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Leishmaniasis

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  • 1. Leishmaniasis By: Dr Osman Sadig
  • 2.
    • The leishmaniasis are a group of diseases
    • with a variety of clinical manifestations
    • 1- Visceral leishmaniasis VL/ PKDL
    • 2- Cutaneous leishmaniasis CL
    • 3- Mucocutaneous leishmaniasis MCL
    • 4- Diffuse cutaneous leishmaniasis DCL
    • Over 20 pathogenic sp of leish parasites
    • are known:
    • 1- L donovani 2- L infantum
    • 3- L archibaldi 4- L chagasi
  • 3.
    • 5- L tropica 6- L major
    • 7- L ethiopica 8- L braziliensis
    • 9- L mexicana
  • 4.  
  • 5.  
  • 6.
    • The outcome of the infection depends on :
    • 1- Parasite invasiveness & pathogenicity
    • 2- dose of inoculum
    • 3- parasite tropism
    • 4- genetically determined host immune
    • response A single leish sp can produce diff clinical syndromes and each of the syndromes can be caused by more than one sp e.g. Viscerotropic L tropica
  • 7.
    • Visceral leishmaniasis
    • VL is usually fatal disease without TR.
    • Epidemiology
    • - About 500 000 new cases annually, 90%
    • in India & Sudan
    • - Infection is endemic in India, China
    • Central Asia, East Africa, Middle east,
    • Medit region and Latin America
    • - VL is endemic in Sudan & has been
    • reported since early 19 th century.
  • 8.
    • - Main endemic areas in Sudan are :
    • 1- Eastern Sudan along Atbara & Rahad
    • rivers
    • 2- Sinnar & Blue Nile states
    • 3- Upper Nile state
    • 4- Eastern Equatoria around Kapoita
    • 5- South Kordofan
    • 6- South Darfor
    • - VL is caused by L. donovani (LDB), L. infantum, L. chagasi & L. tropica ( usually mild disease)
  • 9.
    • - More than 24 600 cases & 1193 deaths
    • had been reported in Sudan during
    • 1996—2001. This is only reported cases
    • and does not reflect actual dis transmiss
    • - The dis affects mainly children & young
    • adults and is commoner among poor people, farmers, labourers, malnourished, people visiting endemic areas for the 1 st time and in the immunosuppressed
    • - Leishmania exists in 2 different forms:
  • 10.
    • Leishmania exists in 2 different forms :
    • 1- Promastigote in the vector developing
    • from amastigotes through series of
    • intermediate stages in the digestive tract
    • eventually migrating to the proboscis and
    • inoculated to the skin of the host with the blood meal. It is pearl or spindle shaped 10—15 mc with flagellum .
    • 2- Amastigote : develops in the human- being from promastigote & proliferate
    • in the R/E system within macrophages. It is oval in shape.
  • 11.  
  • 12.  
  • 13.
    • The vector is Female sand fly - Phlebotomus orientalis
    • - Phl martini (termite hill dweller)
    • - Phl lutzomyia in new world leishma
    • The reservoir
    • - Depends on the leish sp & the vector
    • - Rodents, dogs, wild animals & patients
    • with VL (PKDL)
  • 14.  
  • 15.
    • Transmission
    • Depends on the presence of suitable reservoir , vector and susceptible human host
    • 1- H uman to human ( anthroponotic) e.g. India (causing epidemics)
    • 2- A nimal reservoir to human ( zoonotic transmission) e.g. dogs in the ME and Mediterranean where the dis. is sporadic in children and opportunistic in immunosuppressed – HIV patients
    • 3- Congenital, sexual & BT are rare.
  • 16.
    • Out breaks
    • - Mellut town 1940
    • - Southern Fung 1956
    • - Jum jum tribe 1958 (Satti)
    • - Western Upper Nile 1984—1994
    • - Gedarif state 1996—200-
  • 17.
    • Immunity
    • Out come of infection depends on the
    • interplay between protective CMI respon
    • at one hand & dis enhancing immune
    • response on the other hand
    • 1- Th1 CD4 cells are protective by
    • producing IL2 & INF gamma which
    • stimulate macrophage to inhibit the
    • growth of amastigotes
    • 2- Th2 CD4 cells produce IL4,5 which
    • enhance disease progression
  • 18.
    • Leishmania infection results in life long latent immunity. With immunoparesis leishmania can become opportunistic pathogen through reactivation or new infection .
  • 19.
    • Clinical manifestations
    • - Varies from asymptomatic self limitting
    • dis to frank VL which is fatal if untreated ,
    • with mild dis in between.
    • 1- Clinically suspect case is any pat who
    • lives or had traveled to an endemic area
    • presenting with fever of > 2/52 + spleenomegaly and/or Lymphadenopathy in whom malaria is ruled out or treated
  • 20.
