Leishmaniasis is caused by protozoan parasites of the Leishmania species, which are transmitted through the bite of infected sand flies. It manifests clinically in three main forms: cutaneous, mucocutaneous, and visceral leishmaniasis. Cutaneous leishmaniasis causes skin sores, visceral affects internal organs, and mucocutaneous can destroy nasal and oral tissues. It is diagnosed through microscopic identification of the parasite, culture, serology or PCR. Treatment involves antimony- or amphotericin B-based medications. Prevention relies on protective clothing, repellents and reducing exposure to sand fly bites.

1. PAEDIATRIC
SKIN DISORDERS
Richie Chacko
Paediatric & Nonatal Nursing

2. LISHMANIASIS
• The leishmaniasis are a group of vector-
borne protozoan diseases caused by
pathogenic Leishmania species which, if
symptomatic, result in clinical
manifestations that range from localised
cutaneous ulcers to disseminated lethal
infection. video

3. Leishmania Parasites and Diseases
SPECIES DISEASE
Leishmania tropica
Leishmania major
Leishmania aethiopica
Leishmania mexicana
Cutaneous leishmaniasis
Leishmania braziliensis Mucocutaneous leishmaniasis
Leishmania donovani
Leishmania infantum
Leishmania chagasi
Visceral leishmaniasis

4. LIFE CYCLE
• The organism is transmitted by the bite of several
species of blood-feeding sand flies (Phlebotomus)
which carries the promastigote in the anterior gut and
pharynx. It gains access to mononuclear phagocytes
where it transform into amastogotes and divides until
the infected cell ruptures. The released organisms
infect other cells. The sandfly acquires the organisms
during the blood meal, the amastigotes transform into
flagellate promastigotes and multiply in the gut until the
anterior gut and pharynx are packed. Dogs and rodents
are common reservoirs.

7. SAND FLY

8. AMASTIGOTES PROMASTIGOTES

9. ETIOLOGY
• Leishmaniasis is due to protozoan parasites
from the Leishmania species. leishmaniasis
transmits from bite of an infected called sand
fly.

10. RISK FACTORS
• Geography: India, Bangladesh, South Sudan,
Sudan, Brazil, Ethiopia; tropical or subtropical
areas of these countries and regions.
• Socioeconomic Conditions: According to
the World Health Organization (WHO), poverty is
a determining factor for the disease.
• Other Infections: children who have weakened
immune systems are also at increased risk of this
condition.

11. CLASSIFICATION
Categorization by clinical disease:
• leishmaniasis is divided into 3 primary clinical
forms:
1. Cutaneous leishmaniasis: (localized, diffuse
(disseminated), which causes skin sores
2. Visceral leishmaniasis: which affects several
internal organs (usually spleen, liver, and bone
marrow).
3. Mucocutaneous leishmaniasis: lead to partial or
complete destruction of the mucous
membranes found in your nose, throat, and
mouth.

12. Categorization by geographic occurrence:
1. Old World leishmaniasis (caused
by Leishmania species found in Africa
(ethiopia), Asia, the Middle East, the
Mediterranean,), which produces cutaneous
or visceral disease.
2. New World leishmaniasis (caused by
Leishmania species found in Central and
South America), which produces cutaneous,
mucocutaneous, and visceral disease

13. DISTRIBUTION OF MUCOCUTANEOUS
LEISHMANIASIS
• Old World spread of
mucocutaneous leishmaniasis is
via L aethiopica in Ethiopia,
Kenya, and Namibia.

14. SIGNS AND SYMPTOMS
• Cutaneous leishmaniasis :
1. Localized cutaneous leishmaniasis: Crusted papules or
ulcers on exposed skin.
2. Diffuse (disseminated) cutaneous leishmaniasis:
Multiple, widespread nontender, nonulcerating
cutaneous papules and nodules.
3. Leishmaniasis recidivans: Presents as a recurrence of
lesions at the site of apparently healed disease years
after the original infection.
4. Post–kala-azar dermal leishmaniasis: Develops
months to years after the patient's recovery from
leishmaniasis, with cutaneous lesions ranging from
hypopigmented macules to erythematous papules
and from nodules to plaques; the lesions may be
numerous and persist for decades

