Rare Cause of Facial Palsy: Case Report of Tick Paralysis by Ixodes Holocyclus Imported by a Patient Travelling into Singapore from Australia.

BACKGROUND: Ticks are blood-sucking arachnids that feed on all classes of vertebrates, including humans. Ixodes holocyclus, also known as the Australian Paralysis Tick, is capable of causing a myriad of clinical issues in humans and companion animals, including the transmission of infectious agents, toxin-mediated paralysis, allergic and inflammatory reactions, and mammalian meat allergies in humans. The Australian Paralysis Tick is endemic to Australia, and only two other exported cases have been reported in the literature. CASE REPORT: We report the third exported case of tick paralysis caused by I. holocyclus, which was imported on a patient into Singapore. We also discuss the clinical course of the patient, the salient points of management, and the proper removal of this tick species. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: With increasing air travel, emergency physicians need to be aware of and to identify imported cases of tick paralysis to institute proper management and advice to the patient. We also describe the tick identification features and proper method of removal of this tick species.

NT-proBNP and cardiac troponin I concentrations in dogs with tick paralysis caused by Ixodes holocyclus.

OBJECTIVE: The purpose of this study was to determine through measurement of cardiac biomarkers whether there was cardiac involvement in dogs infested with Ixodes holocyclus. METHODS: Dogs with tick paralysis and no-mild (group 1; n = 44) or moderate-severe respiratory compromise (group 2; n = 36) and a control group of dogs (n = 31) were enrolled. Plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP), serum cardiac troponin I (cTnI) and serum creatinine concentrations were determined. For most of the affected dogs SpO2 was determined. RESULTS: SpO2 readings did not differ between groups 1 and 2. Three animals in group 2 had an SpO2 reading <90%. NT-proBNP concentrations were lower in both groups 1 and 2 compared with the control group. There was no difference in cTnI concentrations among groups, although they were elevated in four dogs, including the three dogs in group 2 with SpO2 readings <90%. Creatinine concentrations were within the reference interval for all dogs, but did differ among the groups, with control dogs having the highest values, followed by group 1 and then group 2. CONCLUSION: This study did not detect significant cardiac involvement in dogs with tick paralysis induced by I. holocyclus. Evidence for reduced preload in dogs with tick paralysis was provided by lower NT-proBNP concentrations compared with control dogs. Severe hypoxaemia may not be a significant component of the clinical picture in many of the dogs presenting with tick paralysis. Dogs with severe hypoxaemia may have loss of cardiomyocyte integrity, reflected by elevated cTnI concentrations.

Electrodiagnostic Abnormalities in Tick Paralysis: A Case Report and Review of Literature.

OBJECTIVE: To study the electrodiagnostic abnormalities in tick paralysis. METHODS: A 7-year-old girl with acute onset proximal muscle weakness and an engorged dog tick attached to her scalp was evaluated. RESULTS: The routine motor nerve conduction study showed normal compound muscle action potential amplitude. The stimulated jitter analysis of the orbicularis oculi muscle showed normal jitter with no blocking. The quantitative electromyography of the proximal muscles showed decreased mean duration of the motor unit potentials. CONCLUSION: We propose toxin-mediated direct skeletal muscle involvement as one of the reasons for muscle weakness in tick paralysis.

A Comparative Meta-Analysis of Tick Paralysis in the United States and Australia.

