Leishmaniasis in Emergency Medicine Clinical Presentation

In some endemic areas, natives have recognized that immunity occurs as a natural course of the disease. Some cultures deliberately inoculate their children on a part of the body that is not usually exposed to avoid later development of a disfiguring scar on an exposed part of the body.

• Cutaneous leishmaniasis

  • The broad spectrum of clinical manifestations of cutaneous leishmaniasis is often compared with that of leprosy. Cutaneous leishmaniasis can be simple or diffuse.
  • Different species, as well as host factors, can also affect the clinical picture, where some species cause "wet" ulcers and others "dry" ulcers.
  • After the bite of an infected sandfly, the incubation period is usually several weeks after inoculation, but this incubation period is variable. Initial lesions can appear immediately after a bite, or the incubation period may last for several months. These lesions are usually painless.
  • Skin trauma can result in activation of seemingly latent cutaneous infection long after the initial bite.
  • Over a period of weeks to years, some lesions may resolve spontaneously without pharmacotherapy.
• Mucocutaneous leishmaniasis

  • The incubation period is from 1-3 months. Mucocutaneous leishmaniasis can be the primary manifestation of the disease, but the primary lesions may also be limited to cutaneous manifestations, with mucosal lesions appearing only later in the course of disease when untreated cutaneous lesions progress to involve the oral and nasal surfaces. Cases in which the time between the primary lesion and the appearance of mucosal involvement is up to 2 decades have been reported.
  • Initial symptoms related to mucosal lesions may include nasal obstruction and bleeding.
  • Mucosal lesions become painful gradually and can become sites of infection, sometimes leading to sepsis.
• Visceral leishmaniasis

  • Kala azar is the Indian name for visceral leishmaniasis. The term means "black disease," which is a reference to the characteristic darkening of the skin that is seen in patients with the disease.
  • Many subclinical cases occur and go unrecognized for each clinically recognized case.
  • Malnutrition has been shown to contribute to the development of clinical disease.
  • Like cutaneous leishmaniasis, visceral leishmaniasis can take different forms ranging from asymptomatic or self-resolving disease to fulminant disease.
  • Onset can be insidious or sudden.
  • In endemic areas, kala azar may be suspected in a patient with persistent, irregular, or remittent fever; leukopenia; and splenomegaly. Other accompanying symptoms may be lymphadenopathy and weight loss.
  • Fever can be continuous, intermittent, or remittent, and it can recur at irregular intervals.

• Cutaneous leishmaniasis

  • Systemic signs usually are absent.
  • Initially, the lesion is a small, red papule up to 2 cm in diameter. Over several weeks, the papule becomes darker and will crust in the center, eventually ulcerating to present a typical appearance of an ulcer with raised edges and surrounding dusky red skin. The ulcers can be moist or open with seropurulent exudate or dry with a crusted scab. See the images below. After about 3-6 months, the ulcers heal, leaving a raised border. Leishmaniasis. Photo courtesy of Robert Norris, MD, Stanford University Medical Center. Leishmaniasis. Ethiopian woman with 1-year history of asymptomatic pink-erythematous infiltrative plaque with overlying scale and central crust.
  • Sores usually are found on exposed areas of skin, especially the extremities and face. See an example below.Leishmaniasis. Image courtesy of the CDC Public Health Image Library.
  • Regional adenopathy, satellite lesions, and subcutaneous nodules can be present.
  • Untreated sores can leave depigmented retracted scars.
• Mucocutaneous leishmaniasis

  • Cutaneous lesions can be single or multiple.
  • Secondary mucosal lesions often develop after the primary lesion has healed.
  • Mucosal lesions can progress to involve the entire nasal mucosa and the hard and soft palates. Without treatment, the entire nasal mucosa and palates become deformed with ulceration and erosion of the nasal septum, lips, and palate. The disease attacks cartilaginous areas (as depicted below) but usually spares bony structures, and it can leave extreme disfigurement. Leishmaniasis. Photo courtesy of Robert Norris, MD, Stanford University Medical Center.
  • Signs include gingival edema, periodontitis, and adenopathy.
• Visceral leishmaniasis

  • Bouts of fever occur.
  • Hepatosplenomegaly occurs secondary to compensatory production of phagocytic blood cells.
  • Wasting and weakness are observed.
  • Darkening of the skin is characteristic (thus, the name kala azar or black fever).
  • Diarrhea may occur.
  • Lymphadenopathy is often present.
  • In visceral leishmaniasis, patients may die of hemorrhage (secondary to infiltration of the hematopoietic system), severe anemia, secondary bacterial infections of mucous membranes, bacterial pneumonia, septicemia, tuberculosis, dysentery, or measles.

• Cutaneous leishmaniasis

  • Americas -Leishmania tropica mexicana, Leishmania braziliensis, and Leishmania amazonensis
  • Old World -Leishmania tropica, Leishmania major, L infantum, and Leishmania aethiopica
• Mucocutaneous leishmaniasis

  • Americas -L braziliensis
  • Old World -L aethiopica
• Visceral leishmaniasis

  • India, Kenya -Leishmania donovani
  • South Europe and North Africa -L infantum
  • Americas -Leishmania chagasi
• Risk factors

  • Children are at greater risk than adults in endemic areas.
  • Malnutrition has been shown to contribute to the development of disease.
  • Persons with AIDS are at 100-1000 times greater risk of developing visceral leishmaniasis in certain areas.
  • Incomplete therapy of initial disease is a risk factor for recurrence of leishmaniasis.
  • Some studies have shown protection against cutaneous leishmaniasis with vaccination of killed Leishmania promastigotes and live bacillus Calmette-Guérin (BCG). However, this does not seem to be protective against visceral leishmaniasis.
  • Of note, the bite of one infected sandfly is sufficient to cause the disease, since a sandfly can egest more than 1000 parasites per bite.