1305 Rather than dabbling in social Darwinism and having us believe that trade unionism is a "collective bribery" which is the inheritance of a mammalian tendency toward plunder, preying, and violence, Passmore should leave the world of fresh fruit, early to bed, and outdoor exercise, which he says he learned as a child, and visit the coalmines and steelworks to meet some who had to resort to "collective bribery" to begin to secure those same amenities. A dilettante dissertation by a physiologist on primary care does not deserve to be in the pages of a journal such as The Lancet, which has in the past taken a serious view of the problems of getting care to people. If Passmore finds altruism, compassion, and dedication to meeting people’s needs, however and whenever those needs arise, too difficult to fit into his scheme of orderly, disease specific, practical primary care, then it would be well for him to stick to his experimental preparations, good eating habits, and jogging, and leave the problems of primary care to those of us who are trying to deliver it.
terfere with the natural course of gestation, perhaps prematurely ; this letter may reveal other areas with a similar experience. Exchange of ideas at this stage may help such investigations to be more effective in the endeavour to reduce intra-partum loss of life.
Glyncorrwg Health Centre, near Port Talbot, Glamorgan SA13
First, the consultative document containing the proposals, like all other consultative documents issued by the Commission, serves only to put forward proposals from the Commission on which the views of interested parties are sought. The objective is to see what others concerned think of the proposals, and the proposals made will be reconsidered in the light of the comments received. This leads me to the statement by Dr Freeman and Dr Ingham that the consultative document "does not seem to have been well publicised". The Commission put out a Press notice in the usual way when the document was published and sent out over 800 copies of the notice and the document to the national and regional Press and medical and scientific journals. In addition, the document was sent to some 50 of the professional and scientific bodies concerned, with a request for their comments. I am sorry that, at the time they wrote their letter, Dr Freeman and Dr Ingham had not received the copy of the document they had requested but demand for it has been
3BL
West Sussex Area Health
Authority, Goring-by-Sea, Worthing, West Sussex BN12 4NQ
DANGEROUS PATHOGENS
SIR,-Since my Division of the Health and Safety Executive had some involvement with the recent proposals for regulations to notify H.S.E. of work with dangerous pathogens I would like to comment on the letter from Dr Freeman and Dr
Ingham (Nov. 24, p. 1134).
J. J. FREY
PERINATAL MORTALITY
SIR,-Professor Rooth (Dec. 1, p. 1170) claims that high and maintained standards of obstetric care are responsible for the creditably low perinatal mortality rate (PMR) in Sweden. During the past twenty years we have been accustomed to finding the rate for West Sussex to be at least 10% lower than that for England and Wales. The standardised PMR of this area for the years 1974-78 was calculated by Mallett and Knox’ to be 88.6. This was eleventh in order from the lowest of the ninety health areas. Their thesis is that standardisation of the rate by birthweights eliminates, to an extent, the effects of social background. The performance of obstetricians in West Sussex was, on this measure, of high quality. In 1978, however, the PMR for this area was no better than the national figure of 15-5. It seems that this poor result was not just an occasional variation resulting from small numbers. The four-year moving average of the rate is rising, and the mean for the last four years is just about the present rate in England and Wales. There is a tendency for the rate to increase, contrary to its pattern before the last three years and contrary to the national trend. The stillbirth and early neonatal rates (the two components of the perinatal rate) have both reversed their previous steady improvement. When the rates in the three districts of the area are examined separately, no district is immune from an increase during the past three years. The lowest perinatal mortality and stillbirth rates are achieved in the district with the fewest births for each consultant obstetrician (i.e., the most generous consultant cover); the district with the largest number of all obstetric staff, proportional to the number of births, has the highest stillbirth rate. It may be that when junior staff are available, they take decisions beyond their competence. The evidence for the conclusions is inadequate; the association may occur purely by chance. We are in process of examining the multiple factors which can influence a PMR in order to determine whether the apparent increase truly represents a larger number of unsuccessful pregnancies. It is possible that changes in reporting methods are the only cause of alteration in the rates. We are analysing the characteristics of the mothers who lose babies and categorising the causes of early neonatal death. Our intention had been to present our findings to the obstetric and pxdiatric divisions concerned to open up a discussion on their validity and such changes in practice as might be indicated. Your series of articles on Better Perinatal Health, however, prompts us to in1. Mallett R, Knox EG. Standardized perinatal mortality ratios: utility and interpretation. Commun Med 1979; 1: 6-13.
technique,
S. A. COOPER A. S. HARRIS B. S. HOLMES G. RICHARDS
heavy. .
