The treatment of amoebic liver abscess, if given adequately, is very satisfactory. Most often there is complete resolution.^1-2
A few months or years after the abscess has resolved and the cold area on the scan has cleared, if the clinical features of an abscess reappear and the scan shows a new cold area, the diagnosis of recurrent abscess is most likely. Before the days of scanning, it was difficult to differentiate between relapse and recurrence. However, a recurrent abscess can now be confidently diagnosed since liver scanning is more routinely available. The recurrence can also be confirmed by serological tests which would again show a high titre.
In the world literature, there have been only a few isolated case reports on recurrent amoebic liver abscess, having adequate proof of liver scans and positive serological tests.
Jenkinson³ in 1975 reported a patient who developed abscesses on three separate occasions over a period of five years which were confirmed by scan as well as serological tests. I.H.A. test was positive in high dilution which suggested optimal immunological response. But since it is known that antibodies do not offer long term protection, this patient still developed a recurrent abscess. The authors' analysis showed that to eradicate the intestinal infection their patient had received di-iodohydroxyquin in a dose of 600 mgm. once a day only, for twenty days. In fact the recommended dose of di-iodohydroxyquin is 600 mgm. thrice daily for 20 days.
In 1976, Gregory Peter⁴ reported a case of a proved recurrent amoebic liver abscess who had three episodes in one year. In this case the author analysed that the patient was treated with emetine, chloroquine, metronidazole and tetracycline as recommended by Powell et al⁵ and Manson-Bahr.⁶ These drugs had possibly failed to eradicate intestinal amoebiasis. The patient had not received diiodohydroxyquin which is the drug known to eradicate intestinal infection effectively.
I have treated one case who had three episode of amoebic liver abscess over three years. Although a liver scan was not done during the first attack in October 1975, it appeared clinically that the patient had an abscess in the superior surface of the right lobe which elevated the diaphragm and produces typical appearances in the X-ray chest (Fig. 4).
The fact that during the next attack in April 1976 the right dome was normal (Fig. 5) proved that the present abscess was at a new site. This was confirmed by a scan which showed a cold area in the right lobe posteriorly (Fig. 6). He responded well to treatment and the cold area disappeared within ten weeks.
During the third attack in April 1977, the liver scan showed cold area on the posterior surface at a much lower site (Fig. 7) thus establishing the fact that the abscess had recurred.
In the above case the first recurrence could be explained by the fact that he had not been given di-iodohydroxyquin to eradicate intestinal amoebiasis. It is known that in a small percentage of patients emetine and metronidazole are not enough to sterilise the gut.⁷ The fact that during the second attack his stool showed E. Histolytica proved the point. But the second recurrence was very difficult to explain. Chances of intestinal infection persisting were minimal since stool examination and sigmoidoscopy were negative.
A positive l.H.A. titre, normal serum immunoglobulins and positive mantoux test with P.P.D. showed that he did not have any immunological deficiency. The patient was also not known to be an alcoholic.
The only explanation can be, as Wilmot states,⁸ that certain individuals are particularly susceptible to recurrent amoebic infections. This case was possibly highly susceptible and his antibody levels did not protect him from a recurrence.⁹
On analysis of the clinical material presented by Cook,¹⁰ in the first episode, the patient appeared to have had a superior surface superficial right lobe abscess with pleuropulmonary complications. During the second episode seven months later, the patient presented with epigastric tenderness. Pericarditis as a complication followed and on aspiration, pus was obtained from the left subphrenic space suggesting a left lobe abscess. This strongly, though not conclusively, suggests a recurrence, in spite of the fact that scans of each episode were not available .
In the literature there are a few more reports without scan confirmation. These cases when analysed in detail, do not appear to have suffered from a recurrent abscess.
Archampong¹¹ in 1972 described a case who was operated for peritonitis. At laparotomy amoebic pus was obtained from a large abscess in the left lobe while the right lobe appeared to be normal. The patient gradually recovered. A month later he was readmitted with recurrence of the previous clinical features and was treated with amoebicidal drugs and aspiration. There being no clinical improvement, a second laparotomy was done. A large loculated abscess in the right lobe was evacuated.
As described elsewhere, quite often patients with left lobe abscess have a concurrent one in the right lobe. The short duration between the attacks in this case suggests that on inspection at the first laparotomy the right lobe, though appeared normal, could well have harboured an intrahepatic abscess, possibly in the posterior area where it was missed at that time.
Tsai of Taiwan¹² has mentioned two cases where the patient returned a year later with a recurrence. As no further details were available, we are unable to comment whether these were recurrent abscesses or relapse of the same abscess.
I personally feel that more research work into the subject of recurrence of an amoebic liver abscess is needed. I have seen hundreds of patients who have never had a recurrence even though they were not given adequate doses of luminal amoebicides to eradicate an intestinal focus. The fact remains that little less than fifty percent of the patients of amoebic liver abscess have no intestinal involvement. What then, are we trying to eradicate?
There is no doubt that many clinicians while discharging the patients from the hospitals, do not emphatically advise to continue luminal amoebicides for complete three weeks. Moreover, even when advised, not many of these patients complete this course, Yet, hardly any of these patients return with a recurrence!

References

1. Powell, S J. Wilmot A J, et al, Ann. Trop. Parasitot, 1969, 63,139.
2. Wilmot, A J. Powell, S J, et al, Am. J. Med. Hyg., 1959, 8, 623.
3. Jenkinson, S G. and Margrove, M D, J Med. Ass, 1975, 232, 277.
4. Gregory Peter, B. Gastroent., 1976, 70, 585.
5. Powell, S J, Bult M Y Acad. Med., 1971, 47, 469.
6. Manson-Bahr, P. Brit. Med. J., 1941, 2, 255
7. Weber, D M, J. Am. Med. Ass., 1971, 216, 1339.
8. Wilmot, A J. Clinical Amoebiasis, Blackwell Scientific Publicaitions, Oxford, 1962
9. Elellanti, A, Immunology, W B Saunders & Co., Philad., 1971.
10. Cook, A T. Proc. Roy. Soc. Med., 1970, 63,1312.
11. Archampong E Q. Brit. J. Surg., 1972, 59, 179.
12. Tsai Shen Ho, Am J Trop. Med. Hyg, 1973, 22, 24