15. • Visceral leishmaniasis
1. Potentially lethal widespread systemic
disease characterized by darkening of the
skin as well as fever, weight loss,
hepatosplenomegaly, pancytopenia.
2. Nonspecific abdominal tenderness; fever,
rigors, fatigue, malaise, nonproductive
cough, intermittent diarrhea, headache,
arthralgias, myalgias, nausea, adenopathy,
transient hepatosplenomegaly

16. • Mucocutaneous leishmaniasis
1. Excessive tissue obstructing the nares, septal
granulation, and perforation; nose cartilage
may be involved, giving rise to external
changes known as parrot's beak or camel's
nose .
2. Possible presence of granulation, erosion,
and ulceration of the palate, uvula, lips,
pharynx, and larynx .
3. Gingivitis, periodontitis
4. Localized lymphadenopathy
5. Optical and genital mucosal involvement in
severe cases

18. DIAGNOSIS
Laboratory diagnosis include the following:
• Isolation, visualization, and culturing of the
parasite from infected tissue
• Serologic detection of specific antibodies
• Polymerase chain reaction (PCR) assay for
sensitive, rapid diagnosis of Leishmania
species.
• CBC count, coagulation studies, liver function
tests, peripheral blood smear
• Measurements of lipase, amylase, gamma
globulin, and albumin

19. COMPLICATIONS
• bleeding
• other infections due to a weakened immune
system, which can be life-threatening
• disfigurement

20. MEDICAL MANAGEMENT
• Liposomal amphotericin B and paromomycin
can treat mucocutaneous leishmaniasis.
• Mucocutaneous leishmaniasis disease
responds to a 20-day course of sodium
antimony gluconate; amphotericin B may be
used to treat advanced or resistant cases.
Pentavalent antimony for a course of 4 weeks
has also been recommended.

21. PREVENTION
• Wear clothing that covers as much skin as
possible. Long pants, long-sleeved shirts
tucked into pants, and high socks are
recommended.
• Use insect repellent on any exposed skin and
on the ends of your pants and sleeves.
• Spray indoor sleeping areas with insecticide.
• Sleep on the higher floors of a building. The
insects are poor fliers.
• Avoid the outdoors between dusk and dawn.
• Use a bed net tucked into your mattress.

22. ONYCHOMYCOSIS
• Onychomycosis is a fungal infection of
the toenails or fingernails that may
involve any component of the nail unit,
including the matrix, bed, or
plate. Onychomycosis can cause pain,
discomfort, and disfigurement and may
produce serious physical and
occupational limitations, as well as
reducing quality of life.

23. ETIOLOGY
• The primary causative dermophytes
are Trichophyton rubrum, T. mentagrophytes,
and Epidermophyton floccosum.
• Trichophyton rubrum being by far the most
likely common.

24. TYPES OF ONYCHOMYCOSIS
• Distal lateral subungual
onychomycosis (DLSO)
• White superficial onychomycosis
(WSO)
• Proximal subungual onychomycosis
(PSO)
• Candidal onychomycosis.

25. Distal lateral subungual
onychomycosis (DLSO)
• Most common
• Fungi invade the
hyponychium and
grow in the
substance of nail
plate, causing it to
crumble
• Hyperkeratotic debris
causes nail to
separate from the
bed

26. White superficial onychomycosis
(WSO)
• Commonly Trichophyton
mentagrophytes
• Nail - white
• soft
• powdery
• not thickened
• not separated from the
nail bed.

27. Proximal subungual onychomycosis
(PSO)
• Commonly
Trichophyton Rubrum
• Invade the substance
of nail plate, not the
surface
• Hyperkeratotic debris
causes the nail plate
to separate from the
nail bed

28. Candidal onychomycosis.
• Almost exclusively in
chronic
mucocutaneous
candidiasis
• Generally infect all
fingernails
• Linear yellow or
brown streaks grow
and advance
proximally

29. CLINICAL MANIFESTATION
• Onychomycosis is usually asymptomatic
• interfere with standing, walking, and
exercising.
• Paresthesia, pain, discomfort, and loss of
dexterity.
• The nail shows usually yellow-white in color.
• Nail becomes roughened and crumbles easily.

