EP1015610A2 - Medicament for treating a manifested lyme disease - Google Patents

Abstract

The invention relates to a pharmaceutical composition for treating lyme disease comprising an antibody as an active agent. Said antibody is specifically for the 24kDa-antigen (OspC) from B. burgdorferi, preferably an antibody which is specifically for the 24kDa-antigen (OspC) from B. burgdorferi represented by the sequence corresponding to SEQ ID NO. 2.

Description

Medicines to treat overt Lyme disease

description

The invention relates to a pharmaceutical composition for the treatment of Lyme disease and a vaccine against Lyme disease, as well as a method for obtaining an active substance for treating Lyme disease and a method for obtaining a vaccine for Lyme disease.

Lyme disease is a tick-borne infectious disease caused by Spirochete Borrelia burgdorferi. The disease is a chronic progressive infection that affects many organs, such as the skin, central and peripheral nervous system, heart, liver, kidney, musculoskeletal system, and joints. Various symptoms, such as acute arthritis and neuroborreliosis, can disappear spontaneously, but usually recur episodically. Spirochetes have been isolated from untreated patients repeatedly, and there are numerous signs of persistent infections even after antibiotic therapy. Since reliable treatment of this disease through therapy with antibiotics is therefore difficult, great efforts are made to research the pathogen itself and the host's immune response to infection with B. burgdorferi. In the case of the presons affected by Lyme disease, a high titer of antibodies against B. burgdorferi is usually found in the course of the infection, but this does not provide any protection against the infection.

It was found that the outer surface lipoprotein A (OspA) from B. burgdorferi could be an effective vaccine for the prophylaxis of Lyme disease (EP 0 41 8 827). Laboratory studies in mice have shown that extensive protection against a disease in infection can be obtained by OspA-specific antibodies (Schaible et al., Proc. Natl. Acad. Sci. USA 87 (1 990), 3768-3772) . However, these antibodies are only effective if they are present at the time the pathogen is transmitted. One reason for this could be that OspA is mainly expressed on spirochetes in ticks, but is no longer expressed after transmission to a mammalian host. Consequently, OspA-specific antibodies can be used to prevent the transmission of the disease, but are ineffective and therefore unsuitable for therapeutic applications for the treatment of the outbreak. Recent studies show that after active immunization with recombinant OspC, mice could be protected against a tick-borne infection (Preac-Mursic et al., Infection 20 (1 992), 342-349; RD Gilmore et al., Infect. Immun. 64 (1,996), 2234-2239). However, the immunization protocol used there does not lead to the elimination of infectious spirochetes from the vector, as has been shown by OspA-specific antibodies.

The invention was therefore based on the object of providing a medicament for the treatment of Lyme disease.

This object is achieved according to the invention by a pharmaceutical composition for the treatment of Lyme disease, which is characterized in that it comprises as an active ingredient an antibody which is specific for the 24 kDa antigen (OspC) from B. burgdorferi. Surprisingly, it was found that spontaneous resolution of the disease and / or elimination of spirochetes in various mouse types was achieved using high titers of OspC-specific antibodies. The pharmaceutical composition for the treatment of Lyme disease preferably comprises, as an active ingredient, an antibody which is specific for the 24 kDa antigen (OspC) from B. burgdorferi and which is shown in SEQ ID NO. 2 sequence shown.

Surprisingly, it has been shown that the passive transfer of polyclonal OspC-reactive immune serum into B. burgdorferi-infected scid mice lead to complete resolution of chronic arthritis and carditis, such as elimination of the pathogen. A critical limit of OspC-specific antibodies, which is between 3 and 10 μg anti-OspC antibodies, seems to be important for an effective control of an infection. This means that spirochetes express OspC in the mammalian host and are sensitive to protective antibodies in the affected tissue during infection. Therefore, attacking OspC is relevant for successful therapeutic treatment of Lyme disease.

