2
880 TRANSACTONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE, VOL. 77, No. 6 (1983). CORRESPO~ENCE Ataka mountains, west of the Gulf of Suez, whence he had been admitted to Suez military hospital. He had never left Egypt during his period of service there. Examination confirmed that he appeared to be quite ill, but no obvious cause was found. However, he had slight splenomegaly and a few enlarged lymph nodes in the cervical region. There was only a slight anaemia but a marked leukonenia with a relative lymphocytosis. Plasmaproteins-were low, particularly that of the albumin fraction. The form01 gel test was strongly positive. No leishmania were found in the blood nor in lymph node aspirates. Treatment with pentavalent antimonial drugs produced an immediate and dramatic response. In view of the history, the clinical and pathological findings, and the response to therapy, it was consid- ered that this man represented the first case of visceral leishmaniasis to be found in a West Indian in Eavut. the disease having been acquired in Egypt, even though no infecting organism had been recovered from the patient. This case may support the two cases of visceral leishmaniasis reported by TEWFIK et al. (1983) which appear to have been locally acquired infections within Egypt. 6, Crag Lane, Knaresburough, P. B. ADAMSON North Yorkshire HGS 8EE, UK. Reference Tewfik, S., Kasem, S. A., Aref, M. K., Awadalla, H. N. & Abadir, A. (1983). A preliminaryreport on two cases of visceral leishmaniasis in Egypt. Transactions of the Royal Society of Tropical Medicine and HyRiene, 77, 334335. Accepted for publication I1 th July, 1983. Tropical pericarditis It was encouraging to read the report by CORACHAN et al. (1983) from Papua New Guinea, emphasizing the place of surgery i?i the management of-purulent nericarditis in a trooical environment. We would certainly agreethat surgeonsin the tropics “should be familiar with the technique of pericardiectomy”. On the other hand it was disappointing that a recent review of constrictive pericarditis (Lancet, 1983) ignored the problems of pericarditis in the tropics, where the disease is now most common, and where paradoxically the surgical facilities are least adequate. It may be of interest to others in a similar environment to offer the following observations from our 10 years’ continuous experience with 80 patients in Zaria, in Northern Nigeria (MABOGUNJE et al., 1981; LAWRIE, 1982). (1) The diagnosis is overlooked as the most frequent presenting feature is ascites, and these natients are labelled “?cirrhosis”. The dvspnoea and gredness are of such insidious onset that patients in a rural environment do not complain of these speci- fically. (2) “Aggressive” surgical treatment, advocated in Papua New Guinea is not a pericardial window. Windows are no better than large tube drainage via trocar and canula, and are dangerous, being done with poor visibility and with risk of tearing the myocar- dium. Three of our patients died partly asthe result of making windows and we no longer do this. Pericar- diectomy should be considered if tube drainage proves inadequate. (3) “Primary” pericardiectomy has a useful place in the treatment of purulent and effusive pericarditis, before constriction has developed, and before “secon- dary” pericardiectomy becomes obligatory. (4) “Radical” pericardiectomy is not necessarily the ideal operation as this requires wide exposure, sternal splitting and accurate assessment and control of respiration-rarely available. In two of our patients who died, sternal splitting and attempted radical dissection were contributory factors, (5) “Partial” pericardiectomy with wide release and clearance of the anterior surface, the left side of the heart, the apex, and with excision of the pericardium posterior to the left phrenic nerve, can all be carried out rapidly and safely through a left thoractomy, with no special facilities or intensive care. We have patients restored from moribund to normal life after this procedure. (6) The pathological conundrum, for which it is difficult to offer hard evidence, is-which patients with pericarditis, purulent or effusive! go on to constrict, and whtch resolve and heal leavmg a normal mobile pericardial space?It is attractive to consider purulent pericarditis, pericarditis with effusion, con- strictive pericarditis and calcified pericarditis, all as a spectrum of one disease process. From our experience of tropical pericarditis at least, we consider this to be so. Unfortunately these various manifestations of pericardial diseasetend to be studied and reported in isolation, on the supposition that they are separate disease entities. (7) Finally, we need an explanation for the finding in some, but not all, of an inner, thinner, tough, but defimtely constricting myoepicardial layer. This is discovered at operation when division and initial separation of the thick, obvious, outer pericar- dium does not release the heart. Some patients have this pathology obviously. But could this develop later, as part of the continuing disease process? Could it be a factor in the development of “recurrent” pericardial constriction? As tropical pericarditis is now probably the most common form of this crippling but treatable disease, these points seem to us to deservemore attention from surgical groups working in the under-doctored reg- ions of the tropical world. Department of Surgery, Ahmadu Belle University, Zaria, Nigeria JAMES LAWRIE References Corachan, M., Poore, P., Hadley, G. P. & Tanner, A. (1983) Purulent pericarditis in Papua New Gumea: Report of 12 cases and review of the literature in a tropical environment. Transactions of the Royal Societyof Tropical Medicine and Hygiene, 77, 341-343. Lancet (1983). Constrictive Pericarditis (Leading Article). Lancer, i, 1313-1314.

