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Case report: TBE-virus infections concurrently acquired by father and son in Northern Germany
Zent.bl. Bakteriol. 289, 628-631 (1999) © Urban & Fischer Verlag http://www.nrbanfischer.de/jonrnals/zblbakteriol
Zentralblatt fUr
Extended Summary
Case Report: TBE-virus Infections Concurrently Acquired by Father and Son in Northern Germany Michael Krebs, Sebastian Pornschlegel, and Bernd Holdorff Department of Neurology, Schlosspark-Klinik Berlin, Germany
In the last few years, reports on tick-borne encephalitis (TBE) in Germany have been noted mostly from Bavaria and Baden-Wiirttemberg (4) (Fig. 1). Few cases were reported from elsewhere, e. g. from the Saarland (6, 7) and Hesse (3). After a period of high morbidity between 1960 and 1970 the prev alence of TBE-infections and TBE-virus in Ixodes ricinus is now very low in eastern Germany (5). Although antibodies against TBE-virus were detected in roe deer (2), clinical cases of TBE in humans have not been found in Berlin. Also, no TBE-infections have been reported from Schleswig-Holstein. We report on a 49-year-old male from Berlin who was on a sailing-trip to gether with his son at the Baltic Sea coast of Schleswig-Holstein in May 1998. About 2 weeks later, the patient developed fever up to 39°C, cephalgia and arthralgia and was admitted to the medical department of the Free University of Berlin. The patient did not remember a tick-bite. In cerebrospinal fluid (CSF) a pleocytosis of up to 305/fll was found, so a meningitis was diagnosed. Serum tests showed a significant increase in TBE antibody titers (Table 1): In itial TBE-IgM was positive and TBE-IgG negative, 10 days later both IgM and IgG were positive. In CSF TBE-antibodies were negative. No significant titers of neurotropic viruses (CMV, EBV, VZV, HSV, ECHO, Coxsackie A and B, enterovirus, influenza virus A and B, polio, HAV, HBV and HCV) were found. In the EEG, a mild to moderate slowing of the background activity was found. Cranial CT and MRI showed normal findings. A few days later the patient complained about sciatica, and a prolapsed intervertebral disc L4/5 was seen on MRI. Because of a potential simultaneous infection with B. burgdorferi, the patient was treated with ceftriaxone for 3 weeks, after which he recovered from meningitis and was discharged from the hospital. Five weeks after onset of meningitis, the patient developed problems with orientation and problem-solving as well as exhibiting hyperphagia. Further0934-8840/99/289/5-7-628 $12.00/0
TBE case report
629
endemic areas of TBE-infections single cases of TBE-infections regions where our patient possibly acquired his TBE-infection Fig.1. Clinical cases of TBE in Germany; based on (1).
more, he had intensive sexual imaginations and developed increased sexual activities, such as frequent masturbation. On the day of admission he felt worse and was referred to our hospital by his neurologist. The patient had a history of ascending cholangiohepatitis in 1970 and an endogenous depres sion in 1994 which had been treated with tricyclic antidepressants. On neuro logical examination the patient showed only signs of a radicular L5-syndrome
630
M. Krebs et al.
Table 1. The patient's serum titers of TBE-antibodies 26.6.98 TBE-CFT TBE-IgM (ELISA) TBE-IgG (ELISA)
29.6.98
06.7.98
1:10
1 :20
1:40
+
+ (+)
+ +
31.7.98
+ +
+ positive; (+) borderline; - negative.
