Neuropsychiatric presentation of Lyme disease in Australia

To the Editor

Lyme disease is not currently well documented in Australia, though it is a relatively common diagnosis in the US. It is named after the town of Lyme in Connecticut, USA where a number of patients with this illness were identified in 1975. This spirochetal multi-system illness often adversely affects the CNS, with up to 40% of patients developing neuropsychiatric symptoms, within a few weeks of the initial skin infection, subsequent to a bite from an infected female Ixodes tick. The infective spirochaetes were identified in 1981 by Willy Burgdorfer, whose name was subsequently given to the aetiological agent (Fallon and Nields, 1994; Strijdom and Berk, 1996).

Like syphilis, Lyme disease can have a latency period of months to years before later neuropsychiatric symptoms present. A wide spectrum of psychiatric symptoms can include psychosis, presenting both with schizophrenic or bipolar-type symptoms, depression and anxiety disorders and, more rarely, a secondary dementia. Rates of depressive symptoms in patients suffering from a late Lyme disease infection can range from 26% to 66%. The microbiology of Borrelia burgdorferi is complex and is thought to contribute to an autoimmune-type process (Fallon and Nields, 1994). Subtle cognitive problems, including difficulties with concentration and short-term memory, are common, as is marked fatigue. Neurological symptoms are also common, including gait difficulties, leg weakness, facial palsy, bladder problems, headaches, paraesthesia, vertigo and back pain. Somatoform symptoms, depersonalization and derealisation are described. Somatosensory symptoms including light and sound sensitivity, tinnitus and visual disturbances are well described.

We present the case of a young woman with neuropsychiatric complications of Lyme disease. The patient, aged 18 years old, had always lived with her parents in rural Victoria on a farm with mixed livestock. The patient herself had, from a young age, been actively involved with caring for the animals and was a keen horsewoman. Collateral information as to her neuropsychiatric symptoms was obtained from her mother, a qualified nurse. At the age of 2 years, she had a presumed herpes zoster infection, presenting with shingles down her left leg. The mother was unable to remember an encephalitic process at the time. At the age of 10 years, she had a pyrexia of unknown origin (PUO) for a week and, thereafter, especially at high school, had experienced regular presumed viral illnesses requiring considerable time from school, but had still passed her year 12 examinations in 2011 and been accepted into veterinary school for 2013. These illnesses had precipitated a chronic fatigue-type syndrome. During October to December 2011, she had two episodes of severe generalized body pain, for which no cause had been found, and she was diagnosed with fibromyalgia. Neither the patient nor her mother could remember a tick bite.

Her presentations were confounded by an episode of tiredness being linked to a family argument and she was treated with fluoxetine in 2010 without any improvement – but later she spontaneously improved. She had been treated with escitalopram in 2011 and her mother reported that her mood had lifted but she had developed alopecia, attributed to the escitalopram, which was then stopped.

On admission in June 2012, she was acutely psychotic with auditory hallucinations and paranoid ideas. The symptoms were linked with a recent change in her antidepressant medication from paroxetine to duloxetine a week previously. The presentation was further complicated by information that her elderly grandmother had recently been diagnosed as suffering from a bipolar disorder. She was treated with quetiapine and diazepam and rapidly settled within 3 days. As the patient settled she reported the following longstanding complaints, which pre-dated her psychosis: ongoing severe arthritic pains in her hands, auditory hyperacusis, poor concentration, longstanding irritability and emotional lability, and profound fatigue with episodic sleep disturbances.

Following peer review discussion, she was tested for Lyme disease, amongst other laboratory tests, with the following results: B. burgdorferi IgG titre = 80 and IgM titre = 10, indicating past Lyme disease.

It is always a caveat of case reports that causal associations cannot be confirmed. Nevertheless, this report highlights the need to consider Lyme disease, in Australia, when reviewing the diagnosis of a patient presenting with longstanding complex neuropsychiatric symptoms, where people are from a rural background, especially where there is exposure to livestock (Mayne, 2011).