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Tick-borne encephalitis complicated by monoplegia and sensorineural deafness
Journal of Infection (1991) 22, 81-86
CASE REPORT T i c k - b o r n e e n c e p h a l i t i s c o m p l i c a t e d by m o n o p l e g i a and s e n s o r i n e u r a l deafness A. N. B. McNair and J. L. Brown
Department of Medicine, St Mary's Hospital Medical School (Imperial College of Science, Technology and Medicine), Praed Street, London W2 I N Y , U.K. Accepted for publication 3 July 199o Summary Tick-borne encephalitis (TBE) is rarely seen in Britain. We report a case of TBE in a 44-year-old Swedish woman presenting to an accident and emergency department in London. The clinical features of the case, while in many ways typical, were nonspecific and led to difficulty in early diagnosis. The course of the illness was complicated by monoplegia and evidence of bulbar involvement with sensorineural deafness. The last is a very rare manifestation of TBE. With increasing foreign travel, TBE is likely to present more commonly in the U.K. and should be considered in any case of febrile illness with neurological complications following travel abroad. Serological tests to aid early diagnosis should be more readily available.
Introduction Acute encephalitis is characterised by fever, headache, depression of consciousness, seizures and pleocytosis in the CSF. T w o forms of the disease exist u acute viral encephalitis, an inflammatory disease of the grey matter, and post-infectious encephalomyelitis, a demyelinative disease of the white matter. O f the agents k n o w n to cause these disorders, herpes simplex virus accounts for about IO % of cases but 5o % of the fatalities. M o s t of the remaining fatalities are caused by the a r t h r o p o d - b o r n e viruses (alpha-, flavi- and bunyaviridae). Poliomyelitis is n o w rare in the developed world. I n the past, post-infectious encephalomyelitis accounted for about o n e - t h i r d of cases of encephalitis, having been associated with vaccinia, measles, varicella and rubella. T o d a y , in the developed world, the condition is m o r e often associated with u p p e r respiratory tract infection and varicella. 1 Flavivirus infections are transmitted to h u m a n beings by mosquitoes (eg, yellow fever, dengue fever and Japanese B encephalitis) or by ticks ( T B E and some haemorrhagic fever viruses) (Table I). Central E u r o p e a n T B E is endemic f r o m Scandinavia to the western U.S.S.R. Cases in Scandinavia were originally described in the i94os, 2 the causative agent having been first isolated from the vector, Ixodes ricinus, in I959 .3 T h e proportion of ticks carrying the T B E virus varies considerably but m a y be as high as r in 2oo. 4 T h e illness classically follows a diphasic course. T h e first phase arises after an incubation period of 7-IO days and is characterised by fever, headache, o163-4453/91/oioo8I +06 $03.00/0 4
© I99I The British Society for the Study of Infection JIN 22
82
A. N. B. M C N A I R A N D J. L. B R O W N
Table I Tick-borne flaviviruses Viruses Louping ill Central European tick-borne Far eastern Russian Langat Powassan Negishi Omsk haemorrhagicfever Kyasanur forest
Presentation
Geographical distribution
Encephalitis Encephalitis Encephalitis Encephalitis Encephalitis Encephalitis Haemorrhagic fever Haemorrhagic fever
British Isles Central Europe Eastern U.S.S.R. Malaysia North America Japan Central U.S.S.R. India
malaise and myalgia. These symptoms persist for 5-Io days and are followed by an asymptomatic interval of up to 25 days. T h e major symptoms, which constitute the second phase, include reduced consciousness, meningism and focal neurological signs. Cases are seen in which either the first or second phase is inapparent. In the latter instance, the infection is abortive. Asymptomatic infection appears to be common. 3 L u m b a r puncture, E M G and E E G findings are all non-specific, although diagnosis is readily confirmed by demonstration of an IgM antibody response to the virus. While the mortality from TBE is low at I or 2 %2.5 its morbidity is high and long-term sequelae including lethargy, depression and complete paralysis of limbs occasionally occur. We describe a case of TBE presenting in the U.K. and which was initially difficult to diagnose. T h e clinical features, differential diagnosis and investigations are discussed. Case report
