Leishmaniosis: DR / Salem Al Bothaigi

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LEISHMANIOSIS

DR / SALEM AL BOTHAIGI
The leishmaniases are a diverse group of diseases caused by intracellular protozoan*
.parasites of the genus Leishmania, which are transmitted by phlebotomine sand flies

Multiple species of Leishmania are known to cause human disease involving the skin and *
mucosal surfaces
.and the visceral reticuloendothelial organs

Cutaneous disease is generally mild but may cause cosmetic disfigurement. Mucosal and*
visceral leishmaniasis is associated with significant morbidity and
.mortality
: Clinical manifestations *

The different forms of the disease are distinct in their causes,


.epidemiologic feature, transmission, and geographic distribution

Visceral Leishmaniasis / 1
VL (kala-azar) typically affects children younger
than 5 yr of age in the New World and Mediterranean region (L.
infantum/chagasi) an older children and young adults in Africa
.and Asia (L. dnovani)
: After inoculation of the organism into the skin by the sandfly, the child may have
:a completely asymptomatic infection -1
.children are transiently seropositive but show no clinical evidence of disease

.an oligo symptomatic illness that either resolves spontaneously or evolves into active kala_azar -2
*Children who are oligo symptomatic have mild constitutional symptoms:
(malaise, intermittent diarrhea, poor activity tolerance) and intermittent fever; most will
have a mildly enlarged liver. In most of these children the illness will resolve
In most of these children the illness will resolvewithout *
therapy, but in approximately 25% it will evolve to active kala-
.azar within 2-8 mo

Extreme incubation periods of several years have rarely been *


described. During the first few wk to months of diseas
evolution the fever is intermittent, there is weakness and loss
.of energy, and the spleen begins to enlarge
The classic clinical features of high fever, marked *
splenomegaly, hepatomegaly, and severe cachexia typically
develop approximately 6 mo after the onset of the illness, but a
rapid clinical course over 1 mo has been noted in up to 20% of
.patients in some series

At the terminal stages of kala-azar the hepatosplenomegaly is massive, there is gross wasting, the *
.pancytopenia is profound, and jaundice, edema, and ascites may be present
Anemia may be severe enough to precipitate heart failure. Bleeding
.episodes, especially epistaxis, are frequent
The late stage of the illness is often complicated by *
secondary bacterial infections, which frequently are a cause of
.death

A younger age at the time of infection and underlying *


malnutrition may be risk factors for the development and more
rapid evolution of active VL. Death occurs in more than 90%
.of patients without specific antileishmanial treatment
VL has been increasing recognized as an opportunistic *
infection associated wit HIV infection

Frequently there is an atypical clinical presentation of VL in *


HIV-infected individuals with prominent involvement of the
gastrointestinal tract and absence of the typical
.hepatosplenomegaly
A small percentage of patients previously treated for VL*
develop diffuse skin lesions, a condition known as post–kala-
azar dermal Leishmaniasis (PKDL ) . These lesions may
appear during or shortly after therapy (Africa) or up to several
.years later (India)
: The lesion of PKDL are *
hypopigmented-1
erythematous -2
nodular -3
.and commonly involve the face and torso
: kala azar ( black sickness ) *
the skin become dry and scaly and may acquire the grey ashen appearance , from which the
. hindi name kala azar is derived

:CUNTANEOUS LEISHMANIASIS /2

after insolation by the bite of an infected sandfly , parasites -


proliferate locally in mononuclear phagocytes leading to an
erythematous macular or nodule , that typically form a shallow
ulcer with raised border
Lesion commonly are located on exposed areas or in face -
and extremities and may be accompanied by satellite lesion
. and regional adenopathy