Tropical pericarditis

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880 TRANSACTONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE, VOL. 77, No. 6 (1983). CORRESPO~ENCE

Ataka mountains, west of the Gulf of Suez, whence he had been admitted to Suez military hospital. He had never left Egypt during his period of service there.

Examination confirmed that he appeared to be quite ill, but no obvious cause was found. However, he had slight splenomegaly and a few enlarged lymph nodes in the cervical region. There was only a slight anaemia but a marked leukonenia with a relative lymphocytosis. Plasma proteins-were low, particularly that of the albumin fraction. The form01 gel test was strongly positive. No leishmania were found in the blood nor in lymph node aspirates. Treatment with pentavalent antimonial drugs produced an immediate and dramatic response.

In view of the history, the clinical and pathological findings, and the response to therapy, it was consid- ered that this man represented the first case of visceral leishmaniasis to be found in a West Indian in Eavut. the disease having been acquired in Egypt, even though no infecting organism had been recovered from the patient. This case may support the two cases of visceral leishmaniasis reported by TEWFIK et al. (1983) which appear to have been locally acquired infections within Egypt.

6, Crag Lane, Knaresburough,

P. B. ADAMSON

North Yorkshire HGS 8EE, UK.

Reference Tewfik, S., Kasem, S. A., Aref, M. K., Awadalla, H. N. &

Abadir, A. (1983). A preliminary report on two cases of visceral leishmaniasis in Egypt. Transactions of the Royal Society of Tropical Medicine and HyRiene, 77, 334335.

Accepted for publication I1 th July, 1983.

Tropical pericarditis It was encouraging to read the report by CORACHAN

et al. (1983) from Papua New Guinea, emphasizing the place of surgery i?i the management of-purulent nericarditis in a trooical environment. We would certainly agree that surgeons in the tropics “should be familiar with the technique of pericardiectomy”. On the other hand it was disappointing that a recent review of constrictive pericarditis (Lancet, 1983) ignored the problems of pericarditis in the tropics, where the disease is now most common, and where paradoxically the surgical facilities are least adequate.

It may be of interest to others in a similar environment to offer the following observations from our 10 years’ continuous experience with 80 patients in Zaria, in Northern Nigeria (MABOGUNJE et al., 1981; LAWRIE, 1982).

(1) The diagnosis is overlooked as the most frequent presenting feature is ascites, and these natients are labelled “?cirrhosis”. The dvspnoea and gredness are of such insidious onset that patients in a rural environment do not complain of these speci- fically.

(2) “Aggressive” surgical treatment, advocated in Papua New Guinea is not a pericardial window.

Windows are no better than large tube drainage via trocar and canula, and are dangerous, being done with poor visibility and with risk of tearing the myocar- dium. Three of our patients died partly as the result of making windows and we no longer do this. Pericar- diectomy should be considered if tube drainage proves inadequate.

