AMEBIC PERFORATION OF THE INTESTINE IN CHILDREN

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AMEBIC

PERFORATION

OF THE

INTESTINE

IN CHILDREN

C. de S. Wijesundera, M.B.B.S. (Ceylon), D.C.H. (Ceylon), and

C. C. de Silva, M.D., F.R.C.P.

Department of Paediatrics, Univers-ity of Ceylon

(Submitted January 31, 1962; accepted June 25, 1962.)

ADDRESS: (C.C.deS.) Department of Paediatrics, University of Ceylon, Colombo 8, Ceylon.

PEDr.rwcs, December 1962

937

S

EVEN PATJENTS with amebic perforation of the intestine were admitted to our unit within a period of 8 months in

1960-1961. We had not previously diagnosed this condition clinically nor seen it at autopsy

in children.

Case 1

REPORT OF CASES

A Tamil male child, aged 2 years and

weighing 8.9 kg, was admitted on July 10, 1960, with a history of diarrhea with blood

and mucus of one week’s and dyspnea of 3 days’ duration. On the first day, the child had passed six stools which were semisolid and offensive with mucus but without

blood. On the second day, the stools had been watery. On the third day, blood had

appeared in the stools; and on the fourth, he had in addition a cough with breathless-ness and fever. These symptoms had

con-tinued until admission to the hospital. There was no previous history of diarrhea with

blood and mucus.

On examination the patient’s temperature

was 38.9#{176}C;he was moderately dyspneic

and mildly dehydrated. The breath sounds were vesicular, and medium crepitations

were heard bilaterally in all zones of the chest. His abdomen was slightly distended without tenderness or rigidity. His stools

were watery with blood and mucus, and the smear showed numerous active troph-ozoites of the Entameba histolytica.

The child was given oxytetracycline (200 mg) and iodochlorhydroxy-quinoline (250 mg) each three times a day. The diarrhea

continued, with three to four daily stools containing blood and mucus which were constantly smeared around the anal orifice.

On July 13, i.e., the fourth day after admis-sion, the abdomen was more distended and moderately tender. Though somewhat

re-sistant, it was not rigid, but the area of liver

dullness was obliterated and peristaltic sounds were not heard. A perforation was

suspected, but the parents refused permis-sion for operation. The patient died on the following morning.

Postmortem examination was done 5

hours after death. When the abdomen was opened, a live round worm was seen in the peritoneal cavity. There was yellow, offen-sive pus in the lower part of the abdominal

cavity, and a loop of small intestine showed

signs of inflammation. There was a

perfora-tion on the lateral side of the middle of the descending-colon, through which blood and mucus exuded. On closer examination, three

perforations were seen close together (Fig.

1). The mucosal surface of the entire large

intestine showed numerous small ulcers which were irregular in shape with

under-mined edges. Ulceration was most extensive

in the cecum, pelvic colon, and rectum. Whipworms were attached to the mucous

membrane of the whole of the large intes-tine. Microscopically the large intestine showed necrosis of the mucous membrane with infiltration of all the coats, especially

the submucosa, with amebae and round cells (Fig. 2). The liver showed fatty in-filtration. The stools did not show any

Salmonella and Shigella organisims on cul-ture.

Case 2

A Sinhalese male child, aged 6 years,

weighing 16.4 kg, was admitted on July

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blood and mucus, vomiting of 2 weeks, and

fever of 9 days’ duration. About 15 days earlier the patient had been given treatment for ascariasis (syrup of piperazine citrate),

and 40 round worms had been passed. On the next day, the child had 10 watery stools and had vomited twice. Tile stools were scanty and offensive with blood and mucus,

and the symptoms persisted in spite of out-door treatment for 5 days. Pyrexia with

profuse sweating had commenced on July

13, with abdominal distension and dyspnea from July 18, without any pain or

tender-ness referred to tile abdomen.

The patient had had a chronic, recurrent cough following an attack of whooping cough at the age of 9 months. No previous

history of diarrhea was elicited from the

parents.

