Leishmaniasis

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Organism

Leishmania (protozoa)

Transmission

Via sandflies
Leishmania anastigotes infect sandflies when they take them up with their blood meal.

Pathogenesis

  • The adult female sand ingests the pathogen in the form as amastigotes when feeding on host blood
  • Amastigotes transform into promastigotes in the stomach of the sandfly
  • These live in the GI tract, reproducing asexually, then migrate to be regurgutated back into a mammal host, when the fly injects its saliva into prey as it bitesàinside the new host they invade macrophages
  • Here they change back into the smaller amastigote form and replicateàeventually burst out into bloodstream and repeat the cycle infecting target tissuesàresponse to infection varies according to the type of immune reaction mounted.
Man with leishmaniasis
Man with leishmaniasis

Comparison of types of infection

CUTANEOUSMUCOCUTANEOUSVISCERAL
(Kala-azar)
EpidemiologyMost common form

Carries 5% rsik of going onto develop mucutaneous disease

Majority of cases are in South america3:1 F:M

90% cases found in India, Bangladesh, Nepal, Sudan, and Brazil

SiteSkinOral and nasal musocaSystemic disease
vital organs
Clinical featuresLesion develops at bite site, beginning as itchy papule, becomes nodule then forms ulcer. Occasionally sore develop on mucous membranes.

Diffuse cutaneous disease:
Closely resembles lepromatous leprosy
(extensive areas of depigmentation)

Leishmaniasis recividans:
Resembles lupus vulgans

Onset a few years after resolution of cutaneous lesion

Can begin with symptoms of chronic nasal congestion but results in longterm cartilaginous destruction and ulceration.

 fever (twice daily peak),
weight loss,
mucosal ulcers,
fatigue,
anaemia and substantial hepatosplenomegaly and lymphadenopathy
ComplicationsCan enlarge to
several cm and persist for years before eventually healing to atrophic scar.
 Can lead to very destructive and disfiguring lesions of the faceUntreated all patients die within approx. 2 years
DiagnosisMicroscopy and culture of aspiration from base of ulcer.Clinical diagnosis
+ PCR (gold standard)
Serology
(may be negative in HIV positive patients)
TreatmentOnly needed if not healed by 6 monthslong courses (e.g. 30 days) sodium stiboglucanate in a high dose (20 mg/kg) –high failure rate
Amphoteracin B is also used.
PreventionPreventing sandfly bites:
Mosquito nets, protective clothing and  insect repellent
Public health measures to reduce the sandfly
There are no vaccine currently availiable
OtherImportant cause of chronic ulcerating skin lesions

Recently seen in soliers retuirning from afganistan

substantial part of the disfigurement is possibly due to immunological mechanismsEven following successful treatment, a secondary form of the disease can develop= post kala-azar dermal leishmaniasis.

Manifests small, skin lesions on the face, which gradually spread over the body forming disfiguring, swollen structures resembling leprosy,

References

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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