862
TROPICAL MYOSITIS WHEN
from para-equatorial South Pacific island tells of the spontaneous onset of severe pain in a single muscle of one limb, and the muscle proves to be firm, tender, and swollen, the likely diagnosis is tropical myositis. But the presentation is often atypical; when the same picture arises in a middle-aged Londoner2 or in a North American3.4 tropical myositis is hardly the first diagnosis which springs to mind. More likely causes are segmental a
young
America, Africa,
man
or a
irritation, Guillain-Barre syndrome, polymyalgia rheumatica (with or without polyarteritis nodosa), intermittent claudication, and anterior-compartment syndrome of the lower leg. Other possibilities are nutritional disturbance and drugs (notably chloroquine), and virus infection-e.g., Coxsackie B and influenza.5,6 Secondary syphilis, trichinosis, toxoplasmosis, trypanosomiasis, and cysticercosis can cause muscle pain, and suppurative myositis sometimes arises from clostridial infections or after penetrating injury. The patient with tropical myositis may recollect a nerve
illness such as a cold, a sore throat, or and some report trauma to the affected area.7,8 There may be arthralgia and signs of pulmonary inflammation or myocarditis, but peripheral neuropathy is absent. In three-quarters of the patients only one muscle is involved. Incision early in the illness reveals oedema of the muscle and its sheath, with fragmentation and separation of myofibrils and an infiltrate of mononuclear cells, lymphocytes, and eosinophils.l Where the disease is sporadic a diagnostic biopsy may be required.9 Excision of the muscle is not indicated. With antibiotics the early lesions may resolve but some progress and suppurate (pyomyositis). Then, copious yellow or brown pus can be drained from within the muscle belly-a feature which distinguishes tropical myositis from guinea-worm abscess, in which the pus is intermuscular. 90% of the positive bacterial cultures grow Staphylococcus aureus, usually phage type II. The anaemia in these patients may be due to staphylococcal hsemolysins or, more prosaically, to hookworm, which has been reported more prevalent in patients with tropical myositis than in unaffected people.10 When there are pulmonary symptoms a chest radiography will possibly show pneumonitis, with abscess or pleural thickening in 5%. The pleura is infiltrated with lymphocytes. If the iliopsoas is involved radiographs of the spine and hip may be required; but the important differential diagnosis here is retrocaecal appendicitis. Serum lactate dehydrogenase and hydroxybutyrate dehydrogenase are initially raised and they return to normal within two weeks of drainage.7 Toxocara skin tests are usually negative but flocculation tests may be
prodromal diarrhoea,
Taylor, J. F., Henderson, B. F. in Medicine in a Tropical Environment (edited by J. W. Kibikamusoke and M. S. R. Hutt). London, 1972. 2. Rogers, D. W. Br. med. J. 1973, iii, 679. 3. Levin, M. J., Gardner, P., Waldwogel, F. A. New Engl. J. Med. 1971, 284, 1.
positive.3 Leptospiral agglutination and malarial antibody studies are negative, as are serological tests for Coxsackie and enteroviruses.7 Toxoplasmosis, helminabscess, and trichomoniasis have been excluded as of tropical myositis;11 there is no histological evidence of autoimmune disease, but some workers have seen vesicles resembling virus particles in non-suppuratthic
causes
ing lesions. 12 In view of the initial influenza-like illness, the lymphocytic infiltration of muscle and pleura, reports of the disease in close contacts,’and reports of minor epidemics,13 the general view is that tropical myositis is
caused by an unknown primary pathogen, the staphylococcal invasion being secondary; the abscess site may, however, be determined by trauma. Smith and his coworkers14 have lately reported on the epidemiology of the disease in Uganda. The geographical distribution does not correlate with filariasis and the age and sex incidence excludes syphilis, nutritional deficiency, and exposure to chemical and plant toxins. Clustering was not striking, and no seasonal effect was noted. They conclude that viruses and migrant hookworm larvee remain candidates for the primary pathogen. If the cause is a virus, this can only be elucidated by ultrastructural studies and examination of paired sera. If hookworm larvx are responsible, serological tests3 should supply the answer.
DIAGNOSIS OF TWINS MULTIPLE
pregnancies
carry
a
perinatal morbidity
and a perinatal mortality three to four times higher than those of singleton pregnancies.1,2 Antenatally, the main
problems are pre-eclamptic toxaemia, placental insufficiency, and prematurity; at delivery they are asphyxia and trauma, especially to the second twin. The prognosis is improved by early diagnosis, but a great many multiple pregnancies go undetected until delivery. At present the best diagnostic method is second-trimester screening by ultrasound, which reveals at least 95% of multiple
pregnancies.3 First-trimester screening gives rise to false positives since several gestation sacs may be displayed but only one continue to grow.4 Unfortunately, many maternity units do not have the benefit of ultrasound; and some of those which do are unable to screen the whole of their obstetric population. For these, immunoassay of pregnancy hormones may aid in early detection of multiple pregnancy.
