- Email: [email protected]
MENINGOCOCCAL DISEASE IN SOUTH-WEST OF ENGLAND
806
blindness, and clinicians have not been encouraged to look for the earlier evidence of disease.l-6 These early and persisting signs and symptoms include chronic backache, shoulder, chest, and hip pains, non-pitting oedema, deep muscle abscesses, enlarged glands in the groin, and patches of epidermal oedema, visible as peau d’orange only when viewed in a cross-light on an otherwise perfectly normal skin. Musculoskeletal symptoms cause a major amount of incapacitating morbidity, especially amongst farmers and manual workers. In an endemic area of Nigeria, when these symptoms were taken as an indication for skin-snips, many puzzling cases were diagnosed for the first time71J and at last given relief. A 46-year-old Nigerian roadworker with a 6-year history of unexplained abdominal discomfort and backache had been labelled "? hypochondriac". He had enlarged lymph glands in the groin and peau d’orange on the abdomen and back. Spinal movements were normal. Skin snips were strongly positive. A course of diethylcarbamazine citrate (DEC) gave him his first real relief in years.
Many cases are missed in Nigeria through waiting for severe dermatitis or ocular problems to appear. How much more likely is the diagnosis to be missed when people return to the west having worked in an endemic area? Looking mainly for late signs is like restricting ourselves to diagnosing syphilis only at the onset of general paralysis of the insane or leprosy only when we can see foreshortened fingers. An obstetrician, who had worked in West Africa for several years, returned to the United States with backache and peau dorange on one hand. A rheumatologist in Washington diagnosed ankylosing spondylitis and a dermatologist at the National Institute of Health diagnosed scleroderma. The obstetrician went to Australia, where visual symptoms developed and microfilariae of 0 volvulus were found in the anterior chamber. DEC cured the eyes, and the musculoskeletal and dermatological symptoms as well, this link being realised only in retrospect. An anthropologist who had worked in an area of East Africa endemic for onchocerciasis had pruritus in Britain 15 months after probable exposure while living in the bush. Symptomatic treatment only was given. 9 months later chronic low backache started and a lumbar support was prescribed. After a further 16 months the pruritus intensified, a rash appeared on her trunk and buttock, and then pains started in the right hip. Now began 9 years of chronic low backache, hip pain, general rheumatic symptoms, pruritus, intermittent dermatitis, and insomnia. Despite many referrals, mainly to orthopaedic surgeons, no all-embracing diagnosis was reached, except a suggestion of hypochondria. Arthropathies developed in the right ankle and left knee, but it was not until itching in the eyes developed, with headache and paraesthesia from behind the eyes, over the head to the back of the neck, that an ophthalmologist was called in, and found signs suggestive of onchocerciasis and a positive filarial antigen test. It had taken 12 years to reach the
diagnosis.
When DEC and suramin was started, there was a strong Mazzotti reaction. Nodules appeared on her chest and right knee, and there was exacerbation of hip pain. Further courses of DEC and suramin were given over the next 2 Y2 years, with diminishing Mazzotti reactions. There was marked improvement not only in the ocular symptoms and pruritus, but also in the musculoskeletal symptoms. The lumbar support, which she had expected to wear for the rest of her life, was discarded 18 months after starting treatment, and she has been free from low back and hip pain since. Once more the significance of this was not realised until later. Onchocerciasis is still endemic over large areas of West and East Africa and Central and South America. All doctors treating patients who have travelled to these countries should be made aware of the early signs and symptoms of the disease. General practitioners,
dermatologists, rheumatologists, and orthopaedic surgeons, should be particularly on the alert, and not just the ophthalmologists and specialists in tropical medicine. 2 Springfield Road, Bury St Edmunds, Suffolk
IP33 3AN
MJ, Gabathuler AW. Report of onchocerciasis (May): 188-95. E Afr Med 1947 J
1. Gabathuler
C. A. PEARSON in the
Ulanga District.
2. 3.
