Got the Travel Bug? A Review of Common Infections, Infestations, Bites, and Stings Among Returning Travelers

Matthew P. Vasievich; Jose Dario Martinez Villarreal; Kenneth J. Tomecki


Am J Clin Dermatol. 2016;17(5):451-462. 

In This Article



Leishmaniasis is a relatively common disease in returning travelers, accounting for approximately 5–10 % of all travel-related diseases.[3] Caused by a protozoan parasite of the genus Leishmania, leishmaniasis is broadly classified into 'Old World' and 'New World' disease. Old World leishmaniasis originates from Africa, Asia, the Middle East, and Southern Europe; New World disease originates in Central and South America, occasionally as far north as Texas.[33–35] Leishmaniasis in returning travelers to the USA has increased in recent years, owing to increased travel abroad and to the activities of the US military and contractors in the Middle East. Old and New World leishmaniasis can be classified into four forms: localized cutaneous, diffuse cutaneous (or diffuse anergic cutaneous), mucocutaneous, and visceral. The progression from one stage to another largely depends on the Leishmania species and host response to the infection.[33]

The life cycle of Leishmania in the human host starts with the bite of the female sandfly of either the Phlebotomus (Old World) or Lutzomyia (New World) genera. The flagellated promastigote form of the protozoa is transferred from the proboscis of the sandfly to the tissue of the host, where it is rapidly phagocytosed by macrophages, dendritic cells, and neutrophils. The parasite then transforms into the non-flagellated amastigote form and multiplies in the cytoplasm of the host cells. If the host is again bitten by a female sandfly, the parasites are transferred to the gut of the fly, transform back into the flagellated promastigote form and subsequently migrate to the proboscis of the fly in preparation to infect the next host. The Leishmania genus is divided into Leishmania and Viannia subgenera if the protozoa replicates in the foregut or mid- to hind-gut of the sandfly, respectively. The fly itself is smaller than a mosquito and inaudible; it has a painless bite that typically occurs on exposed skin of the head, neck, and extremities between dusk and dawn. Animal reservoirs include rodents and dogs.[36]


Global prevalence of both Old World and New World leishmaniasis is estimated at 12 million, with an annual incidence of approximately 2 million, of which 1.5 million are thought to be cutaneous leishmaniasis. Mortality is estimated at 20,000–30,000 annually, second only to malaria for diseases caused by a protozoan.[37] More than 90 % of New World cutaneous disease originates from Brazil and Peru; Old World disease originates mostly from Iran, Afghanistan, Syria, and Saudi Arabia.[38,39] New World disease is typically limited to Central and South America; disease is uncommon in the USA, although occasional case reports have come from Texas and Oklahoma.[40]

Clinical Presentation

Cutaneous leishmaniasis (Fig. 6) begins after a 1- to 2-month incubation period as a solitary well-circumscribed erythematous papule at the site of the sandfly bite. The papule enlarges and forms larger nodules and plaques with indurated borders that may ulcerate. Cutaneous leishmaniasis can be caused by numerous species in both Old World and New World disease.[39] Diffuse (anergic) cutaneous leishmaniasis (Fig. 7) is a more extensive form of cutaneous leishmaniasis characterized by disseminated flesh-colored papules or nodules; however. Leishmania mexicana usually causes an ulcer. Primarily a New World disease, diffuse cutaneous leishmaniasis is caused by L. mexicana, L. amazonensis, and L. venezuelensis species.[33,41] Mucocutaneous leishmaniasis is a rare form, almost exclusively in New World disease, and can occur 1–2 years after the onset of primary cutaneous disease. Signs and symptoms of mucocutaneous disease include upper respiratory congestion and hoarseness, often epistaxis with erythematous, edematous, and boggy mucosa with purulent drainage. This can lead to mutilating destruction of the mucous membranes and surrounding cartilage; most classically, ulceration of the septal mucosae. Progression rates to mucocutaneous leishmaniasis range from 1 to 10 %.[37,42,43] The disseminated form of leishmaniasis, known as visceral disease or Kala-azar (black sickness) is caused by migration of infected tissue macrophages through the reticuloendothelial system. Patients exhibit fever, weight loss, weakness, pallor, hepatosplenomegaly, and lymphadenopathy. Visceral leishmaniasis can originate from either Old or New World disease, with patients from Bangladesh, Brazil, Ethiopia, India, Sudan, and South Sudan accounting for >90 % of cases.[37]

Figure 6.

Cutaneous leishmaniasis

Figure 7.

Diffuse anergic cutaneous leishmaniasis

The differential diagnosis for cutaneous leishmaniasis is broad and includes malignancy, mycobacterial, non-mycobacterial, and fungal infections of the skin and arthropod assault. A good travel history is essential for making the diagnosis. Skin biopsy reveals a dense dermal mixed infiltrate with histiocytes, lymphocytes, neutrophils, and plasma cells. Intracellular amastigotes may be present within inflammatory cells, though sensitivity for the organism is highly variable, ranging from 19 to 77 %.[37,44] Polymerase chain reaction (PCR) helps to confirm the diagnosis, either with a skin biopsy specimen or fine needle aspirate. PCR can also identify the organism, which can guide choice of treatment.[45]


Treatment of leishmaniasis can be difficult. As a general rule, pentavalent antimonials—either intravenous sodium stibogluconate or intramuscular meglumine antimoniate, both 20 mg/kg/day for 3–4 weeks—are preferred therapy for cutaneous leishmaniasis. This depends somewhat on the infecting species, as determined by PCR results, and risk of progression to mucocutaneous disease.[46] All patients with New World leishmaniasis should receive systemic therapy as well as disseminated mucocutaneous or visceral Old World leishmaniasis. Side effects of antimonial treatment include nausea, vomiting, diarrhea, fatigue, pancreatitis, cytopenias, and reversible electrocardiogram (ECG) changes. Cure rates can range widely from 52 to 95 % with antimonials.[47–49] Oral miltefosine may also be used in both Old World and New World disease as it has been shown to be efficacious and relatively well tolerated compared with antimonials.[50] As second-line therapy, liposomal or non-liposomal amphotericin B are effective in patients who are non-responsive to antimonials. Liposomal amphotericin B is preferred because of its shorter dosing regimen and better side effect profile. For uncomplicated localized disease in Old World leishmaniasis, topical therapies such as paromomycin, cryotherapy, or intra-lesional antimonials can be effective and helpful.[51,52]