Demonstration of pus is one of the criteria for making a definite diagnosis of amoebic liver abscess. Some facts about the physical characteristics of the pus are mentioned below.

Colour
The colour has by common usage been described as "like anchovy sauce".^1-7 in countries like India although anchovy sauce (Fig. 1) is not available, medical students and doctors often tend to use this word without understanding its meaning. In my experience rarely have I seen typical anchovy sauce like pus (Fig. 1). On the other hand on half a dozen occasions, I have seen "so called" anchovy sauce-like pus, when it turned out to be non-amoebic. For instance, one of my patients was diagnosed as a case of ruptured liver abscess because typical pus was aspirated from the peritoneal cavity when a diagnostic tap was done. At autopsy, peritonitis due to perforated typhoid intestinal ulcer was found. Another patient of right sided empyema was diagnosed as "amoebic" because of the so called "anchovy sauce" like pus (Fig. 2). Liver scan and l.H.A. test were negative and culture of the pus showed Klebsiella organisms. Therefore, it is worth remembering that anchovy sauce-like pus is not always amoebic,⁸ it is not typical of amoebic liver abscess and has been overstressed in the past.
The pus is usually "chocolate" coloured^8-13 or pinkish brown (Figs. 3 a,b). However, pus of different colours has been aspirated from patients in whom the diagnosis of amoebic liver abscess was finally confirmed by various other methods such as surgery, post-mortem examination, serological tests and therapeutic response. The colour may be dirty yellowish^6,13,15 (Fig. 4) (like pus elsewhere) or it may even be ivory⁵ (creamy white) (Fig. 5), grey^9-12 or greenish.^3,14,16-19 Figures 6,7,8,9,10 & 11 show, some of the other colours commonly seen by us. Very often in the same patient, the initial colour of the pus changes as aspiration proceeds^1,20,21 (Fig. 12). Often specks of blood or necrotic tissue are seen floating in the pus (Figs. 13 a, b). Also the colour changes to a darker shade after it is exposed to air for sometime.
The red brown hue¹⁴ may be derived from the necrosed liver tissue or due to admixture of blood^2,13,22 (Fig. 14). As the abscess is actually formed by liquefaction of the necrotic tissue, either of these possibilities may be correct. Previously it was believed that the pus appears yellowish only if there is secondary infection^2,3,14 but some workers have found thin yellow pus even in the absence of secondary infection.¹⁶ This is more common in patients having a chronic amoebic liver abscess (Fig. 15) .
(Greenish colour of the pus may be due to admixture with bile.^17,20 Fariss²⁰ and Viana²¹ have found direct communication between the abscess cavity and the bile ductules^20,21 (Figs. 16 a,b).
It is a common observation that on successive aspirations the nature of the pus changes. It becomes thinner,^1,18 clearer and its colour changes from brownish pink to greenish yellow. It is possible that in the past in some of these patients, secondary infection by anaerobic bacteroids was missed, because routine culture for these organisms was not done. Thus, the pus was wrongly labelled as sterile.

Odour
The pus is usually odourless¹² except when secondarily infected. Some authors have described a musty smell.²³

Consistency
The pus is usually very thick or glutinous in consistency (Fig. 17). so often we have felt that the similarity between amoebic pus and anchovy sauce is more in consistency than in the colour. In fact sometimes it is described as a "paste".
If serial aspirations are done, the consistency of the pus becomes much thinner,^1,18 and it can be aspirated more easily. The explanation for this is not forthcoming.

Viscosity
Paul has compared the viscosity of amoebic pus to that of thick lubricating oil. Because of this quality, the pus can flow easily through a small bore of a cannula-a fact which many clinicians have also observed now and again.
Some clinicians feel that if pus is not removed, it again becomes semi-solid or like 'putty^1,17 This stage however can be seen only after cure takes place with medical therapy (without aspiration). it is but natural therefore that this phenomenon has rarely been recognised at autopsy.

Taste
Patients of pulmonary amoebiasis, who expectorate this pus, have occasionally complained of taste of 'liver' in the sputum. At other times the taste could be bitter because of admixture with bile.

Quantity
The quantity of pus will naturally vary according to the size of the abscess. There are reports in the literature of three and a half litres of pus having been removed at a single tapping.^2,6
Often the pus is under pressure and comes out in a aush.^15,24 specially on initiating the tap.

Mircroscopy
On microscopic examination the pus may show dead and deformed hepatocytes (although often they are not recognisable as liver cells), R.B.Cs.¹³ and a few polymorphs.¹³ The trophozoites of E. Histolytica are usually present in the wall of the abscess.^18,25,26 Hence it is not surprising that many authors report their total absence or very low incidence,^27,28 on examination of the pus. However, when the pus is examined carefully, they are found in 15-25% of cases.^16,10,14,29 The organism is more likely to be found in the terminal part of the aspirate. Samples should be obtained in small containers at intervals (Fig. 12) during aspiration. Thus, the last fraction which is usually mixed with blood and is most likely to contain amoebae will not be diluted by the main mass of the aspirate.
It is interesting to note that examination of the exudate a few days after open drainage, may reveal the organisms much more readily. Whether this reappearance of the amoebae in the aspirate is due to changes in the oxygen availability, pressure levels or vascularity, is not known.³⁰

Microbiology of pus
The pus is usually sterile^{2,10,14,24,31} but secondary infection can occur, the rate varying from 7.8% to 25%.",^11,14 This was more common when open surgical drainage of the abscess used to be carried out. Infection occurs more commonly on successive aspirations.¹ Culture of the pus for aerobic and anaerobic organisms would help to identify the organism responsible for the secondary infection. Cocci,¹ E. Coli, para colon and proteus bacilli have been cultured from amoebic pus.²⁵ in some studies anaerobic bacteroides have been isolated in as many as 26% cases. If facilities are available, culture for E. Histolytica may be asked for.