Previous studies have shown that immune sera from B. burgdorferi-infected mice only provided complete protection against disease and infection if they were administered before, but not if they had been inoculated with the pathogen. In the present invention it is shown that the spontaneous resolution of the infection with antibodies against OspC is possible, the spirochetes being inactivated in the vertebrate. Furthermore, it was found that it is possible to dissolve both arthritis and carditis using polyclonal OspC-specific immune sera and to cure existing spirochetin infections in CB-17 scid mice, regardless of whether the antibodies were present before the onset (e.g. 1 0 Days before infection) or, alternatively, at a time when the disease broke out completely (on the ninth day after infection) or it was a chronic illness (day 60 after infection). The complete resolution of the disease and elimination of the pathogen was dose-dependent and was achieved with 1 μg to 10 mg anti-OspC antibody / mouse, preferably 5 μg to 20 μg anti OspC antibody / mouse.

Inflammatory lesions on joints or in the heart of B. burgdorferi-inoculated scid mice were counteracted by polyclonal immune sera

Fully dissolved OspC, even if administered at a time. were sufficient for which there was a chronic illness, ie on the 60th day pi

The invention is explained below with reference to the figures in the drawing and the examples.

Figure description:

FIG. 1 shows a Western blot analysis of NMS and IS, which were used for passive immunization of C. B.-1 7 scid mice. Lane 1 shows a standard of mouse mAbs against Hsp70 (70 kDa), Hsp60 (60 kDa), Flagellin (41 kDa), OspB (34 kDa), OspA (31 kDa), OspC (24 kDa), pLA7 (20 kDa) and p7.5 (7.5 kDa). Lane 2: NMS collected from naive BALB / c mice. Lane 3: Polyclonal immune serum, formed in BALB / c mice, immunized with rLip-OspA in ABM2 adjuvant. Lane 4: Polyclonal IS generated in BALB / c mice immunized with rOspC in ABM2 adjuvant as described herein.

Figure 2 Kinetics of the occurrence of B. burgdorferi-specific (IgG) or OspC-specific (IgM / IgG) antibodies (A) and correlation analysis of serum contents of either total B. burgdorferi-specific or OspC-specific antibodies (IgG) and elimination of spirochetes from infected mice (B). AKR / N, C57BL / 6 and BALB / c mice (6 to 8 weeks old) were infected by syringe injection with 10 ³ spirochetes in the tail (sc). The levels of B. burgdorferi-specific (IgG) and OspC-specific antibodies (IgM and IgG) in sera from individual mice were determined by ELISA using either whole cell lysates (B. burgdorferi strain ZS7) or rOspC (ZS7) Substrates examined. The data represent the mean of individual serum samples examined (AKR / N and C57BL / c: 10 mice / group; BALB / c: 7 mice; A). Correlation between serum levels of total B. Burgdor feri-specific IgG antibodies, OspC-specific IgG antibodies (day 23 pi) and the ability to recultivate spirochetes from ear tissue (day 90 pi) were analyzed by correlation assay (B).

FIG. 3 shows the DNA sequence and the protein sequence of the 24 kDa antigen (OspC) from B. burgdorferi (SEQ ID NO. 2)

FIG. 4 shows the construction of the plasmid pG OspC-ZS, which contains the OspC gene.

Table 1

Different therapeutic effects of immune sera against OspA and OspC on established B. burgdorferi-

Infections of C.B.-17 scid mice

Table 2

Therapeutic effects of an immune serum against OspC 60 days after infection of C.B.-17 scid mice with

10 ³ B. burgdorferi-ZS7

Table 3

Histopathological examination of affected organs from individual infected scid mice after therapeutic treatment with immune sera

not tested

example 1

Materials and methods

a) Mice and infection with B. burgdorferi. Adult mice of the AKR / N (H-2 ^k ), C57BL / 6 (H-2 ^b ) strains,