On examination the temperature was

37.8#{176}C,and the patient looked very ill. He

was mildly dehydrated. His breath sounds

were vesicular with bilateral coarse

crepita-tions. The abdomen was resistant and

dis-tended without any tenderness. The patient

FIG. 1. Case 1. Mucosal surface of large intestine. The arrows indicate perforations.

Fic. 2. Case 1. Section of large intestine showing

necrotic mucous membrane and numerous amebae in mucosa and submucosa.

vomited twice on the day of admission. He was given oxytetracycline, 200 mg three times a day by mouth, and 300 ml of N/2 saline solution with 12.5% dextrose intrave-nously. On the next day his condition was much worse; the abdomen was now resistant,

tender, and distended; the liver dullness was obliterated, but faint peristalic sounds were heard. On examination ulcers were palpable in the rectum. The patient continued to pass

blood and mucus in the stools, which were swarming with trophozoites of the Entameba histolytica. He was given 200 ml of N/2

saline solution with 12.5% dextrose and 300 ml of N/4 saline solution with 12.5%

dex-trose intravenously. The general condition remained more or less the same but im-proved after a transfusion of 20 ml of

blood. He did not pass any stools that night.

On July 21, 1960, the patient was operated

upon. About % pint (250 ml) of purulent

fluid was found in the peritoneal cavity.

The appendix was gangrenous and

perfor-ated in two places. It was lying against the

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939

Fic. 3. Case 2. Section through the inner muscle layer of the large intestine, stained with a modified P.A.S. stain,17 showing amebae as dark spots

sur-rounded by a clear space. (xllO)

apposition to a perforation of the cecum. The

appendix was removed and the cecal per-foration was closed. A smear from the

per-foration in the appendix showed live E. histolytica. The patient died the same eve-ning without regaining consciousness.

A limited autopsy was done through the operation wound about 14 hours after death;

the lungs were congested, there was cystic bronchiectasis of the lingula of the left

lung. There was extensive ulceration of the

mucosal surface of the large intestine, most marked in the cecum, pelvic colon, and rectum; tile ulcers were irregular with

un-dermined edges, and there were numerous whipworms attached to the mucous

mem-brane of the large intestine.

Histological examination of the large

in-testine silowed necrosis of the mucous

mem-brane and infiltration of all the coats with

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Fic. 5. Case 2. Section through the muscle and peritoneal coats of large in-testine. Arrow indicates an ameba in peritoneal coat. (x 150)

amebae and round cells, with occasional polymorphonuclear leukocytes; mononu-clear cellular infiltration was prominent in

the muscular layer (Figs. 3-6). The stools did not show any Salmonella and Shigella

organisms on culture.

Case 3

A Sinhalese male child, aged 2 years 5

months and weighing 9.6 kg, was admitted

to the hospital on September 23, 1960, with

a history of fever, diarrhea, and vomiting of 12 days’ duration. The stools were semisolid and frothy and contained blood or mucus

for the 5 days prior to admission. The child

had passed seven round worms with the

stools and had vomited seven times. He had

had a similar attack one year ago, which

subsided after a week’s treatment in the

ward.

On examination the child was found to

be moderately well nourished. The

tempera-FIG. 6. Case 2. High magnification of the ameba indicated in Figure 5.

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ture was 37.8#{176}C, but he was not dehy-drated; his tongue was moist and pink, and

angular stomatitis was present. His pulse rate was 142 per minute, and the volume

and tension were good. The examination of

the heart showed nothing abnormal, but there were coarse crepitations over both

lungs. Tile abdomen was firm with

general-ised tenderness, but it was not distended;

peristaltic sounds were not heard, but the

area of liver dullness was not impaired.

From the time of admission the child passed several stools which consisted mostly

of blood-stained mucus. The fecal smears were swarming with very active

tropho-zoites of E. histolytica.

