- Email: [email protected]
SEROLOGICAL DIAGNOSIS OF SALMONELLA INFECTIONS
456 and bilateral hilar nodes, with known date of onset of symptoms. Most were women (166, 89%), with a mean age of 39 years (range 14-67). All cases were white and resident in the same geographical area. In almost half the patients (91) symptoms were first noticed between April and June. This distribution was significantly higher for spring than for the other seasons (p < 0 0001 ), both overall and in most of the years examined. The observation of a seasonal pattern in the frequency of sarcoidosis suggests that an unidentified environmental factor(s), probably of infectious origin, plays a part in the aetiology of this disease.
presented with erythema nodosum
TABLE II-SENSITIVITIES AND SPECIFICITIES OF AGGLUTINATION
TESTS
Hospital de Bellvitge Princeps d’Espanya, L’Hospitalet de Llobregat, Barcelona
FRANCESC BADRINAS
Hospital German Trias i Pujol, Barcelona
JOSEP MORERA
Hospital L’AlianÇa Mataronina, 08301 Mataró, Barcelona, Spain
ENRIQUETA FITÉ
Institut Municipal de la Salut, Barcelona
ANTONI PLASENCIA
Hiraga Y, Odaka M, et al. A cooperative study of sarcoidosis in Asia and Africa: analytic epidemiology. Ann NY Acad Sci 1976; 278: 355-67. 2. Henke CE, Henke G, Elveback LR, Beard CM, Baillard DJ, Kurland LT. The epidemiology of sarcoidosis in Rochester, Minnesota: a population-based study of incidence and survival. Am J Epidemiol 1986; 123: 840-45. 3. Poukkula A, Huhti E, Lilja M, Saloheimo M. Incidence and clinical picture of sarcoidosis in a circumscribed geographical area. Br J Dis Chest 1986; 80: 138-47. 1. Hosoda Y,
SEROLOGICAL DIAGNOSIS OF SALMONELLA INFECTIONS
SIR,-Isomaki and colleagues (June 24, p 1411) suggest the use of enzyme immunoassay (EIA) in the diagnosis of salmonellosis. I report the use of a classic type of Widal test during a continuing outbreak of Salmonella enteritidis phage type 8. The outbreak occurred in a 376-bed hospital for acute and long stay geriatric patients and for psychiatric and psychogeriatric patients. Sera from an
34 of 51 patients, from Jan, 1986, to May, 1986, were examined. The Widal agglutination tests were done with a standardised suspension of the outbreak strain by Cruickshank and colleagues’ method.’ The patients were classified as symptom-free, mildly ill (ie, loose stools only), or ill (frequent watery stools with or without abdominal pain). All initial sera were taken between 7 and 28 days after the onset of symptoms, or, in symptom-free patients, after the first positive stool sample was taken. Sera were also obtained from patients who remained culture negative for Salmonella spp, 19 of whom had diarrhoea and 17 of whom did not. Positive Widal serology correlated strongly with the more serious
type of disease (table I). Isomaki and coworkers defined Widal positivity as a titre of 40 or more. We took our cut-off value at 80 or TABLE I-AGGLUTINATION TESTS IN
SALMONELLOSIS
34 PATIENTS WITH
after assessing the results of the control sera. Table n shows the sensitivities and specificities of the Widal reaction in our study population. Further samples of sera were available from 13 patients with significant positivity in initial specimens (our criteria). These sera were taken between 42 and 113 days from the onset of symptoms. In only 4 (at day 56, 83, 85, and 86) did the sera become negative. In the other 9, 3 had persistent positive stool cultures. In patients with more severe partly invasive salmonellosis serological tests may be helpful, especially if such a diagnosis is attempted more than one month after the initial illness--eg, in reactive arthritis. In this respect the Widal test may be useful if the appropriate antigens are used. However, in mild disease and symptom-free patients such serology may well be negative and therefore would not help to identify epidemics or chronic carriers. Such instances explain why EIA, although undoubtedly more sensitive than the classic agglutination test, was not totally successful in identifying all Salmonella culture-positive patients in Isomaki and colleagues’ series. More importantly, such serological studies may well throw light on the poorly understood pathological processes involved in the various forms of salmonellosis.
more
Department of Pathological Sciences, Division of Bacteriology, University of Manchester, Manchester M13 9PT
SARAH MAXWELL
1. Cruickshank
12rh ed.