Jopling WH. Onchocerciasis presenting without dermatitis. Br Med J 1960; i: 861. Lamp HC. Musculo-skeletal symptoms in onchocerciasis. W Afr MedJ 1967; 16: 60-62.
on an oil palm estate. Trans Roy Soc Trop Med Hyg 1971; 65: 484-89. 5. Buck AA, ed. Onchocerciasis: Symptomatology, pathology, diagnosis. Geneva: World
4. Thomson IG. Onchocerdasis
Health Organisation, 1974: 12. 6. Mahoney JL. Management of onchocerciasis. S Afr Med J 1982; 61: 50-52. 7. Pearson CA. Are we missing cases of onchocerciasis? Trop Doctor 1985; 15: 140-41. 8. Pearson CA, Brieger WR, Ramakrishna J, Kale OO, Adeniyi JD. Improving recognition of onchocerciasis: Non-classical symptoms. Trop Doctor 1985; 15: 160-63.
MENINGOCOCCAL DISEASE IN SOUTH-WEST OF ENGLAND
and co-workers
SIR,-Dr Cartwright (Sept 6, p 558) report a continuing outbreak of sulphonamide-resistant group B type 15 meningococcal disease in Gloucestershire with particular localisation of cases in certain communities. A comparable excess of cases, mostly with the same group and serotype, was seen during a similar period in the Plymouth Health District managed population (figure).
Quarterly
cases
of meningococcal infection in Plymouth Health
District managed population (Plymouth, West and South Devon, and East Cornwall).
The peak incidence in both outbreaks was early, with that of Plymouth in the first quarter and that of Gloucester in the last quarter of 1983. The total number of cases over the period October, 1981, to March, 1986, was also comparable (Gloucester 65, Plymouth 57). We have detailed information on 53 of these 57 cases, 37 of whom (70%) lived within Plymouth city. Although this proportion is similar to that reported from Stroud (66% or 43/65) there was no clustering either within urban Plymouth or in other towns and villages in the area. Until 1986, there was no excess meningococcal activity in other health districts in south-west England. To help general practitioners recognise cases early, bulletins summarising the presenting signs and symptoms and the management of contacts have been issued. Vomiting (86%) and rash (65%) were far more common as presenting features in 51 patients admitted to hospital in 1982-85, headache being recorded in 39%, confusion in 12 %, and joint pains in 10 %. When a vaccine becomes available, priority should be given to high-risk groups. In the absence of other known risk factors, agespecific incidence rates are useful in formulating vaccination policies (table). Despite the wide confidence limits, the priority risk groups for this
area
would be 15-19-year age group, followed
CUMULATIVE AGE-SPECIFIC INCIDENCE RATES (AND
95%
CONFIDENCE LIMITS) OF MENINGOCOCCAL GROUP B 15 AND C INFECTIONS
(1982-85) PER 100 000 MANAGED POPULATION
by
807 ages 0-4 and 10-14. The overlap between confidence limits makes it difficult for individual districts to decide upon their high-risk groups. We hope that national coordination of epidemiological information will reduce this overlap and provide a firmer basis for
preventive measures. Department of Community Health, Plymouth General Hospital
J. A. DAWSON JANET RICKARD
Public Health Laboratory, Demford Hospital,
P. J. WILKINSON
Plymouth PL6 8DH
SIR,-Dr Cartwright and colleagues note that in Gloucestershire only 57 % of cases of meningococcal disease were notified. Since it is reasonable
to assume
that almost all such
cases are
admitted
to
hospital, the laboratory making the bacteriological diagnosis might be the appropriate source for formal notification to originate in. This principle has been followed in this health district for many years. District Headquarters, Worcester and District Health Isaac Maddox House, Shrub Hill Road, Worcester WR4 9RW
Authority,
H. P. FERRER
MENINGOCOCCAL INFECTIONS AND ERADICATION OF THE CARRIER STATE
SiR,—Your Sept 6 editorial on meningococcal meningitis, recommends that in such patients eradication of meningococci from the nasopharynx should be attempted with rifampicin or sulphonamide before the patient is discharged from hospital. Penicillin, the drug of choice for treatment, will not necessarily achieve this.! However, during the initial penicillin therapy meningococci may seem to be eradicated from the nasopharynx, only for the organism to be isolated again several days after cessation of this treatment.2 Eradication of carriage in such patients should therefore be attempted even if the nasopharynx swab culture result is negative. Indeed the collection of nasopharyngeal swabs merely delays the start of such therapy, and swabbing is probably not useful in these circumstances. The choice of antibiotic for eradication should also be carefully considered, especially in view of the emergence of sulphonamide-resistant meningococci3 and the unreliable results from disc testing for sulphonamide sensitivity.4 Department of Microbiology, Medical School, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH
T. S. J. ELLIOTT
Department of Clinical Microbiology, Royal Victoria Infirmary, Newcastle upon Tyne
S.
