13.3 Parasitic Infestations, Arthropod Bites & Cutaneous Leishmaniasis

13.3 Parasitic Infestations, Arthropod Bites & Cutaneous Leishmaniasis

Scabies (Sarcoptes scabiei var. hominis)

Scabies is an intensely pruritic ectoparasitic dermatosis caused by the microscopic human mite Sarcoptes scabiei var. hominis (order Astigmata, family Sarcoptidae). Classified as a Neglected Tropical Disease by the WHO, it remains highly prevalent across Europe, causing frequent community, household, and institutional outbreaks (nursing homes, long-term care facilities, hospitals, asylum-seeker reception centers).

Biology & Pathophysiology

• Transmission: Occurs primarily via direct, prolonged, close skin-to-skin contact (requiring at least 15 to 20 minutes of continuous contact, such as between sexual partners, parents and children, or co-sleeping individuals). Fomite transmission (clothing, bedding) is rare in classic scabies because the mite survives only 24 to 36 hours off the human host at room temperature; however, fomite transmission is an enormous hazard in crusted scabies.
• Mite Life Cycle:
  • The impregnated adult female mite (0.3–0.4 mm long, oval, eyeless, with 4 pairs of short legs) uses its cutting mouthparts (chelicerae) and front legs to burrow into the stratum corneum of the epidermis.
  • It advances at a rate of 0.5 to 5 mm per day, feeding on dissolved keratinocytes.
  • Over her 4-to-6-week lifespan, the female deposits 2 to 3 eggs daily in the burrow floor, alongside dark oval fecal pellets called scybala.
  • Eggs hatch in 3 to 4 days into larvae, which migrate to the skin surface, molt through protonymph and tritonymph stages, and mature into adults in 10 to 14 days.
• Immunological Pathogenesis:
  • In classic scabies, the total mite burden on the entire host body is remarkably low—typically only 10 to 15 live adult female mites.
  • Cutaneous symptoms are entirely driven by a Type IV delayed hypersensitivity immune response directed against mite proteins, salivary secretions, and scybala.
  • Incubation Period: In a primary, first-time infestation, the development of specific T-cell sensitization requires 3 to 6 weeks before pruritus commences. In secondary re-infestation, pre-existing memory T cells trigger intense pruritus within 24 to 48 hours.

Clinical Manifestations

+-------------------------------------------------------------------------+
|                   ANATOMICAL TOPOGRAPHY OF SCABIES                      |
+-------------------------------------------------------------------------+
| ADULTS (Classic Distribution):                                          |
|   - Interdigital web spaces of hands (most common diagnostic site)      |
|   - Flexor aspects of wrists & extensor elbows                          |
|   - Anterior axillary folds & periumbilical ring                        |
|   - Waistline, beltline & lower buttocks                                |
|   - Genitalia: Pathognomonic pruritic nodules on penile shaft & scrotum |
|   - Breasts: Areolae and submammary folds in women                      |
|   * STRICT SPARING of head, neck, face, scalp, and upper back           |
|                                                                         |
| INFANTS & YOUNG CHILDREN (< 2 years):                                   |
|   - LACKS adult head sparing: Involves scalp, face, neck                |
|   - Extensive palm and sole involvement with tense vesiculopustules     |
|   - Generalized eczematisation, secondary impetiginisation             |
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• Intense Nocturnal Pruritus: The clinical hallmark of scabies. Pruritus is characteristically out of proportion to visible skin lesions and worsens dramatically at night in bed (due to warmth stimulating mite motility and nocturnal circadian shifts in cytokine release) and after hot baths.
• Pathognomonic Primary Lesion: The Burrow (Cuniculus):
  • A delicate, thin, whitish, greyish or light-brown, thread-like serpentine (S-shaped or wavy) intra-corneal tunnel measuring 2 to 15 mm in length.
  • Located predominantly in the interdigital web spaces, flexor wrists, ulnar borders of hands, and lateral feet.
  • At the advancing, blind terminus of the burrow, a tiny translucent vesicle or dark pinpoint speck is frequently seen—this speck is the adult female mite.
• Secondary Lesions: Excoriations, erythematous urticarial papules, eczematous plaques, and secondary honey-crusted impetiginisation from scratching.

