- 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
- Range from self healing cutaneous disease-
debilitating mucocutaneous disease- fatal
- Incidence- 2 million cases/ year
- More than 90% of CL occurs in Afghanistan,
Iran, Saudi Arabia, Syria, Brazil, Peru
- no race or sex predilection
- Each species tend to occupy a particular
New world (Central & South America)
Old world ( Mediterranean basin, southern
Europe, central Africa, parts of southern &
- CL &VL are major public health problems in
- There are three forms :
■ Cutaneous leishmaniasis
- most often in the old world
- both skin & mucosal surface
- mostly in the new world
- organ of the mononuclear phagocyte
- Primary reservoirs- wild & domestic animals
- Humans are accidental hosts
- Infection is transmitted by bite of an infected
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
Etiology & lifecycle
- It is a parasitic protozoa
Order – kinetoplastida
- ~ 20 species are pathogenic for humans
- Human leishmania has a wide geographic
- In Old world cutaneous leishmaniasis
• L. major
• L. tropica
• L. aethiopica
• L. infantum
- In New world cutaneous leishmaniasis
• L. mexicana complexes
• L. brasiliensis complexes
- Genera of the sandfly
In New world- phlebotomus
In Old world- Lutzomyia
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
After phagocytosis, promastigotes
changed into amastigotes
Macrophages burst releasing their
amastigotes which in turn infecting
Amastigote- 3-5 μm, ovoid, non-motile intracellular
Promastigote- elongated, motile extracellular form
- 1.5-3.5 by 15-20 μm consisting of a single flagellum
- During inoculation, tear of epidermis & dermal
capillaries to release promastigotes
Promastigote binds to macrophage
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
- 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
- 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
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
☻Dry or urban type
- By L. tropica
- longer IP & course
- dry ulcer
- Lesions start as erythematous papules
- Enlarge over few weeks forming
- These often ulcerate & become crusted
- Ulcerated nodules
- Often covered by an
New world CL
alley sickness, Andean sickness
- Pure cutaneous disease is similar to OW-CL
- Isolated ulcers are the most common
- Half of the lesions caused by L. mexicana
heals within 3 mo
- Those caused by L. braziliensis persist much
Complication / other forms of CL
- Disseminated Cutaneous Leishmaniasis
- Chronic Cutaneous Leihmaniasis - CCL
- Muco - Cutaneous Leishmaniasis - MCL
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
- Mimics Lepromatous Leprosy
-Viscera are not involved
course with relapse after
treatment is classic
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
- In NW-CL by L. braziliensis & L. panamensis
- In OW-CL, by L. aethiopica
- Results from direct extension or
- Mucosal involvement- erythema, edema
- Crusting, ulceration
- Nasal stuffiness, difficulty of breathing
- Bony structures are spared
- Nasal collapse, free hanging nose
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
- In India, 5-10% develop several years after Rx
Diagnosis of CL
● Skin smears
- Stained with Giemsa’s
- Amastigotes seen
- Success rate – 50-80%
- Early lesions & lesions of
DCL –easily identified &
- Late /healing/ lesions-
● Skin biopsy
- In early lesions of CL,
dense & diffuse mixed
- Histiocytes, scattered
cells, lymphocytes &
- Presence of amastigotes- hallmark
/LD bodies/- ~70% of cases
- Epidermal hyperplasia, ulceration
- Later, granuloma
- Novy- MacNeal-
Nicolle media- gold
- Sensitivity- 50%
- Promastigotes seen
after several days up to
- 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
persistent, progressive, deep
risk of MCL
- There are local &
- Local therapy for :
• small lesions
• not progressing
- Systemic treatment is
reserved for :
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
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
- 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
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.
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.
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.
The average number of adult female
mites in common form of scabies is about
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.
Female scabies mite with egg. in potassium
hydroxide wet mount obtained from skin
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.
Incubation period ranges from days to
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
clinical featuresclinical features
Basis for diagnosis
- History pruritus in household members or close personal
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
worsen during night & warm.
persistent during day but tolerable.
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
pruritic papules are
around the axillae,
and on the buttocks &
Vesicles and bullae
particularly on the
palms and fingers.
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.
Crusted scabies (formerly called
- found in individuals with compromised
immune system & decreased sensory
- experience minimal pruritus despite their
highly contagious Patients
-May have thousands of mites on their skin
-live mites from crusted cases can survive
for up to a week in the environment feeding
on the sloughed stratum corneum.
Keraiotosis and crusting
there is involvement of
face and especially scalp,
genitalia and buttocks,
are sites of predilection
for heavy keratotic
The tips of fingers are
nails are distorted.
mite under the
◦ mites, eggs & fecal
2 topical treatments (1 wk apart) with anti
scabietic is recommended
pruritus can and will likely persist for up to
1mth after treatment.