A perforation was suspected, and the

child was prepared for a laparotomy on the

same evening. On palpation under

anes-thesia, there was a lump in the right iliac fossa. On opening into the abdominal

cay-ity through a MacBurney incision, the omentum was seen to be covering the cecal area. On raising the omentum a 2 to 3 in. long strip of the anterior wall of the cecum

and ascending colon between the anterior

and tile medial tenia coli was seen to be sloughing and gangrenous, and the intes-tinal contents with blood and mucus exuded through multiple perforations. The margins

of the healthy portion of the intestine were sutured together, leaving the gangrenous

part everted and not in continuity with the lumen of the intestine.

He was given oxytetracycline, 200 mg, and emetine, 15 mg, intramuscularly about 4 hours before the operation. Administration

of the latter drug was repeated about 1

hour after the operation. Therapy was con-tinued with oxytetracycline, 200 mg three times a day by mouth; emetine, 15 mg

in-tramuscularly once a day; and iodochlor-hydroxyquinoline, 250 mg twice a day. Also,

300 ml of 5% dextrose in N/2 saline and 200

ml of blood were administered intrave-nously during and after the operation. The

same intravenous therapy was continued until September 25; but Darrow’s solution,

200 ml intravenously, was added when

signs of hypokalemia appeared.

The patient continued to show

improve-ment in his general condition, though the

abdomen was distended, with obliteration of the liver dullness. He continued to pass

blood and mucus containing live amebae per rectum. They were, however, less nu-merous and more sluggish in their move-ments. There were also numerous

whip-worm ova in the stools. From September

25 he was given a diet of orange juice and

malted milk. Owing to the persistence of

live amebae in the stools, he was given a chiniofon enema on September 26. On the

following day the patient became much worse. Analysis of the serum for electro-lytes showed sodium, 132 meq/l; potassium, 2.2 meq/l; and chlorides, 92 meq/l. He was

given intravenously 400 ml of normal

sa-line solution wih 5% dextrose and 400 ml of Darrow’s solution. Gastric suction was

in-stituted. He died on September 28, 5 days after the operation. The parents refused

permission for a postmortem examination.

The stools did not show any Salmonella or

Shigella organisms on culture.

Case 4

A Sinhalese male child, aged 1 year 10

months, was admitted to the hospital on

October 29, 1960, with a history of diarrhea

and vomiting of 10 days’ duration. He had

passed 10 to 12 watery stools per day, with

blood and mucus, from the second day of

illness. He had no history of fever or cough,

but edema of the feet was visible since the morning prior to admission.

On examination the child was

comfort-able and did not show any signs of dehy-dration. There were no abnormal findings

in his respiratory or cardiovascular systems.

His abdomen was soft without any

disten-sion or tenderness. His stools were watery with blood and mucus; microscopically

there was no evidence of any parasitic in-festation. The patient was given

sulphadia-zine, 0.5 gm, every 6 hours. Food was

omitted for 8 hours, and intravenous fluids

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no improvement on sulphadiazine therapy,

he was given iodochlorhydroxyquinoline,

125 mg twice daily, and neomycin with

kaopectate, 1 drachm (60 ml) every 8 hours.

On November 5 the stools were positive for

E. histolytica. Round worm ova, whipworm

ova, and Giardia lamblia cysts were found

at subsequent smear examinations. From

November 5 the patient was given emetine,

10 mg intramuscularly per day;

iodochlor-hydroxyqumnoline, 125 mg twice daily; and

oxytetracyclmne, 125 mg twice daily. The

child was drowsy and restless with

abdomi-nal distension from November 6. On the

next day he had slight neck stiffness, but

the cerebrospinal fluid was normal. Tue

stools continued to contain a surfeit of

blood and mucus. Intestinal sounds were

heard. On November 9 the child looked

very toxic, and there was marked

abdomi-nal distension with moderate resistance and

tenderness. The intestinal sounds were no

longer heard. The liver dullness was

ab-sent. A perforation was suspected, and he

was operated on the same evening. There

was pus in the peritoneal cavity. The lateral

wall of the cecum was gangrenous with a

perforation measuring 3 in. diameter. The

appendix was inflamed and friable.

Cecos-tomy was done as a change from the

previ-ous routine of repairing the perforations,

since none of the previous patients

oper-ated on had recovered.

