1. Latent abscess.
2. Silent abscess.
3. OccuIt abscess.
4. Subclinical abscess.
5. Chronic abscess.
6. Residual abscess.
7. Recurrent abscess.
8. Relapse of an abscess.
9. Resistant abscess.
10. Refractory abscess.

Different authors, while describing their cases, have used these terms interchangeably. Patients with a 'recurrence' of symptoms, or unsatisfactory response to therapy have been unfortunately labelled with any one of the above names. Thus, Wilmot¹ states, "very rarely cases are seen which 'relapse"'; later, in the same text, statements like "injecting chloroquine into local abscess cavity may be used in the above 'resistant' cases" and "the abscess may persist and remain 'silent' for long periods" have been made.
The confusion that these terms have created can probably be explained by the fact that in the past, since an abscess could not be visualised (scan, ultrasonography) clinicians could only conjecture as to its presence, depending on the clinical features and available investigatory findings.
The problem is similar to that of a patient diagnosed as having pulmonary tuberculosis. Such a patient may show a good response to therapy and make an apparent recovery. If cough with expectoration recurs in this patient, unless a previous radiograph of the chest is available in addition to a present one, the clinician is unable to differentiate between relapse of the disease, recurrence of tuberculosis or tuberculous bronchiectasis!
Of late, with increased availability of facilities such as isotope liver scan, ultrasonography, peritoneoscopy and serological tests, confusion between these terms should be a thing of the past. In the following discussion an attempt has been made to clarify these concepts.
Terms like latent, silent, occult² or subclinical abscess are synonymous, all indicating the failure of a liver abscess to manifest itself clinically. With the recent availability of imaging devices their existence can immediately be confirmed or refuted.
The term 'chronic' should ideally be used only at autopsy when a well defined fibrous wall surrounds the abscess. Clinically, patients in whom the onset of the disease is gradual (weeks or months) may be considered as having a ‘chronic' abscess. In these patients, the clinical features mimic a hepatoma- low fever, mild pain and hepatomegaly etc. Aspiration usually reveals thin yellow pus. The response to therapy of such abscesses is in no way different from that of other abscesses.
The term 'residual' abscess has been used when a cold area produced by amoebic liver abscess on the liver scan persists for more than three to four months (as discussed in Section IV). If there are no residual clinical features of the liver abscess and the E.S.R. is normal, there is no justification in presuming that the patient has a residual abscess which has not cleared up with the therapy. Why such cold areas persist for so long is not clear, although scarring or some other factors may be responsible.
A few months or years after an amoebic liver abscess is cured and the cold area on the scan has cleared, if clinical features of an abscess reappear and the scan shows a new cold area, this can be considered as a 'recurrent' abscess. This entity has been discussed elsewhere.
The adequacy of therapy has no relevance to the term 'recurrence'. Although the authors reporting such cases always criticise past clinicians for treating such patients inadequately (e.g. not administering luminal amoebicides in the proper dose concurrently), future work may demonstrate some other factors (like immunology) etc. which may be playing a part in recurrence.
'Relapse' and 'Resistance' are pharmacologically, not synonymous. It has been established, for example, that with emetine therapy the 'relapse' rate is 7% whereas with chloroquine it is 25%. However in combination, the relapse rate may be considerably reduced³. On the other hand, in marked contrast to tuberculosis where certain strains of the bacilli are known to be 'resistant' to one or more antitubercular drugs, such a phenomenon has only rarely been described in relation to antiamoebic drugs. Many of these reports are incomplete.^4-5
When a case terminates fatally, inspite of adequate therapy for example with metronidazole, it does not mean that the patient was resistant to this drug^9,12,16,17 (although theoretically this cannot be excluded). It is more probable, however, that the abscess was associated with one of the complications, which was not suspected and thus worsened the prognosis (for example, associated multiple abscesses⁷ or a chest complication¹⁸). The drug cannot be considered as being ineffective if adequate aspiration was not conducted in the hope of the abscess resolving on conservative management.¹²
Thus the term "refractory" rather than "resistant" abscess is more appropriate for the description of such cases.
This brings us to the most important drawback in the evaluation of the adequacy of management of amoebic liver abscess-that is the role of aspiration. Even today, the indications for aspiration remain vague. Which abscess needs aspiration? Should all abscesses be aspirated? How often should aspiration be carried out? These are the questions which plague the minds of every physician even today. Failure to aspirate pus could well mean that a part of the abscess was still solid and at a later date, may even liquefy! It is hoped that scans and ultrasonographs will solve these problems in near future.
All that can be stated at present is that an amoebic liver abscess can persist and not be cured, if patients are given inadequate therapy. For example, if