- 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
◦ 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.
◦ include transient burning, stinging, and pruritus.
◦ 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.
Seizures, slowly metabolized & has a predilection
for storage in fatty tissues, as well as the brain.
CROTAMITON (10% cream)
◦ is a scabicide with some antipruritic
◦ 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.
◦ 12.5% & 25% emulsion lotion overnight
application for three consecutive nights
◦ Adverse reactions were usually limited to skin
6% / 10% precipitated sulfur in a cream
or ointment base.
applied on multiple consecutive days- up
◦ appears to have been relatively safe.
The only well-documented adverse effect
is the drug's obnoxious odor.
◦ 200microgram/kg single oral dose, repeated
◦ Adverse Effects
rare side effects of hypotension, laryngeal edema,
The only oral but highly effective
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
Individuals in close contact with the
person should be treated.
fomites, bed sheets, pillow cases, towels,
and clothes worm during the past 5 days
washed and dried
a chronic parasitic disease
filarial nematode Onchocerca volvulus.
multiple organ systems
cutaneous and ophthalmologic
multiple organ systems
primarily affects people living near fast-
flowing rivers where blackflies breed.
Africa, Central and South America, and the
~ 18 million people are currently infected.
Of those infected:-
◦ about 1.5% are blind,
◦ additional 2.8% have severe visual
◦ Greater morbidity with age is the result of cumulative
exposure in endemic areas.
◦ Blindness tends to occur in adulthood after many
years of infection.
humans are the only definitive hosts.
Simulium black flies - obligate intermediate
The species Simulium damnosum in africa
African Simulium species tend to bite the ribs,
hips, iliac crests and lower limbs,
Female worm length ranges from 30-80
Male adult worms are usually 3-5 cm in
migrate between various subcutaneous
nodules to inseminate females.
life span of up to 14 years for adults
MF live for 6-30 months;
the female worms produce 1000-3000 MF daily.
can migrate throughout the subcutaneous tissues
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
The predominant immune response is production of
antibodies against dead/dying MF
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
fully develop in the labium of the proboscis of the fly
which passes larvae to another human when taking a
In the human host, the larvae developesto male and
female adult worms
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→
vision loss and frank→ blindness
range from early mild inflammatory lesions to chronic
debilitating cutaneous and ophthalmic lesions.
◦ refers to the various cutaneous findings
◦ classified into 6 diseases
1. Acute papular onchodermatitis (APOD)
2. Chronic papular onchodermatitis (CPOD)
3. Lichenified onchodermatitis (LOD)
ACUTE PAPULAR DERMATITISACUTE PAPULAR DERMATITIS
Widespread small pruritic papules that may
progress to vesicles and/or pustules in the most
There may be associated erythema and edema.
most often involves the face, shoulders, trunk, and
CHRONIC PAPULAR DERMATITISCHRONIC PAPULAR DERMATITIS
Larger (3 to 9 mm in diam.), flat-topped,
lichenoid papules distributed
Pruritus is common
may be present.
hyperpigmented papules, regional
lymphadenopathy, and edema
The most commonly affected anatomic
areas are the buttocks, shoulders, and
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
There is often associated lymphadenopathy.
Atrophy, also known as “lizard skin”
degeneration of elastic fibers and other
structural elements of the skin due to
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.
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
Less commonly the buttocks, lateral groin,
and lower abdomen are involved.
Palpable onchocercal nodules containing the
involve the deep dermis and subcutaneous
are typically asymptomatic
occur over bony prominences such as
◦ the skull, -iliac crest,
◦ knee, -rib,
◦ sacrum, -scapula
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
dermatitis, subcutaneous nodules, or ocular lesions.
Peripheral eosinophilia and elevated IgE levels are
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.
◦ Performed when infection is suspected and skin snip test results are
◦ 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
◦ Severe reactions may occur in both the skin and the eyes, and other
adverse effects include vomiting, conjunctivitis, hypotension, and
DEC patch test
◦ A mixture of 10% DEC and Nivea cream is applied under an occlusive
◦ 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%.
Microscopic examination of excised
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
The current mainstay of treatment is
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.
Doxycycline 100 mg/d administered
for 6-8 weeks
targets bacteria of the Wolbachia
species, known endosymbionts in
Reduces microfilarial loads,
sterilizes adult worms,
decreases adult worm viability.
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.
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
Ocular reactions need treatment with
corticosteroid eye drops and mydriatics.
◦ 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.
◦ larvicides to reduce the black fly population.
Mass treatment with ivermectin
◦ is employed in areas of high endemicity
◦ reduces the microfilarial burden in the
Education of people in endemic areas