Servicio de Infectologia y Medicina Tropical, Hospital San Roque, Ministerio de Salud de la Provincia de Jujuy, Jujuy, Argentina
Tick paralysis (TP) occurs worldwide and is caused by a neurotoxin secreted by engorged female ticks that affects the peripheral and central nervous system. The clinical manifestations range from mild or nonspecific symptoms to manifestations similar to Guillain-Barré syndrome, bulbar involvement, and death in 10% of the patients. The diagnosis of TP is clinical. To our knowledge, there are no formal reports of TP in humans in South America, although clusters of TP among hunting dogs in Argentina have been identified recently. In this paper, clinical features of two cases of TP occurring during 1994 in Jujuy Province, Argentina, are described.
Keywords: Tick borne diseases. Tick paralysis. Rickettsioses. Argentina.
A paralisia por carrapatos (PC) ocorre mundialmente e é causada por uma neurotoxina secretada por carrapatos fêmea engolidores de sangue que afeta o sistema nervoso periférico e central. As manifestações clínicas variam de suave ou sintomas não específicos a manifestações semelhantes à síndrome de Guillain-Barré, envolvimento de bulbar, e morte em 10% dos pacientes. O diagnóstico de PC é clínico. A nosso conhecimento, não há nenhum relatório formal em seres humanos na América do Sul, embora grupos de PC entre cães de caça na Argentina, tenham sido identificados recentemente. Neste artigo, descrevo dois casos de PC ocorridos durante o ano de 1994 na província de Jujuy, Argentina.
Palavras-chaves: Doenças por carrapato. Paralisia por carrapato. Rickettsias. Argentina.
Tick paralysis (TP) occurs worldwide and is caused by a neurotoxins secreted by engorged female ticks that affects the peripheral and central nervous systems; clinical manifestations range from mild or nonspecific symptoms to manifestations similar to Guillain-Barré syndrome, bulbar involvement, and death in a 10% of the patients1. Toxins may derive from a pathogen or symbiotic organism living within the host tick as with organisms that make tetrodotoxin, or from a combination of the host and a symbiotic organism creating a product together, or from the tick itself2.
Although the precise mechanism of action of the neurotoxin is not understood, the tox-ins have been shown to block axonal sodium channels and also inhibit the release of acetylcholine at presynaptic motor nerve terminals, causing total neuromuscular blockade. Clunies Ross provided the ﬁrst deﬁnitive evidence that paralysis was due to a toxin secreted by the tick3. Kaire was able to obtain a partially puriﬁed toxin by homogenizing 350-400 replete ticks. Sub-sequent work by Stone et al. has suggested that it is a protein neurotoxin with a molecular weight of 40,000-80,000. It has been named holocylotoxin or ixovotoxin but its chemical structure has not been fully identiﬁed4.
The diagnosis of TP is clinical and is determined by the exclusion of other known etiologies presenting with the same symptoms5. Although persons of any age may be affected, small children are particularly susceptible6.
In North America, TP is reported most commonly in the Rocky Mountains and northwestern regions of the United States and in Western Canada. To our knowledge, in South America there is a report of a case in Brazil7 and recently was published TP in humans in Mexico8.
At least 15 species of ixodid ticks, including many that harbor rickettsiae of undetermined pathogenicity, are reported to bite humans in Argentina9.
Jujuy Province in Northwest Argentina is a subtropical region, bordering Chile and Bolivia. Geographically, it has four regions: Quebrada and Puna are high and arid areas, and the Valle and the Yungas are tropical rainforest regions. The predominant tick species in Jujuy is Amblyomma cajennense and already has been reported as a vector of authochthonous cases of Rocky Mountain spotted fever (RMSF) in this province10. It is extensively distributed throughout Northwestern Argentina, including Jujuy Province, and nymphs and adults are frequently identified from tick bite surveys of humans9. In Jujuy and throughout Argentina, tick-borne diseases were underestimated by much of the general population and even by the medical community, until we published descriptions of several cases of RMSF and serological evidence of Ehrlichia chaffeensis10.
