INFECTIONS
Tick
in Three Children
Paralysis
The Diversity of Neurologic Presentations Major, U.S.A.F., M.C.,
Richard J. Gorman, D.O.,
O. Carter Snead, M.D.,
Major, U.S.A.F.,
M.C.
3 cases of tick paralysis in children each with a different One child presented with an ascending flaccid weakness, another with weakness and cerebellar signs, and a third with pure cerebellar signs. Ixodes scapularis, the black-legged deer tick, was the offending tick in Case 3 and apparently has not been previously reported to cause paralysis in humans. Because of the potential for a fatal outcome, it is imperative to consider tick paralysis in any child with an ascending flaccid weakness or acute ataxia. Reviewed
are
presentation.
TICK
PARALYSIS has long been recognized in Western United States, the provinces of British Columbia and Alberta in Canada, and in Australia, South Africa and Europe. 1-3 In the United States a variety of ticks have been noted to produce symptoms; the wood tick, Dermacentor andersoni, and the dog tick, D. variabilis, are the chief offenders. The Lone Star tick,5 Amblyomma americanum, and rarely the Gulf Coast tick,’ A. maculatum, also have been incriminated. We here describe tick paralysis in three
patients
seen
over
a
four-year period
at
Keesler Medical Center, Mississippi. The black-legged deer tick, Ixodes scapularis, was identified as the offender in one case (Case 3). To our knowledge, I. scapularis has never before been reported to cause paralysis in human Thpsp r~sps ;ire illustrative of the From the USAF Medical Center Keesler, Keesler AFB,
Mississippi, Department of Pediatrics. Correspondence to: Richard J. Gorman,
HMR Box
1702, USAF Medical Center Keesler, Keesler AFB,
MS 39534.
diverse
neurologic signs produce. Case
that this disease
can
Reports
Case 1. This 5-year-old white boy was admitted the emergency room in June, 1972, with ataxia of 12 hours’ duration. Symptoms had been first noted the evening before admission when he fell while walking to the bathroom. Past medical and family history were negative. On examination, the vital signs and general physical findings were normal. Neurologically the cranial nerves were intact. There was incoordination on finger-to-nose testing. Gait was widebased and ataxic. There was pronounced weakness with absent deep tendon reflexes in the lower extremities. No pathologic reflexes were noted. A large brown tick was found on the left temporal area behind the ear, and removed. In 4 hours after this removal his gait had improved. By next morning all neurologic abnormalities were gone. Case 2. On August 11, 1974, a 3-year-old white girl, was brought to the pediatric clinic with a 12hour history of difficulty in walking. There was no history of exposure to toxins. Past medical history and family history were unremarkable.
through
249
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The vit.al
findings
signs were normal and general physical normal. Neurologically, her cranial
were
nerves were
intact and there
were no
cerebellar
signs. She was unable to stand because of profound muscular weakness in the legs. Deep tendon reflexes were absent in the lower extremities. Two large ticks were noted in the scalp of the occipital region, and removed. By next morning the child could walk without difficulty. She had full muscle strength in the lower extremities, with normal tone and normal deep tendon reflexes
throughout. Case 3. In
boy
was
August, 1976, an 11-year-old white brought to the emergency room because
of inability
to
walk. He had been well until
two
days earlier, when he began complaining of numband tingling over the left parietal area. Durthe next two days he had paresthesias over ing his arms and legs. On the morning of admission, he was unable to stand. Two weeks prior he had been in the woods camping. Past medical and family history were unremarkable. On examination the vital signs and general findings were normal. Cranial nerves were functioning intact. He had marked difficulty with hnger-to-nose and rapid alternating movements bilaterally, and mild difficulty with heel-to-shin movements. There was marked truncal ataxia. His gait was broad-based and ataxic. Deep tendon reflexes were one plus throughout. There were no abnormal reflexes. Sensory testing revealed a diminution to vibratory testing in the lower extremities, with preservation of other modalities. A large engorged tick, subsequently identified as Irc~~~r~.s st~a~~~l~z.~‘i,s, was removed from his left occiput shortly after admission. His disturbances rapidly improved over the next 12 hours, leaving only minimal truncal ataxia. By 48 hours he was completely normal. ness