R, Duguid JP, Marmion BP, Swain RHA. Medical microbiology, vol 2 Edinburgh: Churchill Livingstone, 1975: 416-18.
DERMATOFIBROMAS AND ARTHROPOD BITES
SIR,-Mr Evans and colleagues (July 1, p 36) do not give data on the dermatofibromas and sex distribution in their patients. Since 100 specimens were examined histologically, did each patient questioned have over 3 lesions excised, or were their data retrospective? Dermatofibromas usually occur on the lower extremities and are more common in women than men.1 This latter fact is cited to support the insect-bite theory on the grounds that women tend to have unprotected legs and are therefore more likely to be bitten. Although Evans at al state in their summary that the controls were matched they do not provide details of the characteristics selected. If patients and controls were not age and sex matched the validity of the comparison is questionable. It is not surprising that all the controls recalled being bitten by "insects" several times in one 24-h period at some stage in their lives. This does not address the question whether there was a causal relation between the bite and the subsequent lesion. I have yet to see a patient who has a clear recollection of being bitten at the same site as the dermatofibroma, although many remember being bitten at some time. As Evans et al point out, dermatofibroma is not a foreign-body giant-cell reaction, so it would have been surprising if they had identified arthropod material or chitin residues in serial sections. Perhaps an angiogenic, histiocyte chemotactic peptide regulatory factor will be identified in the saliva of midges. A study of the occurrence of dermatofibromas on the legs of women who habitually wear trousers might keep the argument alive. Institute of Dermatology,
St Thomas’s Hospital, London SE1 7EH 1. Greaves MW.
*Positive result when titre > 40. tPositive result when titre > 80.
C. E. H. GRATTAN
Histiocytic proliferative disorders. In: Rook A, Wilkinson DS, Ebling FJG, Champion RH, Burton JL, eds. Textbook of dermatology, vol 2. Oxford.
Blackwell Scientific Publications, 1986: 1706-08.
presented with erythema nodosum
TABLE II-SENSITIVITIES AND SPECIFICITIES OF AGGLUTINATION
TESTS
Hospital de Bellvitge Princeps d’Espanya, L’Hospitalet de Llobregat, Barcelona
FRANCESC BADRINAS
Hospital German Trias i Pujol, Barcelona
JOSEP MORERA
Hospital L’AlianÇa Mataronina, 08301 Mataró, Barcelona, Spain
ENRIQUETA FITÉ
Institut Municipal de la Salut, Barcelona
ANTONI PLASENCIA
Hiraga Y, Odaka M, et al. A cooperative study of sarcoidosis in Asia and Africa: analytic epidemiology. Ann NY Acad Sci 1976; 278: 355-67. 2. Henke CE, Henke G, Elveback LR, Beard CM, Baillard DJ, Kurland LT. The epidemiology of sarcoidosis in Rochester, Minnesota: a population-based study of incidence and survival. Am J Epidemiol 1986; 123: 840-45. 3. Poukkula A, Huhti E, Lilja M, Saloheimo M. Incidence and clinical picture of sarcoidosis in a circumscribed geographical area. Br J Dis Chest 1986; 80: 138-47. 1. Hosoda Y,
SEROLOGICAL DIAGNOSIS OF SALMONELLA INFECTIONS
SIR,-Isomaki and colleagues (June 24, p 1411) suggest the use of enzyme immunoassay (EIA) in the diagnosis of salmonellosis. I report the use of a classic type of Widal test during a continuing outbreak of Salmonella enteritidis phage type 8. The outbreak occurred in a 376-bed hospital for acute and long stay geriatric patients and for psychiatric and psychogeriatric patients. Sera from an
34 of 51 patients, from Jan, 1986, to May, 1986, were examined. The Widal agglutination tests were done with a standardised suspension of the outbreak strain by Cruickshank and colleagues’ method.’ The patients were classified as symptom-free, mildly ill (ie, loose stools only), or ill (frequent watery stools with or without abdominal pain). All initial sera were taken between 7 and 28 days after the onset of symptoms, or, in symptom-free patients, after the first positive stool sample was taken. Sera were also obtained from patients who remained culture negative for Salmonella spp, 19 of whom had diarrhoea and 17 of whom did not. Positive Widal serology correlated strongly with the more serious