There is not space to deal adequately with some of the other issues in their letter, or with those in your editorial of Nov. 10, and there seems little point in debating further at the moment when we are in fact at a consultative stage and can deal with all these matters as we receive comments on the document. Health & Safety Executive, 25 Chapel Street, London NW1 5DT
K. P.
DUNCAN,
Director of medical services
DELAYED HYPERSENSITIVITY TO CHLAMYDIA TRACHOMATIS: CAUSE OF CHRONIC PROSTATITIS? no specific microbial aetiology for chronic prosbe found treatment is notoriously unsuccessful.’I Mardh et al. suggested that chlamydiae might be a cause but their cultural and serological tests did not confirm this suggestion.3 Delayed hypersensitivity tests to chlamydial antigens are used in the diagnosis of lymphogranuloma venereum, and there is evidence that delayed hypersensitivity may play a role in the manifestations of trachoma.4 We have studied a case of chronic non-bacterial prostatitis which could be a manifestation of delayed hypersensitivity to Chlamydia trachomatis. C. trachomatis strain TE55 (serologically identical to LGVII),
SIR,-When
tatitis
can
kindly provided by
Prof. L. H. Collier (The London
Hospital),
was
1. Feit RM, Fair WR. Prostatitis. Sex Transm Dis 1978; 5: 78-80. P-A, Colleen S, Holmquist B. Chlamydia in chronic prostatitis. Br
2. Mardh
Med J 1972; 4: 361. 3. Mardh P-A, Ripa KT, Colleen S, Treharne JD, Darougar S. Role of Chlamydia trachomatis in non-acute prostatitis. Br J Vener Dis 1978; 54: 330-334. 4. Grayston JT, Wang S-P. New knowledge of chlamydiæ and the diseases they cause. J Infect Dis 1975; 132: 87-105.
1306 grown in
yolk sacs at 35 °C. Chlamydial suspensions were prepareds without the potassium chloride step and the pellet was resuspended in saline, boiled for 30 min, and preserved with 0.3% phenol and 0-1% formaldehyde. Before inactivation the suspension contained 10" inclusion-forming units/ml and 108.s total particles/ml. A control suspension was prepared from the yolk sacs of uninoculated eggs in the same way and adjusted to the same optical density at 350 nm. For skin tests 0. 1 ml of antigen was inoculated intradermally into the flexor aspect of the forearm and reactions were measured at 1 h and 48 h, the surrounding erythematous zone being considered to be non-specific. A positive reaction to chlamydial antigen at 48 h was defined by an induration which was 5 mm or more bigger than that produced by the control preparation. Antigens were injected at previously unused skin sites. Both forearms were used alternatively for chlamydial and control preparations. Anti-chlamydial antibodies were sought by indirect microimmunofluorescence6 and isolation of C. trachomatis was attempted on McCoy tissue-culture cells pretreated with idoxuridine.’ A 36-year-old man complained of painful swollen testes associated with pain in the perineum and low in the back. There was no dysuria or urethral discharge. He also had a low-grade conjunctivitis. His symptoms became chronic, with partial remissions and exacerbations. Clinical examination revealed a tender enlarged prostate and bilateral epididymitis. Urine cultures were negative. He was treated for non-specific epididymitis and prostatitis with short courses of antimicrobial agents, but with no significant improvement. Bilateral epididymectomy was also ineffective. When we saw the patient, 3 years after his illness had started, his condition was unchanged: testes enlarged and tender ; prostate enlarged, tender, and boggy; no urethral discharge ; and low-grade conjunctivitis. Routine blood tests were all normal and bacterial cultures of the urine were negative, as were serological tests for syphilis. Examination of a urethral swab revealed clumps of neutrophils, with occasional lymphocytes, and a conjunctival scraping showed large numbers of plasma cells and lymphocytes; however, culture yielded no growth of C. trachomatis or other microorganisms. Antibodies to oculogenital