31. DIAGNOSIS
• Culture – gold standard
• Histological examination by periodic
acid-Schiff (PAS) staining – equal to
culture

32. Obtaining specimen
Clip the nail for culture
Subungal debris for culture

33. –Antibiotics suppress bacterial
contaminants
–Medium turn from yellow to red in 7-
14 days – alkaline released by
dermatophytes turn phenol (pH
indicator) red
• ID the organism
• PAS staining: stain fungal elements
pinkish-red

34. COMPLICATIONS
• Skin injury adjacent to the nail may
allow organisms to colonize, thereby
increasing the risk of infectious
complications. Reports of
complications with diabetes include
cellulitis, osteomyelitis, sepsis, and
tissue necrosis.

35. MEDICAL MANAGEMENT
• Fluconazole (Diflucan): 150-mg dose each
week for 9 months
• Itraconazole (Sporanox): 200 mg/day for
12 weeks for toenails, 6 weeks for
fingernails.“Pulse dosing”: 400 mg/day for
first week of each.
• Terbinafine: 250 mg/day (12 weeks for
toenails, 6 weeks for fingernails)

36. MECHANICAL REMOVAL
• Surgery: Remove the entire nail or cut the
affected portion, followed by curetting to
normal nail in 7-10 days

37. DERMATOPHYTOSIS
• Dermatophyte infections are common
worldwide, and dermatophytes are the
prevailing causes of fungal infection of the
skin, hair, and nails. These infections lead to a
variety of clinical manifestations, such as tinea
pedis, tinea corporis, tinea cruris.

38. ETIOLOGY
• Dermatophytes are fungi in the genera
Trichophyton, Microsporum, and
Epidermophyton. Dermatophytes
metabolize and subsist upon keratin in the
skin, hair, and nails.

39. RISK FACTORS
• Age (most common in pre-pubescent
children).
• Overcrowding (households or schools).
• Hairdressing salons.
• Use of shared combs.
• Ethnicity.

40. MAJOR CLINICAL SUBTYPES
• Tinea corporis – Infection of body
surfaces other than the feet, groin, face,
scalp, hair, or beard hair.
• Tinea pedis – Infection of the foot.
• Tinea cruris – Infection of the groin.

41. TINEA PEDIS
• Tinea pedis (also known as athlete's foot)
is the most common dermatophyte
infection. Tinea pedis may manifest as an
interdigital, hyperkeratotic, or
vesiculobullous eruption, and rarely as an
ulcerative skin disorder.

42. ETIOLOGY
• Tinea pedis usually occurs in adults and
adolescents (particularly young men) and
is rare prior to puberty Common causes
are T. rubrum, T. interdigitale (formerly T.
mentagrophytes), and E. floccosum.

43. CLINICAL FEATURES
• Interdigital tinea pedis – Interdigital tinea pedis
manifests as pruritic, erythematous erosions or scales
between the toes, especially in the third and fourth
digital interspaces. Associated interdigital fissures may
cause pain.
• Hyperkeratotic tinea pedis – Hyperkeratotic tinea
pedis is characterized by a diffuse hyperkeratotic
eruption involving the soles and medial and lateral
surfaces of the feet, There is a variable degree of
underlying erythema.
• Vesiculobullous (inflammatory) tinea pedis –
Vesiculobullous tinea pedis is characterized by a
pruritic, sometimes painful, vesicular or bullous
eruption with underlying erythema . The medial foot is
often affected.

45. DIAGNOSIS
• The diagnosis is confirmed with the detection
of fungi in skin scrapings from an affected area
with a potassium hydroxide (KOH) preparation
• A fungal culture is an alternative diagnostic
procedure.

46. TREATMENT
• Topical antifungal therapy include azoles,
allylamines, butenafine, ciclopirox, tolnaftate,
and amorolfine applied once or twice daily and
continued for four weeks.
• Hyperkeratotic tinea pedis can benefit from
combining antifungal treatment with a topical
keratolytic, such as salicylic acid. Burow's (1%
aluminum acetate or 5% aluminum subacetate)
wet dressings.
• Placing gauze or cotton between toes may be
helpful as an adjunctive measure for patients
with vesiculation.
• Treatment of shoes with antifungal powder, and
avoidance of occlusive footwear.

47. TINEA CORPORIS
• Tinea corporis is a cutaneous
dermatophyte infection occurring in sites
other than the feet, groin, face, or hand.