BALB / c (H-2 ^d ) and CB-1 7 se (H-2 ^d ) were grown under specific pathogen-free conditions. Female animals between 6 and 8 weeks old were used for the experiments. The mice were subcutaneously (sc) with 1 × 10 ³ low-passage (two to four in vitro passages) organisms B. burgdorferi of the strain ZS7 (Schaible et al., Proc. Natl. Acad. Sci. USA 87 (1 990), 3768-3772) vaccinated in the tail.

b) Recombinant antigens. A complete recombinant lipidated OspA (rLip-OspA) from B. burgdorferi, strain ZS7, was prepared as described (Gern et al., Immunol. Lett. 39 (1 994), 249-258). A B. burgdorferi strain ZS7, a glutathione-S-transferase OspC fusion protein (rOspC), was prepared using known techniques (R. Wallich et al., Infect. Immun. 64 (1,995), 3327-3353).

c) Polyclonal immune serum.

BALB / c mice were inoculated with either 10 μg rLip-OspA or 10 μg rOspC in 1 00 / vl ABM2 adjuvant (Sebak, Aldenbach, Germany) and injected twice with the same antigen preparation

Refreshed every 10 days. The immune serum (IS) was collected over a period of approximately 2 months after the last refreshment and contained the following concentrations of OspA or OspC-specific antibodies (Ak), as with an ELISA using rLip-OspA or rOspC as Substrate was determined: Anti-OspA IS, 3.2 mg / ml or Anti-OspC IS, 300 / yg / ml. Normal mouse serum (NMS) was collected from naive BALB / c mice. The specificities the immune sera and NMS generated were verified by Western blot analysis. As shown in Figure 1 (lanes 3, 4), a polyclonal immune serum from either OspA or OspC-immunized mice reacted selectively with proteins with 31 kDa (OspA) or 24 kDa (OspC) from a total cell lysate of ZS7 spirochetes. No reactivity with NMS was found (Figure 1, lane 2).

d) Analysis of serum antibodies by ELISA and Western blot.

Serum antibodies against B. burgdorferi OspA or OspC were quantified by a solid phase ELISA as described in the prior art (Kramer et al., Immunobiol. 1 81 (1 990), 357-366), 1 μg / ml total cell lysate B. burgdorferi, strain ZS7, rLip-OspA (ZS7) or rOspC (ZS7) were used as substrates. Western blot analysis was carried out as described in the prior art (MM Simon et al., J. Infect. Dis. 1 64 (1 991), 1 23-1 32) using a total cell lysate from B. burgdorferi Strain ZS7 performed as an antigen preparation.

e) Passive transfer of immune serum to protect against and treat an infection.

For passive protection, 6-8 week old female CB-17 scid mice were injected intraperitoneally (ip) with either an OspA or an OspC-reactive polyclonal immune serum 1 hour before infection. Control mice received 100 // I NMS. For infection, the mice were injected into the tail with 1 × 10 ³ B. burgdorferi ZS7 organisms. Alternatively, for the passive treatment of an existing infection, scid mice were first infected with 1 × 10 ³ ZS7 spirochetes (sc), and then they were repeatedly administered (four times at 3 to 4 day intervals) different amounts of polyclonal immune serum, which was either OspA or Ospc specific (ip), starting on day 1 0, 1 9 or 60 after infection (pi). The animals were evaluated for the development of clinical arthritis in the tibiotarsal joints observed. The hardness of arthritis in the right and left tibiotarsal joints was assessed as follows: 4- 4-, severe; + moderately difficult; ±, mild swelling; (±), redness; -, no clinical signs.

At the indicated times, the mice were examined for the presence of spirochetes by culturing ear tissue samples, following the procedure described in the prior art (Sinsky et al., J. Clin. Microbiol. 27 (1 989), 1 723- 1 727).

