July, 1950] AMOEBIC ABSCESS OF THE BRAIN : KOSHY 287

Original Articles

AMCEBIC ABSCESS OF THE BRAIN I !

By P. KOSHY, b.a., m.d.

(Department of Medicine, Christian Medical College, Vellorc)

Amebic abscess of the brain is one of the

rarest and most fatal of the complications of

amoebiasis. In the majority of cases described brain abscess has followed an abscess of the liver or lung. Craig (1944), in his forty years of

study of amoebiasis, says he never saw a case

of amoebic abscess of the brain except as a

museum specimen. The statistics of the Medical College Hospital,

Vellore, show from 1944 to 1949 there were

2,275 cases treated for amoebic dysentery and there were 166 cases of amoebic abscess of the liver among them. During this period there was not a single case of amoebic abscess of brain

recorded. Of the 561 post mortems performed in the above hospital there were only 8 cases of amoebic dysentery and one of amoebic abscess of the liver.

Reddy and Thangavelu (1948) in an analysis of 2,64l' cases of dysenteries treated in Madras General Hospital recorded 1,011 cases of

amoebic dysentery of which 44 came for post mortem and found no case of amoebic abscess of

the brain. In a recent review of 104 post mortems of metastatic brain abscess by Qates ct al. (1950) there is not a single case mentioned of amoebic abscess of the brain.

Amoebic abscess of the lung may be primary, reaching the organ through the blood stream, or

secondary to an amoebic abscess of the liver. It occurs in 10 per cent (Kartulis, 1904) to 20

per cent (Rogers, 1922) of liver abscess cases.

Craig quotes the incidence as 3 in his series of 26 cases of liver abscess and in 5 cases liver

abscess ruptured into 'pleural cavity producing empyema.

Well known among the complications of

amoebic colitis is abscess of the liver. Accord- ing to Simonds (1843) its incidence ranges from 3.48 in surviving patients to 42.36 per cent in

cases in which necropsies were performed. Involvement of the brain is a rare complica-

tion and is usually preceded by similar involve- ment of the liver or of the lungs or both. To date not less than 62 cases of abscess of brain have been reported. Among them involvement ?f brain without evidence of involvement of liver or lungs are not more than five. Of the latter two were reported by Kartulis (loc. cit.), a third by Putney and Baker (1938), a fourth by

Stein and Kazan (1942) and a fifth by Halpert and Ashley (1944). One more is added to this from.the following record.

Case report A 60-year-old man was admitted to the

Christian Medical College Hospital, Vellore, on 24th June, 1949, with a history of cedema of the legs and distension of the abdomen lasting 45

days. Breathlessness and diarrhoea for one

month with blood and mucus in stools. Occasional fever with chills.

On admission he had ascites, soft pitting cedema of both legs, pallor, emaciation, well- marked clubbing of fingers. Pulse rate 80/m., regular. Heart not enlarged, no murmur. Blood

pressure 95/60. Lungs : impaired resonance at both bases with diminished air entry. Nervous

system : cranial nerves nothing abnormal, sensations normal, motor power normal, reflexes normal, abdominals difficult to elicit and plantar response flexor.

Laboratory examination.?Hb., 6.25 gm. W.B.C. 5,100 per cubic millimetre with a

differential count of 84 per cent polymorphs and 16 per cent lymphocytes. Stool showed R.B.C. and pus cells in plenty with macrophages, no E.H. or E.H. cysts. Urine was of alkaline

reaction; specific gravity 1025, albumin found in trace and deposits showed R.B.C., pus cells and granular casts. With sulphaguanidine the diarrhoea improved.

Paracentesis of the abdomen done on 28th of June and pints of straw-coloured fluid

removed, the albumin content of the fluid

being 0.35 per cent with a few lymphocytes and polymorphs. With a diet rich in milk his general condition seemed to improve. On the 5th July at 11.30 a.m. the patient

developed an attack of Jacksonian epilepsy. He cried out hysterically iust before the attack, then the fit started with twitching of the face muscle followed by conjugate deviation of the eyes to the right and frothing at the mouth. The fits followed one after the other at fairly

frequent intervals till 6 p.m. when they appeared to be controlled. The next day he appeared somewhat stuporose. On 7th he had another attack of Jacksonian epilepsy. Thereafter he remained in a state of coma until the 14th July when he died of pulmonary cedema. Examination following the initial attack of fits

showed left pupil larger than the right and not responding to light; right pupil showed sluggish reaction. Ocular media were not quite clearly seen due to sclerosis of the lens. No papill- oedema made out. There were arteriosclerotic

changes but no haemorrhages or exudates. Deep reflexes all over were exaggerated, plantar flexor; Kernig's absent. Roentgenographs examination of skull revealed no abnormality. Blood urea was 45 mg. and blood sugar 82 mg. per cent.