Special Clinical Variants

1. Scabietic Nodules (Nodular Scabies):
   • Firm, exquisitely pruritic, reddish-brown or violaceous nodules (5–12 mm) that develop primarily on the male genitalia (shaft of penis, scrotum), groin, and axillary folds.
   • Represent a chronic, persistent, exaggerated hypersensitivity granulomatous reaction to retained dead mite parts and antigens.
   • Critical Clinical Pitfall: Nodules frequently persist for weeks to several months after successful microbiological eradication of live mites. They do not signify active persistent infestation unless new linear burrows or mites are identified.
   • Treatment: Potent topical corticosteroids (clobetasol propionate) or intralesional triamcinolone acetonide.
2. Infantile Scabies:
   • Occurs in neonates and children under 2 years of age.
   • Differs markedly from adult scabies: involves the scalp, face, neck, palms, and soles, presenting with prominent inflammatory pustules, blisters, and widespread weeping eczema. Often misdiagnosed as infantile atopic dermatitis or dyshidrotic eczema.
3. Crusted Scabies (Norwegian Scabies):
   • A severe, highly debilitating variant resulting from a profound defect in host cell-mediated immunity or inability to scratch.
   • Seen in patients with HIV/AIDS, organ transplant recipients on immunosuppression, hematological malignancies, severe neurological deficits (paraplegia, stroke, dementia), Down syndrome, and leprosy.
   • Due to the absence of protective cellular immune containment and mechanical scratching, mites proliferate unchecked into hundreds of thousands or millions of live mites.
   • Clinical Features: Extensive, thick, adherent, yellow-brown to grey, hyperkeratotic, fissured, psoriasiform crusted plaques on hands, feet, extensor joints, scalp, and face. Dystrophic, thickened, subungual hyperkeratosis in nails. Can progress to full-body erythroderma. Secondary bacterial superinfections (S. aureus, S. pyogenes) frequently cause life-threatening bacteremia and sepsis.
   • Paradoxical Presentation: Pruritus is typically minimal or entirely absent due to blunted immune reactivity.
   • Extreme Contagiousness: Highly infectious. Transmission occurs readily through brief, casual non-intimate contact or contact with shedded scales on furniture, clothing, and bedding, frequently sparking explosive institutional ward epidemics.

Diagnostic Techniques

1. Dermoscopy (Epiluminescence Microscopy) - The "Delta-Wing Jet" Sign:
   • Dermoscopy is the diagnostic standard of care in European clinics, achieving sensitivity and specificity > 90%.
   • Under 10× to 20× magnification, the clinician identifies the "delta-wing jet plane" sign (also termed the "hang-glider" sign or "triangle" sign):
     • A tiny, dark, pigmented, brownish triangular structure at the apex of the burrow, which represents the anterior head, mouthparts (chelicerae), and two front pairs of legs of the mite.
     • The translucent, wavy, whitish trailing line represents the burrow ("jet contrail"), often containing dark oval pellets (scybala).
2. Microscopic Examination (Skin Scraping):
   • Definitive gold standard. Mineral oil or 10% KOH is placed on a scalpel blade (#15) and used to gently scrape the roof of a burrow containing a terminal speck.
   • Scrapings are placed on a glass slide with a coverslip and examined under light microscopy (10× and 40× objective).
   • Confirmed by identifying: (a) adult mites, (b) oval translucent eggs, (c) empty hatched egg shells, or (d) dark brown oval scybala.
3. Burrow Ink Test: Surgical marking pen or fountain pen ink rubbed over a suspected lesion and wiped with an alcohol swab; ink penetrates the defective burrow roof, outlining the tunnel as a dark zigzag line.

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European Guideline Management of Scabies (IUSTI / EADV)

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|              EUROPEAN GUIDELINE SCABIES MANAGEMENT PROTOCOL                       |
+-----------------------------------------------------------------------------------+
| 1. FIRST-LINE TOPICAL THERAPY:                                                    |
|    - Permethrin 5% Dermal Cream                                                   |
|    - Apply thoroughly to entire body from neck down to tips of toes               |
|      (Include scalp, face, neck in infants, young children, and elderly)          |
|    - Leave on for 8 to 14 hours (overnight); wash off thoroughly                  |
|    - MANDATORY SECOND APPLICATION: Repeat 7 to 14 days later (ideally Day 7-10)   |
|      *Rationale: Permethrin is not fully ovicidal; repeat kills newly hatched      |
|                  larvae before they can mature and lay new eggs.                  |
|                                                                                   |
| 2. FIRST-LINE SYSTEMIC THERAPY:                                                   |
|    - Oral Ivermectin: 200 mcg/kg as a single oral dose taken with food            |
|    - MANDATORY SECOND DOSE: Repeat 7 to 14 days later                             |
|    - Indications: Institutional outbreaks, mass eradication, non-compliance,     |
|      severe eczema/broken skin, failed topical therapy, crusted scabies.          |
|    - Contraindications: Infants < 15 kg (or < 2 yrs), pregnancy, lactation.       |
|                                                                                   |
| 3. CRUSTED (NORWEGIAN) SCABIES PROTOCOL:                                          |
|    - COMBINED MULTIMODAL THERAPY:                                                 |
|      * Oral Ivermectin (200 mcg/kg) on Days 1, 2, 8, 9, 15 (and 22, 29 if severe) |
|      * PLUS Daily Topical Permethrin 5% cream for 7 days, then 2x/week            |
|      * PLUS Keratolytics (5% Salicylic acid or 40% Urea) to dissolve crusts       |
|      * Strict contact isolation in private room                                   |
|                                                                                   |
| 4. MANDATORY CONTACT TRACING & HYGIENE DECONTAMINATION:                           |
|    - SIMULTANEOUS TREATMENT of all household members, sexual partners, and close  |
|      personal contacts, REGARDLESS of whether they have symptoms!                 |
|    - Wash all clothes, bed linens, towels used in prior 3-4 days at >= 60°C       |
|      OR seal in airtight plastic bags for at least 72 hours (7 days for crusted). |
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Alternative Therapies & Post-Scabetic Management