Immunology of pus
It is hardly surprising that immunological tests of the pus show the presence of amoebic antigen.³² T his test can be of great diagnostic significance. The work of Sherry et al³³ serves to explain the coarse clumpy character of anchovy sauce type of aspirate. They stained the aspirated material by Feulgen method and demonstrated the presence of D.N.A. material.³³

Amoebic fluid
Although there is no mention of it in the literature, on half a dozen occasions I have seen 10 to 20 ml. Of brownish or dark pink fluid obtained during hepatic aspiration (Fig. 18). Usually in these cases if the direction of the needle is changed, amoebic pus is tapped. In one patient, 250 ml. of such fluid was tapped. After five days, the second aspiration showed typical amoebic pus.
Amoebic fluid is always transparent. Its consistency is not viscous, like blood, but watery. If kept for some time a few solid particles, found floating in it, settle down (Fig. 18). These consist of dead, deformed hepatocytes which may be identified during the microscopic examination with H & E stain. Amoebic fluid is thus a stage in the life history of amoebic pus. Amoebic fluid may be simulated by the following:

1. Fluid aspirated from hepatoma-It is thick, bloody and opaque (Fig. 19). A careful microscopic examination may show malignant cells.
2. Fluid aspirated inadvertently from a liver cyst. This could be brownish red (Fig. 20), but is absolutely clear. There are no floating particles.
3. Haemangioma of the liver if aspirated inadvertently will show blood (Fig. 21).
4. Vascular tumours following oral contraceptives would show a bloody fluid.

References

1. Rogers, L, Brit. Med. ., 1902, 2, 844.
2. Lamont, N M, and Pooler, N R. Quart J. Med., 1958, 27, 389.
3. Purandare, N M, and Deoras, S M, Ind J Med. Sci., 1955, 9, 1
4. Clinico-Pathological Conference Touro-lnfirmary, New Orleans, Am. J. Gastroent., 1964, 41, 64
5. Sheehy, T W. Parmley, L F. et al, Gastroent, 1968, 55, 26.
6. Nadkarni, S V, and Parashar, S K, et al, Int. Surg., 1973, 58, 112.
7. Uthman, S M, Am J. Proct., 1973, 24, 228.
8. Reddy, D C, and Subramaniam, K, Ind J. Med. Sci., 1962, 16, 203.
9. Turrill, F L, and Burnham, J R. Am. J Surg., 1966, 111, 424.
10. Crane, P S. Lee, Y T. et al, Am J. Surg., 1972, 123, 332.
11. Tsai Shen Ho, Am. J. Trop. Med. Hyg., 1973, 22, 24.
12. Cain, C D, Moore. P. et al, Am J Dig. Dis, 1968, 13, 709.
13. Paul, M, Brit J Surg., 1960, 47, 502.
14. DeBakey, M E, and Ochsner, A, Surg. Gyn Obst (I A S ), 1951, 92, 209.
15. Paul, M, Brit J Surg., 1959, 47, 502.
16. Clark, H C, Am J Trop Med. 1925, 5. 157
17. Wilcocks, Charles, and Manson-Bahr, P E C, Manson'sTropicalDiseases", 7thEdition, Williams & Wilkins Co., Baltimore, USA, 1972.
18. Rasaretnam, R. Paul, A T S. et al, Brit J. Surg., 1974, 61, 713.
19. Sharma, B N. J. Ass. Phys. Ind., 1972, 20, 519
20. Fariss, B L, and Captain, M C, Am J. Gastroent., 1965, 44, 559
21. Viana, R 1, Gut, 1966, 7, 285.
22. Meleney, H E, J Am. Med Ass, 1934, 103, 121:1
23. Charles, R H. Anderson, A R S. et al, Brit. Med. J . 1908, 2, 1235.
24. Datta D V J. Ass. Phys. Ind 1977. 25, 907
25. Malhotra, K C, Singh Amarjit, et al, J. Ass. Phys Ind, 1966, 16, 603.
26. Bhaskara Reddy, C, Sumathikumari, B. et al, Ind. J Path Bact, 1969, 12, 104.
27. Wright Ralph, Brit Med. J., 1966, 1, 957
28. Islam, N. Alam, K S. et al, J Trop. Med Hyg., 1960, 63, 131.
29. Sengupta, P C, Ind. J Path Bact., 1969, 12, 68.
30. Anderson, N H. Bostick W L, et al, Amoebiasis, Pathology, Diagnosis and Chemotherapy, Charles C. Thomas Publication, Springfield, 1953
31. Reynold, T B. Gastroent., 1971, 60, 952.
32. Mahajan, R C, Ganguly, N K, et al, Ind J. Med Res, 1975, 63, 229.
33. Sherry, S. McCatty, W R. et al, Arch Int Med., 1951, 88, 752.