CONTEXT: Tick paralysis is a neurotoxic envenoming that mimics polio and primarily afflicts children, especially in hyperendemic regions of the Western United States of America (US) and Eastern Australia. OBJECTIVE: To compare the epidemiology, clinical and electrodiagnostic manifestations, and outcomes of tick paralysis in the US versus Australia. METHODS: A comparative meta-analysis of the scientific literature was conducted using Internet search engines to identify confirmed cases of tick paralysis in the US and Australia. Continuous variables including age, time to tick removal, and duration of paralysis were analyzed for statistically significant differences by unpaired t-tests; and categorical variables including gender, regional distribution, tick vector, tick attachment site, and misdiagnosis were compared for statistically significant differences by chi-square or Fisher exact tests. RESULTS: Tick paralysis following ixodid tick bites occurred seasonally and sporadically in individuals and in more clusters of children than in adults of both sexes in urban and rural locations in North America and Australia. The case fatality rate for tick paralysis was low, and the proportion of misdiagnoses of tick paralysis as Guillain-Barré syndrome (GBS) was greater in the US than in Australia. Although electrodiagnostic manifestations were similar, the neurotoxidromes differed significantly with prolonged weakness and even residual neuromuscular paralysis following tick removal in Australian cases compared with US cases. DISCUSSION: Tick paralysis was a potentially lethal envenoming that occurred in children and adults in a seasonally and regionally predictable fashion. Tick paralysis was increasingly misdiagnosed as GBS during more recent reporting periods in the US. Such misdiagnoses often directed unnecessary therapies including central venous plasmapheresis with intravenous immunoglobulin G that delayed correct diagnosis and tick removal. CONCLUSION: Tick paralysis should be added to and quickly excluded from the differential diagnoses of acute ataxia with ascending flaccid paralysis, especially in children living in tick paralysis-endemic regions worldwide.

Neurotoxin-induced paralysis: a case of tick paralysis in a 2-year-old child.

BACKGROUND: Tick paralysis is an arthropod-transmitted disease causing potentially lethal progressive ascending weakness. The presenting symptoms of tick paralysis overlap those of acute inflammatory diseases of the peripheral nervous system and spinal cord; thus, the condition is often misdiagnosed, leading to unnecessary treatments and prolonged hospitalization. PATIENT: A 2-year-old girl residing in northern New York and having no history of travel to areas endemic to ticks presented with rapidly progressing ascending paralysis, hyporeflexia, and intact sensory examination. Investigation included blood and serum toxicology screens, cerebrospinal fluid analysis, and brain imaging. With all tests negative, the child's condition was initially mistaken for botulism; however, an engorged tick was later found attached to the head skin. Following tick removal, the patient's weakness promptly improved with no additional interventions. CONCLUSION: Our patient illustrates the importance of thorough skin examination in all cases of acute progressive weakness and the necessity to include tick paralysis in the differential diagnosis of paralysis, even in nonendemic areas.

Tick paralysis caused by Amblyomma maculatum on the Mexican Pacific Coast.

Tick paralysis is a rare entity in which it is necessary to identify the cause and remove the arthropod to have a rapid remission of symptoms. In the absence of an early diagnosis, the outcome can be fatal, as toxins are released from the tick's saliva as it feeds. To the best of the authors' knowledge, this is the first clinical report of the disease in Mexico and Latin America. A 22-year-old man from a rural area, who was in contact with cattle, developed ascending flaccid paralysis secondary to Amblyomma maculatum tick toxin. He presented flaccid paraplegia and arreflexia that progressed until causing dyspnea. The clinical symptoms subsided 48 h after the ticks spontaneously detached. The ticks were discovered by nursing personnel while the patient was being transferred to a regional hospital with the diagnosis of Guillain-Barré syndrome. The patient was asymptomatic on discharge from hospital and showed no further motor deterioration at a 1-month follow-up.

Conduction block and impaired axonal function in tick paralysis.

Tick paralysis (TP) is an uncommon disorder caused by a neurotoxin secreted by engorged female ticks. The cause of TP remains unclear, although alterations in axonal ion channel function and neuromuscular transmission have been proposed. In the present case, nerve excitability techniques, which provide information regarding axonal ion channel function, were used to elucidate the mechanism underlying weakness in a 45-year-old man who presented with weakness following a tick bite in the lateral aspect of the left axilla. Standard clinical nerve conduction studies were undertaken during the acute phase of symptoms and following clinical recovery. Nerve excitability studies were performed to investigate possible changes in ion channel properties distal to the site of conduction failure. Nerve conduction studies and electromyography suggested the possibility of a lesion involving the lower trunk of the left brachial plexus. Nerve excitability studies distal to the site of the tick bite demonstrated an abrupt increase in refractoriness, a marker of recovery from inactivation of Na(+) channels. There was normalization of both nerve conduction and nerve excitability parameters associated with clinical recovery. The alteration in refractoriness is similar to that noted in disorders involving the terminal portion of the motor nerve. The changes raise the possibility that TP may cause weakness through impairment of distal neural transmission.