A 44-year-old Swedish nurse was admitted to hospital with an 8 days' history of headache and a z days' history of weakness in the right arm. She had arrived in England 2 days before her admission to hospital. Twelve days earlier, after walking in a wood outside Stockholm, she had discovered a hard tick adherent to the left side of her neck. Two days later, she felt generally unwell with headache, mild photophobia and anorexia, but her symptoms improved enough for her to visit the U.K. Shortly after arrival, the symptoms returned and were accompanied by weakness of the right arm. On the day of admission, the headache had become more severe and she had vomited four times. T h e rigt~t arm had become weaker and also numb and she had numbness around the nose. There was no medical history of note, although she was uncertain about polio vaccination. She was not taking any medication but had a history of allergy to chloroquine, which had caused pruritus, and to penicillin, which had caused an urticarial skin rash. On examination, the patient was flushed, with a temperature of 37"5 °C. T h e cardiovascular and respiratory systems and the abdomen were normal. She
Complications of tick-borne encephalitis
83
was orientated and alert without neck stiffness. Fundoscopic examination of the eyes was normal. T h e r e was n u m b n e s s to light touch and pin-prick over the nose, right arm and shoulder. T h e power of all right arm movements was reduced to 3/5. T h e biceps and supinator reflexes on the right side were absent while the triceps reflex was reduced. A full blood count as well as urea and electrolyte values and a chest radiograph were all normal. At lumbar puncture the CSF pressure was I8 cm water and examination of the fluid revealed a white cell count of 250 × IO6/1 (35 % lymphocytes), IO x ion/1 red cells, a glucose concentration of 3"3 mmol/1 (blood glucose concentration 5"8 mmol/1) and a protein concentration of o'94 g/1. Organisms were not seen. In view of the history of contact with a tick, an initial diagnosis of lymphocytic meningo-radiculitis due to Borrelia burgdorferi infection (Bannwarth's syndrome) was made, although viral illness with radiculoneuropathy (possibly due to Epstein-Barr virus 6 or HIV) or atypical Guillain-Barr6 syndrome were also considered. T h e incubation period of B. burgdorferi infection, however, would have required the patient to have been bitten earlier in the year by an infected tick. T h e following day she had become drowsy and confused, with a temperature of 39 °C and obvious neck stiffness. Power in the right arm was lost altogether and she developed bilateral facial and ocular palsies. A C T scan of the brain was normal and an E E G performed at this time did not show any specific abnormalities. Repeated lumbar puncture demonstrated a rise in CSF pressure to 33 cm water, 74 × Io6/1 white cells (95 % lymphocytes), a protein concentration of I'2 g/1 and no visible organisms. T h e revised differential diagnoses for this case are shown in Table II. Viral encephalitis, probably tick-borne, seemed to be the most likely cause of the illness, but consideration was given to tuberculous meningitis, listeria rhombencephalitis and herpes encephalitis, since these alternatives were treatable. T h e patient therefore received intravenous cefotaxime (for neuroborreliosis), chloramphenicol (for listeriosis in view of known penicillin allergy), acyclovir, rifampicin and intramuscular isoniazid and streptomycin (75o mg od). Pyrazinamide and pyridoxine were given through a nasogastric tube as short-course chemotherapy for tuberculous meningitis. 7 T h e results of blood and CSF cultures were negative while poliovirus was not detected in the faeces and V D R L / T P H A tests were negative. Serological tests for 'atypical pneumonias', B. burgdorferi (ELISA) and Epstein-Barr virus (IgM) infections were negative also. T h e r e were no risk factors in the patient's history to suggest a diagnosis of dumb rabies. Over the next 3 days, the patient's level of consciousness improved with resolution of the facial and ocular palsies. Even so, she complained of deafness in the right ear, and weakness of the arm persisted. Antituberculous therapy was discontinued as the speed of recovery was believed to be incompatible with mycobacterial infection. An audiogram demonstrated hearing loss at all frequencies [Fig. I(a)], inconsistent with streptomycin ototoxicity. Electromyography showed absence of spontaneous motor activity and suggested neuropraxic rather than axonal nerve damage, the former having a more favourable prognosis. 4-2
h.