The large placental mass associated with multiple pregnancy produces increased amounts of the pregnancy-specific proteins human placental lactogen (H.P.L.), human chorionic gonadotrophin (H.C.G.) and pregnancy-specific -glycoprotein (P.S.B.G.). Most women with multiple pregnancies will produce increased amounts of placental proteins. Their major disadvantage in diagnosis is the overlap with singleton pregnancies. H.P.L.
196.
Echeverria, P., Vaughn, M. C. Am. J. Dis. Child. 1975, 129, 856. 5. Dietzman, D. E., Schaller, J. G., Ray, G., Reed, M. E. Pediatrics, 1976, 57,
85,
11. Elmes, B. C. T., McAdam, P. W. J. Ann. trop. Med. Parasitol. 1954, 48, 1. 12. Taylor, J. F., Fluck, D., Fluck, D. J. clin. Path. 1976,29,1081. 13. Horn, C. V., Masters, S. E. Afr. med. J. 1968, 45, 463. 14. Smith, P. G., Pike, M. C., Taylor, E., Taylor, J. F. Trans. R. Soc. trop. Med.
Taylor, J. F., Shaw, B., Bluming, A., Briers, P., Friedman, E., Henderson, B., Horn, C., Mohan, S., Pike, M. Afr. J. med. Sci. 1973, 4, 409. 8. Penman, H. G., Rothwell, A. G. N.Z. med. J. 1968, 68, 246.
1. Brown, E. J., Dixon, H. G. J. Obstet. Gynæc. Br. Emp. 1963, 70, 251. 2. Powers, W. Obstet. Gynec. 1973, 42, 795. 3. Grennent, L, Persson, P. H., Gennser, G. Kullander, S., Thorelli, J. Lancet,
4.
255. 6.
Greco, T. P., Askenase, P. W., Kashgarian, M. Ann.
intern.
Med. 1977,
193. 7.
9. Heffner, R. R., Armbrustmacher, V. W., Earle, K. M. Cancer, 1977, 40, 301. 10. Burkitt, R. T. J. trop. Med. Hyg. 1947, 50, 71
Hyg. 1978, 71, 46.
1976, i, 4. 4. Robinson, H.
P., Caines, J. S. Br. J. Obstet. Gynæc. 1977, 84, 22.
TROPICAL MYOSITIS WHEN
from para-equatorial South Pacific island tells of the spontaneous onset of severe pain in a single muscle of one limb, and the muscle proves to be firm, tender, and swollen, the likely diagnosis is tropical myositis. But the presentation is often atypical; when the same picture arises in a middle-aged Londoner2 or in a North American3.4 tropical myositis is hardly the first diagnosis which springs to mind. More likely causes are segmental a
young
America, Africa,
man
or a
irritation, Guillain-Barre syndrome, polymyalgia rheumatica (with or without polyarteritis nodosa), intermittent claudication, and anterior-compartment syndrome of the lower leg. Other possibilities are nutritional disturbance and drugs (notably chloroquine), and virus infection-e.g., Coxsackie B and influenza.5,6 Secondary syphilis, trichinosis, toxoplasmosis, trypanosomiasis, and cysticercosis can cause muscle pain, and suppurative myositis sometimes arises from clostridial infections or after penetrating injury. The patient with tropical myositis may recollect a nerve
illness such as a cold, a sore throat, or and some report trauma to the affected area.7,8 There may be arthralgia and signs of pulmonary inflammation or myocarditis, but peripheral neuropathy is absent. In three-quarters of the patients only one muscle is involved. Incision early in the illness reveals oedema of the muscle and its sheath, with fragmentation and separation of myofibrils and an infiltrate of mononuclear cells, lymphocytes, and eosinophils.l Where the disease is sporadic a diagnostic biopsy may be required.9 Excision of the muscle is not indicated. With antibiotics the early lesions may resolve but some progress and suppurate (pyomyositis). Then, copious yellow or brown pus can be drained from within the muscle belly-a feature which distinguishes tropical myositis from guinea-worm abscess, in which the pus is intermuscular. 90% of the positive bacterial cultures grow Staphylococcus aureus, usually phage type II. The anaemia in these patients may be due to staphylococcal hsemolysins or, more prosaically, to hookworm, which has been reported more prevalent in patients with tropical myositis than in unaffected people.10 When there are pulmonary symptoms a chest radiography will possibly show pneumonitis, with abscess or pleural thickening in 5%. The pleura is infiltrated with lymphocytes. If the iliopsoas is involved radiographs of the spine and hip may be required; but the important differential diagnosis here is retrocaecal appendicitis. Serum lactate dehydrogenase and hydroxybutyrate dehydrogenase are initially raised and they return to normal within two weeks of drainage.7 Toxocara skin tests are usually negative but flocculation tests may be
prodromal diarrhoea,
Taylor, J. F., Henderson, B. F. in Medicine in a Tropical Environment (edited by J. W. Kibikamusoke and M. S. R. Hutt). London, 1972. 2. Rogers, D. W. Br. med. J. 1973, iii, 679. 3. Levin, M. J., Gardner, P., Waldwogel, F. A. New Engl. J. Med. 1971, 284, 1.