(slight paresis of the right extensor hallucis longus muscle; reduced perception on the medial side of the right foot). Furthermore he showed reduced atten tion, concentration and drive, as well as having mild deficits in his short-term memory. His mood was elevated. On thinking, he showed flightiners of ide as, as well as loosening of associations and ideas of reference. No manifest psychotic symptoms like delusions or hallucinations were detected. On serum tests for neurotropic viruses, TBE-IgM and TBE-IgG were positive (Table 1). A positive B. burgdorferi-IgM was detected. B. burgdorferi-IgG was negative as well as B. burgdorferi-IgM-Western blot. No acute infection with CMV, EBV, VZV, HSV, LCM, HIV 1 and 2 was detected. In CSF a slight pleocyto sis was found 12.3/f.,l1 (normal <5/f.,l1), total protein was 59 mg/dl (normal <45 mg/dl). Protein electrophoresis of the CSF revealed 2 possible bands; no bands were detected in serum. In CSF B. burgdorferi antibody-titers (IgM and IgG) were negative. A cranial MRI including MRI-angiography showed nor mal findings. On EEG we found a theta-focus over the occipital part of the left hemisphere. Because of the significant increase of TBE-antibody-titers (Table 1) we diagnosed an encephalitis due to TBE-infection; meninigitis complications could not be found on MRI. During the stay in our hospital the patient developed psychotic symptoms such as derealization and ideas of ref erence and became agitated and panic stricken. After treatment with haloper idole was initiated, the psychotic symptoms disappeared but the patient still showed mild cognitive deficits. The patient made a good recovery after par ticipating for 6 weeks in an intensive neuropsychological training programme. Interestingly, the patient's 18-year-old son had had a meningitis due to TBE virus infection with significant TBE-titer-increase two weeks earlier than the father. The son remembered the bite of a tick which was removed by his father during the sailing trip. Both denied a stay in TBE-endemic areas, e. g. south ern Germany, at the likely time of TBE-infection so both probably acquired their infection in Berlin or on a sailing trip at the Baltic Sea coast of Schleswig Holstein. This case underlines the possibility of an acquisition of TBE-infection in "untypical" areas of Germany such as Berlin or Schleswig-Holstein (Fig. 1). The concurrent manifestation in both father (meningoencephalitis) and son (meningitis) seems to be important for the estimate of infectivity. In "non endemic" areas, an encephalitis due to TBE-infection should only be diag-
TBE case report
631
nosed after careful exclusion of other possible causes like meningitis-compli cations and infections with neurotropic viruses (e. g. CMV, HSV, HIV). Key words: TBE-infection; northern Germany
References 1. Immuno-Baxter: FSME in Deutschland~Naturherdgebiete des FSME-Virus (1998) 2. Kahl, O. and A. C. Radda: Occurrence of tick-borne encephalitis (TBE) virus in Ber lin (West). Zentralbl. Bakteriol. Mikrobiol. Hyg. (A) 268 (1988) 482-486 3. Gzdemir, F. A., F. Rosenow, W. Slenczka, T. O. Kleine, and W. H. Oertel: Friihsom mermeningoenzephalitis (FSME) - Ausbreitung des Endemiegebietes nach Mittel hessen. Nervenarzt 70 (1999) 119-122 4. Roggendorf, M., P. Lenz, R. Kaiser, and G.]ager: Epidemiologische Situation der FSME in Bayern und Baden-Wiirttemberg. In: Durch Zecken iibertragbare Erkran kungen - FSME und Lyme-Borreliose, 3. Potsdamer Symposium. U. Siiss, ed.), pp. 7-19. Weller-Verlag: Schriesheim (1995) 5. Siiss, ]., H. Sinnecker, R. Sinnecker, D. Berndt, E. Zilske, G. Dedek, and L. Apitzsch: Epidemiology and ecology of tick-borne encephalitis in the eastern part of Germa ny between 1960 and 1990 and studies on the dynamics of a natural focus of tick borne encephalitis. Zbl. Bakt. 277 (1992) 224-235 6. Treib, j.: First case of tick-borne encephalitis (TBE) in the Saarland. Infection 22 (1994) 368-369 7. Treib, j., A. Haass, N. Mueller-Lantzsch, H. Ehrfeld, D. Mueller-Rheiland, R. Woes sner, G. Holzer, and K. Schimrigk: Tick-borne encephalitis (TBE) in the Saarland and the Rhineland-Palatinate. Infection 24 (1996) 242-244 Corresponding author: Michael Krebs, Dept. Neurology, SchlofSpark-Klinik Berlin, Germany
