Leishmaniasis

Original article by Lilly Stanley | Last updated on 27/5/2014
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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.

Comparison of types of infection

   
CUTANEOUS
 
 
MUCOCUTANEOUS
 
VISCERAL
(Kala-azar)
 
Epidemiology
 
Most common form
 
Carries 5% rsik of going onto develop mucutaneous disease
 
Majority of cases are in South america
3:1 F:M
 
90% cases found in India, Bangladesh, Nepal, Sudan, and Brazil
Site
 
Skin Oral and nasal musoca Systemic disease
vital organs
 
Clinical features
 
Lesion 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
 
Complications
 
Can enlarge to
 several cm and persist for years before eventually healing to atrophic scar.
 
 Can lead to very destructive and disfiguring lesions of the face Untreated all patients die within approx. 2 years
 
Diagnosis
 
Microscopy and culture of aspiration from base of ulcer. Clinical diagnosis
+ PCR (gold standard)
Serology
(may be negative in HIV positive patients)
 
Treatment
 
Only needed if not healed by 6 months long courses (e.g. 30 days) sodium stiboglucanate in a high dose (20 mg/kg) –high failure rate
Amphoteracin B is also used.
Prevention Preventing sandfly bites:
Mosquito nets, protective clothing and  insect repellent
Public health measures to reduce the sandfly
There are no vaccine currently availiable
 
Other Important cause of chronic ulcerating skin lesions
 
Recently seen in soliers retuirning from afganistan
 
substantial part of the disfigurement is possibly due to immunological mechanisms
Even 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,