Tick paralysis as a cause of autonomic dysfunction in a 57-year-old female.

Both Guillain-Barré and tick paralysis can present with ataxia and acute, ascending, flaccid motor paralysis. While autonomic dysfunction has been identified in Guillain-Barré, it has never been reported in association with tick paralysis--possibly due to the rapid recovery of tick paralysis patients after removal of the tick. We present a case report of a patient with ascending weakness, ocular disturbances, ataxia, weakness, tachycardia and new hypertension who was initially thought to have Guillain-Barré syndrome with autonomic dysfunction. On hospital day two, a tick was removed, and the patient's symptoms of paralysis and autonomic dysfunction began to resolve. To our knowledge, this is the first reported case of autonomic dysfunction associated with tick paralysis.

Tick paralysis.

Tick paralysis results from inoculation of a toxin from tick salivary glands during a blood meal. It is a relatively uncommon neuromuscular disease with a higher prevalence among young girls, although older men who get exposed to ticks may also be affected. It typically presents as an acute ascending paralysis occurring a few days after tick attachment and may result in respiratory failure and death. Patients may report minor sensory symptoms but constitutional signs are usually absent. Deep tendon reflexes are usually hypoactive or absent and ophthalmoplegia and bulbar palsy can occur. Children may be ataxic. Electromyographic studies usually show a variable reduction in the amplitude of compound muscle action potentials but no abnormalities of repetitive nerve stimulation studies. These appear to result from a failure of acetylcholine release at the motor nerve terminal level. There may be subtle abnormalities of motor nerve conduction velocity and sensory action potentials. Removal of the tick results in the very rapid reversal of clinical and physiologic deficits, quicker with North American ticks than with the Ixodes species seen in Australia.

Tick paralysis presenting in an urban environment.

We report the case of a 17-month-old female with tick paralysis presenting to an urban Los Angeles emergency department. The tick was later identified as the North American wood tick, Dermacentor andersoni, and was likely obtained while the family was vacationing on a dude ranch in Montana. We discuss the epidemiology of tick paralysis, a differential diagnosis for health care providers, and methods of detection and removal. Given the increasing popularity of outdoor activities and ease of travel, tick paralysis should be considered in cases of acute or subacute weakness, even in an urban setting.

Effects of the paralysis tick, Ixodes holocyclus, on the electrocardiogram of the Spectacled Flying Fox, Pteropus conspicillatus.

OBJECTIVE: To evaluate cardiac electrical function in the Spectacled Flying Fox (bat) infested with Ixodes holocyclus. DESIGN: Prospective clinical investigation of bats treated for naturally occurring tick toxicity. PROCEDURE: ECGs were performed on bats with tick toxicity (n = 33), bats that recovered slowly (n = 5) and normally (n = 5) following treatment for tick toxicity, and on normal bats with no history of tick toxicity (n = 9). RESULTS: Bats with tick toxicity had significantly prolonged corrected QT intervals, bradycardia and rhythm disturbances which included sinus bradydysrhythmia, atrial standstill, ventricular premature complexes, and idioventricular bradydysrhythmia. CONCLUSIONS: The QT prolongation observed on ECG traces of bats with tick toxicity reflected delayed ventricular repolarisation and predisposed to polymorphic ventricular tachycardia and sudden cardiac death in response to sympathetic stimulation. The inability to document ventricular tachycardia in bats shortly before death from tick toxicity may be explained by a lack of sympathetic responsiveness attributable to the unique parasympathetic innervation of the bat heart, or hypothermia-induced catecholamine receptor down-regulation. Bradycardia and rhythm disturbances may be attributable to hypothermia.