The clinical manifestation of old and new world are similer -

Cutaneous resolution of lesion may take from weeks to years -


. and usually results in a flat atrophic scar
: MUCOSAL LEISHMANAISIS /3
from the initial cutaneous infection be leishmania
brazilienisis or relater to new world species parasites may
disseminate to midline facial mucosa in some patient
granulomatous ulceration follows leading to facial
.disfigurement
secondary infection and mucosal perforation months to -
. years after the cutaneous lesion heal
Localized Cutaneous Leishmaniasis /4
LCL (Oriental sore) can affect individuals of any age,-
but children are the primary victims in many endemic regions.
It may present as 1 or a few papular, nodular, plaquelike, or
ulcerative lesions that are usually located on exposed skin,
.such as the face and extremities
:ETIOLOGY *
in the human host leishmania species are obligate intercellular parasites of mononuclear phagocytes -
a single leishmania species can produce different clinical syndromes and each syndrome can be -
. caused by different species
: for example *
, cutaneous leishmanisis typically is caused by L-tropica - 1
L – majora , L – ocethiopica ( old world species ) , and by L – Mexicana , L – amazonensis , L –
braziliensis , L – panamensis ( new world species )
visceral leishmaniasis is caused by L- donovani , L- infatum , also cause old world cutaneous -2
. leishmanisis
: EPIDEMIOLOGY*
leishmaniosis typically is a zoonosis with a varity of -
mammalian reserve hosts including carmines and rodents , the
vectors are phlebotomine sand fly , the distribution of old
world cutaneous leishmaniosis include the middle east , some
. Asian and African countries and sporadically South Europe
New world cutaneous leishmaniosis is found in areas -
. extending from México to northen amentina
mucosal leishmaniosis occurs primarily in the amazon -
basin and central plains of brazil , in south and central America
.
The distribution of visceral leishmaniosis in the old world -
include southern Europe , the Mediterranean basin , the middle
. east , east Africa , china and the Indian subcontinent

endemic foci in the new world are found in south and central -
. America , particularly in brazil
: The incubation periods *

The incubation period for the different forms of leishmaniosis -


. request from serval days to months

in cutaneous leishmaniosis primary skin lesion typically appear with -


. in serval weeks

in visceral leishmaniosis the incubation take for 6 weeks to 6 months -


, however incubation period from 10 days to 10 years have been
reported and reactivation of previously asymptomatic latent infection
. can occur in immunosuppressed patients
:DIAGNOSIS *
is by microscopic identification of intracellular -
leishmanial organism on wright or Giemsa stains of smears or
. histologic sections of infective tissue
: in cutaneous disease - 1
tissue can be obtained by 3 mm punch biopsy ,
lesion scraping or needle aspiration of the raised non necrotic
. edge ( not the centre ) of the lesion
: in visceral lesion -2
the organism can be identified in the spleen and
less commonly from bone marrow and liver also in lymph
. node
Blood culture has been positive in some Indian patient and in HIV -
. infected patient

The diagnosis of VL and some cutaneous infection can also be -


aided by serologic or P.C.R testing , however a negative serologic
test result should never be interpreted as excluding the possibility of
. L infection

false positive serologic results may occur , occasional in serum -


. simples of patients with other infection diseases ( Chagas disease )
: DIFFERENTIAL DIAGNOSIS *

: Local Cutaneous L /1
include sporotrichosis, blastomycosis, chromomycosis, lobomycosis cutaneous tuberculosis,
.atypical mycobacterial infection, leprosy, ecthyma, syphilis, yaws, and neoplasms

: mucosal L /2
as syphilis, tertiary yaws, histoplasmosis, paracoccidioidomycosis, as well as
sarcoidosis, Wegener granulomatosis, midline granuloma, and carcinoma , may have clinical features
.similar to those of ML
: visceral L /3

malaria, typhoid fever, miliary tuberculosis, schistosomiasis, brucellosis, amebic liver-


.abscess, infectious mononucleosis, lymphoma, and leukemia

diagnosis by : reticuloendothelial cell hyperplasia in the spleen , bone marrow and lymph -
. nodes

