Leishmaniasis + scabies + onchocerciasis


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Leishmaniasis + scabies + onchocerciasis

  1. 1. Cutaneous leishmaniasisCutaneous leishmaniasis
  2. 2. Leishmaniasis - A group of disease caused by several species of the genus leishmania - Named after W.B.Leishman who identified the organism in 1901 - the spectrum of disease depends on the species - Range from self healing cutaneous disease- debilitating mucocutaneous disease- fatal visceral involvement
  3. 3. Epidemiology - Incidence- 2 million cases/ year - More than 90% of CL occurs in Afghanistan, Iran, Saudi Arabia, Syria, Brazil, Peru - no race or sex predilection
  4. 4. - Each species tend to occupy a particular geographical zone New world (Central & South America) Old world ( Mediterranean basin, southern Europe, central Africa, parts of southern & central Asia) - CL &VL are major public health problems in Ethiopia
  5. 5. - There are three forms : ■ Cutaneous leishmaniasis - skin - most often in the old world ■ Mucocutaneous - both skin & mucosal surface - mostly in the new world ■ Visceral - organ of the mononuclear phagocyte system
  6. 6. Cutaneous leishmaniasis - Primary reservoirs- wild & domestic animals (canine, rodents) - Humans are accidental hosts - Infection is transmitted by bite of an infected phelebotomine sandfly
  7. 7. Epidemiology in Ethiopia - CL is wide spread through out high lands at altitude between 1500- 2650m. - mainly caused by L.aethiopica, L.major, L tropica& L. donovani. (CL,MCL& DCL) - The vector is phlebotomous martini - Along the lake Abaya, Omo river plains, Metema & Humera plains in NW Ethiopia
  8. 8. Etiology & lifecycle - It is a parasitic protozoa Phylum- Sarcomastigophora Subphylum- Mastigophora Order – kinetoplastida Family- Trypanosomatidae Genus- Leishmania - ~ 20 species are pathogenic for humans
  9. 9. - Human leishmania has a wide geographic distribution - In Old world cutaneous leishmaniasis • L. major • L. tropica • L. aethiopica • L. infantum - In New world cutaneous leishmaniasis • L. mexicana complexes • L. brasiliensis complexes
  10. 10. - Genera of the sandfly In New world- phlebotomus In Old world- Lutzomyia
  11. 11. Infected macrophages taken up by fly during blood meal Amastigotes released in the stomach Transformation into promastigotes Migrate to the alimentary tract & multiply by binary fission Changed into infective form When infectious sandfly feeds, release promastigotes After phagocytosis, promastigotes changed into amastigotes Macrophages burst releasing their amastigotes which in turn infecting others.
  12. 12. Amastigote- 3-5 μm, ovoid, non-motile intracellular form Promastigote- elongated, motile extracellular form - 1.5-3.5 by 15-20 μm consisting of a single flagellum
  13. 13. Pathogenesis - During inoculation, tear of epidermis & dermal capillaries to release promastigotes Promastigote binds to macrophage Phagocytosis Formation of phagolysosome Transformation into amastigote Leishmania antigen presented on cell surface by MHC II molecules T cells bind to antigen Th1 or Th2 response
  14. 14. - A dominant Th1 response resulting in the production of IFN & NO → leishmanicidal state of macrophages → subclinical infection or self healing CL - A dominant Th2 responses – progressive disease; DCL
  15. 15. Clinical findings - The clinical spectrum includes: ○ Localized CL ○ Disseminated (DCL, MCL & VL) - Most cases of CL heal spontaneously within one year - cute CL - Disease lasting more than a year- chronic CL
  16. 16. Old world CLOld world CL Oriental sore, Baghdad boil,Aleppo boilOriental sore, Baghdad boil,Aleppo boil - Two major types: ☻ Moist or rural type - typically by L. major - short IP - 1 wk-3 mo - rapid & mild course - often heal within 6 mo ☻Dry or urban type - By L. tropica - longer IP & course - dry ulcer
  17. 17. - Lesions start as erythematous papules - Enlarge over few weeks forming nodules/plaques - These often ulcerate & become crusted
  18. 18. - Ulcerated nodules - Often covered by an adherent crust
  19. 19. New world CL alley sickness, Andean sickness - Pure cutaneous disease is similar to OW-CL - Isolated ulcers are the most common presentation - Half of the lesions caused by L. mexicana heals within 3 mo - Those caused by L. braziliensis persist much longer