    • 2 - Probable case : suspect case + leucopenia
    • 3 - Confirmed case : suspect case + positive parasitology
    • Presentation
    • - IP : 1—2/12 (2/52—10 years)
    • - Onset : insidious , but may be acute
    • - Fever (95%) : prolonged fever without rig
    • It may be intermittent, remittent wz doubl
    • spike or contin. Fever is well tolerated.
  • 21.
    • - Splenomegaly (95%)
    • - Wt loss (80%) & wasting later
    • - Anaemia (75%): chronic dis, bleeding,
    • hemolysis, BM infilt wz parasites, hypresp
    • haemodilution.
    • - Hepatomegaly (60%) - LN (75%)
    • - cough (75%) - anorexia (70%)
    • - epistaxis (50%) - diarhoea (40%)
    • - vomiting (15%) - jaundice (5%)
    • - edema (5%) - ascites.
  • 22.
    • - skin pigmentation : The skin is dry, thin, scaly with sparse hair.
    • Atypical cases present with: - mild symptoms and/or isolated splenomegaly
    • - lymphadenopathy may be the sole
    • presentation in India
    • - Some present with PKDL
    • - Some show sub clinical sero conversion
    • - In immunosuppressed (e.g AIDS) fever and spleenomegaly may be absent
  • 23.
    • Differential diagnosis
    • - Malaria must be ruled out
    • - Enteric fever
    • - H/S schistosomiasis - African trypansom
    • - Miliary Tb
    • - Brucellosis & relapsing fevers
    • - AIDS
    • - Liver abscess
  • 24.
    • - Histoplasmosis - infectious mononucleos
    • - Other causes of gross splenomegaly - Malnutrition
  • 25.
    • Laboratory & diagnosis:
    • - CBC & ESR:
    • - anaemia (60-90%)
    • - leucopenia (84%)
    • - thrombocytopenia (73%)
    • - high ESR
    • - Liver biochemstry:
    • albumin < 30 g/l (88%), globulin >30 g/l (78%), elevated ser bilirubin, transaminases and ALP
    • - Renal profile & ECG
  • 26.
    • - Specific diagnosis depends on clinical suspicion & either 1- parasitology OR 2- serology .
    • 1- Parasitology : specimen obtained from:
    • - Gland puncture is easy & safe with
    • 50—65% sensitivity
    • - BM aspirate require trained person,
    • painful & require sp needle wz
    • 64—92% sensitivity
    • - Splenic puncture : invasive & hazardous
    • with 90—95% sensitivity
  • 27.
    • - rarely from puffy coat layer of blood - Culture in NNN media
    • * Negative splenic aspirate does not
    • exclude diagnosis
    • * Parasitology is the only diagnostic method in relapse, HIV pat & infants < 6/12
  • 28.
    • 2- Serology : in clinically suspected cases
    • (FAT, DAT, ELIZA, Latex Agg test, PCR)
    • - DAT is sensitive, specific, simple and
    • can be easily performed under field
    • conditions, but needs trained staff.
    • Not useful for relapse diagn or TOC. Positive DAT (>1:64000) combined with negative LST in a clinical suspect is diagnostic. Positive LST rules out active VL even if DAT is positive.
  • 29.
    • - Katex detects Ag in urine, sensitive and specific
    • - ICT 3 LST: measures type 1V hypersensitivity .
    • It is negative in active VL, but becomes
    • positive in 80% 3—6 months after TR
    • It is valuable in epidemiological studies and augments DAT in the diagnosis if it is negative.
  • 30.
    • Treatment of VL: ( supportive/ specific)
    • - TR ideally given to confirmed cases in
    • hospital settings under med supervision
    • - Trial of TR is only considered if there are
    • no lab. facilities & after exclusion of
    • other infections and occasionally in
    • highly suspected cases despite –Ve lab.
    • 1- Supportive TR include nutritional care,
    • oral hygiene, Fe, folic acid, multivit, TR
    • of infections, BT & correction of flu & E
  • 31.
    • 2- Specific TR :-
    • A- First line drugs:
    • 1 - Sod stibogluconate is pentaval antimony (SSG) in 100mg/ml. Dose 20 mg/kg/d IV or IM for 30 days.
    • - SE: include A,N,V, fatigue, headache arthralgia myalgia, cough, cardiotoxicity, renal damage
    • pancreatitis, elevated ser amylase and transaminases, and local pain
  • 32.
    • - CI : cardiac dis, liver dis, renal fail,
    • moribund pat & full blown AIDS.