serotypes of C. trachomatis were detected in the serum at 1:16 but there were no antibodies to either endemic trachoma and lymphogranuloma venereum serotypes or to selected C. psittaci strains. No antibody was detected in eye secretions. These results pointed to exposure to an oculogenital serotype of C. trachomatis. The chlamydial skin test was strongly positive at 48 h. Antibodies to oculogenital serotypes of C. trachomatis were also found in the serum of the patient’s wife, but the organism could not be isolated from her cervix. She was not skin tested. The patient was treated with erythromycin stearate, 500 mg every 6 h for 5 zmonths. After 3 weeks the patient experienced an acute exacerbation of symptoms, which subsided after 2 weeks. Subsequently, his symptoms improved and at 2 months his prostate was clinically normal and the conjunctivitis had disappeared; the testes, however, remained enlarged. Skin tests became negative (see table). The patient’s wife was given erythromycin for 3 weeks. Three lines of evidence lead to the idea that chronic nonbacterial prostatitis may, in some cases, be the result of delayed hypersensitivity to C. trachomatis. The first is the evidence that these organisms produce genital-tract disease.8 Secondly, prostatitis, usually asymptomatic, sometimes accompanies acute non-specific urethritis and may occasionally
J, Blyth WA. Interactions between trachoma organisms and macrophages. In: Nichols RL, ed. Trachoma and related disorders caused by chlamydial agents. Amsterdam, Netherlands: Excerpta Medica, 1971:
5. Taverne
88-107.
JD, Darougar S, Jones BR. Modifications of the microimmunofluorescence test to provide a routine serodiagnostic test for chlamydial infection. J Clin Path 1977; 30: 510-17. 7. Reeve P, Owen J, Oriel JD. Laboratory procedures for the isolation of Chlamydia trachomatis from the human genital tract. J Clin Path 1975; 28: 910-14. 8. Schachter J. Chlamydial infections. N Engl J Med 1978; 298: 428-35. 6. Treharne
CLINICAL RESPONSE
(RECTAL EXAMINATION) AND RESULTS OF
CHLAMYDIAL SKIN TESTS DURING TREATMENT WITH
ERYTHROMYCIN
I
Clinical* Skin testt
I
I
I
+
14
I
i
I
I
+ — — — — —
9
..
6
4
4
signs of prostatitis, -- no signs of prostatitis. tMean diameter of induration (mm). A mean diameter
terfere with the natural course of gestation, perhaps prematurely ; this letter may reveal other areas with a similar experience. Exchange of ideas at this stage may help such investigations to be more effective in the endeavour to reduce intra-partum loss of life.
Glyncorrwg Health Centre, near Port Talbot, Glamorgan SA13
First, the consultative document containing the proposals, like all other consultative documents issued by the Commission, serves only to put forward proposals from the Commission on which the views of interested parties are sought. The objective is to see what others concerned think of the proposals, and the proposals made will be reconsidered in the light of the comments received. This leads me to the statement by Dr Freeman and Dr Ingham that the consultative document "does not seem to have been well publicised". The Commission put out a Press notice in the usual way when the document was published and sent out over 800 copies of the notice and the document to the national and regional Press and medical and scientific journals. In addition, the document was sent to some 50 of the professional and scientific bodies concerned, with a request for their comments. I am sorry that, at the time they wrote their letter, Dr Freeman and Dr Ingham had not received the copy of the document they had requested but demand for it has been
3BL
West Sussex Area Health
Authority, Goring-by-Sea, Worthing, West Sussex BN12 4NQ
DANGEROUS PATHOGENS
SIR,-Since my Division of the Health and Safety Executive had some involvement with the recent proposals for regulations to notify H.S.E. of work with dangerous pathogens I would like to comment on the letter from Dr Freeman and Dr
Ingham (Nov. 24, p. 1134).