• Benzyl Benzoate 25% Lotion: Applied for 24 hours on consecutive days (diluted to 10%–12.5% in children); highly effective European second-line agent, though produces skin irritation.
• Sulfur Ointment (5%–10% in petrolatum): Applied once daily for 3 consecutive nights; an alternative for infants under 2 months of age, for whom permethrin is not licensed. Permethrin remains the preferred option in pregnancy and breastfeeding.
• Post-Scabetic Pruritus: Patients must be warned in advance that itching frequently persists for 2 to 4 weeks after successful cure, resulting from persistent dead mite antigens within the stratum corneum. Manage with emollients, oral non-sedating H1-antihistamines, and moderate-potency topical corticosteroids. Re-treatment is indicated only if new burrows or live mites are verified.

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Pediculosis (Louse Infestations)

Lice are obligate, blood-sucking, host-specific, wingless human insects.

• Maculae Caeruleae (Tâches Bleues): Pathognomonic slate-grey or bluish, non-palpable, asymptomatic macules (0.5–1.5 cm) on the lower abdomen, thighs, and buttocks of patients infested with Phthirus pubis. Caused by the enzymatic conversion of host bilirubin and hemoglobin by louse salivary secretions injected during blood feeding.

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Cutaneous Leishmaniasis

Cutaneous leishmaniasis is a vector-borne protozoal infection caused by obligate intracellular parasites of the genus Leishmania, transmitted to humans through the bite of an infected female phlebotomine sandfly (Phlebotomus species in the Old World; Lutzomyia species in the New World).

Life Cycle & Pathogenesis

1. During a blood meal, the female sandfly injects flagellated, motile promastigotes from its proboscis into the host's dermis.
2. Promastigotes are phagocytosed by dermal macrophages, dendritic cells, and neutrophils.
3. Inside the phagolysosome, promastigotes lose their flagella and transform into non-motile, oval amastigotes (measuring 2 to 4 µm in diameter), historically termed Leishman-Donovan (LD) bodies.
4. Amastigotes replicate by binary fission within macrophages until the host cell ruptures, releasing amastigotes to infect adjacent reticuloendothelial cells.

Clinical Classification: Old World vs New World Leishmaniasis

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|                     CUTANEOUS LEISHMANIASIS CLASSIFICATION                           |
+--------------------------------------------------------------------------------------+
| 1. OLD WORLD CUTANEOUS LEISHMANIASIS:                                                |
|    - Geography: Mediterranean basin, Middle East, North Africa, Central Asia         |
|    - Vectors: Phlebotomus sandflies                                                  |
|    - Major Species:                                                                  |
|      * L. major: Rural/zoonotic (rodents); acute "wet" rapidly ulcerating lesions     |
|      * L. tropica: Urban/anthroponotic; chronic "dry" indolent ulcers                |
|      * L. infantum: Mediterranean basin; solitary papule/ulcer, children             |
|    - Course: Solitary, painless "oriental sore"; heals spontaneously in 6-18 months |
|      leaving cribriform, depressed, tissue-paper scar. Mucosal spread is rare.      |
|                                                                                      |
| 2. NEW WORLD CUTANEOUS LEISHMANIASIS:                                                |
|    - Geography: Central and South America (neotropical forests)                      |
|    - Vectors: Lutzomyia sandflies                                                    |
|    - Major Species:                                                                  |
|      * L. mexicana complex: Chiclero ulcer (painless, destructive ulcer of ear pinna) |
|      * L. braziliensis complex (Subgenus Viannia): L. braziliensis, L. panamensis    |
|    - SEVERE DANGER: High risk of hematogenous / lymphatic dissemination to           |
|      naso-oropharyngeal cartilage -> MUCOCUTANEOUS LEISHMANIASIS ("ESPUNDIA")       |
|      * Occurs months to years after healing of initial skin ulcer; destroys nasal    |
|        septum, palate, larynx ("tapir nose" deformity). Mandatory systemic therapy! |
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Clinical Morphology of the "Oriental Sore"