Tick paralysis is caused by over 40 species of ticks worldwide. Hard and soft bodied female ticks are thought to produce a neurotoxin capable of causing paralysis. In North America, tick paralysis in humans is usually caused by Dermacentor andersoni or Dermacentor variabilis5. In Australia, Ixodes holocyclus is responsible for most cases10. In Mexico tick paralysis caused by Amblyomma maculatum8. In Brazil TP was reported in cattle, sheep and goats, cajennense as the causative agent11. Clusters of TP among hunting dogs in Misiones Province, Argentina, have been also identified recently (Available from: http://www.misionesonline.net).
In this paper, clinical features of two cases of TP occurring during 1994 in Jujuy Province are described. Both patients were medical doctors who developed neurological symptoms associated with tick bite.
Patient 1 was a 40 year-old woman who experienced headache, facial numbness, dizziness, and malaise four days after visiting a tick-infested area in Jujuy. Physical examination revealed no fever, a right Bell’s palsy, and a small crusted lesion on her scalp where she had removed a tick two days earlier. A complete blood cell count, erythrocyte sedimentation rate, chemistry profiles, and urinalysis were normal. Clinical improvement occurred after the fourth day of tick removal.
Patient 2 was a 41-year-old woman who experienced dizziness, irritability, slurred speech, and partial recent memory loss five days after removing a tick. She subsequently developed gait instability, inability to walk and drive her car, followed by severe malaise, arthromyalgias, headache, hypoacusia, blurred vision, and diplopia. On physical examination, she was afebrile, alert, and cooperative but bradypsychic, hypoacusic, and dysarthric. Her third, sixth, and eighth cranial nerves were affected. Horizontal nystagmus was present. There was a small scar behind the right ear where she had removed the tick. No meningeal signs were present; she was bradykinetic and ataxic, with abnormal gait and unable to walk and with a positive Romberg’s test and abnormal coordinating tests. A mild left upper limb palsy, hyporreflexia and mild hepatomegaly was present. A complete blood cell count, erythrocyte sedimentation rate, chemistry profiles, and urinalysis were normal. Blood cultures were negative. She has recovered after twenty days after onset of symptoms. See below neurological manifestations (Table 1).
In contrast to the dramatic, life threatening symptoms that follow soon after snake or spider bite, tick paralysis evolves slowly but it can be equally deadly in a 10% of the patients1.
Tick paralysis has been frequently misdiagnosed, and this envenomation syndrome must be included in the differential diagnoses of any patient presenting with an ascending symmetrical paralysis.
The spectrum of neurological manifestations described for both of the patients, occurring two days after tick bite or exposure, the absence of fever, and the presence of normal laboratory values are keys to diagnosis TP. It is important to emphasize that the diagnosis is entirely clinical, as are the diagnoses of Kawasaki disease or rheumatic fever and several other syndromes. In Jujuy Province, we also must consider other endemic diseases, including lactrodectism, rickettsioses, Guillain-Barré syndrome, rabies, heavy metal intoxication, and insecticide poisoning.
The two patients visited tick-infected areas within 10km of each other as was described in Colorado, USA. Case 1 presented with an isolated facial Bell’s palsy, which has been described in other cases of TP6. Case 2 presented with a more severe clinical picture that included gait instability, inability to walk, muscular hypotonia, and hyporeflexia as reported previously1. The clinical course of paralysis produced by this tick is different from that of ticks in other continents. Australian TP differs from the North American variety in that patients are more acutely ill, paralysis may continue and progress for 48 hours after tick removal, and recovery also is prolonged5. Some patients become worse after tick removal1. Both cases described here showed features compatible with Australian variety of TP5.
Cases of tick paralysis are not very common in humans compared to animals2. Many times, the tick is not identified therefore, just demonstrating the presence of a tick on the body is not sufficient to make a defin-itive diagnosis of tick paralysis3. Until now we do not know the cusative agent of TP in Argentina.
I thank Christopher D. Paddock, Centers for Disease Control and Prevention, Atlanta, Georgia, USA. Research Medical Officer, Infectious Disease Pathology Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, for critically reviewing the manuscript.
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Received in 30/08/2011
Accepted in 14/12/2011