J. J. FREY
PERINATAL MORTALITY
SIR,-Professor Rooth (Dec. 1, p. 1170) claims that high and maintained standards of obstetric care are responsible for the creditably low perinatal mortality rate (PMR) in Sweden. During the past twenty years we have been accustomed to finding the rate for West Sussex to be at least 10% lower than that for England and Wales. The standardised PMR of this area for the years 1974-78 was calculated by Mallett and Knox’ to be 88.6. This was eleventh in order from the lowest of the ninety health areas. Their thesis is that standardisation of the rate by birthweights eliminates, to an extent, the effects of social background. The performance of obstetricians in West Sussex was, on this measure, of high quality. In 1978, however, the PMR for this area was no better than the national figure of 15-5. It seems that this poor result was not just an occasional variation resulting from small numbers. The four-year moving average of the rate is rising, and the mean for the last four years is just about the present rate in England and Wales. There is a tendency for the rate to increase, contrary to its pattern before the last three years and contrary to the national trend. The stillbirth and early neonatal rates (the two components of the perinatal rate) have both reversed their previous steady improvement. When the rates in the three districts of the area are examined separately, no district is immune from an increase during the past three years. The lowest perinatal mortality and stillbirth rates are achieved in the district with the fewest births for each consultant obstetrician (i.e., the most generous consultant cover); the district with the largest number of all obstetric staff, proportional to the number of births, has the highest stillbirth rate. It may be that when junior staff are available, they take decisions beyond their competence. The evidence for the conclusions is inadequate; the association may occur purely by chance. We are in process of examining the multiple factors which can influence a PMR in order to determine whether the apparent increase truly represents a larger number of unsuccessful pregnancies. It is possible that changes in reporting methods are the only cause of alteration in the rates. We are analysing the characteristics of the mothers who lose babies and categorising the causes of early neonatal death. Our intention had been to present our findings to the obstetric and pxdiatric divisions concerned to open up a discussion on their validity and such changes in practice as might be indicated. Your series of articles on Better Perinatal Health, however, prompts us to in1. Mallett R, Knox EG. Standardized perinatal mortality ratios: utility and interpretation. Commun Med 1979; 1: 6-13.
technique,
S. A. COOPER A. S. HARRIS B. S. HOLMES G. RICHARDS
heavy. .
There is not space to deal adequately with some of the other issues in their letter, or with those in your editorial of Nov. 10, and there seems little point in debating further at the moment when we are in fact at a consultative stage and can deal with all these matters as we receive comments on the document. Health & Safety Executive, 25 Chapel Street, London NW1 5DT
K. P.
DUNCAN,
Director of medical services
DELAYED HYPERSENSITIVITY TO CHLAMYDIA TRACHOMATIS: CAUSE OF CHRONIC PROSTATITIS? no specific microbial aetiology for chronic prosbe found treatment is notoriously unsuccessful.’I Mardh et al. suggested that chlamydiae might be a cause but their cultural and serological tests did not confirm this suggestion.3 Delayed hypersensitivity tests to chlamydial antigens are used in the diagnosis of lymphogranuloma venereum, and there is evidence that delayed hypersensitivity may play a role in the manifestations of trachoma.4 We have studied a case of chronic non-bacterial prostatitis which could be a manifestation of delayed hypersensitivity to Chlamydia trachomatis. C. trachomatis strain TE55 (serologically identical to LGVII),
SIR,-When
tatitis
can
kindly provided by
Prof. L. H. Collier (The London
Hospital),
was
1. Feit RM, Fair WR. Prostatitis. Sex Transm Dis 1978; 5: 78-80. P-A, Colleen S, Holmquist B. Chlamydia in chronic prostatitis. Br
2. Mardh
Med J 1972; 4: 361. 3. Mardh P-A, Ripa KT, Colleen S, Treharne JD, Darougar S. Role of Chlamydia trachomatis in non-acute prostatitis. Br J Vener Dis 1978; 54: 330-334. 4. Grayston JT, Wang S-P. New knowledge of chlamydiæ and the diseases they cause. J Infect Dis 1975; 132: 87-105.