For histopathological examinations, the mice were sacrificed at the times indicated after the infection. The tibiotarsal joint, the heart, the liver and the muscles adjacent to the tibiotarsal joint were fixed in 10% formaldehyde, embedded in paraffin and stained with hematoxylin and eosin. The inflamed lesions were rated as follows: 4- 4- 4-, very severe; 4- 4-, difficult; 4-, moderate; ±, mild; -, no.

Example 2 Results:

Three inbred mouse strains, AKR / N, BALB / c and C57BL / 6 with different sensitivity to a B. burgdorferi-induced disease (UE Schaible et al., Eur. J. Immunol. 21 (1 991), 2397- 2405) were infected with 1 0 ³ spirochetes. The kinetics of the specific antibody responses, the development of arthritis and the resistance of spirochetes were observed up to 90 days after infection. All animals vaccinated with B. burgdorferi were infected as shown by seroconversion (Figure 2A). All animals produced similar amounts of B. burgdorferi-specific IgG antibodies, which were first detectable on the 1st day after the infection and rose continuously during the entire observation period. Furthermore developed all mice have significant but variable amounts of OspC-specific IgM and IgG antibodies (Figure 2A). OspC-specific IgM antibodies were first detectable on the 4th day after the infection, peaked on the 1st day after the infection and then decreased to baseline values on the 24th day after the infection. OspC-specific IgG antibodies were first observed on day 1 pi with a peak on day 23 pi (maximum values for AKR / N, C57BL / 6: about 8 // g / ml; BALB / c: about 3 μg / ml). Antibody titers in AKR / N and C57BL / 6 mice decreased over time, but remained at detectable levels (approximately 3 // g / ml) up to 90 days pi. In contrast, BALB / c mice formed lower levels of OspC-specific IgG antibodies in the early phase of infection, but serum titers increased over time after infection. As expected from previous studies (Schaible et al., Immunol. Lett. 36 (1,993), 21 9-226; L. Gern et al., J. Infect. Dis. 1 67 (1 993), 971-975 ) antibodies to OspA were not detected in any of the sera from infected mice during the entire 90-day observation period, neither by ELISA nor by Western blot analysis using spirochetal lysate or recombinant OspA.

A close correlation between serum titers of anti-OspC antibodies and spontaneous resolution of the infection was found. As shown in Figure 2B, the amount of OspC-specific IgG antibodies in the 8 mice from which spirochetes could not be recultivated was considerably higher than in those from which positive cultures were obtained (10 ± 5 // g / ml versus 4.8 ± 2.8 / g / ml). On the other hand, no correlation was found between the total content of B. burgdorferi-specific IgG antibodies and the elimination of spirochetes. This shows that OspC-specific antibodies are able to inactivate spirochetes in vertebrates and fight infection. Example 3

Passive transfer experiments were performed to investigate whether it is possible to cure a proven B. burgdorferi infection in scid mice with polyclonal IS, which is specific for rOspC. A polyclonal immune serum specific for rLip-OspA served as a control. It was found that different dose amounts of OspC-specific antibodies were necessary for the prevention or treatment of the infection. Passive transfer of 3 μg OspC-specific antibodies in scid mice 1 hour before infection resulted in complete protection against the disease and infection in all examined mice (Table 1). As shown previously, complete protection was also observed with 3 μg OspA-specific antibodies, but not with normal mouse serum under similar conditions (Table 1 and MM Simon et al., J. Infect. Dis. 1 64 (1 991 ), 1 23-1 32). In contrast, repeated administration of 3 // g / mouse prevented OspC-specific antibodies (4 × at 3 to 4 day intervals), starting on the 10th day after the infection, a point in time when spirochetes spread and the inflammation of the joints and heart begins, only partially the development of clinical arthritis. Spirochetes could not be inactivated in this amount.