  20. 20. Complication / other forms of CL - Disseminated Cutaneous Leishmaniasis -DCL - Chronic Cutaneous Leihmaniasis - CCL - Muco - Cutaneous Leishmaniasis - MCL
  21. 21. Diffuse Cutaneous Leishmaniasis DCL - Rare anergic form of CL - Deficient in cell mediated immunity - L. aethiopica, L. amazonensis - Disseminated non-ulcerated nodules without internal organ involvement - On the extremities, face /may give leonine facies/ - Mimics Lepromatous Leprosy
  22. 22. -Viscera are not involved - progressive/chronic course with relapse after treatment is classic
  23. 23. Mucocutaneous Leishmaniasis /MCL/ - Chronic, progressive spread of CL of the nasal, laryngeal & buccal mucosa - Often a complication of CL - Several years after resolution or while lesions present - In NW-CL by L. braziliensis & L. panamensis - In OW-CL, by L. aethiopica - Results from direct extension or hematogenous/lymphatic spread
  24. 24. - Mucosal involvement- erythema, edema - Crusting, ulceration - Nasal stuffiness, difficulty of breathing - Bony structures are spared - Nasal collapse, free hanging nose
  25. 25. Post Kalazar Dermal Leishmaniasis /PKDL/ - A complication of VL caused by L. donovani develop during or after treatment - Macule, papule, nodule which starts on the face and involve the extremities, trunk - Symmetrical & non itchy - In Sudan, 50% of pts develop within 6 mo after Rx - In India, 5-10% develop several years after Rx
  26. 26. Diagnosis of CL ● Skin smears - Stained with Giemsa’s stain - Amastigotes seen - Success rate – 50-80% - Early lesions & lesions of DCL –easily identified & confirmed - Late /healing/ lesions- difficult
  27. 27. ● Skin biopsy - In early lesions of CL, dense & diffuse mixed inflammatory cells infiltrates - Histiocytes, scattered multinucleated giant cells, lymphocytes & plasma cells
  28. 28. - Presence of amastigotes- hallmark /LD bodies/- ~70% of cases - Epidermal hyperplasia, ulceration - Later, granuloma
  29. 29. ● Culture - Novy- MacNeal- Nicolle media- gold standard - Sensitivity- 50% - Promastigotes seen after several days up to 4 weeks
  30. 30. Treatment - Should be individualized - Patients should be monitored until lesions have completely healed - An expectant management in cases caused by L. major & L. mexicana - Treatment should be started in: cosmetically or functionally important sites multiple lesions persistent, progressive, deep risk of MCL
  31. 31. - There are local & systemic therapy - Local therapy for : • small lesions • non-inflammed • not progressing - Systemic treatment is reserved for : ▫ DCL ▫ CCL ▫ MCL
  32. 32. Systemic Therapy Pentavalent antimonials compounds - first line drugs sodium stibogluconate 20 mg/kg for 20 days for CL & 28 days MCL meglumine antimoniate20 mg/kg for 20 days
  33. 33. Amphotericin B Deoxylate & its lipid formulation- 0.5-1.0mg/kg for up to 8 weeks Pentamidine isethionate- 3 mg/kg on alter. days x4 or 2 mg/kg on alter. days x 7d Fluconazole 200mg daily for 6 wks Ketoconazole 400mg daily for 6 wks Itraconazole 7mg/kg/d for 3 wks Allopurinol 15mg/kg/d for 21 days
  34. 34. Prevention - Promotion of personal protective measures use of protective clothing use of insect repellents permethrin-treated bed nets & clothings - Use of insecticides - Destruction of animal reservoirs
  35. 35. Cutaneous leishmaniasis Localized cutaneous leishmaniasis Diffuse cutaneous leishmaniasis Mucocutaneous leishmaniasis Post kalazar dermal leishmaniasis Leishmania recidivans
  36. 36. ScabiesScabies
  37. 37. EPIDEMIOLOGY 300 million people worldwide are infected with scabies mite. Scabies is most common in children & young adults but may occur at any age.  sex incidence is equal. All racial groups are susceptible.  Higher incidences occur with overcrowding. Scabies
  38. 38. EtiologyEtiology  caused by mites of family Sarcoptidae, which includes Sarcoptes scabiei,var.hominis. host specific - they survive for only a short period on another host. Morphology of scabies mite ◦ has an ovoid body, flattened dorsoventrally. ◦ There are 4 pairs of short legs; the anterior 2 pairs end in broad.