288 THE INDIAN MEDICAL GAZETTE [July, 1950

Autopsy findings : (1) Alimentary canal.? The peritoneal cavity contained one pint of clear straw-coloured fluid. The colon was very much thickened. The mucous membrane of the caecum and colon showed many flask-shaped ulcers with necrotic base and typical

' dark hair ' appearance. The edges of the ulcers were necrosed and covered by exudate, due to

secondary infection.

Microscopically, the ulcers showed necrosis of the submucosa, and sometimes of the muscularis, with mononuclear infiltration. This picture was altered in many ulcers, due to secondary infection. Here, the surface layers and the area around the ulcers showed fibrinous exudate with

polymorph infiltration. Amoebae were found in the base and sides of ulcers.

(2) Liver.?The liver was slightly smaller in size, light brown in colour, coarsely granular and firm. It weighed 750 gm.

Microscopic appearance was that of the portal type of cirrhosis. The whole liver was sliced into thin pieces and no evidence of amoebic abscess found.

(3) Spleen.?Was slightly enlarged and covered by fibrinous deposit. The capsule was thick and consistency firm. It weighed 300 gm.

Microscopically, there was increase in the fibrous trabeculae and atrophy of the lymph follicles.

(4) Respiratory system.?Both the pleural spaces were obliterated by moderately firm fibrous adhesions.

The lungs showed basal oedema with emphy- sema of the remaining portions. There was no evidence of amoebic abscess.

(5) Heart.?Foramen ovale not patent. (6) Brain.?There was an area of hemorrhage

and softening in the lower part of the left frontal lobe about 5 cm. in diameter. The affected part was gelatinous?the typical

1 red currant jelly

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appearance (figure 1, plate XLII). Microscopically, there was haemorrhage and

necrosis with amoebae at the edge (figure 2, plate XLII).

Discussion

The route by which E. histolytica reaches the brain is by no means clear, particularly in those rare instances where, as in the case reported here, the liver and lungs are not involved. It has been claimed that amoeba can pass through the capillaries of the liver and lung and reach the brain. Further, a healed lesion in the liver with a subsequent lesion in the brain without involvement of the lung has been considered by some as a possibility. There is some difficulty in comprehending how the amoeba can pass through the capillaries in the liver and lungs without being arrested in them. The more probable route which it takes from the intestines to brain is the one suggested by Stein and Kazan (loc. cit,),

the vertebral system of veins which has been demonstrated by Batson (1940). This mechanism of spread makes it easier to under- stand how these rare complications of intestinal amebiasis can occur.

Collis (1944) in exhaustive review of all the theories on the pathogenesis of metastatic brain abscess from thoracic disease came to the con- clusion that the method of spread is a retrograde passage of infected material from the thoracic wall to the paravertebral plexus of veins and thence J:o the cerebrum. He further demon- strated how the reversal of flow in the spinal system of veins is facilitated by the patient lying flat on his back.

More interesting however is Batson's demon- stration how by coughing and sneezing with

consequent changes in pressure inside the abdomen blood may be squeezed from the intra- abdominal veins into the vertebral system of veins. It is therefore possible that paravertebral plexus of veins may be the source of spread to the brain in the rare cases of isolated metastatic brain abscess complicating amcebic dysentery. My thanks arc due to the Pathology Department of

the Christian Medical College Hospital, Vellore, and

particularly to Dr. M. Asirvadham who has been kind enough to provide me with the post-mortem report and the photographs.

I am specially indebted to Dr. P. Kutumbiah, M.D., m.r.c.p., for the stimulus and direction in preparing this article.

REFERENCES

Batson, C. V. (1940) .. Ann. Surg., 112, 138. Collis, J. L. (1944) .. ,/. Thoracic. Surg., 13, 445. Craig, C. F. (1944) .. /Etiology, Diagnosis and

Treatment of Amcebiasis. Williams and Wilkins Co..

1 Baltimore. Gates, E. M., Kernohan, Medicine, 29, 91.

J. W., and Craig, W. M. (1950).

Hai.pert, B., and Ashley, Arch. Path., 38, 112. J. D. (1944).

Kartulis, S. (1904) .. Zentralbl. Bakt., 37, 527. Putney, F. J., and Dis. Chest, 4, 20.

Baker, D. C. (1938). Reddy, D. G., and Indian Med. Gaz., 83, 557. Thangaveiaj, M. (1948).

Rogers, L. (1922) .. Brit. Med. J., i, 224. Simonds, J. P. (1843) .. Bull. North Western Univer-

sity Med. School, 17, 25.

Stein, A., and Kazan, J. ' Neuropath, and Expcr.

? A. (1942). Neurol, 1, 32.

Plate XLI1

AMCEBIC ABSCESS OF THE BRAIN : P. KOSHY. (O, A.) PAGE 287

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