Journal of the Royal Society of Medicine Volume 83 October 1990 Behset's disease in our country is apparently extremely rare. The response to treatment with IVIgG and aspirin demonstrated by this case should be evaluated on a larger scale. References 1 Cobby M, Higgs CMB, Hall CL. Beh$et's syndrome presenting as intracranial hypertension in a Caucasian. J R Soc Med 1988;81:478-9 2 Editorial. Beh$et's disease. Lancet 1989;i:761-2 3 Masuda K, Urayama A, Kogure M, Nakajima A, Nakae K, Inaba G. Double-masked trial of cyclosporin versus colchicine and long-term open study of cyclosporin in Beh$et's disease. Lancet 1989;i:1093-6 4 Sultan Y, Kazatchkine MD, Maisonneuve P, Njddeger UE. Anti-idiotypic suppression of autoantibodies to factor VIII
Transverse myelitis following cholera, typhoid and polio vaccination
D F D'Costa MRCP
A Cooper MB Chir
I F Pye MD FRCP Department of Neurology, Leicester Royal Infirmary, Leicester LEI 5WW Keywords: transverse myelitis; vaccination
Active immunization with various vaccines is carried out internationally. Cholera and typhoid vaccines are recommended to most travellers to the East. Post vaccination myelitis has been documented following triple vaccine', rubella2, rabies3, diphtheria, tetanus and polio vaccines. We report a case of transverse myelitis TM)occurring after cholera, typhoid and polio vaccines. We believe the association of TM with the former two has not been documented previously.
Case report A 24-year-old woman was admitted as an emergency with a 24 h history of paraesthesiae and weakness in her legs. Two days previously, she had been inoculated with inactivated typhoid and cholera vaccines. She also received live oral polio vaccine. She had been unwell with an upper respiratory tract infection and pharyngitis for 5 weeks and at the time of vaccination was pyrexial. One day postvaccination, she developed malaise, fever and inflammation of both injection sites. At 2 days, paraesthesiae developed in her feet and then there was rapid progression over 24 h to a flaccid paraplegia, retention of urine and sensory loss below T10. There was no faecal incontinence. Her reflexes were preserved throughout and the plantar responses remained flexor. Neurological and general examinations were otherwise normal. Investigations showed a normal peripheral white cell count. Cerebrospinal fluid was clear, acellular with a protein of 0.1 gll and culture was sterile. Oligoclonal bands were not detected. Virology of the cerebrospinal fluid and throat were normal. Complement fixation tests against several viral antigens including tests for Epstein-Barr virus did not demonstrate any significant titres. Spinal X-rays were normal. A myelogram was not performed. Nerve conduction studies were normal and the electromyogram (EMG) was suggestive of pyramidal dysfunction with an element of radiculopathy. A catheter was inserted on admision but normal bladder function returned after 3 days. A steroid pulse of prednisolone 500 mg intravenously was given for 5 days. She received prolonged physiotherapy and 3 months later there
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8
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(antihaemophilic factor) by high-dose intravenous gammaglobulin. Lancet 1984;ii:765-8 Kimberly RP, Salmon JE, Bussel JB, Kuntz Crow M, Hilgartner MW. Modulation of mononuclear phagocyte function by intravenous -y-globulin. JImmunol 1984;132:745-50 Lewis MA, Priestley BL. Transient neonatal Behcet's disease. Arch Dis Child 1986;61:805-6 Head JR, Billingham RE. In: Lachmann PJ, Peters DK, eds. Clinical aspects of immunology. Oxford: Blackwell Scientific 1982:273 Wilson AP, Efthimiou J, Betteridge DJ. Decreased prostacyclin sensitivity of platelets in patients with Behcet's syndrome. Eur J Clin Invest 1988;18:410-14