  39. 39. Copulation occurs in a small burrow excavated by the female. After fertilization female burrows into stratum corneum &deposits her eggs. The adult male mite dies after copulation.
  40. 40. The average number of adult female mites in common form of scabies is about 12 [13-15]. Approximately 40-50 eggs are laid during a lifespan of 4-6 wks. After 3-4 days larvae emerge. Later adult males and females develop.
  41. 41. Female scabies mite with egg. in potassium hydroxide wet mount obtained from skin scrapings.
  42. 42.  contagious disease Scabies is usually transmitted by close physical contact, such as prolonged hand-holding or the sharing of bed. Indirect spread by clothing or bedding. Away from the host, scabies mites survive for 24-36 hr in room condition.
  43. 43. Incubation period ranges from days to months both immediate & delayed type hypersensitivity are involved & result pruritus and cutaneous lesions.  subsequent infestation is usually recognized within 24-48 hrs. Asymptomatic scabies-infested individuals “carriers”.
  44. 44. clinical featuresclinical features  Basis for diagnosis - History pruritus in household members or close personal contacts  Distribution and types of lesions. - interdigital web ,flexor aspect of wrists, axillae, areolae, umbilicus, lower abdomen, genitals, and buttocks. - circle of Hebra(nipple,axillae,elbow,wrists,hand&crotch/groin) -In adults scalp & face are usually spared. - In infants lesions are commonly present over entire cutaneous surface.  Itching worsen during night & warm. persistent during day but tolerable.
  45. 45. The pathognomonic sign is the burrow. ◦ a thin, thread-like, linear structure. 1-10 mm in length. vesicle or pustule containing mite may be noted at end of burrow.
  46. 46. pruritic papules are predominantly present around the axillae, periareolar regions, periumbilical region, and on the buttocks & thighs. Vesicles and bullae may develop particularly on the palms and fingers.
  47. 47. Nodular scabies Dull red nodules appear during active scabies or after treatment. represent exaggerated reaction to scabetic antigens.  3- 5 mm in diameter.  May or may not itch. No organisms are found in the lesions.  scrotum, penis, and vulva.  Intralesional steroids, tar or excision are methods of treatment.
  48. 48. Crusted scabies (formerly called Norwegian scabies) - found in individuals with compromised immune system & decreased sensory function. - experience minimal pruritus despite their highly contagious Patients -May have thousands of mites on their skin surface. -live mites from crusted cases can survive for up to a week in the environment feeding on the sloughed stratum corneum.
  49. 49.  Show erythema,hyper- Keraiotosis and crusting  there is involvement of face and especially scalp, genitalia and buttocks,  Pressure-bearing areas are sites of predilection for heavy keratotic lesions.  The tips of fingers are swollen&crusted.  nails are distorted.
  50. 50. DiagnosisDiagnosis demonstration of mite under the microscope ◦ mites, eggs & fecal product (scybala).