84
hi. B. MCNAIR
AN])
]. L. BROWN
Table II Possible infectious aetiologies for the case
reported
Bacterial Lymphocytic meningoradiculitis due to Borrelia burgdorferi infection Tuberculous meningitis Listeria rhombencephalitis Neurosyphilis Mycoplasma or Coxiella infection
Viral/viral-related Tick-borne encephalitis (Central European type) Other acute viral encephalitides (herpes, dumb rabies) Enteroviral meningomyelitis (polio virus, coxsackie virus) Viral illness with radiculoneuropathy (Epstein-Barr virus, HIV) Atypical Guillain-Barr6 syndrome
(a) 0 I0 20 :50 40 50 60 70 80 90 I00 I10
o
b)
IO 2o 30 40 50 60 70
I
I
128 256
1
I
I
I
I
512 1024 20484096 8192.
8o 9o i ioo Ii tlO~
I
I
128 256
I
I
I
I
I
512 1024 2048 4096 8192
Frequency(Hz)
Fig. L Audiograms showing (a) hearing loss at all frequencies in the case described and (b) typical hearing loss at high frequencies in aminoglycoside ototoxicity. ( - - O - - ) , Right ear; ( - - x - - ) , left ear.
On the patient's return to Sweden, an I g M E L I S A in respect of T B E virus was found to be strongly positive. Discussion T h i s case illustrates many of the characteristic features of tick-borne encephalitis. T h e history of a tick bite, present in approximately I / 2 cases of T B E , was typical. Moreover, the illness ran a diphasic course as reported in about 3 / 4 cases.5 Headache, neck-stiffness (usually not marked), an altered level of consciousness, high fever ( > 39 °C) and lymphocytosis in the C S F were other c o m m o n features present in this case. T h e proportion of cases developing paresis has been reported as 5 % in one series from Finland s and 25 % in another from Sweden. 5 It may depend on the virulence of local strains of the virus. Paralysis is usually confined to one arm and is transient, although involvement of cranial nerves, the legs and the autonomic nervous system have all been described. Occasionally, weakness is permanent. 9
Complications of tick-borne encephalitis
85
In our case, there were several u n c o m m o n features. Firstly, the patient presented in D e c e m b e r whereas most infections in Scandinavian countries (over 8o %) appear from July to September. ~ A second atypical feature was the sensorineural deafness. Cranial nerve m o t o r involvement, particularly affecting the eye, facial and pharyngeal m u s c u l a t u r e is not u n c o m m o n but sensory manifestations are rare, while sensorineural deafness has not previously been reported. T h e audiogram was typical of an auditory n e u r o p a t h y but did not suggest damage induced by streptomycin, which p r e d o m i n a n t l y affects the high frequencies [Fig. I (b)]. T h e dose of streptomycin we used was low, the duration of therapy was short and the patient's renal function was normal. T h i s case illustrates the difficulties in establishing the diagnosis, since the clinical features were non-specific and the critical serological test was not readily available. Neuroborreliosis could not at first be excluded despite the absence of a history of a rash which is not always present. 1° F u r t h e r m o r e , although the time course would have been atypical, earlier tick bites m a y have gone unnoticed. Listeriosis n and tuberculosis m a y both give rise to focal neurological signs and be accompanied by C S F findings similar to those in this case. On the patient's r e t u r n to Sweden, the diagnosis was confirmed by a strongly positive test for I g M antibody to T B E . I f such a test had been more readily available in the U . K . , the need for potentially h a r m f u l empirical antibiotic t h e r a p y m i g h t have been avoided. Indeed, there is evidence to suggest that some aminoglycoside antibiotics, including streptomycin, m a y exert an activating effect on T B E virus. 12 Finally, we wish to draw attention to the apparent absence of an adequate facility for the rapid diagnosis of this infection in the U . K . at the present time. References I. Johnson RT, Griffin DE, Gendleman HE. Postinfectious encephalomyelitis. Semin Neuro I985; 5: 18°-19o-
2. Wahlberg P, Saikku P, Brummer-Korvenkontio M. Tick-borne encephalitis in Finland. The clinical features of Kumlinge disease during 1959 to 1987. J Intern Med 1989; 225: I73-I77.