(Accepted 4 December 1989)
has been a marked recovery in both sensory and motor function such that she walks independently and sensation is normal. Discussion Although the plantar responses remained flexor and there were some EMG features suggesting a possible element of radiculopathy, the preservation of the tendon reflexes in the presence of profound weakness, the clear cut sensory level and the bladder dysfunction pointed to a transverse myelitis as the predominant lesion. Neurological complications of vaccination include fits, coma, hemiparesis, myelitis, blindness and multiple cranial palsies'. The majority of these occur within 24 hours. Symptoms began in our patient 36 h after immunization and progressed to maximal neurological deficit over the next 24 h. It is difficult, if not impossible, to discount the temporal relationship between vaccination and the onset of a transverse myelitis here. The possibility cannot be ruled out that the neurological picture resulted from a viral infection responsible for the febrile illness at the- time of vaccination. No virus was identified and we suggest that vaccination triggered the development of transverse myelitis; the fever may have played a secondary role by increasing susceptibility to such a complication1. As the patient received all three vaccines simultaneously, it is impossible to implicate an individual one specifically. However, polio is unlikely since she had been given this on several previous occasions without ill effects. The pathogenesis of transverse myelitis is unknown but it has been postulated that direct invasion of the nervous system followed by an antigen-antibody reaction may be responsible'. The prognosis of post-vaccination transverse myelitis is uncertain but has tended to be unfavourable in the reported cases'4. Our patient has shown a steady improvement which continues with every indication of making a good functional recovery. 'Transverse myelitis following cholera or typhoid vaccination has not been documented previously. We believe that there is a causal relationship between vaccination and its development in this patient. In these days of ever increasing foreign travel, this experience is a reminder of the need for caution when performing immunization and reemphasizes that intercurrent illness is a contraindication.
References 1
Kulenkampff M, Schwartzman JS, Wilson J. Neurological complicationso pertussisinoculation. Arch Dis Child 1974;4&:46
2 HoltS, Hudgins D, KRishnniR, Critchley EMR Diffse myelitis associated with rubella vaccination. BMJ 1976;30.1037-8 3 Label LS, Batts DH. Transverse myelitis caused by duck embryo rabies vaccine. Arch Neurol 1982;39:.426-30 4 Whittle E, Roberton NRC. Transverse myelitis after diphtheria, tetetnss and polio nnation. BMJ 1977;1:1450 5 Croft PB. Para-infectious and post-vaccinal encephalomyelitis.
Postgrad Med J 1969;45:392-400 (Accepted 8 December 1989)
0141-0768/90/
100653-01/$02.00/0 © 1990 The Royal Society of Medicine
Transverse myelitis following cholera, typhoid and polio vaccination
D F D'Costa MRCP
A Cooper MB Chir
I F Pye MD FRCP Department of Neurology, Leicester Royal Infirmary, Leicester LEI 5WW Keywords: transverse myelitis; vaccination
Active immunization with various vaccines is carried out internationally. Cholera and typhoid vaccines are recommended to most travellers to the East. Post vaccination myelitis has been documented following triple vaccine', rubella2, rabies3, diphtheria, tetanus and polio vaccines. We report a case of transverse myelitis TM)occurring after cholera, typhoid and polio vaccines. We believe the association of TM with the former two has not been documented previously.