  51. 51. ComplicationComplication Secondary impetiginization. Eczematization.
  52. 52. TreatmentTreatment 2 topical treatments (1 wk apart) with anti scabietic is recommended pruritus can and will likely persist for up to 1mth after treatment. In adults - apply to entire body except face and scalp. children and crusted scabies. ◦ the face and scalp should also be treated. ◦ family members and close contacts has to be treated simultaneously.
  53. 53. PERMETHRIN  ADMINISTRATION ◦ A weeek apart two applications of 5% cream is applied to the body from the neck down, left on for 8-14 hours,then washed off.  Adverse reactions ◦ include transient burning, stinging, and pruritus.
  54. 54. LINDANE ◦ single application to the entire body from neck down, left for 8-12 hr then washed off. Patients should be retreated only if active mites can be demonstrated, and never within 1 wk of initial treatment. ◦ ADR  Seizures, slowly metabolized & has a predilection for storage in fatty tissues, as well as the brain.
  55. 55. CROTAMITON (10% cream) ◦ is a scabicide with some antipruritic properties. ◦ applications to the entire body from chin down at 24hr intervals, with a cleansing bath 48 hr after the last application for 3days ◦ Allergic contact hypersensitivity and primary irritation may occur, necessitating discontinuance of therapy.
  56. 56. Benzyl Benzoate ◦ 12.5% & 25% emulsion lotion overnight application for three consecutive nights ◦ Adverse reactions were usually limited to skin irritation.
  57. 57. Precipitated Sulfur 6% / 10% precipitated sulfur in a cream or ointment base.  applied on multiple consecutive days- up to 7days ◦ appears to have been relatively safe. The only well-documented adverse effect is the drug's obnoxious odor.
  58. 58. Ivermectin ◦ 200microgram/kg single oral dose, repeated 10-14day. ◦ Adverse Effects  Infrequent  rare side effects of hypotension, laryngeal edema, and encephalopathy.
  59. 59. The only oral but highly effective scabicide shouldn`t be used in children <5 years or during pregnancy or lactation.  In crusted scabies the combination of ivermectin and a topical anti-scabicidies often used.
  60. 60. PreventionPrevention Individuals in close contact with the infected person should be treated. fomites, bed sheets, pillow cases, towels, and clothes worm during the past 5 days should be washed and dried
  62. 62. ONCHOCERCIASISONCHOCERCIASIS Synonyms  Onchocercosis  Blinding filariasis  River blindness
  63. 63. a chronic parasitic disease filarial nematode Onchocerca volvulus. multiple organ systems cutaneous and ophthalmologic complications. multiple organ systems primarily affects people living near fast- flowing rivers where blackflies breed.
  64. 64. EPIDEMIOLOGYEPIDEMIOLOGY occurs worldwide  Africa, Central and South America, and the Middle East. ~ 18 million people are currently infected. Of those infected:- ◦ about 1.5% are blind, ◦ additional 2.8% have severe visual impairment.
  65. 65. ◦ Greater morbidity with age is the result of cumulative exposure in endemic areas. ◦ Blindness tends to occur in adulthood after many years of infection.