Discussion Tick
occurs when a gravid-entick a neurotoxin that can releases gorged cerebellar produce dysfunction or an ascendweakness. The ing process is reversible with no apparent sequelae, once the tick is discovered and removed. A mortality rate of 13 per cent has been reported in children.3 Girls are affected twice as often as boys/1 probably because it is more difficult to detect ticks in the long hair of girls. Laboratory data including CSF studies are usually normal, a lymphocytic pleocytosis sometimes although occurs.2 After the tick becomes attached to the skin there usually is a latent period of 4 to 7 days prior to symptoms of restlessness, irritability,
paralysis
flaccid paralysis. These progress rapidly through a few days with bulbar involvement, respiratory paralysis, and finally death if the tick is not detected. The mechanism of action of the tick toxin is poorly understood. The toxin produces a conduction block in the peripheral branches of motor fibers which results in a failure of liberation of acetylcholine at the neuromuscular junction7; however, central sites of action have been postulated to explain the cerebellar dysfunction produced by this and
an
ascending
symptoms
can
toxin.&dquo;
paralysis occurs when a gravidengorged tick releases a neurotoxin that can produce cerebellar dysfunction or an ascending weakness. Tick
Each of our patients had a different combination of symptoms. One presented with an ascending flaccid weakness, a second with weakness and cerebellar signs, and a third with pure cerebellar signs. The truncal ataxia in the third patient is convincing evidence of cerebellar involvement. Cerebellar signs are often not clear because peripheral weakness may, in and of itself, produce wide-based gait and apparent intention tremor. The parasthesia prior to the onset of neurologic dysfunction in Patient 3 as well as the loss of vibratory sense in the lower extremities was most unusual. These findings led us to suspect the Guillain-Barr6 syndrome in this patient before the tick was found. It is of interest that the patient with the atypical presentation is the one with whom the Ixodes scapularis was identified. Although other species of Ixodes, most not-2 ably the holocyclus and ricinus in Australia,~ have been identified as offenders in tick paralysis in humans, I. scapularis has not heretofore been known to cause this disease. This black-legged deer tick can be found from Southern Massachusetts to Florida and from Indiana south to Louisiana and Texas.~4 The atypical presentation with pure ataxia is
250
Downloaded from cpj.sagepub.com at Purdue University on May 24, 2015
of a different mode of action of its toxin. The most recent report of a patient who presented with pure ataxia failed to identify the offending tick.’ D. variabilis was identified as the agent in an older report of a patient with clinical presentation similar to our case three.9 It is imperative to consider tick paralysis in the differential diagnosis of any child with an ascending flaccid paralysis or acute onset of ataxia. This is a treatable disease, but may prove fatal when the offending agent is allowed to remain.
suggestive
References Abbott, K. H.: Tick paralysis: A review. Proc. Mayo Clin. 18 : 39, 1943. 2. Stanbury, J. B., and Huyck, J. H.: Tick paralysis. : 219, 1954. 24 Medicine 3. Schmitt, N.: Tick paralysis in British Columbia. Can. Med. Assoc. J. 94: 417, 1969. 4. Bishop, F. C., and Trembley, H. L.: Distribution and 1.
5.
615,
6.
°
Acknowledgment
7. 8.
We thank Dr. John Ouzts, School of Arts and Sciences and Head, Department of Biological Sciences, Delta State University for his identification of the tick and Mrs. L. G. Malig for her technical assistance.
hosts of certain North American ticks. J. Parasitol. 31: 1, 1945. Henderson, F.: Tick paralysis: Report of a case in 1961. Florida. JAMA 175: Bennett, I. L.: Tick bite and tick paralysis. In: Harrison’s Principles of Internal Medicine. New York, McGraw-Hill Co., 6th ed., 1970, p. 695. Murnaghan, M.: Site and mechanism of tick paralysis. Science 131: 418, 1960. Lagos, J. C., and Thies, R. E.: Tick paralysis without muscle weakness. Arch. Neurol. 21: 471, 1969. Mulherin, P. A.: Ataxia due to the bite of the American dog tick (Dermacentor variabilis . J. ) Pediatr. 16: 86, 1940.
9.
