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MEDIAN-NERVE PALSY FOLLOWING BEE-STINGS
619
Further, the action of lippia is
a
strong argument
hypothesis that the direct diazo reaction against (Hijmans van den Bergh’s direct reaction) is peculiar to bilirubin which has passed the liver cells. For the jaundiced plasma in the lippia-poisoned sheep gave a strong direct diazo reaction although it did not pass into the bile. the
County Hospital, Svendborg, Denmark.
TORBEN K. WITH.
MEDIAN-NERVE PALSY FOLLOWING BEE-STINGS SiR,-The report of Mr. Bailey and Mr. Bolton Carter (March 12) on two cases of median-nerve palsy complicating hand infections reminded me of a personal experience of median-nerve palsy resulting from bee-stings. Last summer, when manipulating a vicious stock of bees, was stung badly on the front of both wrists-parts’ of the body singularly attractive to bees. The attack was concentrated and localised. There were few stings on the fingers (because they were smeared with dimethyl phthalate) and none above the wrists (I was wearing elastic cuffs). There was little visible swelling, but I was kept awake that night ,by intense tingling in the thumb and in the index and middle fingers. Next day the fingers were flexed and any attempt to straighten them, actively or passively, was very painful. The little finger was normal. About 48 nours later, while I was still wondering what had happened, the symptoms began
I
to subside
’
rapidly.
I looked upon it as an acute carpal-tunnel syndrome, and the cases reported last week support the idea that the median nerve was involved in deep-seated oedema resulting from the
stings. Chase Farm Hospital, Enfield, Middlesex.
C. ALLAN BIRCH.
INFECTION WITH CRYPTOCOCCUS NEOFORMANS SiR,_The report last week of two cases of cryptococcosis by Dr. Beck and his colleagues raises interesting
problems.
They state that ease 1 was originally diagnosed as Hodgkin’s by cervical lymph-node biopsy, but that the developrevealed the ment of a terminal cryptococcal meningitis true nature of the disease." They thus imply that the disease
.,
lesions arose as a result of cryptococcal infection. Yet the lesions described were typical of Hodgkin’s disease in their microscopical appearance and showed no cryptococci, while the histology of the meningitis, where cryptococci were abundant, was that of chronic inflammation. It is difficult to accept that an organism can produce an inflammatory condition of the meninges at the same time as a Hodgkin’s-like picture elsewhere. It would seem more likely that this infection arose as a terminal event in the course of typical Hodgkin’s disease. This view is supported by the fact that the lymph-node enlargement preceded the cryptococcal meningitis clinically, and at necropsy the Hodgkin’s lesions were extensive, while the meningeal inflammatory infiltrate was sparse.
Hodgkin’s
The explanation for the association between these two diseases may be connected with the breakdown of certain
immunity mechanisms that is known to occur in Hodgkin’s disease. It was discovered many years ago that the proportion of tuberculin-positive reactors is much lower in Hodgkin’s disease than in the general population 1;
and Dubin2 has shown that the incidence of in Negro patients with Hodgkin’s disease is significantly lower than in the Negro population in general. It is possible that natural antibodies giving resistance to cryptococcal infection in healthy people are absent or reduced in cases of Hodgkin’s disease. Both the patients described by Dr. Beck and his Direct colleagues had heavy doses of antibiotics. stimulation of fungal growth by antibiotics has been shown to take place in the case of JtfoMtMtt albicans,3 but so far no work has been published in this connection with regard to torulosis.
Wasserman-positivity
’
1. 2. 3.
Reed,
D. M. M. Foley, C. C.,
Dubin, I.
Johns Hopk. Hosp. Rep. 1902, 10, 133. Ann. intern. Med. 1947, 27, 898. Winter, W. O. J. infect. Dis. 1949, 85,
was given intrathecal penicillin and streptomycin well as these antibiotics systemically and sulphonamides orally. The patient’s condition deteriorated rapidly, and he died after a week of this treatment.
C’ase 1
as
Eighteen months ago I saw in this hospital a case in which the cryptococcosis presented as a terminal septicaemia, with no focal lesions, in a patient with advanced Hodgkin’s diseased The patient had been treated with large quantities of sulphonamides, penicillin, streptomycin, and chloramphenicol during the three months before death. Here too it was possible that stimulation of cryptococcal growth by these antibiotics might have been the cause of the unusually acute infection.