• Initial Lesion: Weeks to months following a sandfly bite on an exposed body area (face, neck, arms, legs), an asymptomatic, firm, pink-to-violaceous erythematous papule develops.
• Evolution: Slowly expands into a firm, indurated plaque (1–5 cm), which breaks down centrally to produce a painless, shallow ulcer with a raised, indurated, rolled, violaceous border ("volcano" or "crater" morphology).
• Crust: The ulcer base is covered by an adherent, yellowish-grey, hyperkeratotic crust. If the crust is removed, projecting keratin plugs on the undersurface leave tiny pits ("tin-tack sign" or "carpet-tack sign"). Satellite papules may surround the primary ulcer.
• Special Forms:
  • Leishmaniasis Recidivans (Lupoid Leishmaniasis): Chronic recurrence of new granulomatous papules and nodules within or around the margin of a previously healed, scarred lesion, mimicking lupus vulgaris.
  • Post-Kala-Azar Dermal Leishmaniasis (PKDL): Sequela of visceral leishmaniasis (L. donovani), presenting with widespread macular hypopigmented lesions and succulent nodules.

Diagnostic Evaluation

• Direct Slit-Skin Smear: Slit scraping from the indurated active ulcer border stained with Giemsa stain. Microscopy (oil immersion 1000×) shows pathognomonic intracellular amastigotes (LD bodies) within the cytoplasm of large macrophages. Each amastigote is an oval body (2–4 µm) containing a distinct rounded nucleus and a characteristic rod-shaped, dark-staining kinetoplast.
• Histopathology: Dense diffuse dermal lymphohistiocytic and plasma cell infiltrate containing intracellular amastigotes within macrophages (in early lesions); evolving into well-formed epithelioid granulomas with scarce amastigotes in late stages.
• PCR (Polymerase Chain Reaction): Diagnostic gold standard with sensitivity >95%. Essential for species identification, which is clinically mandatory for all New World leishmaniasis cases to determine the risk of mucosal metastasis (L. braziliensis).
• Culture: Inoculation of aspirate onto Novy-MacNeal-Nicolle (NNN) biphasic medium incubated at 22°C to 26°C; yields flagellated promastigotes within 1 to 3 weeks.

European Guideline Management

1. Local Therapy (Indications: Simple Old World CL: ≤ 3-4 small [< 4 cm] lesions, non-facial, non-joint, immunocompetent host, low-risk species):

• Intralesional Pentavalent Antimonials: Meglumine antimoniate (Glucantime) or Sodium stibogluconate (Pentostam). 0.5 to 2.0 mL infiltrated directly into the indurated borders and base until the entire lesion blanches pale; repeated every 3 to 7 days for 3 to 5 sessions.
• Cryotherapy: Liquid nitrogen applied as a double freeze-thaw cycle (15–20 seconds freeze), either alone or immediately preceding intralesional antimonial injection (synergistic efficacy).
• Topical Paromomycin 15% ointment: Applied twice daily for 20 days.

2. Systemic Therapy (Indications: Complex CL: > 4 lesions, lesions > 4–5 cm, lesions on face/ears/fingers/toes, failure of local therapy, immunocompromised host, and ALL cases of New World Leishmania Viannia subgenus [L. braziliensis] to prevent mucocutaneous leishmaniasis):

• Intravenous or Intramuscular Pentavalent Antimonials: Meglumine antimoniate or Sodium stibogluconate at 20 mg Sb⁵⁺/kg/day for 20 to 28 consecutive days.
  • Toxicity Monitoring: Mandatory baseline and weekly ECG (pentavalent antimonials cause dose-dependent cardiotoxicity: QTc prolongation, T-wave inversion, life-threatening ventricular arrhythmias), serum amylase/lipase (raised pancreatic enzymes are common; clinical pancreatitis is less frequent), liver transaminases, and renal parameters.
• Liposomal Amphotericin B: 3 mg/kg/day IV on days 1–5, 14, and 21 (total cumulative dose 18–21 mg/kg). First-line in antimony resistance, pregnancy, renal/cardiac contraindications, or severe mucosal disease.
• Oral Miltefosine: 2.5 mg/kg/day (50 mg orally 2–3 times daily) for 28 days. First oral agent approved for leishmaniasis; highly active against L. braziliensis and L. panamensis. Strict teratogen (requires a negative pregnancy test and effective contraception during therapy and for 5 months afterwards under US labelling); frequent gastrointestinal intolerance.