Therefore, immune sera containing 10 μg anti-OspC antibodies were used for the passive transfer experiments. As shown in Table 1, such repeatedly administered immune serum (10 µg, 4 times at 3 to 4 day intervals), starting on either the 10th or the 9th day after infection, completely prevented and healed Clinical arthritis occurred in all infected scid mice. Spirochetes could not be recultivated from the ear tissue samples. In contrast, and as expected from previous studies (Schaible et al., Proc. Natl. Acad. Sci. USA 87 (1 990), 3768-3772) had repeated passive transfer of similar amounts of anti-OspA- specific antibodies on day 10 or day 9 no effect on clinical arthritis and infection. It is highly remarkable and surprising that anti-OspC-specific antibodies were able to resolve a chronic illness and infection in mice. This is illustrated by the fact that the passive transfer of the respective immune serum, starting on day 60 pi, led to a considerable reduction in clinical arthritis within 10 days after treatment and to a practically complete dissolution in the following 30 days (Table 2 ). While the pathogen from the ear tissues of all infected scid mice could be recultivated prior to treatment (on day 38 pi), none of the samples contained the same animals taken on day 20 after antibody transfer (day 80 pi) detectable amounts of spirochetes. No relapse of clinical arthritis was observed up to 40 days after treatment, regardless of whether the immune serum (1 0 // g / mouse anti-OspC-specific antibody) transferred pi on the 1 0th, 1 9th or 60th day has been.

Example 4

The therapeutic effect of a polyclonal immune serum directed against OspC on an existing disease and infection of scid mice was further confirmed by histopathological examinations of the organs affected. As shown in Table 3, significant histopathological changes were found in the joints, heart, liver and muscle of infected but otherwise untreated scid mice or those that received only NMS. As previously shown (UE Schaible et al., Am. J. Pathol. 1 37 (1 990), 81 1 -820), chronic progressive inflammatory changes were most commonly found in tibiotarsal joints, in the heart and in the liver and passed throughout the observation period (45 days pi). Mice that received immune serum that either for OspC or OspA (3 μg specific antibodies / mouse) 1 hour before infection showed no pathological changes in any of the four organs when examined on day 45 pi. In addition, mice that received an immune serum directed against OspC (10 μg specific antibodies / mouse) on the 10th or 19th day after the inoculation showed, if at all, only slight inflamed lesions in joints, heart, liver and muscle. In contrast, immune serum directed against OspA (10 μg specific antibody / mouse) had no effect on the development or progression of inflammation in the affected organs (day 1 9 pi).

Example 5

Production of OspC-GST fusion protein and purification of rec. OspC

The cloning of OspC into the expression vector pGEX-2T was carried out as follows:

1) Amplification of the OspC gene from amino acid 20-21 1 using PCR

(Primer: ATGGATCCAATAATTCAGGAAAAGATGGG and ATGAATTCCTAAGGTTTTTTTGGACTTTCTACC)

2) Cloning of the PCR fragment in pGEX-2T after BamHI / EcoRI digestion

3) Transformation of E.coii DH5a

4) Expression rec. OspC-GST according to the manufacturer's instructions (Pharmacia Biotech)

5) Enrichment of OspC-GST via Gluthatione Seph. 4B columns

6) Cleavage of OspC-GST using thrombin and purification. For this purpose, four OspC-GST protein preparations were digested with thrombin protease overnight and OspC from GST via a glutation Seph. 4B column separated.