May I therefore suggest that until exact knowledge is obtained on this point it would be as well to withhold local and systemic antibiotics in the treatment of torulosis, unless laboratory tests have shown that the cryptococcus is sensitive to any particular antibiotic. Department of Pathology, Crumpsall Hospital,
B.C.G. VACCINATION SiR,-Dr. Webster (March 5) hits the nail on the head when he says that the fundamental question to which we do not know the answer is whether a positive skin reaction is really very important in immunity to tuberculosis." "
A positive skin reaction is a measure of hypersensitivity and not of immunity, though of course5 immunity and hypersensitivity may be related. Brownlee has emphasised that the characteristic widespread tissue destruction of tuberculosis follows the conditioned hypersensitivity. Hypersensitivity without immunity is clearly undesirable. We know that a negative skin reaction can often be converted into a positive one by infection with tubercle bacilli, We also know that a B.C.G., or other related organisms. positive reactor can be converted into a negative one by desensitisation with either old tuberculin or purified protein derivative. But we do not know whether there is any difference between the negativereactor who has never been positive and the- negative reactor who went through a positive phase and became negative as a result of therapeutic or natural desensitisation. If we accept Godlowski’s6 enzymatic concept of allergy, the distinction between these two types of negative reactor is clear-cut.. The negative reactor who has never been through a positive phase has tissues which are insensitive to the particular antigen of the tubercle bacillus which causes hypersensitivity. The negative reactor who has been positive and has become negative through desensitisation produces sufficient antibody to destroy the antigen before it can reach the interior of the sensitised cells. Godlowski’s hypothesis also explains why in some cases of sarcoidosis the reaction cannot be converted from negative to positive with B.C.G. Such patients are negative reactors because they have been desensitised naturally, and although their tissues are still sensitive to antigen they do not exhibit hypersensitivity because the antigen is neutralised by antibody before it can do its destructive work. Professor Heaf (Feb. 12) points out that the evidence is that B.C.G. vaccination does offer considerable protection against the development of primary tuberculosis but exerts little control over the development of postprimary lesions. Whether primary or postprimary tuberculosis is the more lethal or crippling disease in this age of chemotherapy is undecided. But the wisdom of protecting the population against primary tuberculosis and leaving it susceptible to postprimary tuberculosis is doubtful. As Professor Heaf so rightly says, " Perhaps the greatest disadvantage associated with B.C.G. vaccination is the unwarranted confidence that it has inspired in laymen in many countries."
It would seem that what is required is a vaccine which will confer immunity and will at the same time desensitise the patient. When we are satisfied that B.C.G. does confer some degree of immunity, subsequent desensitisa4. 5.
268.
L. MICHAELS Registrar in Pathology.
Manchester.
Levene, M., Michaels, L. J. clin. Path. (in the press). Brownlee, G. Irish J. med. Sci. October, 1951, p. 495. 6. Godlowski, Z. Z. Enzymatic Concept of Anaphylaxis and
Allergy. Edinburgh, 1953.
Further, the action of lippia is
a
strong argument
hypothesis that the direct diazo reaction against (Hijmans van den Bergh’s direct reaction) is peculiar to bilirubin which has passed the liver cells. For the jaundiced plasma in the lippia-poisoned sheep gave a strong direct diazo reaction although it did not pass into the bile. the
County Hospital, Svendborg, Denmark.
TORBEN K. WITH.
MEDIAN-NERVE PALSY FOLLOWING BEE-STINGS SiR,-The report of Mr. Bailey and Mr. Bolton Carter (March 12) on two cases of median-nerve palsy complicating hand infections reminded me of a personal experience of median-nerve palsy resulting from bee-stings. Last summer, when manipulating a vicious stock of bees, was stung badly on the front of both wrists-parts’ of the body singularly attractive to bees. The attack was concentrated and localised. There were few stings on the fingers (because they were smeared with dimethyl phthalate) and none above the wrists (I was wearing elastic cuffs). There was little visible swelling, but I was kept awake that night ,by intense tingling in the thumb and in the index and middle fingers. Next day the fingers were flexed and any attempt to straighten them, actively or passively, was very painful. The little finger was normal. About 48 nours later, while I was still wondering what had happened, the symptoms began
I
to subside
’
rapidly.
I looked upon it as an acute carpal-tunnel syndrome, and the cases reported last week support the idea that the median nerve was involved in deep-seated oedema resulting from the
stings. Chase Farm Hospital, Enfield, Middlesex.
C. ALLAN BIRCH.
INFECTION WITH CRYPTOCOCCUS NEOFORMANS SiR,_The report last week of two cases of cryptococcosis by Dr. Beck and his colleagues raises interesting
problems.
They state that ease 1 was originally diagnosed as Hodgkin’s by cervical lymph-node biopsy, but that the developrevealed the ment of a terminal cryptococcal meningitis true nature of the disease." They thus imply that the disease
.,
lesions arose as a result of cryptococcal infection. Yet the lesions described were typical of Hodgkin’s disease in their microscopical appearance and showed no cryptococci, while the histology of the meningitis, where cryptococci were abundant, was that of chronic inflammation. It is difficult to accept that an organism can produce an inflammatory condition of the meninges at the same time as a Hodgkin’s-like picture elsewhere. It would seem more likely that this infection arose as a terminal event in the course of typical Hodgkin’s disease. This view is supported by the fact that the lymph-node enlargement preceded the cryptococcal meningitis clinically, and at necropsy the Hodgkin’s lesions were extensive, while the meningeal inflammatory infiltrate was sparse.