Zentralblatt fUr
Extended Summary
Case Report: TBE-virus Infections Concurrently Acquired by Father and Son in Northern Germany Michael Krebs, Sebastian Pornschlegel, and Bernd Holdorff Department of Neurology, Schlosspark-Klinik Berlin, Germany
In the last few years, reports on tick-borne encephalitis (TBE) in Germany have been noted mostly from Bavaria and Baden-Wiirttemberg (4) (Fig. 1). Few cases were reported from elsewhere, e. g. from the Saarland (6, 7) and Hesse (3). After a period of high morbidity between 1960 and 1970 the prev alence of TBE-infections and TBE-virus in Ixodes ricinus is now very low in eastern Germany (5). Although antibodies against TBE-virus were detected in roe deer (2), clinical cases of TBE in humans have not been found in Berlin. Also, no TBE-infections have been reported from Schleswig-Holstein. We report on a 49-year-old male from Berlin who was on a sailing-trip to gether with his son at the Baltic Sea coast of Schleswig-Holstein in May 1998. About 2 weeks later, the patient developed fever up to 39°C, cephalgia and arthralgia and was admitted to the medical department of the Free University of Berlin. The patient did not remember a tick-bite. In cerebrospinal fluid (CSF) a pleocytosis of up to 305/fll was found, so a meningitis was diagnosed. Serum tests showed a significant increase in TBE antibody titers (Table 1): In itial TBE-IgM was positive and TBE-IgG negative, 10 days later both IgM and IgG were positive. In CSF TBE-antibodies were negative. No significant titers of neurotropic viruses (CMV, EBV, VZV, HSV, ECHO, Coxsackie A and B, enterovirus, influenza virus A and B, polio, HAV, HBV and HCV) were found. In the EEG, a mild to moderate slowing of the background activity was found. Cranial CT and MRI showed normal findings. A few days later the patient complained about sciatica, and a prolapsed intervertebral disc L4/5 was seen on MRI. Because of a potential simultaneous infection with B. burgdorferi, the patient was treated with ceftriaxone for 3 weeks, after which he recovered from meningitis and was discharged from the hospital. Five weeks after onset of meningitis, the patient developed problems with orientation and problem-solving as well as exhibiting hyperphagia. Further0934-8840/99/289/5-7-628 $12.00/0
TBE case report
629
endemic areas of TBE-infections single cases of TBE-infections regions where our patient possibly acquired his TBE-infection Fig.1. Clinical cases of TBE in Germany; based on (1).
more, he had intensive sexual imaginations and developed increased sexual activities, such as frequent masturbation. On the day of admission he felt worse and was referred to our hospital by his neurologist. The patient had a history of ascending cholangiohepatitis in 1970 and an endogenous depres sion in 1994 which had been treated with tricyclic antidepressants. On neuro logical examination the patient showed only signs of a radicular L5-syndrome
630
M. Krebs et al.
Table 1. The patient's serum titers of TBE-antibodies 26.6.98 TBE-CFT TBE-IgM (ELISA) TBE-IgG (ELISA)
29.6.98
06.7.98
1:10
1 :20
1:40
+
+ (+)
+ +
31.7.98
+ +
+ positive; (+) borderline; - negative.