  66. 66. PATHOPHYSIOLOGYPATHOPHYSIOLOGY humans are the only definitive hosts. Simulium black flies - obligate intermediate hosts The species Simulium damnosum in africa African Simulium species tend to bite the ribs, hips, iliac crests and lower limbs,
  67. 67. Female worm length ranges from 30-80 cm, Male adult worms are usually 3-5 cm in length migrate between various subcutaneous nodules to inseminate females. life span of up to 14 years for adults MF live for 6-30 months;
  68. 68. the female worms produce 1000-3000 MF daily. can migrate throughout the subcutaneous tissues and skin; they have a particular affinity for ocular tissues.  most die without completing their life cycle. with heavy infection, as many as 100,000 MF die each day. The predominant immune response is production of antibodies against dead/dying MF
  69. 69. LIFE CYCLELIFE CYCLE  Blackflies bite an individual infected with O.volvulus.  Fly saliva acts as a chemoattractant for microfilariae in the surrounding subcutaneous tissues  The microfilariae develope in the thoracic muscles within the blackfly,  in a 2- to 3-week period they become infective-stage larvae.  fully develop in the labium of the proboscis of the fly  which passes larvae to another human when taking a blood meal.  In the human host, the larvae developesto male and female adult worms
  70. 70. CLINICALCLINICAL  years after initial infection.  initial bite go unnoticed.  A 1- to 2-year latent period afer initial bite  Pruritus is the most common early symptom  Lymphadenopathy inguinal and femoral regions→ .  Subcutaneous nodules → (onchocercomata)  Visual symptoms itching, redness, photophobia, and→ blurred vision vision loss and frank→ blindness
  71. 71. PHYSICAL FINDINGS  diverse  range from early mild inflammatory lesions to chronic debilitating cutaneous and ophthalmic lesions.
  72. 72.  OnchodermatitisOnchodermatitis ◦ refers to the various cutaneous findings ◦ classified into 6 diseases 1. Acute papular onchodermatitis (APOD) 2. Chronic papular onchodermatitis (CPOD) 3. Lichenified onchodermatitis (LOD) 4. Atrophy 5. Depigmentation 6. onchocercomata
  73. 73. ACUTE PAPULAR DERMATITISACUTE PAPULAR DERMATITIS  Widespread small pruritic papules that may progress to vesicles and/or pustules in the most severe cases.  There may be associated erythema and edema.  most often involves the face, shoulders, trunk, and extremities.
  74. 74. CHRONIC PAPULAR DERMATITISCHRONIC PAPULAR DERMATITIS Larger (3 to 9 mm in diam.), flat-topped, lichenoid papules distributed symmetrically Pruritus is common post-inflammatory hyperpigmentation may be present. hyperpigmented papules, regional lymphadenopathy, and edema The most commonly affected anatomic areas are the buttocks, shoulders, and waist area.
  75. 75. LICHENIFIED ONCHODERMATITISLICHENIFIED ONCHODERMATITIS  an intensely pruritic dermatitis  excoriations and hyperpigmented and hyperkeratotic papules and plaques.  Become lichenified in time  The plaques have an asymmetric distribution  lower extremity is the most commonly affected anatomic location.  There is often associated lymphadenopathy.
  76. 76. ATROPHYATROPHY  Atrophy, also known as “lizard skin”  degeneration of elastic fibers and other structural elements of the skin due to chronic infection.  The skin appears wrinkled and thin  most commonly the buttocks and, less commonly, the extremities.  It may develop after any of the patterns described previously, or arise de novo.
  77. 77. DEPIGMENTATIONDEPIGMENTATION  is also known as “leopard skin.”  common finding in advanced onchocerciasis.  lesions resemble vitiligo  is ass. with perifollicular pigmentation  Pruritus is rarely seen  commonly found on the shins bilaterally.  useful method to screen for onchocerciasis in endemic areas.  Less commonly the buttocks, lateral groin, and lower abdomen are involved.
  78. 78. ONCHOCERCOMATAONCHOCERCOMATA Palpable onchocercal nodules containing the adult worm, involve the deep dermis and subcutaneous tissue. are typically asymptomatic occur over bony prominences such as ◦ the skull, -iliac crest, ◦ knee, -rib, ◦ sacrum, -scapula ◦ trochanter.