Claims

claims 1. Pharmaceutical composition for the treatment of Lyme disease, due to the fact that it comprises as an active ingredient an antibody which is specific for the 24 kDa antigen (OspC) from B. burgdorferi. 2. Pharmaceutical composition for the treatment of Lyme disease, due to the fact that it comprises as an active ingredient an antibody which is specific for the 24 kDa antigen (OspC) from B. burgdorferi with the sequence shown in SEQ ID NO.2. 3. Pharmaceutical composition according to claim 1 or 2, d a d u rc h g e k e n e i c h n et that it comprises a polyclonal antibody specific for OspC. 4. The pharmaceutical composition according to claim 1 or 2, which also comprises one or more monoclonal antibodies specific for OspC. 5. Pharmaceutical composition according to one of the preceding claims, dadu rc hgekenn ze ichn et that it comprises as an active ingredient an antibody which is specific for recombinant OspC from B. burgdorferi of the strain ZS7. 6. Pharmaceutical composition according to one of the preceding claims, d a d u rc h g e k e n n z e i c h n et that it comprises antibodies of the class IgG and / or IgM as an active ingredient. 7. Pharmaceutical composition according to one of the preceding claims, d a d u rc h g e k e n n z e i c h n e t that it is intended for intraperetoneal administration. 8. Pharmaceutical composition according to one of the preceding claims, d a d u rc h g e k e n n z e i c h n e t that it comprises 1 μg to 10 mg of antibody as an active ingredient. 9. Pharmaceutical composition according to one of the preceding claims, d a d u rc h g e k e n n e e c h e d that they prevent the progression of arthritis and carditis in immunodeficient experimental animals that have been infected with viable pathogenic B. burgdorferi organisms. 10. Pharmaceutical composition according to one of the preceding claims, that it prevents the progression of arthritis and carditis in immunodeficient Scid mice which have been infected with viable pathogenic B. burgdorferi organisms of the ZS7 strain. 11. Pharmaceutical composition according to one of the preceding claims, dadu rc hgekennzeichn et that it leads to the healing of arthritis and carditis in immunodeficient experimental animals, which were infected with viable pathogenic B. burgdorferi organisms. 12. Pharmaceutical composition according to one of the preceding claims, d a d u rc h g e k e n n z e i c h n et that it leads to inactivation of the spirochetes in immunodeficient experimental animals that have been infected with viable pathogenic B. burgdorferi organisms. 13. Vaccine against Lyme disease, due to the fact that it comprises an antibody as an active ingredient which is specific for the 24 kDa antigen (OspC) from B. burgdorferi. 14. Vaccine against Lyme disease, due to the fact that it comprises as an active ingredient an antibody which is specific for the 24 kDa antigen (OspC) from B. burgdorferi with the sequence shown in SEQ ID NO.2. 15. Vaccine according to claim 13 or 14, d a d u r c h g e k e n e z e i c h n e t that it comprises a specific against OspC polyclonal antibody. 16. Vaccine according to claim 13 or 14, characterized in that it comprises one or more monoclonal antibodies specific for OspC. 17. Vaccine according to any one of claims 13 to 16, d a d u r c h g e k e n n z e i c h n et that it comprises antibodies that are specific for recombinant OspC from B. burgdorferi of the strain ZS7. 18. Vaccine according to one of claims 13 to 17, which also includes antibodies of the class IgG and / or IgM as active ingredient. 19. Vaccine according to one of claims 13 to 18, which also means that it prevents the formation of arthritis and carditis in immunodeficient experimental animals that have been infected with viable pathogenic B. burgdorferi organisms. 20. Vaccine according to any one of claims 13 to 19, so that it comprises 0.1 μg to 1 mg of antibody as an active ingredient. 21. Vaccine according to any one of claims 13 to 20, which also means that it further comprises antibodies which are specific for the 31 kDa antigen (OspA) from B. burgdorferi. 22. A method for obtaining an active ingredient for the treatment of Lyme disease from a test animal, that is to say that the test animal is vaccinated with OspC antigen and an immune serum is obtained which is specific for the OspC antigen Contains antibodies. 