1. the dose of emetine is inadequate¹⁹ (many clinicians fear cardiac toxicity and hence administer a smaller dose).
2. the dose of chloroquine or metronidazole is inadequate¹⁷ (clinicians fearing the occurrence of 'nausea' usually reduce the dose).
3. Drug combinations are avoided.⁹
4. Aspiration is not carried out due to:

1. over-confidence in conservative management.
2. impaired liver functions when one may prefer to postpone the procedure to avoid a possible haemorrhage.
3. half-hearted unsuccessful attempts at aspiration or as is more often, the clinician being satisfied with aspiration of a few hundred ml. of pus.

5. even after the development of a subphrenic abscess, an empyema or a localised collection of pus in the lesser sac, conservative management is continued and aspiration or surgery is not carried out.¹⁹

Finally, besides these recognised factors there are many unknown factors which decide the total response of the patient to therapy. Why some patients having a similar type of abscess need one drug, others need two and yet others require additional aspiration is not understood. Usually in such patients if features like tender hepatomegaly, raised E.S.R., radiological signs in the chest etc. persist, the clinicians label them as "resistant".
While, if after a few days, (usually from 10 days to 3 months)^6,14,19-22 the patient again complains of symptoms of fever or recurrence of pain etc., he is labelled as a case of "Relapse".

Table I shows the details of some of the refractory or resistant cases reported in the literature. While going through the table, it will be noticed that refractoriness or resistance to all the drugs-emetine, chloroquine or metronidazole has been noted. Moreover though some patients responded to the change of the drug, others required aspiration or surgical drainage.

Table II shows the details of some reports of 'relapse' of an amoebic liver abscess. Some of these authors have loosely reported these cases as 'recurrent' abscesses.

References

1. Wilmot, A J. Clinical Amoebiasis, Blackwell Scientific Publications, Oxford, 1962.
2. Sharma, B N. J. Ass. Phys. Ind., 1972, 20, 519
3. Wilmot, A J. Powell, S J. et al, Am. J. Trop Med. Hyg, 1959, 8, 623.
4. Adesola, A O. Tropical Surgery, McGraw-Hill Publications, New York, 1971, 13, 323
5. Conan, N J. Am. J. Med., 1949, 6, 309
6. Crane, P S. Lee, Y T. et al, Am J. Surg, 1972,123
7. Datta, D V, Singh, A K, et al, Am. J. Trop. Med. Hyg., 1974, 23, 566.
8. Emmett, J. J. Am. Med. Ass 1949, 141, 22.
9. Griffin, F M, New Eng J. Med. 1973, 288, 1397.
10. Griffin, F M, New Eng J. Med., 1973, 289,869
11. Healy, G R. Bull. N. Y. Acad. Med. 1971, 47, 494
12. Henn, R M, Collin, D B. et al, J. Am. Med. Ass. 1973, 224, 1395
13. Juniper, K, Am. J. Trop. Med. Hyg, 1972, 21,
14. Manson-Bahr, P. J Trop. Med. Hyg, 1949, 52,
15. Murgatroyd, F. and Kent, R P. Trans. Roy. Soc Trop. Med. Hyg., 1948, 42, 15.
16. Vigg, B L, Sahay, B K, et al, J. Ass. Phys. Ind. 1971, 19, 515.
17. Wilde, M, New Eng J. Med., 1973, 289, 378.
18. Stillman, A E, Alvarez, V, et al, J. Am. Med. Ass 1974, 229, 71
19. Sharma, L R. Sunder Rao, A R. et al, Ind Med. Gaz., 1951, 86, 6.
20. Powell, S J. Wilmot, A J. et al, Ann. Trop. Med. Parasitol., 1967, 61, 511.
21. Rao, S V, Satyanarayana, D, et al, J. Ind Med. Ass., 1968, 51, 450.
22. Sodeman, W A, Doerner A A, et al, Ann. Int Med., 1951, 35, 33.