    • 2- Meglumine antimoniate is similar to SSG
    • but in 85 mg/ ml
    • B- Second line drugs :
    • 1- Amphotericin B 1mg/kg EOD for 30 days Nephrotoxic. 2 nd line drug. 2 - Ambisome (amphotericin B lipid complex) is alternative 1 st line drug. 50 dollars for 50 mg vial & 600 dollars total TR. Dose 20—30 mg/kg over 2/52 in doses of 3—5 mg/ kg with
  • 33.
    • TOC in day 21. It is reconstituted and diluted in 5% dextrose and infused over 30—6o min. Main indications of ambisome are: - unresponsiveness to SSG - 3 rd relapse
    • - cardiac disease - hepatic & renal impairment
    • - moribund patients . 3- Pentamidine 3—4 mg/kg EOD for 10 doses 2 nd line drug
  • 34.
    • 4- Paromomycin (aminosidine) 15mg/kg for 17 days IM or IV diluted in NS over 90 min. Usually used in combin with SSG. Oto/ Nephrotoxic.
    • 5- Miltefosine : anti neoplastic. Oral, sp
    • used in India
    • 6- Allopurinol 7- ketoconazole 8- INF gamma
  • 35.
    • Follow up:
    • - gen condition, temp, spleen, Wt, CBC
    • - TOC at 25—30 day of TR to asses the parasitological cure. GP in routine use. - Initial cure = clinical cure + parasitologic
    • cure by the end of TR
    • - Definite cure = absence of symptoms
    • and signs 6/12 after initial cure
    • - Follow up at 3, 6, 12 M & if symptoms rec
  • 36.
    • - slow responder = pat with no clinical
    • response & low grade parasitaemia
    • after 30/d of TR. Extend TR to 60 days or
    • until 2 consecutive –ve TOC - Non responder = patient with no clinical
    • response & high grade parasitology after
    • 30 days TR with SSG. Combine SSG + paramomycin OR go to ambisome for TR.
  • 37.
    • - Relapse (5%) = pat with clinical and parasitological confirmed case & past history of TR of VL. 1 st , 2 nd and 3 rd relapse - For 1 st relapse: SSG for 60 days or till
    • 2 consecutive –ve TOC OR SSG + paramomycin
    • - For 2 nd relapse: SSG + parmomycin OR
    • go to ambisome
    • - For 3 rd relapse ambisome Screen for HIV for non resp and relapse cases
  • 38.
    • Complications of VL
    • - Intercurrent infections (Tb, otitis M, canc
    • oris, pyoderma, viral)
    • - Malnutrition & anaemia
    • - Bleeding, hepatic failure
    • - Neurological (P. neuropathy, GB, ataxia
    • myelopathy, deafness)
    • - PKDL : usually follows TR but can occur
    • during TR or wz out history of clinical VL.
  • 39.
    • PKDL - grade 1 PKDL = rash on the face +/-
    • upper chest & arms
    • - grade 2 PJDL = dense rash most of the
    • face, on the trunk, arm & legs.
    • When extensive & black nodule = grade
    • 2 severe
    • - grade 3 = dense rash most of the body
    • including hands & feet. Ulceration, crust
    • scaling & mucosal spread (PKML) can
    • occur.
  • 40.  
  • 41.  
  • 42.
    • - Parasites are scanty in PKDL which may serve as a reservoir of infection - PKDL should be differentiated from L. leprosy, measels, fungal infections, syphilis, yaws & T versecolor
    • - TR is given for grade 3 & 2 severe. Dose 20 mg/k SSG daily till clinical cure up to 2/12
  • 43.
    • Causes of death in VL - intercurrent infection including HIV - hepatic failure - renal failure
    • - bleeding - malnutrition - severe anaemia
    • - cancrum oris - HF or cardiac arrest (SSG)
  • 44.
    • VL & HIV Co infection
    • - Both are associated wz immune suppres
    • and potentiate each other - Suspected in VL pat wz high parasitaemia , non responders & in relapsers
    • - Clinical diagn may be diff . Fever, spleno
    • and pancytopenia may not be present
    • and clinical suspicion may be obscured by opportunistic infections . Presentation may be atypical .
  • 45.
    • - VL may be rapidly progressive & may
    • have predominant GIT symptoms - CD4 < 200 & associated opportunistic
    • infections are common - Serology is –ve in up to 50% due to
    • depressed immune response
    • - Diagn by parasitology . Parasites are
    • abundant in LN or BM aspirates. It is +ve in 50% in the buffy coat of blood
    • - TR is diff. Relapse rate & mortality high
  • 46.
    • and drug SE are more severe . - Combined anti leish & anti retroviral
    • drugs for TR.
    • - Response to anti leishmanial TR is poor
    • due to depressed immune resp & increas
    • parasite load. Relapse in 50% & relapses
    • should only be treated if symptoms are
    • severe