J. PEDLER
1. Foster MT Jr, Sanders E, Ginter M. Epidemiology of sulfonamide-resistant meningococcal infection in a civilian population. Am J Epidemiol 1971; 93: 346-53. 2 Abramson JS, Spika JS. Persistence of Neisseria meningitidis in the upper respiratory tract after intravenous antibiotic therapy for systemic meningococcal disease. J Infect Dis 1985; 151: 370-71. 3. Poolman JT, Lmd I, Jonsdottir K, Oddvar Froholm L, Jones DM, Zahen HC. Meningococcal serotypes and serogroup B disease in North-West Europe. Lancet
1986; ii: 555-58. 4. Garrod LP, Lambert HP, O’Grady F. Antibiotic and chemotherapy, 5th ed.
Edinburgh Churchill Livingstone, 1981: 475-76.
MENINGOCOCCAL SEROTYPES AND SEROGROUP B DISEASE IN NORTH-WEST EUROPE
SiR,—To expand the information presented by Dr Poolman and p 555) on meningococcal serotypes and serogroup B disease in North-West Europe data for Scotland (population 5145 000) are relevant (see figure). As in other countries of North-West Europe group B meningococci predominated through the 1970s but were virtually equalled in number by serogroup C in 1985, this trend being maintained in the first half of 1986. Serogroup A meningococci outnumbered group C meningococci throughout most of the 1970s but have now fallen to a very low level.1,2 The picture with respect to serotypes of group B meningococci is different from that in the countries reviewed by Poolman et al in that the proportion of type
colleagues (Sept 6,
Incidence; relative contributions of serogroups A,B, and C; and relative of serotypes 2 and 15.
contributions
15 strains of group B meningococci has fluctuated over the period 1976-85. In the late 1970s, as in other countries, the proportion of type 2 meningococci fell profoundly but since then has shown an inverse relationship to the proportion of type 15 strains isolated, so that in the years when type 15 formed only a small proportion of serotypes type 2 have been increased in number and vice versa.3 In 1986, the proportion of strains belonging to type 15 has dropped yet again. Thus, the apparently unremitting increase in the proportion of group B strains of type 15 appearing in other North-West European countries has not been seen in Scotland. As elsewhere, the B:15:P1.16 strains have been sulphonamide resistant and, as noted in England and Wales,4 these strains have tended to be associated with disease in adolescents and young adults rather than with children under 5 years, the group in which most group B disease is
normally seen. The incidence rate of disease is higher than that seen in England and Wales and may be due to the fact that after 1974 instead of only confirmed cases of cerebrospinal fever being notified, notifications in Scotland have been of all meningococcal infections. The picture in Scotland with regard to serotypes 2 and 15 shows that the epidemiology of these serotypes may not necessarily always be the same in North-West Europe and emphasises the need for continuing surveillance, especially when decisions have to be made about the composition of vaccines directed against group B meningococci of different serotypes. The figures for notifications were provided by Mrs Anne Carey of the Communicable Diseases (Scotland) Unit and were based on Scottish Health Statistics and data from the Information Services Division of the Common Services Agenc;y.
