The causative agent of Lyme disease, Borrelia burgdorferi, is endemic to Canada, the northeastern United States, northern California, and temperate European regions. It is rarely associated with a travel-related exposure. In this report, we describe a resident of southern Ontario, Canada who developed rash, fever, and cranial nerve VII and XII palsies following a 12 day trip to Ecuador and the Galapagos islands approximately four weeks prior to referral to our center. Comprehensive microbiological work-up was notable for reactive Borrelia burgdorferi serology by modified two-tier testing (MTTT), confirming a diagnosis of Lyme disease. This case highlights important teaching points, including the classic clinical presentation of acute Lyme disease with compatible exposure pre-travel in a Lyme-endemic region of Ontario, initial manifestations during travel following acquisition of arthropod bites in Ecuador, and more severe manifestations post-travel. Given the travel history to a South American country in which Lyme disease is exceedingly uncommon, consideration of infections acquired in Ecuador necessitated a broad differential diagnosis and more comprehensive microbiological testing than would have been required in the absence of tropical travel. Additionally, cranial nerve XII involvement is an uncommon feature of Lyme neuroborreliosis, and therefore warranted consideration of an alternative, non-infectious etiology such as stroke or a mass lesion, both of which were excluded in this patient through neuroimaging.

Manchineel dermatitis, caused by the sap of the manchineel tree native to the coastlands of the Caribbean, West Africa, and Central America, has received limited attention in the literature despite significant morbidity. The toxic sap causes a burning, blistering rash and conjunctivitis, while ingestion of the fruit may lead to oropharyngeal pain, hemodynamic instability, and gastrointestinal distress. Tourists unfamiliar with the manchineel tree may be exposed through exposure to the tree’s sap, contaminated rainwater, or ingestion of the apple-like fruit. We herein present a case of a patient who experienced prolonged symptoms of manchineel toxicity after ingestion of the manchineel fruit for several weeks. Antihistamines, corticosteroids, and a PPI were ineffective. The symptoms eventually resolved after discarding clothing and towels that had come in contact with the tree, raising the possibility that toxins may linger on fabrics. Travellers to regions in the Caribbean or Central America are at particular risk for toxicity from the Manchineel tree if unfamiliar with the associated dangers and should be counselled to avoid contact with the tree or ingesting any unfamiliar fruit on the ground. When exposures do occur, it may be reasonable to dispose of potentially contaminated fabrics to avoid recurrent exposures, particularly if recurrent symptoms are observed, as in our patient. We further contextualize manchineel toxicity within a comparative review of select tropical foodborne intoxications of plant origin (ackee, lychee, cassava, papain) and marine origin (ciguatera, scombroid, neurotoxic and diarrhetic shellfish poisonings, tetrodotoxin), distinguishing manchineel’s local irritant mechanism from the systemic toxidromes of these comparators and underscoring the absence of a specific antidote.