(slight paresis of the right extensor hallucis longus muscle; reduced perception on the medial side of the right foot). Furthermore he showed reduced atten tion, concentration and drive, as well as having mild deficits in his short-term memory. His mood was elevated. On thinking, he showed flightiners of ide as, as well as loosening of associations and ideas of reference. No manifest psychotic symptoms like delusions or hallucinations were detected. On serum tests for neurotropic viruses, TBE-IgM and TBE-IgG were positive (Table 1). A positive B. burgdorferi-IgM was detected. B. burgdorferi-IgG was negative as well as B. burgdorferi-IgM-Western blot. No acute infection with CMV, EBV, VZV, HSV, LCM, HIV 1 and 2 was detected. In CSF a slight pleocyto sis was found 12.3/f.,l1 (normal <5/f.,l1), total protein was 59 mg/dl (normal <45 mg/dl). Protein electrophoresis of the CSF revealed 2 possible bands; no bands were detected in serum. In CSF B. burgdorferi antibody-titers (IgM and IgG) were negative. A cranial MRI including MRI-angiography showed nor mal findings. On EEG we found a theta-focus over the occipital part of the left hemisphere. Because of the significant increase of TBE-antibody-titers (Table 1) we diagnosed an encephalitis due to TBE-infection; meninigitis complications could not be found on MRI. During the stay in our hospital the patient developed psychotic symptoms such as derealization and ideas of ref erence and became agitated and panic stricken. After treatment with haloper idole was initiated, the psychotic symptoms disappeared but the patient still showed mild cognitive deficits. The patient made a good recovery after par ticipating for 6 weeks in an intensive neuropsychological training programme. Interestingly, the patient's 18-year-old son had had a meningitis due to TBE virus infection with significant TBE-titer-increase two weeks earlier than the father. The son remembered the bite of a tick which was removed by his father during the sailing trip. Both denied a stay in TBE-endemic areas, e. g. south ern Germany, at the likely time of TBE-infection so both probably acquired their infection in Berlin or on a sailing trip at the Baltic Sea coast of Schleswig Holstein. This case underlines the possibility of an acquisition of TBE-infection in "untypical" areas of Germany such as Berlin or Schleswig-Holstein (Fig. 1). The concurrent manifestation in both father (meningoencephalitis) and son (meningitis) seems to be important for the estimate of infectivity. In "non endemic" areas, an encephalitis due to TBE-infection should only be diag-
TBE case report
631
nosed after careful exclusion of other possible causes like meningitis-compli cations and infections with neurotropic viruses (e. g. CMV, HSV, HIV). Key words: TBE-infection; northern Germany
References 1. Immuno-Baxter: FSME in Deutschland~Naturherdgebiete des FSME-Virus (1998) 2. Kahl, O. and A. C. Radda: Occurrence of tick-borne encephalitis (TBE) virus in Ber lin (West). Zentralbl. Bakteriol. Mikrobiol. Hyg. (A) 268 (1988) 482-486 3. Gzdemir, F. A., F. Rosenow, W. Slenczka, T. O. Kleine, and W. H. Oertel: Friihsom mermeningoenzephalitis (FSME) - Ausbreitung des Endemiegebietes nach Mittel hessen. Nervenarzt 70 (1999) 119-122 4. Roggendorf, M., P. Lenz, R. Kaiser, and G.]ager: Epidemiologische Situation der FSME in Bayern und Baden-Wiirttemberg. In: Durch Zecken iibertragbare Erkran kungen - FSME und Lyme-Borreliose, 3. Potsdamer Symposium. U. Siiss, ed.), pp. 7-19. Weller-Verlag: Schriesheim (1995) 5. Siiss, ]., H. Sinnecker, R. Sinnecker, D. Berndt, E. Zilske, G. Dedek, and L. Apitzsch: Epidemiology and ecology of tick-borne encephalitis in the eastern part of Germa ny between 1960 and 1990 and studies on the dynamics of a natural focus of tick borne encephalitis. Zbl. Bakt. 277 (1992) 224-235 6. Treib, j.: First case of tick-borne encephalitis (TBE) in the Saarland. Infection 22 (1994) 368-369 7. Treib, j., A. Haass, N. Mueller-Lantzsch, H. Ehrfeld, D. Mueller-Rheiland, R. Woes sner, G. Holzer, and K. Schimrigk: Tick-borne encephalitis (TBE) in the Saarland and the Rhineland-Palatinate. Infection 24 (1996) 242-244 Corresponding author: Michael Krebs, Dept. Neurology, SchlofSpark-Klinik Berlin, Germany