Meningococcus Reference Laboratory (Scotland), Ruchill Hospital, R. J. FALLON Glasgow G20 9NB 1. Fallon RJ. Meningococcal infections in Scotland, first and second quarters 1986. Commun Dis Scot Weekly Rep 1986; 34: 5-10.
blindness, and clinicians have not been encouraged to look for the earlier evidence of disease.l-6 These early and persisting signs and symptoms include chronic backache, shoulder, chest, and hip pains, non-pitting oedema, deep muscle abscesses, enlarged glands in the groin, and patches of epidermal oedema, visible as peau d’orange only when viewed in a cross-light on an otherwise perfectly normal skin. Musculoskeletal symptoms cause a major amount of incapacitating morbidity, especially amongst farmers and manual workers. In an endemic area of Nigeria, when these symptoms were taken as an indication for skin-snips, many puzzling cases were diagnosed for the first time71J and at last given relief. A 46-year-old Nigerian roadworker with a 6-year history of unexplained abdominal discomfort and backache had been labelled "? hypochondriac". He had enlarged lymph glands in the groin and peau d’orange on the abdomen and back. Spinal movements were normal. Skin snips were strongly positive. A course of diethylcarbamazine citrate (DEC) gave him his first real relief in years.
Many cases are missed in Nigeria through waiting for severe dermatitis or ocular problems to appear. How much more likely is the diagnosis to be missed when people return to the west having worked in an endemic area? Looking mainly for late signs is like restricting ourselves to diagnosing syphilis only at the onset of general paralysis of the insane or leprosy only when we can see foreshortened fingers. An obstetrician, who had worked in West Africa for several years, returned to the United States with backache and peau dorange on one hand. A rheumatologist in Washington diagnosed ankylosing spondylitis and a dermatologist at the National Institute of Health diagnosed scleroderma. The obstetrician went to Australia, where visual symptoms developed and microfilariae of 0 volvulus were found in the anterior chamber. DEC cured the eyes, and the musculoskeletal and dermatological symptoms as well, this link being realised only in retrospect. An anthropologist who had worked in an area of East Africa endemic for onchocerciasis had pruritus in Britain 15 months after probable exposure while living in the bush. Symptomatic treatment only was given. 9 months later chronic low backache started and a lumbar support was prescribed. After a further 16 months the pruritus intensified, a rash appeared on her trunk and buttock, and then pains started in the right hip. Now began 9 years of chronic low backache, hip pain, general rheumatic symptoms, pruritus, intermittent dermatitis, and insomnia. Despite many referrals, mainly to orthopaedic surgeons, no all-embracing diagnosis was reached, except a suggestion of hypochondria. Arthropathies developed in the right ankle and left knee, but it was not until itching in the eyes developed, with headache and paraesthesia from behind the eyes, over the head to the back of the neck, that an ophthalmologist was called in, and found signs suggestive of onchocerciasis and a positive filarial antigen test. It had taken 12 years to reach the
diagnosis.
When DEC and suramin was started, there was a strong Mazzotti reaction. Nodules appeared on her chest and right knee, and there was exacerbation of hip pain. Further courses of DEC and suramin were given over the next 2 Y2 years, with diminishing Mazzotti reactions. There was marked improvement not only in the ocular symptoms and pruritus, but also in the musculoskeletal symptoms. The lumbar support, which she had expected to wear for the rest of her life, was discarded 18 months after starting treatment, and she has been free from low back and hip pain since. Once more the significance of this was not realised until later. Onchocerciasis is still endemic over large areas of West and East Africa and Central and South America. All doctors treating patients who have travelled to these countries should be made aware of the early signs and symptoms of the disease. General practitioners,
dermatologists, rheumatologists, and orthopaedic surgeons, should be particularly on the alert, and not just the ophthalmologists and specialists in tropical medicine. 2 Springfield Road, Bury St Edmunds, Suffolk
IP33 3AN
MJ, Gabathuler AW. Report of onchocerciasis (May): 188-95. E Afr Med 1947 J
1. Gabathuler
C. A. PEARSON in the
Ulanga District.
2. 3.