251
Downloaded from cpj.sagepub.com at Purdue University on May 24, 2015
Tick
in Three Children
Paralysis
The Diversity of Neurologic Presentations Major, U.S.A.F., M.C.,
Richard J. Gorman, D.O.,
O. Carter Snead, M.D.,
Major, U.S.A.F.,
M.C.
3 cases of tick paralysis in children each with a different One child presented with an ascending flaccid weakness, another with weakness and cerebellar signs, and a third with pure cerebellar signs. Ixodes scapularis, the black-legged deer tick, was the offending tick in Case 3 and apparently has not been previously reported to cause paralysis in humans. Because of the potential for a fatal outcome, it is imperative to consider tick paralysis in any child with an ascending flaccid weakness or acute ataxia. Reviewed
are
presentation.
TICK
PARALYSIS has long been recognized in Western United States, the provinces of British Columbia and Alberta in Canada, and in Australia, South Africa and Europe. 1-3 In the United States a variety of ticks have been noted to produce symptoms; the wood tick, Dermacentor andersoni, and the dog tick, D. variabilis, are the chief offenders. The Lone Star tick,5 Amblyomma americanum, and rarely the Gulf Coast tick,’ A. maculatum, also have been incriminated. We here describe tick paralysis in three
patients
seen
over
a
four-year period
at
Keesler Medical Center, Mississippi. The black-legged deer tick, Ixodes scapularis, was identified as the offender in one case (Case 3). To our knowledge, I. scapularis has never before been reported to cause paralysis in human Thpsp r~sps ;ire illustrative of the From the USAF Medical Center Keesler, Keesler AFB,
Mississippi, Department of Pediatrics. Correspondence to: Richard J. Gorman,
HMR Box
1702, USAF Medical Center Keesler, Keesler AFB,
MS 39534.
diverse
neurologic signs produce. Case
that this disease
can
Reports
Case 1. This 5-year-old white boy was admitted the emergency room in June, 1972, with ataxia of 12 hours’ duration. Symptoms had been first noted the evening before admission when he fell while walking to the bathroom. Past medical and family history were negative. On examination, the vital signs and general physical findings were normal. Neurologically the cranial nerves were intact. There was incoordination on finger-to-nose testing. Gait was widebased and ataxic. There was pronounced weakness with absent deep tendon reflexes in the lower extremities. No pathologic reflexes were noted. A large brown tick was found on the left temporal area behind the ear, and removed. In 4 hours after this removal his gait had improved. By next morning all neurologic abnormalities were gone. Case 2. On August 11, 1974, a 3-year-old white girl, was brought to the pediatric clinic with a 12hour history of difficulty in walking. There was no history of exposure to toxins. Past medical history and family history were unremarkable.
through
249
Downloaded from cpj.sagepub.com at Purdue University on May 24, 2015
The vit.al
findings
signs were normal and general physical normal. Neurologically, her cranial
were
nerves were
intact and there
were no
cerebellar
signs. She was unable to stand because of profound muscular weakness in the legs. Deep tendon reflexes were absent in the lower extremities. Two large ticks were noted in the scalp of the occipital region, and removed. By next morning the child could walk without difficulty. She had full muscle strength in the lower extremities, with normal tone and normal deep tendon reflexes
throughout. Case 3. In
boy
was
August, 1976, an 11-year-old white brought to the emergency room because
of inability
to
walk. He had been well until
two
days earlier, when he began complaining of numband tingling over the left parietal area. Durthe next two days he had paresthesias over ing his arms and legs. On the morning of admission, he was unable to stand. Two weeks prior he had been in the woods camping. Past medical and family history were unremarkable. On examination the vital signs and general findings were normal. Cranial nerves were functioning intact. He had marked difficulty with hnger-to-nose and rapid alternating movements bilaterally, and mild difficulty with heel-to-shin movements. There was marked truncal ataxia. His gait was broad-based and ataxic. Deep tendon reflexes were one plus throughout. There were no abnormal reflexes. Sensory testing revealed a diminution to vibratory testing in the lower extremities, with preservation of other modalities. A large engorged tick, subsequently identified as Irc~~~r~.s st~a~~~l~z.~‘i,s, was removed from his left occiput shortly after admission. His disturbances rapidly improved over the next 12 hours, leaving only minimal truncal ataxia. By 48 hours he was completely normal. ness
