Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Live vaccine in immunodeficient patients
- M J Hobbs (20 April 1999)
-
Vaccine-associated paralytic poliomyelitis
- Samuel Sepkowitz (10 May 1999)
-
Paralytic poliomyelitis
- C L Crawford (2 August 1999)
-
Vaccine associated paralytic poliomyelitus.
- Thea Gregg (26 November 1999)
|
|
|||
|
M J Hobbs
Send response to journal:
|
Title: Paralytic poliomyelitis associated with live oral poliomyelitis vaccine in a child with HIV infection in Zimbabwe Chitsike and van Furth1 refer to a report of a patient with HIV infection who developed poliomyelitis after oral poliomyelitis vaccine. Our concern about the 'administration of live virus to those with immunodeficiencies, especially those that are HIV positive' is already on record2, supporting Kroon et al's3 conclusion that any live vaccine is contraindicated in HIV infection. We dispute Chitsike and van Furth's conclusion that the 'benefits of vaccination outweigh the risk of infection with wild poliomyelitis virus', especially in southern Africa where the annual incidence of poliomyelitis before mass vaccination was only 1 per 100000.4 Before the current polio vaccination campaign in developing countries the wild virus would have been encountered in infancy, when it did not cause paralysis but resulted in permanent immunity. Now, however, as in Namibia the wild virus would have been virtually removed as a result of vaccination. If the wild virus were reintroduced, as appears to have been done from neighbouring Angola, then older children not fully protected by vaccination would be liable to develop paralysis. This appears to be what has happened in Namibia where 27 children developed poliomyelitis, including three with bulbar paralysis.5 We were puzzled that in describing their patient Chitsike and van Furth resorted to magnetic resonance imaging to detect wasting when this could be observed by simple observation - surely a matter of considerable relevance in a developing country, given the comparative expense. C L Crawford, Honorary Lecturer M J Hobbs, Lecturer Division of Neuroscience, Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF 1 Chitsike N, van Furth R. Paralytic poliomyelitis associated with live oral poliomyelitis vaccine in child with HIV infection in Zimbabwe: case report. BMJ 1999; 318: 841-3. (27 March.) 2 Crawford CL, Hobbs MJ. Eliminating the poliovirus: is the strategy wrong? Neurol Infections and Epidemiol 1996; 1: 3-9. 3 Kroon FP, van Dissel JP, Labadie J, van Loon AM, van Furth R. Clin Infect Dis 1995; 21: 1197-203. 4 Crawford CL, Hobbs MJ. Poliomyelitis in southern Africa. S Afr Med J 1997; 87:1706. 5 van Niekerk ABW, Vries JB, Baard J, Schoub BD, Chezzi C, Blackburn NK. Outbreak of paralytic poliomyelitis in Namibia. Lancet 1994; 344: 661-4. |
|||
|
|
|||
|
Samuel Sepkowitz
Send response to journal:
|
Dear Sir; A report such as this, one that has associated oral polio vaccine with flaccid paralysis, has prompted many countries to reduce or eliminate the use of oral vaccine altogether or to consider discontinuing its use.1 A case of flaccid paralysis developed in a child with HIV disease in Zimbabwe who had received oral polio vaccine. The paralysis was attributed to the vaccine. The possibility that HIV could have been responsible was not considered, certainly, not discussed. The one previous case of paralysis associated with oral polio vaccine in a child with HIV infection, a report from Romania, also failed to consider the possibility that HIV caused the flaccid paralysis.2 In both cases neurovirulence reversion has been assumed. HIV infection is one of a host of infections than can result in acute flaccid paralysis.3 HIV is a neurotropic virus infection with a variety of clinical manifestations. Neurologic symptoms may occur at any time during the infection. A chronic inflammatory demyelinating polyneuropathy (CIPD) tends to occur before other clinical manifestations.4 In addition, metabolic disorders, drugs, organic substances, toxins, metals, pesticides, as well as unknown or multiple causes of paralysis have been responsible for paralysis. Acute flaccid paralysis may be inherited or congenital, but not necessarily diagnosed at birth.3 Shortly after licensure of oral polio vaccine, cases of paralysis that were consistent with poliomyelitis were considered vaccine induced if these cases "did not exclude a possible causal relationship to the administration of the oral vaccine".3 By definition, an acute flaccid paralysis with evidence of polio vaccine administration or exposure, directly or indirectly, must be diagnosed as vaccine induced. The diagnosis is unavoidable if a patient with a flaccid paralysis has been vaccinated or has been in contact with someone who has been shedding the virus. Vaccine-associated paralysis trumps any other diagnosis. The benefits and advantages of oral polio vaccine have been well presented in a Commentary that questioned the advisability of changing from the oral vaccine for routine immunization.5 Add to their arguments, the weakness of a contrived diagnosis that marks every case of acute flaccid paralysis to be the result of oral polio vaccine unless the vaccine can be excluded as a cause. Those who maintain that vaccine- associated polio exists cannot, as yet, bring themselves to alter the diagnosis to vaccine-caused paralysis.3 Samuel Sepkowitz, M.D. Clinical Professor of Pediatrics University of Oklahoma Health Sciences Center REFERENCES 1 Chitsike I, van Furth R. Paralytic poliomyelitis associated with live oral poliomyelitis vaccine in child with HIV infection in Zimbabwe: case report. BMJ 1999;318:841-3. 