3- Oker-Blom N, Kaarlainen L, Brummer-Korvenkontio Met al. Isolation and occurrence of viruses of the tick-borne encephalitis complex in Finland. In: Libikova H, Ed. Biology of viruses of the tick-borne encephalitis complex. New York: Academic Press, I96O : II, 423-429. 4. Brummer-Korvenkontio M, Saikku P, Korhonen P e t al. Arboviruses in Finland. I. Isolation of TBE viruses from arthropods, vertebrates and patients. Am J Trop Med Hyg 1973; 22: 382-389. 5. Zeipel GV, Svedmyr A, Holmgren B, Lindahl J. Tick-borne meningoencephalomyelitis in Sweden. Lancet 1959 : ii: IO4. 6. Brown J. Brachial neuritis following infection with Epstein-Barr virus. J Infect I987; 15: I73-I76. 7. Phuapradit P, Vejjajiva A. Treatment of tuberculous meningitis: role of short-course chemotherapy. Q J Med 1987; 62 (new series): 249-258. 8. Wahlberg P, Salminen A, Weckstrom Pet al. Diphasic tick-borne meningoencephalitis, Kumlinge Disease, in the Aland Islands. Diagnosis, clinical features and epidemiology. Acta Medica Scand 1964; 412 (Suppl): 275-286. 9. Grandstrom M, Gradien M, Saikku P. Early diagnosis of tick-borne encephalitis by demonstration of specific IgM antibodies. Scand J Infect Dis I978 ; IO : 97-1oo.
86
A . N . B . M c N A I R AND J. L. B R O W N
IO. Steere AC. Medical congress: Lyme disease. N EnglJ Med 1989; 327 (9): 586-596. II. Pollock S, Pollock T, Harrison M. Infection of the central nervous system by Listeria monocytogenes : a review of 54 adult and juvenile cases. Q J Med I n (new series) : 331-34o. 12. Malenko GV, Pogodina VV. The search for antibiotics not exerting activating action in the persistence of the tick-borne encephalitis virus. Vopr Virusol 1989; 34 (2): 197-2oo (Russian).
CASE REPORT T i c k - b o r n e e n c e p h a l i t i s c o m p l i c a t e d by m o n o p l e g i a and s e n s o r i n e u r a l deafness A. N. B. McNair and J. L. Brown
Department of Medicine, St Mary's Hospital Medical School (Imperial College of Science, Technology and Medicine), Praed Street, London W2 I N Y , U.K. Accepted for publication 3 July 199o Summary Tick-borne encephalitis (TBE) is rarely seen in Britain. We report a case of TBE in a 44-year-old Swedish woman presenting to an accident and emergency department in London. The clinical features of the case, while in many ways typical, were nonspecific and led to difficulty in early diagnosis. The course of the illness was complicated by monoplegia and evidence of bulbar involvement with sensorineural deafness. The last is a very rare manifestation of TBE. With increasing foreign travel, TBE is likely to present more commonly in the U.K. and should be considered in any case of febrile illness with neurological complications following travel abroad. Serological tests to aid early diagnosis should be more readily available.