Hodgkin’s
The explanation for the association between these two diseases may be connected with the breakdown of certain
immunity mechanisms that is known to occur in Hodgkin’s disease. It was discovered many years ago that the proportion of tuberculin-positive reactors is much lower in Hodgkin’s disease than in the general population 1;
and Dubin2 has shown that the incidence of in Negro patients with Hodgkin’s disease is significantly lower than in the Negro population in general. It is possible that natural antibodies giving resistance to cryptococcal infection in healthy people are absent or reduced in cases of Hodgkin’s disease. Both the patients described by Dr. Beck and his Direct colleagues had heavy doses of antibiotics. stimulation of fungal growth by antibiotics has been shown to take place in the case of JtfoMtMtt albicans,3 but so far no work has been published in this connection with regard to torulosis.
Wasserman-positivity
’
1. 2. 3.
Reed,
D. M. M. Foley, C. C.,
Dubin, I.
Johns Hopk. Hosp. Rep. 1902, 10, 133. Ann. intern. Med. 1947, 27, 898. Winter, W. O. J. infect. Dis. 1949, 85,
was given intrathecal penicillin and streptomycin well as these antibiotics systemically and sulphonamides orally. The patient’s condition deteriorated rapidly, and he died after a week of this treatment.
C’ase 1
as
Eighteen months ago I saw in this hospital a case in which the cryptococcosis presented as a terminal septicaemia, with no focal lesions, in a patient with advanced Hodgkin’s diseased The patient had been treated with large quantities of sulphonamides, penicillin, streptomycin, and chloramphenicol during the three months before death. Here too it was possible that stimulation of cryptococcal growth by these antibiotics might have been the cause of the unusually acute infection.
May I therefore suggest that until exact knowledge is obtained on this point it would be as well to withhold local and systemic antibiotics in the treatment of torulosis, unless laboratory tests have shown that the cryptococcus is sensitive to any particular antibiotic. Department of Pathology, Crumpsall Hospital,
B.C.G. VACCINATION SiR,-Dr. Webster (March 5) hits the nail on the head when he says that the fundamental question to which we do not know the answer is whether a positive skin reaction is really very important in immunity to tuberculosis." "
A positive skin reaction is a measure of hypersensitivity and not of immunity, though of course5 immunity and hypersensitivity may be related. Brownlee has emphasised that the characteristic widespread tissue destruction of tuberculosis follows the conditioned hypersensitivity. Hypersensitivity without immunity is clearly undesirable. We know that a negative skin reaction can often be converted into a positive one by infection with tubercle bacilli, We also know that a B.C.G., or other related organisms. positive reactor can be converted into a negative one by desensitisation with either old tuberculin or purified protein derivative. But we do not know whether there is any difference between the negativereactor who has never been positive and the- negative reactor who went through a positive phase and became negative as a result of therapeutic or natural desensitisation. If we accept Godlowski’s6 enzymatic concept of allergy, the distinction between these two types of negative reactor is clear-cut.. The negative reactor who has never been through a positive phase has tissues which are insensitive to the particular antigen of the tubercle bacillus which causes hypersensitivity. The negative reactor who has been positive and has become negative through desensitisation produces sufficient antibody to destroy the antigen before it can reach the interior of the sensitised cells. Godlowski’s hypothesis also explains why in some cases of sarcoidosis the reaction cannot be converted from negative to positive with B.C.G. Such patients are negative reactors because they have been desensitised naturally, and although their tissues are still sensitive to antigen they do not exhibit hypersensitivity because the antigen is neutralised by antibody before it can do its destructive work. Professor Heaf (Feb. 12) points out that the evidence is that B.C.G. vaccination does offer considerable protection against the development of primary tuberculosis but exerts little control over the development of postprimary lesions. Whether primary or postprimary tuberculosis is the more lethal or crippling disease in this age of chemotherapy is undecided. But the wisdom of protecting the population against primary tuberculosis and leaving it susceptible to postprimary tuberculosis is doubtful. As Professor Heaf so rightly says, " Perhaps the greatest disadvantage associated with B.C.G. vaccination is the unwarranted confidence that it has inspired in laymen in many countries."
It would seem that what is required is a vaccine which will confer immunity and will at the same time desensitise the patient. When we are satisfied that B.C.G. does confer some degree of immunity, subsequent desensitisa4. 5.
268.
L. MICHAELS Registrar in Pathology.
Manchester.
Levene, M., Michaels, L. J. clin. Path. (in the press). Brownlee, G. Irish J. med. Sci. October, 1951, p. 495. 6. Godlowski, Z. Z. Enzymatic Concept of Anaphylaxis and
Allergy. Edinburgh, 1953.