Tick paralysis in children: electrophysiology and possibility of misdiagnosis.

The authors report six patients with tick paralysis seen over 5 years. Clinical and electrodiagnostic findings failed to adequately distinguish tick paralysis from Guillain-Barré syndrome in these patients. Finding a tick attached to the scalp or the nape of the neck and removing it resulted in rapid clinical improvement.

Pathogenic mechanisms of sand tampan toxicoses induced by the tick, Ornithodoros savignyi.

The tick, Ornithodoros savignyi has been implicated in inducing paralysis and tampan toxicosis. In this study, a basic toxin (TSGP4) was identified and the presence of an acidic toxin (TSGP2) was confirmed. Both basic and acidic toxins were more lethal than previously described, with TSGP4 (34microg) and TSGP2 (24microg) causing mortality of adult mice within 30min. Pathological effects on the cardiac system, notably of salivary gland extract on an isolated rat heart perfusion system and of purified toxins on mouse electrocardiogram patterns could be observed. TSGP4 caused Mobitz type ventricular block, while TSGP2 induced ventricular tachycardia. Conversely, fractions from reversed phase high performance liquid chromatography preparations caused paralysis-like symptoms of the limbs after only 48h. The toxins also differ from previously described tick paralysis toxins in terms of molecular behavior and properties. These results indicate that tampan toxicoses and tick paralysis are unrelated pathogenic phenomena.

Clinical and neurophysiological features of tick paralysis.

The clinical and neurophysiological findings in six Australian children with generalized tick paralysis are described. Paralysis is usually caused by the mature female of the species Ixodes holocyclus. It most frequently occurs in the spring and summer months but can be seen at any time of year. Children aged 1-5 years are most commonly affected. The tick is usually found in the scalp, often behind the ear. The typical presentation is a prodrome followed by the development of an unsteady gait, and then ascending, symmetrical, flaccid paralysis. Early cranial nerve involvement is a feature, particularly the presence of both internal and external ophthalmoplegia. In contrast to the experience with North American ticks, worsening of paralysis in the 24-48 h following tick removal is common and the child must be carefully observed over this period. Death from respiratory failure was relatively common in the first half of the century and tick paralysis remains a potentially fatal condition. Respiratory support may be required for > 1 week but full recovery occurs. This is slow with several weeks passing before the child can walk unaided. Anti-toxin has a role in the treatment of seriously ill children but there is a high incidence of acute allergy and serum sickness. Neurophysiological studies reveal low-amplitude compound muscle action potentials with normal motor conduction velocities, normal sensory studies and normal response to repetitive stimulation. The biochemical structure of the toxin of I. holocyclus has not been fully characterized but there are many clinical, neurophysiological and experimental similarities to botulinum toxin.

Enfermedad de Lyme: informe de dos casos / Lyme disease: report of two cases

En el presente trabajo presentamos las características clínicas y de laboratorio que se encontraron en dos pacientes en los que se hizo el diagnóstico de enfermedad de Lyme. Se hace una revisión somera del ciclo biológico y las características clínicas de los diferentes estadios en que se puede identificar al paciente con esta enfermedad. Se mencionan las técnicas de laboratorio útiles en el diagnóstico y la terapéutica actual del padecimiento. Enfermedad de Lyme

Severe tick-bite fever in young children. A report of 3 cases.

Tick-bite fever in young children is usually a mild illness with few complications and no mortality. That it may assume a severe form is illustrated by the occurrence of 3 cases admitted to Johannesburg Hospital within 1 week in which 2 patients, 3 and 5 years old respectively, had severe involvement of the central nervous system with epileptiform fits and deep coma and loss of power of speech on recovering consciousness. The third patient, aged 5 years, developed an incipient haemorrhagic state as well as serious involvement of the central nervous system. The severe form of the disease in these patients appears to have been due to unusually virulent strains of Rickettsia conorii, probably acquired from dog ticks in their homes. All patients recovered on appropriate treatment. Two regained their normal speech after many weeks while the third patient's incipient haemorrhagic state rapidly resolved.