Introduction Acute encephalitis is characterised by fever, headache, depression of consciousness, seizures and pleocytosis in the CSF. T w o forms of the disease exist u acute viral encephalitis, an inflammatory disease of the grey matter, and post-infectious encephalomyelitis, a demyelinative disease of the white matter. O f the agents k n o w n to cause these disorders, herpes simplex virus accounts for about IO % of cases but 5o % of the fatalities. M o s t of the remaining fatalities are caused by the a r t h r o p o d - b o r n e viruses (alpha-, flavi- and bunyaviridae). Poliomyelitis is n o w rare in the developed world. I n the past, post-infectious encephalomyelitis accounted for about o n e - t h i r d of cases of encephalitis, having been associated with vaccinia, measles, varicella and rubella. T o d a y , in the developed world, the condition is m o r e often associated with u p p e r respiratory tract infection and varicella. 1 Flavivirus infections are transmitted to h u m a n beings by mosquitoes (eg, yellow fever, dengue fever and Japanese B encephalitis) or by ticks ( T B E and some haemorrhagic fever viruses) (Table I). Central E u r o p e a n T B E is endemic f r o m Scandinavia to the western U.S.S.R. Cases in Scandinavia were originally described in the i94os, 2 the causative agent having been first isolated from the vector, Ixodes ricinus, in I959 .3 T h e proportion of ticks carrying the T B E virus varies considerably but m a y be as high as r in 2oo. 4 T h e illness classically follows a diphasic course. T h e first phase arises after an incubation period of 7-IO days and is characterised by fever, headache, o163-4453/91/oioo8I +06 $03.00/0 4
© I99I The British Society for the Study of Infection JIN 22
82
A. N. B. M C N A I R A N D J. L. B R O W N
Table I Tick-borne flaviviruses Viruses Louping ill Central European tick-borne Far eastern Russian Langat Powassan Negishi Omsk haemorrhagicfever Kyasanur forest
Presentation
Geographical distribution
Encephalitis Encephalitis Encephalitis Encephalitis Encephalitis Encephalitis Haemorrhagic fever Haemorrhagic fever
British Isles Central Europe Eastern U.S.S.R. Malaysia North America Japan Central U.S.S.R. India
malaise and myalgia. These symptoms persist for 5-Io days and are followed by an asymptomatic interval of up to 25 days. T h e major symptoms, which constitute the second phase, include reduced consciousness, meningism and focal neurological signs. Cases are seen in which either the first or second phase is inapparent. In the latter instance, the infection is abortive. Asymptomatic infection appears to be common. 3 L u m b a r puncture, E M G and E E G findings are all non-specific, although diagnosis is readily confirmed by demonstration of an IgM antibody response to the virus. While the mortality from TBE is low at I or 2 %2.5 its morbidity is high and long-term sequelae including lethargy, depression and complete paralysis of limbs occasionally occur. We describe a case of TBE presenting in the U.K. and which was initially difficult to diagnose. T h e clinical features, differential diagnosis and investigations are discussed. Case report
A 44-year-old Swedish nurse was admitted to hospital with an 8 days' history of headache and a z days' history of weakness in the right arm. She had arrived in England 2 days before her admission to hospital. Twelve days earlier, after walking in a wood outside Stockholm, she had discovered a hard tick adherent to the left side of her neck. Two days later, she felt generally unwell with headache, mild photophobia and anorexia, but her symptoms improved enough for her to visit the U.K. Shortly after arrival, the symptoms returned and were accompanied by weakness of the right arm. On the day of admission, the headache had become more severe and she had vomited four times. T h e rigt~t arm had become weaker and also numb and she had numbness around the nose. There was no medical history of note, although she was uncertain about polio vaccination. She was not taking any medication but had a history of allergy to chloroquine, which had caused pruritus, and to penicillin, which had caused an urticarial skin rash. On examination, the patient was flushed, with a temperature of 37"5 °C. T h e cardiovascular and respiratory systems and the abdomen were normal. She
Complications of tick-borne encephalitis