1306 grown in
yolk sacs at 35 °C. Chlamydial suspensions were prepareds without the potassium chloride step and the pellet was resuspended in saline, boiled for 30 min, and preserved with 0.3% phenol and 0-1% formaldehyde. Before inactivation the suspension contained 10" inclusion-forming units/ml and 108.s total particles/ml. A control suspension was prepared from the yolk sacs of uninoculated eggs in the same way and adjusted to the same optical density at 350 nm. For skin tests 0. 1 ml of antigen was inoculated intradermally into the flexor aspect of the forearm and reactions were measured at 1 h and 48 h, the surrounding erythematous zone being considered to be non-specific. A positive reaction to chlamydial antigen at 48 h was defined by an induration which was 5 mm or more bigger than that produced by the control preparation. Antigens were injected at previously unused skin sites. Both forearms were used alternatively for chlamydial and control preparations. Anti-chlamydial antibodies were sought by indirect microimmunofluorescence6 and isolation of C. trachomatis was attempted on McCoy tissue-culture cells pretreated with idoxuridine.’ A 36-year-old man complained of painful swollen testes associated with pain in the perineum and low in the back. There was no dysuria or urethral discharge. He also had a low-grade conjunctivitis. His symptoms became chronic, with partial remissions and exacerbations. Clinical examination revealed a tender enlarged prostate and bilateral epididymitis. Urine cultures were negative. He was treated for non-specific epididymitis and prostatitis with short courses of antimicrobial agents, but with no significant improvement. Bilateral epididymectomy was also ineffective. When we saw the patient, 3 years after his illness had started, his condition was unchanged: testes enlarged and tender ; prostate enlarged, tender, and boggy; no urethral discharge ; and low-grade conjunctivitis. Routine blood tests were all normal and bacterial cultures of the urine were negative, as were serological tests for syphilis. Examination of a urethral swab revealed clumps of neutrophils, with occasional lymphocytes, and a conjunctival scraping showed large numbers of plasma cells and lymphocytes; however, culture yielded no growth of C. trachomatis or other microorganisms. Antibodies to oculogenital serotypes of C. trachomatis were detected in the serum at 1:16 but there were no antibodies to either endemic trachoma and lymphogranuloma venereum serotypes or to selected C. psittaci strains. No antibody was detected in eye secretions. These results pointed to exposure to an oculogenital serotype of C. trachomatis. The chlamydial skin test was strongly positive at 48 h. Antibodies to oculogenital serotypes of C. trachomatis were also found in the serum of the patient’s wife, but the organism could not be isolated from her cervix. She was not skin tested. The patient was treated with erythromycin stearate, 500 mg every 6 h for 5 zmonths. After 3 weeks the patient experienced an acute exacerbation of symptoms, which subsided after 2 weeks. Subsequently, his symptoms improved and at 2 months his prostate was clinically normal and the conjunctivitis had disappeared; the testes, however, remained enlarged. Skin tests became negative (see table). The patient’s wife was given erythromycin for 3 weeks. Three lines of evidence lead to the idea that chronic nonbacterial prostatitis may, in some cases, be the result of delayed hypersensitivity to C. trachomatis. The first is the evidence that these organisms produce genital-tract disease.8 Secondly, prostatitis, usually asymptomatic, sometimes accompanies acute non-specific urethritis and may occasionally
J, Blyth WA. Interactions between trachoma organisms and macrophages. In: Nichols RL, ed. Trachoma and related disorders caused by chlamydial agents. Amsterdam, Netherlands: Excerpta Medica, 1971:
5. Taverne
88-107.
JD, Darougar S, Jones BR. Modifications of the microimmunofluorescence test to provide a routine serodiagnostic test for chlamydial infection. J Clin Path 1977; 30: 510-17. 7. Reeve P, Owen J, Oriel JD. Laboratory procedures for the isolation of Chlamydia trachomatis from the human genital tract. J Clin Path 1975; 28: 910-14. 8. Schachter J. Chlamydial infections. N Engl J Med 1978; 298: 428-35. 6. Treharne
CLINICAL RESPONSE
(RECTAL EXAMINATION) AND RESULTS OF
CHLAMYDIAL SKIN TESTS DURING TREATMENT WITH
ERYTHROMYCIN
I
Clinical* Skin testt
I
I
I
+
14
I
i
I
I
+ — — — — —
9
..
6
4
4
signs of prostatitis, -- no signs of prostatitis. tMean diameter of induration (mm). A mean diameter
