pasteurella in animal bites) |
| Comorbidities | HIV status, diabetes, sickle‑cell disease, peripheral vascular disease, chronic steroid use, recent TB treatment, malaria, rheumatic disease | Immunocompromise or vascular disease predisposes to atypical organisms and poorer outcomes |
| Previous skin infection | Recurrence, prior MRSA colonisation, recent antibiotics | Guides likely pathogen and empirical therapy |
| Medication / allergies | Recent antibiotics, immunosuppressants, drug allergies | Influences choice of empiric agents and need for desensitisation |
| Travel / exposure | Recent travel to rural areas, contact with livestock, swimming in fresh water | Raises suspicion for tropical pathogens (e.g., Vibrio, Mycobacterium ulcerans) |
| Vaccination | Tetanus immunisation status | Determines need for tetanus prophylaxis |
Examination findings
- Erythema – hyperemia from inflammatory mediators; extent helps delineate cellulitis vs deeper infection.
- Heat – increased local blood flow; a marker of active inflammation.
- Swelling/induration – edema from increased vascular permeability; firmness may suggest fascial involvement.
- Tenderness – nociceptor activation; severe tenderness out of proportion is a red flag.
- Fluctuance – fluid collection under pressure; indicates abscess formation requiring drainage.
- Bullae or vesicles – toxin‑mediated damage (e.g., Staph aureus exfoliative toxin) or necrotizing infection.
- Necrosis / skin slough – tissue death from vascular thrombosis or bacterial enzymes; hallmark of necrotizing fasciitis.
- Crepitus – gas‑producing organisms (Clostridium, some Gram‑negatives); suggests gas gangrene.
- Lymphangitis – red streaks following lymphatics; indicates spread of infection proximally.
- Regional lymphadenopathy – immune response; may help differentiate cellulitis from deeper abscess.
- Peripheral pulses – assess for arterial compromise, especially in diabetics or sickle‑cell patients.
- Neurological status – sensory loss may indicate compartment syndrome or nerve involvement.
Differential diagnosis
| Condition | Points toward it | Distinguishing feature |
|---|---|---|
| Cellulitis | Warm, tender, expanding erythema, systemic signs | No fluctuance, no necrosis, borders poorly defined |
| Abscess | Localised fluctuant mass, purulent discharge | Presence of fluctuance, often well‑circumscribed |
| Necrotising fasciitis | Severe pain out of proportion, rapid spread, systemic toxicity | Crepitus, bullae, skin necrosis, systemic shock |
| Erysipelas | Sharply demarcated raised erythema, often on face/legs | Upper dermal involvement, raised borders |
| Deep vein thrombosis (leg) | Swelling, pain, risk factors for thrombosis | Positive Homan’s sign, duplex US shows thrombus |
| Venous stasis dermatitis | Chronic edema, hemosiderin staining, varicose veins | History of chronic venous insufficiency, no acute systemic signs |
| Tropical ulcer (Mycobacterium ulcerans) | Rural exposure, painless ulcer with undermined edges | Slow progression, characteristic “cold” ulcer |
| Cutaneous leishmaniasis | Travel to endemic area, papule → ulcer | Presence of sand‑fly bite history, typical lesion morphology |
| Drug reaction (e.g., DRESS) | Recent new drug, widespread rash, eosinophilia | Multisystem involvement, atypical distribution |
| Vasculitis (e.g., PAN) | Purpura, livedo, systemic features | Palpable purpura, biopsy shows vessel inflammation |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Full blood count | Inflammation, anemia, leukocytosis | ↑WBC with left shift → bacterial infection; neutropenia may suggest immunosuppression |
| C‑reactive protein / ESR | Acute phase response | High levels correlate with severity; falling trend indicates response to therapy |
| Blood cultures (2 sets) | Bacteremia, organism identification | Positive → guide targeted antibiotics; negative does not exclude serious infection |
| Wound swab / pus culture | Local pathogen, antibiotic susceptibility | Growth of Staph aureus, Streptococcus pyogenes common; MRSA → need for anti‑MRSA agent |
| Gram stain of pus | Rapid organism clue | Gram‑positive cocci in chains → Streptococcus; clusters → Staph |
| Imaging – Ultrasound | Presence of fluid collection, abscess size | Detects loculated collections needing drainage |
| Imaging – CT (contrast) | Deep fascial involvement, gas, extent | Gas in soft tissue → gas‑forming organisms; fascial thickening → necrotising fasciitis |
| Imaging – MRI | Soft‑tissue detail, early necrosis | Hyper‑intense fascial planes on T2 = necrotising infection |
| HIV test (if unknown) | Immunocompromise status | Positive → higher risk of atypical organisms, may affect prophylaxis |
| HbA1c / glucose | Diabetes control | Poor control predisposes to severe infection |
| Tetanus serology (if indicated) | Immunity status | Non‑immune → need tetanus toxoid booster |
Diagnosis and severity
Diagnosis is made by integrating history, physical exam, and investigations.