(3) “Primary” pericardiectomy has a useful place in the treatment of purulent and effusive pericarditis, before constriction has developed, and before “secon- dary” pericardiectomy becomes obligatory.

(4) “Radical” pericardiectomy is not necessarily the ideal operation as this requires wide exposure, sternal splitting and accurate assessment and control of respiration-rarely available. In two of our patients who died, sternal splitting and attempted radical dissection were contributory factors,

(5) “Partial” pericardiectomy with wide release and clearance of the anterior surface, the left side of the heart, the apex, and with excision of the pericardium posterior to the left phrenic nerve, can all be carried out rapidly and safely through a left thoractomy, with no special facilities or intensive care. We have patients restored from moribund to normal life after this procedure.

(6) The pathological conundrum, for which it is difficult to offer hard evidence, is-which patients with pericarditis, purulent or effusive! go on to constrict, and whtch resolve and heal leavmg a normal mobile pericardial space? It is attractive to consider purulent pericarditis, pericarditis with effusion, con- strictive pericarditis and calcified pericarditis, all as a spectrum of one disease process. From our experience of tropical pericarditis at least, we consider this to be so. Unfortunately these various manifestations of pericardial disease tend to be studied and reported in isolation, on the supposition that they are separate disease entities.

(7) Finally, we need an explanation for the finding in some, but not all, of an inner, thinner, tough, but defimtely constricting myoepicardial layer. This is discovered at operation when division and initial separation of the thick, obvious, outer pericar- dium does not release the heart. Some patients have this pathology obviously. But could this develop later, as part of the continuing disease process? Could it be a factor in the development of “recurrent” pericardial constriction?

As tropical pericarditis is now probably the most common form of this crippling but treatable disease, these points seem to us to deserve more attention from surgical groups working in the under-doctored reg- ions of the tropical world.

Department of Surgery, Ahmadu Belle University, Zaria, Nigeria

JAMES LAWRIE

References Corachan, M., Poore, P., Hadley, G. P. & Tanner, A.

(1983) Purulent pericarditis in Papua New Gumea: Report of 12 cases and review of the literature in a tropical environment. Transactions of the Royal Society of Tropical Medicine and Hygiene, 77, 341-343.

Lancet (1983). Constrictive Pericarditis (Leading Article). Lancer, i, 1313-1314.

Page 2: Tropical pericarditis

TRAN~ACTON~ OF THE ROYAL SOCIETY OP TROPICAL Mmrcrm AND HYGIENE, VOL. 77, No. 6 (1983). CORRESPONDENCE 881

Lawrie, J. H. (1982). Tropical Pericarditis. Proceedings, VZZ Edinburgh Surgical Festival, 34, University of Edin- burgh.

Mabogunje, 0. A., Adesanya, C. O., Khwaja, M. S., Lawrie, J. H. & Edington! G. M. (1981). Surgical management of pericarditis m Zaria, Nigeria. Thorax, 36, 590-595.

itching from any cause would produce a similar picture. The geographical differences in the preva- lence of leopard skin between onchocerciasis areas can be explained by a combination of differences in the biting habits of the Simulium flies, in individual response to the bites, and in the amount of pigment in different tribes or populations.

Accepted for publication 1st August, 1983.

‘Leopard skin’ and onchocerciasis EDUNGBOLA et al. (1983) assessed the endemicity of

onchocerciasis in the Babana district (Sudan savanna) of Kwara State in Nigeria by determining the prevalence of the ‘characteristic-onchocercal depig- mentation’. Biahtlv. thev discussed the validitv of using a clinicalsign for this purpose, especially since the aetiology of this sign remains uncertain. It might be caused either by the bites of the vector, Simulium damnosum, or by the parasite, Onchocerca volvulus, whether the adult worm, its microfilariae, or infective larvae.