positive.3 Leptospiral agglutination and malarial antibody studies are negative, as are serological tests for Coxsackie and enteroviruses.7 Toxoplasmosis, helminabscess, and trichomoniasis have been excluded as of tropical myositis;11 there is no histological evidence of autoimmune disease, but some workers have seen vesicles resembling virus particles in non-suppuratthic
causes
ing lesions. 12 In view of the initial influenza-like illness, the lymphocytic infiltration of muscle and pleura, reports of the disease in close contacts,’and reports of minor epidemics,13 the general view is that tropical myositis is
caused by an unknown primary pathogen, the staphylococcal invasion being secondary; the abscess site may, however, be determined by trauma. Smith and his coworkers14 have lately reported on the epidemiology of the disease in Uganda. The geographical distribution does not correlate with filariasis and the age and sex incidence excludes syphilis, nutritional deficiency, and exposure to chemical and plant toxins. Clustering was not striking, and no seasonal effect was noted. They conclude that viruses and migrant hookworm larvee remain candidates for the primary pathogen. If the cause is a virus, this can only be elucidated by ultrastructural studies and examination of paired sera. If hookworm larvx are responsible, serological tests3 should supply the answer.
DIAGNOSIS OF TWINS MULTIPLE
pregnancies
carry
a
perinatal morbidity
and a perinatal mortality three to four times higher than those of singleton pregnancies.1,2 Antenatally, the main
problems are pre-eclamptic toxaemia, placental insufficiency, and prematurity; at delivery they are asphyxia and trauma, especially to the second twin. The prognosis is improved by early diagnosis, but a great many multiple pregnancies go undetected until delivery. At present the best diagnostic method is second-trimester screening by ultrasound, which reveals at least 95% of multiple
pregnancies.3 First-trimester screening gives rise to false positives since several gestation sacs may be displayed but only one continue to grow.4 Unfortunately, many maternity units do not have the benefit of ultrasound; and some of those which do are unable to screen the whole of their obstetric population. For these, immunoassay of pregnancy hormones may aid in early detection of multiple pregnancy.
The large placental mass associated with multiple pregnancy produces increased amounts of the pregnancy-specific proteins human placental lactogen (H.P.L.), human chorionic gonadotrophin (H.C.G.) and pregnancy-specific -glycoprotein (P.S.B.G.). Most women with multiple pregnancies will produce increased amounts of placental proteins. Their major disadvantage in diagnosis is the overlap with singleton pregnancies. H.P.L.
196.
Echeverria, P., Vaughn, M. C. Am. J. Dis. Child. 1975, 129, 856. 5. Dietzman, D. E., Schaller, J. G., Ray, G., Reed, M. E. Pediatrics, 1976, 57,
85,
11. Elmes, B. C. T., McAdam, P. W. J. Ann. trop. Med. Parasitol. 1954, 48, 1. 12. Taylor, J. F., Fluck, D., Fluck, D. J. clin. Path. 1976,29,1081. 13. Horn, C. V., Masters, S. E. Afr. med. J. 1968, 45, 463. 14. Smith, P. G., Pike, M. C., Taylor, E., Taylor, J. F. Trans. R. Soc. trop. Med.
Taylor, J. F., Shaw, B., Bluming, A., Briers, P., Friedman, E., Henderson, B., Horn, C., Mohan, S., Pike, M. Afr. J. med. Sci. 1973, 4, 409. 8. Penman, H. G., Rothwell, A. G. N.Z. med. J. 1968, 68, 246.
1. Brown, E. J., Dixon, H. G. J. Obstet. Gynæc. Br. Emp. 1963, 70, 251. 2. Powers, W. Obstet. Gynec. 1973, 42, 795. 3. Grennent, L, Persson, P. H., Gennser, G. Kullander, S., Thorelli, J. Lancet,
4.
255. 6.
Greco, T. P., Askenase, P. W., Kashgarian, M. Ann.
intern.
Med. 1977,
193. 7.
9. Heffner, R. R., Armbrustmacher, V. W., Earle, K. M. Cancer, 1977, 40, 301. 10. Burkitt, R. T. J. trop. Med. Hyg. 1947, 50, 71
Hyg. 1978, 71, 46.
1976, i, 4. 4. Robinson, H.
P., Caines, J. S. Br. J. Obstet. Gynæc. 1977, 84, 22.