83
was orientated and alert without neck stiffness. Fundoscopic examination of the eyes was normal. T h e r e was n u m b n e s s to light touch and pin-prick over the nose, right arm and shoulder. T h e power of all right arm movements was reduced to 3/5. T h e biceps and supinator reflexes on the right side were absent while the triceps reflex was reduced. A full blood count as well as urea and electrolyte values and a chest radiograph were all normal. At lumbar puncture the CSF pressure was I8 cm water and examination of the fluid revealed a white cell count of 250 × IO6/1 (35 % lymphocytes), IO x ion/1 red cells, a glucose concentration of 3"3 mmol/1 (blood glucose concentration 5"8 mmol/1) and a protein concentration of o'94 g/1. Organisms were not seen. In view of the history of contact with a tick, an initial diagnosis of lymphocytic meningo-radiculitis due to Borrelia burgdorferi infection (Bannwarth's syndrome) was made, although viral illness with radiculoneuropathy (possibly due to Epstein-Barr virus 6 or HIV) or atypical Guillain-Barr6 syndrome were also considered. T h e incubation period of B. burgdorferi infection, however, would have required the patient to have been bitten earlier in the year by an infected tick. T h e following day she had become drowsy and confused, with a temperature of 39 °C and obvious neck stiffness. Power in the right arm was lost altogether and she developed bilateral facial and ocular palsies. A C T scan of the brain was normal and an E E G performed at this time did not show any specific abnormalities. Repeated lumbar puncture demonstrated a rise in CSF pressure to 33 cm water, 74 × Io6/1 white cells (95 % lymphocytes), a protein concentration of I'2 g/1 and no visible organisms. T h e revised differential diagnoses for this case are shown in Table II. Viral encephalitis, probably tick-borne, seemed to be the most likely cause of the illness, but consideration was given to tuberculous meningitis, listeria rhombencephalitis and herpes encephalitis, since these alternatives were treatable. T h e patient therefore received intravenous cefotaxime (for neuroborreliosis), chloramphenicol (for listeriosis in view of known penicillin allergy), acyclovir, rifampicin and intramuscular isoniazid and streptomycin (75o mg od). Pyrazinamide and pyridoxine were given through a nasogastric tube as short-course chemotherapy for tuberculous meningitis. 7 T h e results of blood and CSF cultures were negative while poliovirus was not detected in the faeces and V D R L / T P H A tests were negative. Serological tests for 'atypical pneumonias', B. burgdorferi (ELISA) and Epstein-Barr virus (IgM) infections were negative also. T h e r e were no risk factors in the patient's history to suggest a diagnosis of dumb rabies. Over the next 3 days, the patient's level of consciousness improved with resolution of the facial and ocular palsies. Even so, she complained of deafness in the right ear, and weakness of the arm persisted. Antituberculous therapy was discontinued as the speed of recovery was believed to be incompatible with mycobacterial infection. An audiogram demonstrated hearing loss at all frequencies [Fig. I(a)], inconsistent with streptomycin ototoxicity. Electromyography showed absence of spontaneous motor activity and suggested neuropraxic rather than axonal nerve damage, the former having a more favourable prognosis. 4-2
h.
84
hi. B. MCNAIR
AN])
]. L. BROWN
Table II Possible infectious aetiologies for the case
reported
Bacterial Lymphocytic meningoradiculitis due to Borrelia burgdorferi infection Tuberculous meningitis Listeria rhombencephalitis Neurosyphilis Mycoplasma or Coxiella infection
Viral/viral-related Tick-borne encephalitis (Central European type) Other acute viral encephalitides (herpes, dumb rabies) Enteroviral meningomyelitis (polio virus, coxsackie virus) Viral illness with radiculoneuropathy (Epstein-Barr virus, HIV) Atypical Guillain-Barr6 syndrome
(a) 0 I0 20 :50 40 50 60 70 80 90 I00 I10
o
b)
IO 2o 30 40 50 60 70
I
I
128 256
1
I
I
I
I
512 1024 20484096 8192.
8o 9o i ioo Ii tlO~
I
I
128 256
I
I
I
I
I
512 1024 2048 4096 8192
Frequency(Hz)
Fig. L Audiograms showing (a) hearing loss at all frequencies in the case described and (b) typical hearing loss at high frequencies in aminoglycoside ototoxicity. ( - - O - - ) , Right ear; ( - - x - - ) , left ear.