Jopling WH. Onchocerciasis presenting without dermatitis. Br Med J 1960; i: 861. Lamp HC. Musculo-skeletal symptoms in onchocerciasis. W Afr MedJ 1967; 16: 60-62.
on an oil palm estate. Trans Roy Soc Trop Med Hyg 1971; 65: 484-89. 5. Buck AA, ed. Onchocerciasis: Symptomatology, pathology, diagnosis. Geneva: World
4. Thomson IG. Onchocerdasis
Health Organisation, 1974: 12. 6. Mahoney JL. Management of onchocerciasis. S Afr Med J 1982; 61: 50-52. 7. Pearson CA. Are we missing cases of onchocerciasis? Trop Doctor 1985; 15: 140-41. 8. Pearson CA, Brieger WR, Ramakrishna J, Kale OO, Adeniyi JD. Improving recognition of onchocerciasis: Non-classical symptoms. Trop Doctor 1985; 15: 160-63.
MENINGOCOCCAL DISEASE IN SOUTH-WEST OF ENGLAND
and co-workers
SIR,-Dr Cartwright (Sept 6, p 558) report a continuing outbreak of sulphonamide-resistant group B type 15 meningococcal disease in Gloucestershire with particular localisation of cases in certain communities. A comparable excess of cases, mostly with the same group and serotype, was seen during a similar period in the Plymouth Health District managed population (figure).
Quarterly
cases
of meningococcal infection in Plymouth Health
District managed population (Plymouth, West and South Devon, and East Cornwall).
The peak incidence in both outbreaks was early, with that of Plymouth in the first quarter and that of Gloucester in the last quarter of 1983. The total number of cases over the period October, 1981, to March, 1986, was also comparable (Gloucester 65, Plymouth 57). We have detailed information on 53 of these 57 cases, 37 of whom (70%) lived within Plymouth city. Although this proportion is similar to that reported from Stroud (66% or 43/65) there was no clustering either within urban Plymouth or in other towns and villages in the area. Until 1986, there was no excess meningococcal activity in other health districts in south-west England. To help general practitioners recognise cases early, bulletins summarising the presenting signs and symptoms and the management of contacts have been issued. Vomiting (86%) and rash (65%) were far more common as presenting features in 51 patients admitted to hospital in 1982-85, headache being recorded in 39%, confusion in 12 %, and joint pains in 10 %. When a vaccine becomes available, priority should be given to high-risk groups. In the absence of other known risk factors, agespecific incidence rates are useful in formulating vaccination policies (table). Despite the wide confidence limits, the priority risk groups for this
area
would be 15-19-year age group, followed
CUMULATIVE AGE-SPECIFIC INCIDENCE RATES (AND
95%
CONFIDENCE LIMITS) OF MENINGOCOCCAL GROUP B 15 AND C INFECTIONS
(1982-85) PER 100 000 MANAGED POPULATION
by
807 ages 0-4 and 10-14. The overlap between confidence limits makes it difficult for individual districts to decide upon their high-risk groups. We hope that national coordination of epidemiological information will reduce this overlap and provide a firmer basis for
preventive measures. Department of Community Health, Plymouth General Hospital
J. A. DAWSON JANET RICKARD
Public Health Laboratory, Demford Hospital,
P. J. WILKINSON
Plymouth PL6 8DH
SIR,-Dr Cartwright and colleagues note that in Gloucestershire only 57 % of cases of meningococcal disease were notified. Since it is reasonable
to assume
that almost all such
cases are
admitted
to
hospital, the laboratory making the bacteriological diagnosis might be the appropriate source for formal notification to originate in. This principle has been followed in this health district for many years. District Headquarters, Worcester and District Health Isaac Maddox House, Shrub Hill Road, Worcester WR4 9RW
Authority,
H. P. FERRER
MENINGOCOCCAL INFECTIONS AND ERADICATION OF THE CARRIER STATE
SiR,—Your Sept 6 editorial on meningococcal meningitis, recommends that in such patients eradication of meningococci from the nasopharynx should be attempted with rifampicin or sulphonamide before the patient is discharged from hospital. Penicillin, the drug of choice for treatment, will not necessarily achieve this.! However, during the initial penicillin therapy meningococci may seem to be eradicated from the nasopharynx, only for the organism to be isolated again several days after cessation of this treatment.2 Eradication of carriage in such patients should therefore be attempted even if the nasopharynx swab culture result is negative. Indeed the collection of nasopharyngeal swabs merely delays the start of such therapy, and swabbing is probably not useful in these circumstances. The choice of antibiotic for eradication should also be carefully considered, especially in view of the emergence of sulphonamide-resistant meningococci3 and the unreliable results from disc testing for sulphonamide sensitivity.4 Department of Microbiology, Medical School, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH
T. S. J. ELLIOTT
Department of Clinical Microbiology, Royal Victoria Infirmary, Newcastle upon Tyne
S.