Case report A 24-year-old woman was admitted as an emergency with a 24 h history of paraesthesiae and weakness in her legs. Two days previously, she had been inoculated with inactivated typhoid and cholera vaccines. She also received live oral polio vaccine. She had been unwell with an upper respiratory tract infection and pharyngitis for 5 weeks and at the time of vaccination was pyrexial. One day postvaccination, she developed malaise, fever and inflammation of both injection sites. At 2 days, paraesthesiae developed in her feet and then there was rapid progression over 24 h to a flaccid paraplegia, retention of urine and sensory loss below T10. There was no faecal incontinence. Her reflexes were preserved throughout and the plantar responses remained flexor. Neurological and general examinations were otherwise normal. Investigations showed a normal peripheral white cell count. Cerebrospinal fluid was clear, acellular with a protein of 0.1 gll and culture was sterile. Oligoclonal bands were not detected. Virology of the cerebrospinal fluid and throat were normal. Complement fixation tests against several viral antigens including tests for Epstein-Barr virus did not demonstrate any significant titres. Spinal X-rays were normal. A myelogram was not performed. Nerve conduction studies were normal and the electromyogram (EMG) was suggestive of pyramidal dysfunction with an element of radiculopathy. A catheter was inserted on admision but normal bladder function returned after 3 days. A steroid pulse of prednisolone 500 mg intravenously was given for 5 days. She received prolonged physiotherapy and 3 months later there
5 6 7
8
653
(antihaemophilic factor) by high-dose intravenous gammaglobulin. Lancet 1984;ii:765-8 Kimberly RP, Salmon JE, Bussel JB, Kuntz Crow M, Hilgartner MW. Modulation of mononuclear phagocyte function by intravenous -y-globulin. JImmunol 1984;132:745-50 Lewis MA, Priestley BL. Transient neonatal Behcet's disease. Arch Dis Child 1986;61:805-6 Head JR, Billingham RE. In: Lachmann PJ, Peters DK, eds. Clinical aspects of immunology. Oxford: Blackwell Scientific 1982:273 Wilson AP, Efthimiou J, Betteridge DJ. Decreased prostacyclin sensitivity of platelets in patients with Behcet's syndrome. Eur J Clin Invest 1988;18:410-14
(Accepted 4 December 1989)
has been a marked recovery in both sensory and motor function such that she walks independently and sensation is normal. Discussion Although the plantar responses remained flexor and there were some EMG features suggesting a possible element of radiculopathy, the preservation of the tendon reflexes in the presence of profound weakness, the clear cut sensory level and the bladder dysfunction pointed to a transverse myelitis as the predominant lesion. Neurological complications of vaccination include fits, coma, hemiparesis, myelitis, blindness and multiple cranial palsies'. The majority of these occur within 24 hours. Symptoms began in our patient 36 h after immunization and progressed to maximal neurological deficit over the next 24 h. It is difficult, if not impossible, to discount the temporal relationship between vaccination and the onset of a transverse myelitis here. The possibility cannot be ruled out that the neurological picture resulted from a viral infection responsible for the febrile illness at the- time of vaccination. No virus was identified and we suggest that vaccination triggered the development of transverse myelitis; the fever may have played a secondary role by increasing susceptibility to such a complication1. As the patient received all three vaccines simultaneously, it is impossible to implicate an individual one specifically. However, polio is unlikely since she had been given this on several previous occasions without ill effects. The pathogenesis of transverse myelitis is unknown but it has been postulated that direct invasion of the nervous system followed by an antigen-antibody reaction may be responsible'. The prognosis of post-vaccination transverse myelitis is uncertain but has tended to be unfavourable in the reported cases'4. Our patient has shown a steady improvement which continues with every indication of making a good functional recovery. 'Transverse myelitis following cholera or typhoid vaccination has not been documented previously. We believe that there is a causal relationship between vaccination and its development in this patient. In these days of ever increasing foreign travel, this experience is a reminder of the need for caution when performing immunization and reemphasizes that intercurrent illness is a contraindication.
References 1
Kulenkampff M, Schwartzman JS, Wilson J. Neurological complicationso pertussisinoculation. Arch Dis Child 1974;4&:46
2 HoltS, Hudgins D, KRishnniR, Critchley EMR Diffse myelitis associated with rubella vaccination. BMJ 1976;30.1037-8 3 Label LS, Batts DH. Transverse myelitis caused by duck embryo rabies vaccine. Arch Neurol 1982;39:.426-30 4 Whittle E, Roberton NRC. Transverse myelitis after diphtheria, tetetnss and polio nnation. BMJ 1977;1:1450 5 Croft PB. Para-infectious and post-vaccinal encephalomyelitis.
Postgrad Med J 1969;45:392-400 (Accepted 8 December 1989)
0141-0768/90/
100653-01/$02.00/0 © 1990 The Royal Society of Medicine