On the patient's return to Sweden, an I g M E L I S A in respect of T B E virus was found to be strongly positive. Discussion T h i s case illustrates many of the characteristic features of tick-borne encephalitis. T h e history of a tick bite, present in approximately I / 2 cases of T B E , was typical. Moreover, the illness ran a diphasic course as reported in about 3 / 4 cases.5 Headache, neck-stiffness (usually not marked), an altered level of consciousness, high fever ( > 39 °C) and lymphocytosis in the C S F were other c o m m o n features present in this case. T h e proportion of cases developing paresis has been reported as 5 % in one series from Finland s and 25 % in another from Sweden. 5 It may depend on the virulence of local strains of the virus. Paralysis is usually confined to one arm and is transient, although involvement of cranial nerves, the legs and the autonomic nervous system have all been described. Occasionally, weakness is permanent. 9
Complications of tick-borne encephalitis
85
In our case, there were several u n c o m m o n features. Firstly, the patient presented in D e c e m b e r whereas most infections in Scandinavian countries (over 8o %) appear from July to September. ~ A second atypical feature was the sensorineural deafness. Cranial nerve m o t o r involvement, particularly affecting the eye, facial and pharyngeal m u s c u l a t u r e is not u n c o m m o n but sensory manifestations are rare, while sensorineural deafness has not previously been reported. T h e audiogram was typical of an auditory n e u r o p a t h y but did not suggest damage induced by streptomycin, which p r e d o m i n a n t l y affects the high frequencies [Fig. I (b)]. T h e dose of streptomycin we used was low, the duration of therapy was short and the patient's renal function was normal. T h i s case illustrates the difficulties in establishing the diagnosis, since the clinical features were non-specific and the critical serological test was not readily available. Neuroborreliosis could not at first be excluded despite the absence of a history of a rash which is not always present. 1° F u r t h e r m o r e , although the time course would have been atypical, earlier tick bites m a y have gone unnoticed. Listeriosis n and tuberculosis m a y both give rise to focal neurological signs and be accompanied by C S F findings similar to those in this case. On the patient's r e t u r n to Sweden, the diagnosis was confirmed by a strongly positive test for I g M antibody to T B E . I f such a test had been more readily available in the U . K . , the need for potentially h a r m f u l empirical antibiotic t h e r a p y m i g h t have been avoided. Indeed, there is evidence to suggest that some aminoglycoside antibiotics, including streptomycin, m a y exert an activating effect on T B E virus. 12 Finally, we wish to draw attention to the apparent absence of an adequate facility for the rapid diagnosis of this infection in the U . K . at the present time. References I. Johnson RT, Griffin DE, Gendleman HE. Postinfectious encephalomyelitis. Semin Neuro I985; 5: 18°-19o-
2. Wahlberg P, Saikku P, Brummer-Korvenkontio M. Tick-borne encephalitis in Finland. The clinical features of Kumlinge disease during 1959 to 1987. J Intern Med 1989; 225: I73-I77.
3- Oker-Blom N, Kaarlainen L, Brummer-Korvenkontio Met al. Isolation and occurrence of viruses of the tick-borne encephalitis complex in Finland. In: Libikova H, Ed. Biology of viruses of the tick-borne encephalitis complex. New York: Academic Press, I96O : II, 423-429. 4. Brummer-Korvenkontio M, Saikku P, Korhonen P e t al. Arboviruses in Finland. I. Isolation of TBE viruses from arthropods, vertebrates and patients. Am J Trop Med Hyg 1973; 22: 382-389. 5. Zeipel GV, Svedmyr A, Holmgren B, Lindahl J. Tick-borne meningoencephalomyelitis in Sweden. Lancet 1959 : ii: IO4. 6. Brown J. Brachial neuritis following infection with Epstein-Barr virus. J Infect I987; 15: I73-I76. 7. Phuapradit P, Vejjajiva A. Treatment of tuberculous meningitis: role of short-course chemotherapy. Q J Med 1987; 62 (new series): 249-258. 8. Wahlberg P, Salminen A, Weckstrom Pet al. Diphasic tick-borne meningoencephalitis, Kumlinge Disease, in the Aland Islands. Diagnosis, clinical features and epidemiology. Acta Medica Scand 1964; 412 (Suppl): 275-286. 9. Grandstrom M, Gradien M, Saikku P. Early diagnosis of tick-borne encephalitis by demonstration of specific IgM antibodies. Scand J Infect Dis I978 ; IO : 97-1oo.
86
A . N . B . M c N A I R AND J. L. B R O W N
IO. Steere AC. Medical congress: Lyme disease. N EnglJ Med 1989; 327 (9): 586-596. II. Pollock S, Pollock T, Harrison M. Infection of the central nervous system by Listeria monocytogenes : a review of 54 adult and juvenile cases. Q J Med I n (new series) : 331-34o. 12. Malenko GV, Pogodina VV. The search for antibiotics not exerting activating action in the persistence of the tick-borne encephalitis virus. Vopr Virusol 1989; 34 (2): 197-2oo (Russian).