- Cellulitis: diffuse erythema, warmth, tenderness, no fluctuance, supported by leukocytosis and elevated CRP.
- Abscess: localized fluctuance or collection on imaging, purulent material on aspiration.
- Necrotising fasciitis: pain out of proportion, rapid spread, systemic toxicity, imaging showing fascial gas or thickening, often elevated LRINEC score (if calculated).
Severity grading (adapted for resource‑limited settings):
| Category | Clinical criteria | Management implication |
|---|---|---|
| Mild | Limited (<5 cm) erythema, no systemic signs, stable vitals | Oral antibiotics, outpatient follow‑up if reliable |
| Moderate | Erythema >5 cm, fever, tachycardia, elevated CRP, no organ dysfunction | IV antibiotics, consider short inpatient stay, monitor labs |
| Severe | Hypotension, tachypnea, altered mental status, extensive necrosis, gas on imaging, LRINEC ≥8 | Immediate IV broad‑spectrum antibiotics, surgical consultation for debridement, ICU support if needed |
| Life‑threatening | Septic shock, multi‑organ failure, rapidly progressing necrosis | Aggressive resuscitation, broad‑spectrum IV therapy, emergent surgical exploration, intensive monitoring |
Prompt recognition of severity guides the need for hospitalization, surgical intervention, and level of monitoring. Early escalation improves outcomes, especially in necrotising infections where delay beyond 6 hours markedly increases mortality.
Management
Immediate stabilisation
- Airway, Breathing, Circulation – ensure patent airway; give supplemental O₂ if SpO₂ < 94 %; establish IV access, give isotonic crystalloid bolus for hypotension or sepsis.
- Pain control – fast‑acting opioid or NSAID (if no contraindication) to allow adequate examination.
- Sepsis bundle – obtain blood cultures before antibiotics, give broad‑spectrum IV antibiotics within one hour, monitor lactate, urine output and mental status.
Definitive treatment
| Clinical pattern | First‑line antimicrobial class* | Adjunctive measures |
|---|---|---|
| Uncomplicated cellulitis (non‑purulent) | β‑lactam (penicillin / cephalosporin) covering streptococci | Elevation, warm compresses, analgesia |
| Purulent cellulitis / abscess | Anti‑staphylococcal (cloxacillin, dicloxacillin, cefazolin) ± MRSA‑active (clindamycin, doxycycline, TMP‑SMX) if risk factors | Incision & drainage (I&D) of any fluctuant collection |
| Necrotising fasciitis / severe SSTI | Carbapenem or β‑lactam/β‑lactamase inhibitor + clindamycin + MRSA‑active agent | Urgent surgical debridement, ICU support, IV immunoglobulin (if streptococcal toxic shock) |
| Diabetic foot infection (moderate‑severe) | Broad‑spectrum covering gram‑positive, gram‑negative and anaerobes (e.g., amoxicillin‑clavulanate or carbapenem) | Off‑loading, wound care, glycaemic optimisation, possible surgical debridement |
| HIV‑related extensive cellulitis | Same as above but low threshold for MRSA coverage and for opportunistic pathogens (e.g., atypical mycobacteria) | CD4 count, antiretroviral optimisation |
\*Specify drug class; exact agents can be chosen according to local formulary and resistance patterns.
Monitoring
- Vital signs q1‑2 h (first 24 h), pain score, wound dimensions, drainage amount.
- Laboratory: CBC, CRP/ESR daily, renal & liver function (for drug toxicity), electrolytes, blood glucose (especially in diabetics).
- Imaging (repeat US/CT) if clinical deterioration or inadequate response.
Safety & contraindications
- Avoid NSAIDs in patients with renal insufficiency, active peptic ulcer disease or severe heart failure.
- Reserve clindamycin for toxin‑mediated disease (e.g., necrotising streptococcal infection) – beware of C. difficile risk.
- MRSA agents contraindicated in pregnancy (e.g., doxycycline) – use β‑lactam plus vancomycin if needed.
- Surgical debridement contraindicated only when patient is unstable for anesthesia; in such cases, aggressive medical therapy and ICU support first.
Complications and prognosis
- Local: abscess formation, ulceration, chronic sinus tract, lymphangitis, compartment syndrome.