23. The method according to claim 22, d a d u rc h g e k e n n z e i c h n e t that the test animal is vaccinated with recombinant OspC. 24. The method according to claim 23, and in that vaccinating BALB / c mice with recombinant OspC three times at intervals of 10 days and collecting the immune serum over a period of 2 months after the last administration of the antigen. 25. A method for obtaining a vaccine against Lyme disease from a test animal, ie by inoculating the test animal with OspC and obtaining an immune serum which contains antibodies specific for OspC. 26. The method according to claim 25, d a d u rc h g e k e n n z e i c h n et that the test animal is vaccinated with recombinant OspC. 27. The method according to claim 26, d a d u rc h g e k e n n z e i c h n et that vaccinated BALB / c mice with recombinant OspC three times at intervals of 10 days and the immune serum via one Period of 2 months after the last administration of the antigen wins. 28. Polyclonal antibody obtainable according to one of claims 22 to 26, characterized in that it is specific for OspC. 29. Polyclonal antibody, obtainable according to one of claims 22 to 26, that a d u rc h g e k e n n ze i c h n et that it is specific for OspC with the sequence shown in SEQ ID NO.2. 30. Monoclonal antibody against OspC. 31. Monoclonal antibody against OspC of the sequence shown in SEQ ID NO.2. 32. Antigen, d a d u rc h g e k e n n z e i c h n et that it reacts immune with an antibody against OspC according to one of claims 1 to 21. 33. Antigen according to claim 32, d a d u rc h g e k e n n ze i c h n et that it is the in Seq. ID NO.2 comprises amino acid sequence or an immunogenic epitope from this sequence. 34. Recombinant DNA, which means that it codes for an antigen according to one of claims 26 or 27 and (1) the in Seq. ID NO. 1 nucleic acid sequence shown, (2) a sequence corresponding here in the context of the degeneration of the genetic code or (3) a sequence which hybridizes with the sequence from (1) or / and (2) under stringent conditions. 35. Recombinant vector, dadu rc hgekennzeichn et, that it contains one or more copies of a recombinant DNA according to claim 34. 36. Method for obtaining antigens according to one of claims 32 or 33, characterized in that a B. burgdorferi gene bank with one or more antibodies according to one of claims 1 to 18 is examined and the clones which are isolated with the or the Antibodies show a positive immune response. 37. A method for obtaining a pharmaceutical composition for the treatment of Lyme disease or a vaccine against Lyme disease, so that test animals are immunized with an antigen according to claim 32 or 33 and from the immunized test animal Protective, polyclonal or monoclonal antibodies against OspC wins in the usual way. 38. Use of a pharmaceutical composition which comprises as an active ingredient an antibody which is specific for the 24kDa antigen (OspC) from B. burgdorferi for the treatment of Lyme disease. 39. Use of a pharmaceutical composition which comprises as an active ingredient an antibody which is specific for the 24kDa antigen (OspC) from B. burgdorferi, as a vaccine against Lyme disease. 40. Use according to one of claims 38 or 39, d ad u rc h g e k e n n ze i c h n et that the active ingredient is a polyclonal antibody. 41. Use according to one of claims 38 or 39, d ad u rc h g e k e n n z e i c h n et that the active ingredient is a monoclonal antibody. 42. Use of a pharmaceutical composition which comprises as an active ingredient an antibody which is specific for the 24kDa B. burgdorferi antigen (OspC), for the manufacture of a medicament for the treatment of Lyme disease. 43. Use of a pharmaceutical composition which comprises as an active ingredient an antibody which is specific for the 24kDa B. burgdorferi's antigen (OspC) is used to manufacture a medicament as a vaccine against Lyme disease. 44. The method according to any one of claims 42 or 43, d a d u rc h g e k e n n z e i c h n e t that the active ingredient is a polyclonal antibody. 45. The method according to any one of claims 42 or 43, d a d u rc h g e k e n n z e i c h n e t that the active ingredient is a monoclonal antibody. 46. Method for the treatment of Lyme disease, characterized in that a patient suffering from Lyme disease is administered a pharmaceutical preparation which comprises as an active ingredient an antibody which is specific for the 24kDa antigen (OspC) of B. burgdorferi is. 7. A method for the prevention of Lyme disease, ie the fact that a patient is given a vaccine which comprises an antibody as an active ingredient which is specific for the 24kDa antigen (OspC) from B. burgdorferi.