type of disease (table I). Isomaki and coworkers defined Widal positivity as a titre of 40 or more. We took our cut-off value at 80 or TABLE I-AGGLUTINATION TESTS IN
SALMONELLOSIS
34 PATIENTS WITH
after assessing the results of the control sera. Table n shows the sensitivities and specificities of the Widal reaction in our study population. Further samples of sera were available from 13 patients with significant positivity in initial specimens (our criteria). These sera were taken between 42 and 113 days from the onset of symptoms. In only 4 (at day 56, 83, 85, and 86) did the sera become negative. In the other 9, 3 had persistent positive stool cultures. In patients with more severe partly invasive salmonellosis serological tests may be helpful, especially if such a diagnosis is attempted more than one month after the initial illness--eg, in reactive arthritis. In this respect the Widal test may be useful if the appropriate antigens are used. However, in mild disease and symptom-free patients such serology may well be negative and therefore would not help to identify epidemics or chronic carriers. Such instances explain why EIA, although undoubtedly more sensitive than the classic agglutination test, was not totally successful in identifying all Salmonella culture-positive patients in Isomaki and colleagues’ series. More importantly, such serological studies may well throw light on the poorly understood pathological processes involved in the various forms of salmonellosis.
more
Department of Pathological Sciences, Division of Bacteriology, University of Manchester, Manchester M13 9PT
SARAH MAXWELL
1. Cruickshank
12rh ed.
R, Duguid JP, Marmion BP, Swain RHA. Medical microbiology, vol 2 Edinburgh: Churchill Livingstone, 1975: 416-18.
DERMATOFIBROMAS AND ARTHROPOD BITES
SIR,-Mr Evans and colleagues (July 1, p 36) do not give data on the dermatofibromas and sex distribution in their patients. Since 100 specimens were examined histologically, did each patient questioned have over 3 lesions excised, or were their data retrospective? Dermatofibromas usually occur on the lower extremities and are more common in women than men.1 This latter fact is cited to support the insect-bite theory on the grounds that women tend to have unprotected legs and are therefore more likely to be bitten. Although Evans at al state in their summary that the controls were matched they do not provide details of the characteristics selected. If patients and controls were not age and sex matched the validity of the comparison is questionable. It is not surprising that all the controls recalled being bitten by "insects" several times in one 24-h period at some stage in their lives. This does not address the question whether there was a causal relation between the bite and the subsequent lesion. I have yet to see a patient who has a clear recollection of being bitten at the same site as the dermatofibroma, although many remember being bitten at some time. As Evans et al point out, dermatofibroma is not a foreign-body giant-cell reaction, so it would have been surprising if they had identified arthropod material or chitin residues in serial sections. Perhaps an angiogenic, histiocyte chemotactic peptide regulatory factor will be identified in the saliva of midges. A study of the occurrence of dermatofibromas on the legs of women who habitually wear trousers might keep the argument alive. Institute of Dermatology,
St Thomas’s Hospital, London SE1 7EH 1. Greaves MW.
*Positive result when titre > 40. tPositive result when titre > 80.
C. E. H. GRATTAN
Histiocytic proliferative disorders. In: Rook A, Wilkinson DS, Ebling FJG, Champion RH, Burton JL, eds. Textbook of dermatology, vol 2. Oxford.
Blackwell Scientific Publications, 1986: 1706-08.