- Systemic: sepsis, septic shock, bacteremia (especially with Streptococcus pyogenes or MRSA), toxic shock syndrome, acute kidney injury, disseminated intravascular coagulation.
- Long‑term: scarring, contractures, functional limitation (especially after necrotising fasciitis).
- Prognosis: Prompt antibiotics and source control give >90 % cure in uncomplicated cellulitis. Necrotising fasciitis carries mortality 20‑30 % despite aggressive care; early surgery is the single most important determinant of survival.
High‑yield exam points
- Look‑alike conditions: cellulitis vs. deep vein thrombosis, erysipelas vs. contact dermatitis, necrotising fasciitis vs. severe cellulitis, mycetoma vs. chronic abscess.
- Common wrong first step: prescribing oral antibiotics without obtaining cultures in a patient with systemic signs or purulent drainage.
- Examiner bedside questions:
- “What feature on inspection makes you think of necrotising fasciitis?” (pain out of proportion, rapid progression, bullae, skin discoloration).
- “How would you differentiate cellulitis from DVT on exam?” (presence of warmth, spreading erythema, lymphangitic streaks vs. unilateral calf swelling, Homan’s sign).
- “Why is incision and drainage preferred over antibiotics alone for a fluctuant abscess?” (drainage removes nidus of infection, antibiotics alone have poor penetration).
Clinical case
Case: A 42‑year‑old man with poorly controlled diabetes presents with a 3‑day history of a painful, swollen left lower leg. Examination shows a 6 cm erythematous, warm area with central fluctuance, fever 38.9 °C, pulse 112 bpm, and blood glucose 280 mg/dL. No peripheral pulses are diminished.
Questions
- What is the most appropriate next step?
Answer: Perform incision and drainage of the abscess, obtain pus for Gram stain and culture, and start broad‑spectrum IV antibiotics covering gram‑positive, gram‑negative and anaerobes.
- Which organism is most likely responsible in this diabetic patient?
Answer: Polymicrobial flora including Staphylococcus aureus (including MRSA) and anaerobes such as Bacteroides spp.
- What key feature would prompt you to suspect necrotising fasciitis rather than a simple abscess?
Answer: Pain that is disproportionate to the visible skin changes, rapid progression, presence of bullae or skin necrosis, and systemic toxicity.
Practice questions
Question 1
A 28‑year‑old woman with HIV (CD4 = 150 cells/µL) presents with a rapidly enlarging, tender erythematous area on her forearm, fever 39 °C, and a violaceous bullae. What is the most urgent next step?
A. Start oral flucloxacillin
B. Obtain a wound swab and discharge with oral analgesia
C. Immediate surgical consultation for possible debridement
D. Give a single dose of intramuscular penicillin
Answer: C. Immediate surgical consultation for possible debridement
Explanation: Rapid progression, bullae and systemic signs raise suspicion for necrotising fasciitis; surgery cannot be delayed.
Question 2
A child presents with a well‑demarcated, bright‑red, raised rash on the face that spares the area around the mouth. Which diagnosis is most likely?
A. Cellulitis
B. Erysipelas
C. Contact dermatitis
D. Impetigo
Answer: B. Erysipelas
Explanation: Erysipelas classically has sharp borders, facial predilection and spares the perioral region.
Question 3
In a patient with a non‑purulent cellulitis of the lower leg, which of the following is least appropriate?
A. Elevate the limb above heart level
B. Empiric oral penicillin‑based therapy
C. Immediate incision and drainage
D. Monitor for systemic signs
Answer: C. Immediate incision and drainage
Explanation: Non‑purulent cellulitis lacks a collection to drain; I&D is unnecessary and may cause harm.
Question 4
A 55‑year‑old man with chronic venous insufficiency develops a painful, erythematous swelling of the calf. There is no fluctuance, but a tender cord is palpable along the medial aspect. What is the most likely diagnosis?
A. Cellulitis
B. Deep vein thrombosis
C. Necrotising fasciitis
D. Lymphedema
Answer: B. Deep vein thrombosis
Explanation: Tender, cord‑like thrombosed vein (Homan’s sign) points to DVT rather than cellulitis.
Question 5
Which adjunctive therapy has proven mortality benefit in streptococcal toxic shock syndrome associated with necrotising fasciitis?
A. High‑dose intravenous vitamin C
B. Clindamycin
C. Oral metronidazole
D. Topical mupirocin
Answer: B. Clindamycin
Explanation: Clindamycin suppresses toxin production and improves outcomes in streptococcal toxic shock.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.