Case 2: A seven-year-old girl with diplopia

In late August, a seven-year-old, otherwise healthy girl developed one day of fever followed by ongoing fatigue, nausea, periumbilical pain and nonbilious emesis. She was briefly admitted to hospital with a presumed diagnosis of gastroenteritis. She received intravenous rehydration and her emesis improved, but her abdominal pain and fatigue persisted. Two weeks after discharge, she returned to the emergency department with a three-day history of diplopia. On examination, she was afebrile and her vital signs were normal. She had esotropia of her left eye and horizontal binocular diplopia. Fundoscopy revealed blurred disc margins and disc hyperemia, consistent with papilledema. There was no nuchal rigidity. The remainder of her physical examination was normal. Investigations revealed a hemoglobin level of 107 g/L, leukocyte count 8.7×109/L and platelet count 436×109/L. Magnetic resonance imaging/magnetic resonance venography of the head and spine were normal. One week before the onset of her abdominal symptoms, she had visited a day camp in the Thousand Islands region, outside of Kingston, Ontario. She had no other recent travel. She resided in a city, drank municipal water and was not exposed to any unusual foods. She had no history of insect bites, rashes or other skin findings. Further investigations revealed the diagnosis. Serum antibody testing was sent for West Nile virus, toxoplasmosis, herpes simplex virus, cytomegalovirus and Lyme disease. Lumbar puncture revealed a normal opening pressure of 22 cmH2O and cerebrospinal fluid (CSF) pleocytosis of 57×106/L, with 81% lymphocytes, a normal glucose level (3.9 mmol/L) and normal protein level (0.29 g/L). CSF was sent for bacterial culture and polymerase chain reaction analysis for herpes simplex, varicella zoster, enterovirus, parechovirus and flavivirus. The patient was started on ceftriaxone. Five days later, serum antibody testing for Lyme immunoglobulin M and immunoglobulin G was reported to be positive. Given her positive Lyme antibody tests, clinical history and CSF pleocytosis, a diagnosis of Lyme neuroborreliosis was made. The remaining tests from the serum and CSF were negative. By day 6 of her admission, her diplopia and abdominal pain had resolved. She did not exhibit any cardiac symptoms. She completed a 14-day course of ceftriaxone and, when seen one month later, her symptoms had completely resolved. Dilated fundoscopy at that time revealed healthy-looking optic disks with no signs of papilledema. Lyme disease, or Lyme borreliosis, is a tick-borne bacterial infection. In North America, the causative pathogen is Borrelia burgdorferi. Ticks contract B burgdorferi by feeding on mice, squirrels and other small animals carrying the bacteria. Lyme disease is then transmitted to humans through an infected tick bite, most commonly from the blacklegged tick species Ixodes scapularis and Ixodes pacificus in Canada (1). If untreated, Lyme disease can progress through three stages. Following a tick bite, individuals may develop an acute localized infection with an erythema migrans skin rash and/or flu-like symptoms. The disease may then progress to an early disseminated infection with rheumatological, cardiac and/or neurological involvement, followed by persistent complications in late disseminated infection (2). Neurological symptoms of Lyme disease, or Lyme neuroborreliosis, first appear in the early disseminated stage of the disease. Among children with untreated Lyme disease, as many as one in five may experience Lyme neuroborreliosis, with the development of a cranial nerve palsy, Lyme meningitis or both (2). Facial nerve palsy is more common, but cranial nerve six can also be affected, as in the present case. Other, more rare complications include encephalopathy, meningoencephalitis or pseudotumour cerebri (2). In Lyme meningitis, CSF findings include pleocytosis (primarily lymphocytic or monocytic), elevated protein level, and a normal or decreased glucose level. Papilledema and increased intracranial pressure may also be present (2). Similar to the present case, many children with Lyme meningitis do not exhibit typical meningitis symptoms and have no known history of a tick bite or erythema migrans. Lyme neuroboreliosis is generally treated with 14 to 28 days of intravenous ceftriaxone. With appropriate treatment, most children experience resolution of their symptoms (2). Over the past two decades, tick populations of I scapularis have expanded into Canada from the United States. There are now established populations of blacklegged ticks in British Columbia, Manitoba, Ontario, Quebec, New Brunswick and Nova Scotia (3). Part of the Thousand Islands National Park, where the patient visited, is a known Lyme-endemic area (1). In addition to land travel, ticks may also be transported to nonendemic areas via attachment and carriage by migratory birds. Therefore, there is a risk of contracting Lyme disease even in nonendemic areas. Due to these trends, the incidence of Lyme disease in Canada has been increasing. From 2009 to 2011, the annual number of Canadian cases almost doubled from 144 to 258 (1). With the geographical expansion of tick populations, the incidence of Lyme disease is expected to continue to rise. The incidence of Lyme disease is rising in Canada due to expanding populations of blacklegged ticks in both endemic and nonendemic areas of the country. Not all patients with Lyme disease present with an erythema migrans rash. In fact, most children with Lyme neuroborreliosis have no history of erythema migrans. Clinicians should familiarize themselves with local Lyme disease epidemiology and have an increased index of suspicion for Lyme disease when patients present with compatible symptoms.

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