2 Ion-Nedelcu N, Dobrescu A, Strebel PM, Sutter RW. Vaccine-associated paralytic poliomyelitis and HIV infection. Lancet 1994;343:51-2. 3 Sutter RW, Cochi SL, Melnick JL. Live attenuated polio virus vaccine. In Plotkin SA, Orenstein WA, eds. Vaccines. 3rd edition. Philadelphia: W. B. Saunders, 1999:364-408. 4 Chaisson RE, Volverding PA. Clinical manifestations of HIV infections. In Mandell GL, Bennet JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Disease, 4th ed. New York: Churchill Livingstone, 1995:1217-38. 5 Heath P, Maclennan JM, Moxon ER. Commentary. Arch Dis Child 1998;78:573 -4. I have no competing interests. |
|||
|
|
|||
|
C L Crawford Division of Neuroscience, Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF
Send response to journal:
|
Paralytic poliomyelitis associated with live oral poliomyelitis vaccine in a child with HIV infection in Zimbabwe Chitsike and van Furth1 refer to a report of a patient with HIV infection who developed poliomyelitis after oral poliomyelitis vaccine. Our concern about the 'administration of live virus to those with immunodeficiencies, especially those that are HIV positive' is already on record2, supporting Kroon et al's3 conclusion that any live vaccine is contraindicated in HIV infection. We dispute Chitsike and van Furth's conclusion that the 'benefits of vaccination outweigh the risk of infection with wild poliomyelitis virus', especially in southern Africa where the annual incidence of poliomyelitis before mass vaccination was only 1 per 100000.4 Before the current polio vaccination campaign in developing countries the wild virus would have been encountered in infancy, when it did not cause paralysis but resulted in permanent immunity. Now, however, as in Namibia the wild virus would have been virtually removed as a result of vaccination. If the wild virus were reintroduced, as appears to have been done from neighbouring Angola, then older children not fully protected by vaccination would be liable to develop paralysis. This appears to be what has happened in Namibia where 27 children developed poliomyelitis, including three with bulbar paralysis.5 We were puzzled that in describing their patient Chitsike and van Furth resorted to magnetic resonance imaging to detect wasting when this could be observed by simple observation - surely a matter of considerable relevance in a developing country, given the comparative expense. C.L.Crawford, Honorary Lecturer M.J.Hobbs Lecturer Division of Neuroscience, Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF 1 Chitsike N, van Furth R. Paralytic poliomyelitis associated with live oral poliomyelitis vaccine in child with HIV infection in Zimbabwe: case report. BMJ 1999; 318: 841-3. (27 March.) 2 Crawford CL, Hobbs MJ. Eliminating the poliovirus: is the strategy wrong? Neurol Infections and Epidemiol 1996; 1: 3-9. 3 Kroon FP, van Dissel JP, Labadie J, van Loon AM, van Furth R. Clin Infect Dis 1995; 21: 1197-203. 4 Crawford CL, Hobbs MJ. Poliomyelitis in southern Africa. S Afr Med J 1997; 87:1706. 5 van Niekerk ABW, Vries JB, Baard J, Schoub BD, Chezzi C, Blackburn NK. Outbreak of paralytic poliomyelitis in Namibia. Lancet 1994; 344: 661-4. |
|||
|
|
|||
|
Thea Gregg
Send response to journal:
|
Chitsike nad van Furth’s report of a patient with HIV infection, who developed poliomyelitis following vaccination, with live polio virus. I was surprised by the lack of detail in the clinical information reported. The use of the word leg being used synonymously when referring to the lower limb was inaccurate and confusing. (The anatomical leg being from knee to ankle). It is mentioned that there was diminished, tone, power and reflexes, but no description of the muscles affected, or muscles wasted. Two reflexes are normally tested in the lower limb, being the knee and the ankle reflexes. It was unclear whether both were diminished. If only the knee reflex was compromised, it would suggest a dysfunction of the quadriceps muscles. That is the action of extension, being diminished. This, would lead me to conclude that a segmental lesion in the anterior horns of L3, L4 was present. If the ankle reflex were diminished It would suggest that the segmental lesion would affect the dorsiflexors of the ankle and be a L4, L5 lesion. Wasting in the corresponding muscles would be present to confirm this diagnosis. This would help to reassure Professor. Sepkowitz’s that his theory that the paralysis was indeed polio and not HIV related as suggested (10th May 1999). As a second year osteopathy student I feel that a full clinical examination based on sound anatomical knowledge would provide enough information to forsake the expense of an MRI. Thea Gregg |
|||