1. The damage done to the liver in an amoebic live abscess is far in excess of the number of amoebae present. As the quantum of enzyme produced by individual amoebae is very little,¹ there must be some other factors which act synergistically.
2. Recurrences of amoebic liver abscess are so rare that they only appear as care reports.^2-5 Absence of recurrence, in all probability indicates immunological protection.
3. A simple spread of infection is obviously not the only factor and always obtained.^6-17 Post mortem studies show colonic lesions in only 12.2¹⁸ - 90%^12,19-21 of amoebic liver abscesses. Proctoscopic²² and sigmoidoscopic examinations give similar results.^6,23.
4. There is a very long disease-free interval between an attack of amoebic colitis and amoebic liver abscess.^24-26 This silent gap says a lot in favour of immunological response. This disease free interval may be the time taken by the body to develop immunological reaction to the antigen of the amoebae. Hence while colitis is due to simple infection, hepatic abscess may be the effect of immunological reaction to the presence of amoebae in the liver.
5. Production of an amoebic liver abscess in experimental animals is very difficult. Suppression of the immunological system by various methods makes it easier to produce an amoebic liver abscess in an animal.²⁷ It is known that it is easier to produce a hepatic lesion by injecting amoebae in the portal radicle of animals with chronic amoebic colitis rather than in those without colitis.^28-30 On examination of the colon of patients who died as a result of amoebic liver abscess, Rogers found fresh colonic lesions in only 20% and chronic lesions in 77.8%.
6. In patients with intestinal amoebiasis and amoebic liver abscess a high percentage of positivity is found to intradermal injection of amoebic antigen,^31-34 including immunological response.

Research in this field was first started in the direction of humoral immunity. By using different methods like indirect haemagglutination,^35-40 complement fixation,⁴¹ immunoelectrophoresis,⁴² immunofluorescence,^37,43 gel diffusion precipitin,⁴⁴ counter-immunoelectrophoresis,^45-47 latex agglutination,^47-48 bentonite flocculation,^37-44 amoeba immobilsation,³⁷ indirect fluorescent antibody,^39,43 it was observed that the body does produce anti-bodies against the amoebic antigen. The I.H.A. test is positive in very high dilutions in patients with amoebic liver abscess. This indicates that the anti-bodies are produced in large quantities in this group of patients. Levels of immunoglobulins G, A, and C3 are also found to be raised in them,²⁷,^49-51
The humoral system usually functions to protect an individual from a particular infection. In vitro studies carried out with immune sera (collected from patients with amoebic liver abscess) show complete inhibition of growth of axenically grown E. Histolytica.^27,52 The immune sera are also found to neutralise virulence of pathogenic cultures of E. Histolytica.²⁷ They also exert direct cytolytic effect on the trophozoites.²⁷ (They require complement for this effect.) However, a patient of amoebic dysentery forms and anti-bodies against the amoebae and yet is afflicted with amoebic liver abscess. Thus, the question which arises, is does the humoral system participate in abscess formation? The antigen (the amoeba) is present in the liver. The antigen-antibody reaction takes place in the liver. Theoretically it may bring about deposition of complement in that organ. Severe hepatolysis can occur by the action of this enzyme system. To prove this hypothesis, studies like immunofluorescent staining for identifying the presence of complement in the livers with amoebic abscesses will have to be done.
The role of cell-mediated immunological system has also been tested. Tests to show presence of migration inhibition factor have been found to be positive.²⁷ Tests for observing blast transformation have been carried out in experimental animals as well as in patients suffering from amoebic liver abscess. Lesser number of cells are transformed to be blast stage in patients with amoebic liver abscess as compared to controls.²⁷ Some workers have noted that after the acute stage of the disease (amoebic liver abscess) passes off, the blast transformation returns to a stage comparable with that in normal controls. Other workers have reported results to the contrary.⁵³ They have noted increased activity of the T cells in the form of blastogenic transformation both in animal models as well as in patients with amoebic liver abscess. The thymidine incorporation (as an indicator of blast transformation) is maximum in patients with amoebic liver abscess as compared to those suffering from amoebic dysentery, cyst passers or controls.⁵⁴
The controversial results of the tests of C.M.I. are better understood by studies carried out during the various stages of the amoebic liver abscess. During the early stages the tests indicate a suppression of the functions of C.M.I. system. However, when the same tests are repeated after the disease has advanced or is cured, the tests show proof of sensitisation and effective functioning of the C.M.I. system.³³
The cytoxic effect of the sensitised lymphocytes on the antigenic cells is the most conclusive proof of the effective sensitization of the cell mediated immunological system. Guerrero et al⁵⁵ conducted a series of experiments to study the phagocytic effect of trophozoites and lymphocytes on each other. When lymphocytes of controls or of patients in the initial stage of amoebic infection were used, all the lymphocytes were phagocytosed by the trophozoites. However, the results were reversed when lymphocytes of patients who have recovered were tested. The cells or even their supernatant had cytotoxic effects on the trophozoites. All the trophozoites were destroyed within 24 hours. This definitely indicates that the C.M.I. system must be getting sensitised and activated after the cure of an initial attack. Thus, the infrequency of recurrence of an amoebic liver abscess is now explained.
To summarise the highest peaks of antibody and B cell reactivity are found during the active process of the disease. We still cannot say with certainty whether these anti-bodies give protection of participate in the destruction of the hepatocytes. The cell mediated immunological system seems to render protection only after the acute stage passes away. How fare does the C.M.I. help in final resolution is also not known.

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