  79. 79. OCULAR FINDINGSOCULAR FINDINGS ◦ MF enter the eye by direct invasion from the conjunctiva into the sclera or cornea. ◦ inflammatory responses to MF ◦ intense host immune inflammatory reaction ◦ intensifies when MF die. ◦ causes the following ocular findings, which are typically bilateral:-
  80. 80. →Punctate keratitis →Sclerosing keratitis. →Anterior uveitis → Posterior segment lesions →optic neuritis
  81. 81. DDX.DDX.  hypersensitivity reactions Leprosy Yaws Pinta Treponematosis (endemic syphilis) Vit. A deficiency Atopic dermatitis Contact dermatitis Insect bites Scabies Chronic eczema Superficial mycoses Glaucoma Trachoma Vitiligo
  82. 82. DIAGNOSISDIAGNOSIS  dermatitis, subcutaneous nodules, or ocular lesions.  Peripheral eosinophilia and elevated IgE levels are common  Identification of the MF in a skin snip (100% specific)  6 samples are usually obtained: 1 from each scapula, iliac crest, and lateral calf  Demonstration of adult worms in an excised nodule.  Free floating MF can easily be seen in the anterior chamber of the eye on slit- lamp examination.
  83. 83. DIAGNOSIS…DIAGNOSIS…  Mazzotti test ◦ Performed when infection is suspected and skin snip test results are negative. ◦ 6 mg of DEC is administered ◦ Pt. observed for development of pruritus with or without erythema ◦ indicates the death of microfilariae in the skin. ◦ The reaction may occur from 15 minutes to 24 hours after DEC administration. ◦ Severe reactions may occur in both the skin and the eyes, and other adverse effects include vomiting, conjunctivitis, hypotension, and sudden death.  DEC patch test ◦ A mixture of 10% DEC and Nivea cream is applied under an occlusive dressing; ◦ the occurrence of a localized inflammatory response indicates a positive test result. ◦ This test is a safer alternative to the Mazzotti test. ◦ sensitivity is 30-80%.
  84. 84. Histologic Findings:-  Microscopic examination of excised onchocercomata reveals  cross-sections of adult worms and a collection of eosinophils and lymphocytes at the periphery of the nodule. and sometimes giant cells tend to accumulate around the worms. Calcification may also be seen
  85. 85. TREATMENTTREATMENT The current mainstay of treatment is ivermectin. Mass treatment campaigns (WHO) ◦ ivermectin is a microfilaricide ◦ and does not kill adult worms, ◦ does not cure the disease. ◦ significantly reduces microfilarial burden ◦ decreases transmission and ◦ 150 mcg/kg/d PO as single dose q6-12mo ◦ administered for the life span of the adult worm.
  86. 86. Doxycycline 100 mg/d administered for 6-8 weeks targets bacteria of the Wolbachia species, known endosymbionts in O.volvulus. Reduces microfilarial loads, sterilizes adult worms, decreases adult worm viability.
  87. 87. Treatment…Treatment… Diethyl carbamazine kills the MF and is given as follows:- first 3 days 1mg/kg body weight once; Next 4 days 2mg/kg body weight once; second week 4mg/kg body weight three times a day; third week 4mg/kg body weight three times a day.
  88. 88. Treatment…Treatment… In heavily infected patients,  or in those with severe dermatitis  or with eye involvement,  prednisone 40mg should be given at a daily dose in adults, starting the day before DEC and continuing for a few days until the reaction has settled.  Ocular reactions need treatment with corticosteroid eye drops and mydriatics.
  89. 89. Treatment…Treatment…  Suramin ◦ Extremely toxic ◦ in selected individuals for curative treatment of severe hyperreactive onchodermatitis uncontrolled by repeated ivermectin treatment. ◦ is a drug that kills adult worms and MF ◦ Parenteral/IV: >60 kg: 0.2 g week 1; 0.4 g week 2; 0.6 g week 3; 0.8 g week 4; 1 g week 5 and 6; total dose 4 g  nodulectomy, usually combined with a microfilaricide.
  90. 90. PREVENTIONPREVENTION Vector control ◦ larvicides to reduce the black fly population. Mass treatment with ivermectin ◦ is employed in areas of high endemicity ◦ reduces the microfilarial burden in the population. Education of people in endemic areas
  91. 91. Mass RMass Rxx