Discussion Tick
occurs when a gravid-entick a neurotoxin that can releases gorged cerebellar produce dysfunction or an ascendweakness. The ing process is reversible with no apparent sequelae, once the tick is discovered and removed. A mortality rate of 13 per cent has been reported in children.3 Girls are affected twice as often as boys/1 probably because it is more difficult to detect ticks in the long hair of girls. Laboratory data including CSF studies are usually normal, a lymphocytic pleocytosis sometimes although occurs.2 After the tick becomes attached to the skin there usually is a latent period of 4 to 7 days prior to symptoms of restlessness, irritability,
paralysis
flaccid paralysis. These progress rapidly through a few days with bulbar involvement, respiratory paralysis, and finally death if the tick is not detected. The mechanism of action of the tick toxin is poorly understood. The toxin produces a conduction block in the peripheral branches of motor fibers which results in a failure of liberation of acetylcholine at the neuromuscular junction7; however, central sites of action have been postulated to explain the cerebellar dysfunction produced by this and
an
ascending
symptoms
can
toxin.&dquo;
paralysis occurs when a gravidengorged tick releases a neurotoxin that can produce cerebellar dysfunction or an ascending weakness. Tick
Each of our patients had a different combination of symptoms. One presented with an ascending flaccid weakness, a second with weakness and cerebellar signs, and a third with pure cerebellar signs. The truncal ataxia in the third patient is convincing evidence of cerebellar involvement. Cerebellar signs are often not clear because peripheral weakness may, in and of itself, produce wide-based gait and apparent intention tremor. The parasthesia prior to the onset of neurologic dysfunction in Patient 3 as well as the loss of vibratory sense in the lower extremities was most unusual. These findings led us to suspect the Guillain-Barr6 syndrome in this patient before the tick was found. It is of interest that the patient with the atypical presentation is the one with whom the Ixodes scapularis was identified. Although other species of Ixodes, most not-2 ably the holocyclus and ricinus in Australia,~ have been identified as offenders in tick paralysis in humans, I. scapularis has not heretofore been known to cause this disease. This black-legged deer tick can be found from Southern Massachusetts to Florida and from Indiana south to Louisiana and Texas.~4 The atypical presentation with pure ataxia is
250
Downloaded from cpj.sagepub.com at Purdue University on May 24, 2015
of a different mode of action of its toxin. The most recent report of a patient who presented with pure ataxia failed to identify the offending tick.’ D. variabilis was identified as the agent in an older report of a patient with clinical presentation similar to our case three.9 It is imperative to consider tick paralysis in the differential diagnosis of any child with an ascending flaccid paralysis or acute onset of ataxia. This is a treatable disease, but may prove fatal when the offending agent is allowed to remain.
suggestive
References Abbott, K. H.: Tick paralysis: A review. Proc. Mayo Clin. 18 : 39, 1943. 2. Stanbury, J. B., and Huyck, J. H.: Tick paralysis. : 219, 1954. 24 Medicine 3. Schmitt, N.: Tick paralysis in British Columbia. Can. Med. Assoc. J. 94: 417, 1969. 4. Bishop, F. C., and Trembley, H. L.: Distribution and 1.
5.
615,
6.
°
Acknowledgment
7. 8.
We thank Dr. John Ouzts, School of Arts and Sciences and Head, Department of Biological Sciences, Delta State University for his identification of the tick and Mrs. L. G. Malig for her technical assistance.
hosts of certain North American ticks. J. Parasitol. 31: 1, 1945. Henderson, F.: Tick paralysis: Report of a case in 1961. Florida. JAMA 175: Bennett, I. L.: Tick bite and tick paralysis. In: Harrison’s Principles of Internal Medicine. New York, McGraw-Hill Co., 6th ed., 1970, p. 695. Murnaghan, M.: Site and mechanism of tick paralysis. Science 131: 418, 1960. Lagos, J. C., and Thies, R. E.: Tick paralysis without muscle weakness. Arch. Neurol. 21: 471, 1969. Mulherin, P. A.: Ataxia due to the bite of the American dog tick (Dermacentor variabilis . J. ) Pediatr. 16: 86, 1940.
9.
251
Downloaded from cpj.sagepub.com at Purdue University on May 24, 2015