48. ETIOLOGY
• T. rubrum is the most common cause
of tinea corporis. Other notable
causes include T. Interdigitale & T.
Tonsurans.

49. CLINICAL FEATURES
• Tinea corporis often begins as a pruritic, circular
or oval, erythematous, scaling patch or plaque
that spreads centrifugally. The result is an annular
(ringshaped)plaque from which the disease
derives its common name (ringworm).
• Pustules occasionally appear, intensely
inflammatory.
• Extensive tinea corporis should raise concern for
an underlying immune disorder; HIV & Diabetes

51. DIAGNOSIS
• The diagnosis is confirmed with the detection
of fungi in skin scrapings from an affected area
with a potassium hydroxide (KOH) preparation
• A fungal culture is an alternative diagnostic
procedure.

52. TREATMENT
• Topical antifungal drugs, such as azoles,
allylamines, butenafine, ciclopirox, and
tolnaftate once or twice per day for one to
three weeks.
• Topical corticosteroids for inflammation.

53. TINEA CRURIS
• Tinea cruris (also known as jock itch)
is a dermatophyte infection involving
the crural fold.

54. ETIOLOGY
• The most common cause is T. rubrum.
Other frequent causes include E.
floccosum and T. interdigitale
• Common in men than women.
• Predisposing factors include copious
sweating, obesity, diabetes, and
immunodeficiency.

55. CLINICAL FEATURES
• The infection spreads centrifugally, with
partial central clearing and a slightly
elevated, erythematous, sharply
demarcated border that may have tiny
vesicles on the proximal medial thigh.
• Infection may spread to the perineum
and perianal areas, into the gluteal cleft,
or onto the buttocks. In males, the
scrotum is typically spared.

57. DIAGNOSIS
• The diagnosis is confirmed with the detection
of fungi in skin scrapings from an affected area
with a potassium hydroxide (KOH) preparation
• A fungal culture is an alternative diagnostic
procedure.

58. TREATMENT
• Topical therapy with antifungal agents such as
azoles, allylamines, butenafine, ciclopirox, and
tolnaftate is effective
• daily use of desiccant powders in the inguinal
area and avoidance of tightfitting clothing and
noncotton underwear

59. TINEA CAPITIS
• Tinea capitis, or scalp ringworm, is an
exogenous infection caused by the
dermatophytes Microsporum .
and Trichophyton . These originate from a
number of possible sources children or adults
(anthropophilic), animals (zoophilic) or soil
(geophilic).

60. CLINICAL FEATURES
• Infection in the hair and scalp skin is
associated with symptoms and signs of
inflammation and hair loss (mainly in
prepubertal children). The main signs are
scaling and hair loss but acute
inflammation with erythema and pustule
formation can occur..
• tinea capitis can affect nails and skin in
other parts of the body (only very rarely
the feet or groins).

63. DIAGNOSIS
• Scalp scrapings - including hairs and hair
fragments.
• Microscopic examination of the infected hairs
may provide immediate confirmation of the
diagnosis of ringworm .
• Culture may take several weeks. Culture
provides precise identification of the species
• Ultraviolet light (Wood's light) Fluorescence is
produced by the fungus.

64. MANAGEMENT
• Topical treatment (usually selenium sulfide or
ketoconazole shampoo but, occasionally, also
topical antifungals like terbinafine cream
• Children - griseofulvin (1 month-12 years 15-
20 mg/kg, maximum 1 g) once daily or in
divided doses.
• Fluconazole2-5 mg/kg/day. Weekly treatment
with 8 mg/kg may be as effective.

65. COMPLICATIONS
• Severe hair loss.
• Scarring alopecia.
• Psychological impact (ridicule, bullying,
isolation, emotional disturbance, family
disruption).
• The main complication is secondary bacterial
infection.
• Pain and difficulty with shoes.

66. PROGNOSIS
• Excellent with good compliance and
subsequent precautions to avoid repeat
infection.

67. PREVENTION
• Good skin hygiene.
• Good nail hygiene.
• Avoiding prolonged wetting or dampness of the
skin and feet.
• Avoiding trainers, which can retain sweat and
promote a warm, moist environment.
• Treatment of tinea pedis - helps prevent
onychomycosis.[8]
• Wearing clean, loose-fitting underwear.