J. PEDLER
1. Foster MT Jr, Sanders E, Ginter M. Epidemiology of sulfonamide-resistant meningococcal infection in a civilian population. Am J Epidemiol 1971; 93: 346-53. 2 Abramson JS, Spika JS. Persistence of Neisseria meningitidis in the upper respiratory tract after intravenous antibiotic therapy for systemic meningococcal disease. J Infect Dis 1985; 151: 370-71. 3. Poolman JT, Lmd I, Jonsdottir K, Oddvar Froholm L, Jones DM, Zahen HC. Meningococcal serotypes and serogroup B disease in North-West Europe. Lancet
1986; ii: 555-58. 4. Garrod LP, Lambert HP, O’Grady F. Antibiotic and chemotherapy, 5th ed.
Edinburgh Churchill Livingstone, 1981: 475-76.
MENINGOCOCCAL SEROTYPES AND SEROGROUP B DISEASE IN NORTH-WEST EUROPE
SiR,—To expand the information presented by Dr Poolman and p 555) on meningococcal serotypes and serogroup B disease in North-West Europe data for Scotland (population 5145 000) are relevant (see figure). As in other countries of North-West Europe group B meningococci predominated through the 1970s but were virtually equalled in number by serogroup C in 1985, this trend being maintained in the first half of 1986. Serogroup A meningococci outnumbered group C meningococci throughout most of the 1970s but have now fallen to a very low level.1,2 The picture with respect to serotypes of group B meningococci is different from that in the countries reviewed by Poolman et al in that the proportion of type
colleagues (Sept 6,
Incidence; relative contributions of serogroups A,B, and C; and relative of serotypes 2 and 15.
contributions
15 strains of group B meningococci has fluctuated over the period 1976-85. In the late 1970s, as in other countries, the proportion of type 2 meningococci fell profoundly but since then has shown an inverse relationship to the proportion of type 15 strains isolated, so that in the years when type 15 formed only a small proportion of serotypes type 2 have been increased in number and vice versa.3 In 1986, the proportion of strains belonging to type 15 has dropped yet again. Thus, the apparently unremitting increase in the proportion of group B strains of type 15 appearing in other North-West European countries has not been seen in Scotland. As elsewhere, the B:15:P1.16 strains have been sulphonamide resistant and, as noted in England and Wales,4 these strains have tended to be associated with disease in adolescents and young adults rather than with children under 5 years, the group in which most group B disease is
normally seen. The incidence rate of disease is higher than that seen in England and Wales and may be due to the fact that after 1974 instead of only confirmed cases of cerebrospinal fever being notified, notifications in Scotland have been of all meningococcal infections. The picture in Scotland with regard to serotypes 2 and 15 shows that the epidemiology of these serotypes may not necessarily always be the same in North-West Europe and emphasises the need for continuing surveillance, especially when decisions have to be made about the composition of vaccines directed against group B meningococci of different serotypes. The figures for notifications were provided by Mrs Anne Carey of the Communicable Diseases (Scotland) Unit and were based on Scottish Health Statistics and data from the Information Services Division of the Common Services Agenc;y.
Meningococcus Reference Laboratory (Scotland), Ruchill Hospital, R. J. FALLON Glasgow G20 9NB 1. Fallon RJ. Meningococcal infections in Scotland, first and second quarters 1986. Commun Dis Scot Weekly Rep 1986; 34: 5-10.