We continued the same drugs and

intra-venous fluid therapy as well as giving a

transfusion with 300 ml of blood. The stools continued to be positive for amebae. He was also given emetine, dissolved in water, via the colostomy tube on November 9. The

patient died on November 12, 3 days after

operation. The stool cultures were negative

for Salmonella and Shigella organisms on

two occasions. No postmortem examination

was allowed.

Case 5

A Sinhalese female child, aged 3 years

3 months and weighing 6.6 kg, was

ad-mitted to the hospital on January 23,

1961, with a history of diarrhea with blood

and mucus of 10 days’ duration and

tem-perature of 37.8#{176}Cwitil dyspnea since the

morning of admission. On examination the patient was in a state of collapse with cold

extremities and an imperceptible pulse.

On examination of the chest the

percus-sion note was resonant and the breath

sounds were vesicular; fine crepitations were heard, especially over the bases; the

ab-domen was distended and soft with general-ized tenderness. The child’s condition be-came worse on the next morning. The liver

dullness was obliterated, and the abdomen was moderately tense. The intestinal sounds

were not heard. There were live E. histo-lytica in the stools. The case was diagnosed

as one of amebic perforation.

In view of Barker’s report, which claimed some recoveries with conservative treatment, we decided to treat this patient in the same manner. She was given neomy-cm witll kaopectate before the amebae were discovered in tile stools and

iodochlorhy-droxyquinoline and oxytetracycline after the positive fecal report. She was also given

200 ml of 10% dextrose solution and 150 ml

of blood intravenously. However her

condi-tion deteriorated rapidly, and she died on the morning of January 24, 1961, the day

after the admission to hospital.

Postmortem examination was done about

3 ilOurs after death. There was fluid with blood and mucus in the peritoneal cavity.

The large intestine was necrotic and friable, with multiple perforations throughout its

length (Fig. 7); the mesenteric glands were enlarged; the mucous membrane was

ex-tensively ulcerated with only a few islands of normal tissue left. There were

whip-worms attached to these intact areas of

mucous membrane. The lungs were con-gested.

Microscopically, section of the large

in-testine showed necrosis throughout the

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943

FIG. 7. Case 5. Open abdomen, showing numerous perforations of large intestines, indicated by white

indicators.

lungs showed areas of congestion collapse

and emphysema, and tile liver showed marked fatty infiltration.

Case 6

A Sinhalese male child, aged 1 year 5 months, was admitted to the hospital on

February 20, 1961, with a history of fever

and diarrhea of 2 weeks’ duration and

dysp-nea of sudden onset since the previous

eve-ning. He had passed three to four watery

stools with blood and mucus per day.

Fic. 8. Necrotic tract through the muscle coat of large intestines.

(x

166)

On examination the patient was cold,

clammy, and collapsed, and his pulse was of low volume and tension; the abdomen was distended and tense.

In the respiratory system, the percussion

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Fic. 10. An ameba in the peritoneal coat shown in Figure 9 under higher magnification. (x750)

note was resonant bilaterally, the breath

sounds were vesicular, and there were fine crepitations on both sides. Continuous gas-tric suction was instituted, and about 4 oz

of “coffee ground” fluid was aspirated from the stomach. The patient died one hour after admission.

Postmortem examination was done about 6 hours after death. The abdomen was

dis-tended. There was purulent fluid in the peritoneal cavity and three perforations in the large intestines (two in the ascending colon and one in the pelvic colon). There was ulceration of the mucous membrane of the large intestine, the ulcers being irregu-lar with undermined edges and intact

mu-cosa between, typical of amebic ulceration.

There were no whipworms to be seen. The liver was enlarged to two fingerbreadths below the costal margin. There was

con-solidation at the base of left lung. Micro-scopically, the liver showed fatty change. There was necrosis of the mucosa of the large intestine with round cell infiltration

and edema of the submucosa. Structures re-sembling amebae were seen infiltrating the submucosa.