I have myself developed the sign on both legs, although, due to my white skin, it is only visible during the summer, when typical patches on both shins fail to tan. During extensive field studies of onchocerciasis in Cameroon from 1970-79, I was often bitten by Simulium flies, especially in the rain-forest, where this sign is common in areas of onchocerciasis. Microfilariae were first demonstrated in skin snips from my left arm and shoulder in 1975, but a heavy infection never developed. Microfilariae have never been demonstrated in the lower part of my body, nor have I had palpable nodules. I have never taken any form of treatment. A Mazzotti test in the autumn of 1982 showed the persistence of microfilariae in the skin over my left shoulder and upper arm.

Fuglsang, H., Anderson, J. & Marshall, T. F. de C. (1979). Studies on onchocerciasis in the United Cameroon Republic. V. A four year follow-up of 6 rain-forest and 6 Sudan-savanna villages. Some changes in skin and lymph nodes. Transactions of the Royal Society of Tropical Medicine and Hygiene, 73, 118-119.

Gibbins, E. G. St Loewenthal, L. J. A. (1973). Cutaneous onchocerciasis in a Simulium damnosum-infected region of Uganda. Annals of Tropical Medicine and Parasitology, 27, 484-496.

Loewenthal, L. J. A. (1939). Diseases of the shin in negroes. Journal of Tropical Medicine and Hygiene, 42, 99-104.

Accepted for publication 11th August, 1983.

Regional variations in serum immunoglobulin levels in South East Asia

During the first years in Africa I did not react to the bites of Simulium in any way, but later I began to itch in the evening after a day of heavy exposure. Particularly memorable was a study in the rain-forest of Cameroon when I received innumerable bites on both legs on consecutive days. The distribution of those bites and the resulting scratch marks corres- ponded to the distribution of the present depigmenta- tion.

It is well established that in many tropical regions the levels of serum immunoglobulins, particularly those in the IgG and IgM classes, are higher than those in temperate regions (GREENWOOD & WHIT- TLE, 1981). Levels of IgA, however, tend to be much more constant. To take one example (WELLS, 1968), the mean levels of IgG, IgM and IgA in a group of healthy inhabitants of New Guinea were 16.5, 3.06

During studies in Cameroon (FUGLSANG et al., 1979) no correlation was found between the incidence of shin depigmentation (leopard skin) and the density of microfilariae in the skin. Furthermore, it was shown that patients who were allergic to S. damnosum bites produced significant reactions when an antigen prepared from the heads of S. damnosum flies, devoid of 0. volvulus larvae, was used in a standard passive cutaneous anaphylactic test.

and 1:95 g. 1-l respectively while the values for a arouo of Australians were 10.2. 1.3 g. 1-l. 1; contrast, the levels of immunoglobulins among inhabitants of peninsular Malaysia (Kuala Lumpur region) were found to be similar to those in temperate regions (YADAV 8c SHAH, 1973). In view of this marked difference in two climatically similar parts of South East Asia, we examined sera from East Java which is situated midway between the two regions.

Since I have only suffered a light infection, confined to my left shoulder, I am convinced that the

Using the technique of laser nephelometry and a set of WHO standard sera. we estimated the concentra-

‘leopard skin’ on both my shins consists of depig- mented scars from scratching after Simulium bites.

tions of immunoglobulin in IgG, IgM and IgA classes

GIBBINS & LOEWENTHAL (1933) and LOEWENTHAL in 186 sera from Indonesian adults (91 men and 95

(1939) were the first to suggest that many of the women; age range 18 to 50 years) resident in and

so-called onchocercal skin changes were in fact due to around the city of Surabaya, East Java. All were

the bites of this fly. The question remains if prolonged clinically healthy and had clear chest radiographs. The mean levels of the three immunoglobulin classes

Langvadvej 60, 7741 Frestrup, Denmark

HARALD FUCLSANG

References Edungbola, L. D., Oni, G. A. & Aiyedun, B. A. (1983).

Babana Parasitic Diseases Project. I. The study area and a preliminary assessment of onchocercal endemicity based on the prevalence of ‘leopard skin’. Transactions of the Royal Society of Tropical Medicine and Hygiene, 77, 303-309.