Amastigotes are abundant in the histocyts and Kopffer’s cell -


results of smears or culture of material from splenic , bone marrow or lymph node aspiration are
. usually diagnostic
laboratory : assonated with classic VL Anemia ( Hb 5 – 8 mg / dl ) -
and thrombocytopenia ,leukopenia ( 2 – 3,000 cells
ml ) , elevated hepatic transaminase levels , and /
. hyperglobulinemia (>5 g/dL) that is mostly IgG
serologic -
,testing by :1- enzyme immunoassay
,indirect fluorescence assay -2
or direct agglutination is very useful in VL because of the very high -3
.level of antileishmanial antibodies
An immunochromatographic strip test using a recombinant antigen (K39) has a diagnostic * -
.sensitivity and specificity for VL of 80-90% and 95%

Serodiagnostic tests have positive findings -


.in only about half of the patients who are confected with HIV
: TREATMENT *

Specific antileismanial therapy is not routinely indicated for uncomplicated LCL caused by -
.strains that have a high rate of spontaneous resolution and self-healing

treatment is indicated when the ulcers are disabling or disfiguring , when healing is delayed or -
. when patients may be infected with L- brazilieness or other species associated with mucosal disease

. drug therapy is always indicated when mucosal or visceral infection are presents -
the standard druge of choice for leishmaniasis is sodium stibogluconate a parenteral pentavalent *
. antimonial that usually is given daily for a minimum 20 days

it generally is well tolerated in young , otherwise healthy patients , but cardiac , pancreatic and *
.hepatotoxic effects can occur

. the related drug Meglumine antimonite is an alternative agents *


.Liposomal amphotericin B is approved for treatment of visceral leishmaniasis *

for patients with disease refractory to antimonial therapy, amphotericin B , liposomal amphotericin *
. B , or pentamidine should be considered

. Also ketocanazol and itraconazol as well as local heat , have been used successfully *
: SOLATION OF THE HOSPITALIZED PATIENTS *
standard precaution are recommended

: control measure /1
in most regions that are endemic for leishmaniasis should be advised to minimize their -
exposure to sand fly bites , by using screened accommodation fine mesh bed mating , protective
.clothing and insect repellent and by minimizing outdoor exposure from dusk to down

. patients infected with leishmania species should not donate blood or organ to other -
: Drugs for treatment of leishmaniosis *
:sodium stibogluconate ) 1
Adult dosage : 20 mg/ kg / day IV or IM for 20-28 day

pediatric dosage : 20 mg/ kg / day IV or IM for 20-28 day

: Meglumine antimonite )2

Adult dosage : 20 mg/ kg / day IV or IM for 20-28 day

pediatric dosage : 20 mg/ kg / day IV or IM for 20-28 day


: Amphotericin B )3
Adult dosage : 0,5 – 1 mg / kg IV daily or every 2 days
up to 8 weeks
pediatric dosage : : 0,5 – 1 mg / kg IV daily or every 2 days
up to 8 weeks

: liposomal Amphotericin B )4
Adult dosage : 3 mg / kg / day for 1-5 days or foe 14-21 days
pediatric dosage : 3 mg / kg / day for 1-5 days or foe 14-21 days
: the dose for HIV patients is *
mg / kg / day for 1-5 days or for ( 10, 17 , 24 , 31 , 38 ) days 4
the relapse rate is high suggesting that maintenance dose
. may be indicated

: Pentamidine )5
Adult dosage : 2-4 mg / kg daily or every 2 days IV or IM
up to 15 days
pediatric dosage : 2-4 mg / kg daily or every 2 days IV or IM
up to 15 days
mg /kg 90 days x 15 doses for L – donovani or 4 *
mg / kg 90 days x 7 doses or 2
. mg /kg 90 days x 4 doses 3

: Paromomycin )5
Adult dosage : topically twice daily x 10 – 20 days
THANK YOU

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