Vol. 17, No. 31
THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Monday, August 10, 1998
A. Provided by David Mann, Division of Outbreak Investigation, Maryland Department of Health and Mental Hygiene.
From July 31, 1998 to August 6, 1998, seven outbreaks were reported to the Maryland Department of Health and Mental Hygiene.
From long term care facilities: one outbreak of influenza-like illness and pneumonia; one outbreak of upper respiratory illness and one outbreak of scabies.
From day care centers: one outbreak of gastroenteritis, presumed viral and one outbreak of scabies.
Foodborne outbreaks: one case of V. cholerae non-01 non-0139 diarrheal disease in a Pennsylvania resident who consumed raw clams at a Maryland restaurant. Patient was hospitalized and has recovered. Isolate was from blood; stool was negative. Risk factor: omeprazole for GERD.
One outbreak of gastroenteritis: 13 cases of gastroenteritis in a group of children ages 1 to 3 with a common restaurant food and restaurant play area exposure. Possibly foodborne but also possibly person to person viral via direct or common surface exposure.
As an update, the case of febrile upper respiratory illness in a day care center reported July 30, 1998 was most likely due to a viral infection, possibly enterovirus. The infectious disease consultant in the community felt that there were a large number of cases in the area consistent with enterovirus, and that the isolates of S. pyogenes and H. influenza from one case in the outbreak were not the true underlying pathogens.
B. The Johns Hopkins Hospital. Information provided by Dr. May Arroyo, Department of Pathology.
Case presentation: A three day old boy was taken to the Emergency Department of an outside hospital with a one day history of reluctance to walk. One day prior to admission the boy had been healthy, with no history of motor disorder, recent trauma, or viral illness. The patient and his family had recently moved from North Carolina to Carroll County. On examination, the patient was afebrile, alert, and demonstrated unsteady gait, symmetric lower extremity weakness, and loss of deep tendon reflexes. The patient exhibited difficulty with heel-to-shin movements as well as finger-to-nose movements. Cranial nerves were intact. Examination of the cerebrospinal fluid revealed a normal protein concentration and no cells. Nine hours after admission, the symptoms had progressed to involve the upper extremities and difficulty in sustaining the head elevated. An EEG was normal. While the EEG was being performed, the mother noted an engorged tick in the right parietal region of the child's scalp. The physician was informed and the tick was carefully removed. By next morning the child had regained all strength.
Organism: The tick was identified as a female Dermacentor variabilis (American dog tick). Various ticks have been shown to cause tick paralysis in both humans and animals. In North America, the most common offenders are D. variabilis and D. andersoni (Rocky Mountain wood tick). Less commonly, Amblyomma americanum (Lone Star tick), A. maculatum (Gulf Coast tick), Ixodes scapularis, and I. pacificus (western black-legged tick). Cases associated with D. andersoni have been reported primarily in the northwestern states and Canada (1). D. variabilis, A. americanum, and A. maculatum have been associated with cases in the eastern and southern states. Tick paralysis has also been recognized in Australia, South Africa, and Europe. In Australia, tick paralysis is most commonly associated with I. holocyclus (Australian scrub tick).
Ticks are most commonly found attached to the scalp or the postauricular area (where are easily concealed). The tick employs its hypostome to penetrate the skin and burrow into the epidermis. Salivary gland fluid containing the toxin is secreted into the site by the tick, and the toxin diffuses both locally and systematically. The toxin presumably acts by diminishing the release of acetylcholine at the motor nerve junction (botulinum-like effect). In addition, nerve conduction velocity appears to be reduced (1). The toxin, however, has not been isolated. Some investigators have proposed that tick paralysis arises in suceptible hosts due to an idiosyncratic reaction to components in the tick's saliva (1).
Clinical presentation: Tick paralysis is characterized by acute, ascending, symmetric flaccid motor paralysis. The disease may also manifest as cerebellar dysfunction. The symptoms generally develop four to seven days after the tick has attached itself and occasionally are preceeded by restlessness and irritability. Complete paralysis can develop within 24 hours of the onset of the initial symptoms and may be fatal in 10% of cases due to bulbar and respiratory failure. The symptoms are quickly reversible with no sequelae following removal of the tick. In contrast, tick paralysis caused by the Australian scrub-tick, I. holocyclus, is characterized by worsening of symptoms following removal of the tick, with symptoms generally peaking 48 hours after removal of the tick and requiring several weeks for resolution (1).
Tick paralysis may also present as facial nerve paralysis. A case presenting with parasthesia and loss of vibratory sense has been described (2).
Treatment: Tweezers should be employed to grasp and remove the mouth parts as close to the skin as possible. One should avoid breaking off the body of the tick, as that will leave the mouth parts embedded in the skin. Gloves should be employed during the procedure in order to avoid exposure to any infectious agent present on the tick. In Australia, a canine anti-tick anti-venom is occasionally administered to patients with severe paralysis and bulbar involvement (3).
Acknowledgements: I would like to thank Dr. Stephens of the Pediatric Infectious Disease Department at Mount Sinai Hospital, Baltimore for sharing this case with us.
References:
1. Kocan, A.A. Tick paralysis. JAVMA 192:1498-1500;1988.
2. Gorman, R.J., and Snead, O.C. Tick paralysis in three children. Clin. Ped. 17:249- 251;1978.
3. Pearn, J. Neuromuscular paralysis caused by tick envenomation. J. of Neurol. Sci. 34:37-42;1977.