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



Scabies is caused by the female mite Sarcoptes scabiei var hominis, which burrows into the stratum corneum after mating and lays eggs in 1–2 days within the burrow. The larvae subsequently hatch within 3 days, emerge from the skin, and then burrow again to mature. The host typically mounts an immune response against the mite, which accounts for the pruritus.[9,10] In naive hosts, symptoms can take 2–6 weeks to occur, whereas in non-naive patients, symptoms typically occur within 12–72 h.[11]


Scabies occurs throughout the world and typically follows close intimate contact with an infested individual. Sexual transmission is common in adults. Mites can be passed from mother to child, particularly in nursing infants. Occasionally, the mite can also be contracted by sleeping in a bed previously used by an infected individual.[12]

Scabies can be fulminant and pronounced as crusted scabies in which the parasite burden grows exponentially and results in thick crusted plaques. Those at risk for crusted scabies include aboriginal Australians; patients with Down's syndrome, leprosy, or human T-lymphotropic virus (HTLV)-1 infection; and those who are immunosuppressed or have a sensorineural deficiency such as patients with spinal cord injury or Parkinson's disease. Patients with crusted scabies are usually asymptomatic as a result of an impaired immune response or itch sensation.[13,14]

Clinical Presentation

Scabies typically presents with erythematous papules or nodules with linear burrows in flexural areas, finger and toe web spaces, and in the groin[9] (Fig. 3). In the crusted variant, thick hyperkeratotic crusted plaques develop on the trunk or extremities. Differential diagnosis for conventional scabies includes dyshidrotic eczema, folliculitis, papular urticaria, cutaneous larva migrans, and arthropod assault. Diagnosis is made by identifying mites, eggs, or feces on a mineral oil prep of the keratotic debris obtained by scraping a burrow with a scalpel blade. Alternatively, a burrow ink test can be conducted by gently rubbing a fountain pen on one of the papules, covering it with ink. When excess ink is wiped away with alcohol-soaked gauze, the remaining ink will track down the scabetic burrow. The head of the mite can be appreciated on dermoscopy; it appears as a black triangular dot, known as the 'delta-wing-jet' sign. The body of the mite is translucent and cannot be seen. A scabies infestation can become superinfected from the persistent scratching or from skin breakdown, especially in crusted scabies.[15]

Figure 3.



Treatment is permethrin 5 % cream applied for 8–12 h from the neck down at bedtime, washed off in the morning, and repeating 1 week later. The reapplication is necessary because the permethrin is not efficacious against eggs of the parasite, only the live mites. Alternatively, ivermectin 200 μg/kg in two doses 2 weeks apart is effective in 90–100 % of patients. Second-line treatment for the infestation includes 10 % topical crotamiton or topical 1 % lindane, though lindane has been associated with neurotoxicity after repeated use. Household contacts also should be treated to prevent re-infection. Patient clothing and bedding should be washed in hot water or sealed in plastic garbage bags for 1 week if laundering the items is not possible. Itch can persist for several weeks after treatment; antihistamines can be used.[16]

For crusted scabies, the United States Centers for Disease Control (CDC) has published a treatment protocol based on expert opinion in which permethrin cream is applied daily for 1 week then twice-weekly coupled with ivermectin 200 μg/kg on days 1, 2, 8, 9, and 15. Ivermectin can also be given on days 22 and 29 if needed. Cure is ascertained by clinical improvement and confirmatory negative skin scrapings.[17]