Case 7

A Muslim male child, aged 4 years and

weighing 9.9 kg, was admitted to the

hos-pital on May 2, 1961, with a history of diarrhea with blood and mucus of three weeks’ duration. He had vomited several

times on the day of admission.

On examination his temperature was

38.3#{176}C. He was moderately well nourished but dehydrated; his tongue was moist and

coated.

In the respiratory system, the percussion

note was resonant, and the breath sounds were vesicular with bilateral coarse

crepi-tations and rlionchi.

In the cardiovascular system, the pulse was regular at 100 per minute, the apex

beat was in the fourth left intercostal space, medial to the midclavicular line; both

sounds were heard and there were no

mur-murs. Tile abdomen was soft but diffusely

tender. The child was given an intravenous

infusion of N/4 saline and 5% dextrose so-lution, 150 ml, followed by 200 ml of 10%

dextrose that night, and oxytetracycline, 150 mg, every 8 hours by mouth. He was

also given Eledon (half-skimmed lactic acid

milk) feedings. The stools were found to be teeming with E. histolytica. On the fol-lowing day the child’s condition became worse, with an anxious look on the face; but his abdomen was not distended though

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(10)

TABLE II PATHOLOGICAL FINDINGS Case Na inber A utopsy; . Operation . . . Perrtonztls . She of .. Perforatlon

3lultiple Stools for

. .

or Slngie Entumeba

. .

Perforatlon IIlstoiytlca

.

Illstology of Large Intestine

1 A P Descemling colon 3 P Infiltration iy round cells & amebae;

necrosis of mucosa

2 0 & A P Cecum & appen(Iix 3 P Inflltrationl)yroundcells &amel)ae; necrosis of mucosa

3 0 P Cecum & ascend- Multiple P Not (lone

ing colon

4 0 P Cecum & appendix Multiple P Not done

.5 A P Entire colon Multiple P Necrosis of wall; infiltration with

alslebae

6 A P Ascending colon Not (lone

1

Infiltration by round cells & amebae;

and necrosis of mucosa

7 A P (?) (?) (i’) Not (lone

was doubtful. Rectal ulcers were palpable

per anum. The abdomen became increas-ingly distended. Intravenous fluids were continued in the form of N/2 saline and 5% dextrose solution, 500 ml, followed by N/4 saline and 5% dextrose, 300 ml. He was

given a single dose of emetine hydrochlo-ride, 10 mg, on May 3.

The child’s condition gradually

deterio-rated on the next day. The abdomen be-came more distended with disappearance of the liver dullness. He was given 10% dextrose, 300 ml, intravenously. He died on the morning of May 5 (on the fourth day

after admission). Permission was not granted for autopsy.

However, a paracentesis of the abdomen immediately after death showed purulent fluid in the peritoneal cavity, teeming with live E. histolytica.

COMMENT

Reports of amebic perforation of the in-testine in children have been rare, but more

and more cases are now being reported. Manson Bahr2 had seen only four cases. Anderson et al. found them in 10.7% of autopsies on all deaths at all ages from ame-biasis. Herrera et al. reported a single case

in a child, while Cordoba et al.5 had a

series of 11 cases of intestinal perforations

due to amebae in children. Ravinna et al.#{176}

reported four fatalities in children due to

amebic perforation. Faust,7 however, in his monograph on amebiasis quotes Armstrong

et al. that 10% of 2,500 Africans in Durban, Natal, who entered the hospital with ful-minating amebic dysentery, died of

perfor-ation and collapse. We have been unable to ascertain how many of these cases, if

any, were in children. Joan Scragg9 from Durban, South Africa, has stated that of

57 deaths from amebiasis in children, 13 (22%) had frank perforations with

perito-nitis; 3 of these 13 had associated liver abscesses. In the Children’s Hospital, Co-lombo, though acute and chronic amebiasis

is very commonly encountered, these seven

cases are so far the only ones to be re-ported. Over the period of 1956-1960 in the

University Unit at the Children’s Hospital, there were 136 cases of amebiasis with 14 deaths (10.3%), which included 4 in 1960 reported here due to perforations. Of these

seven cases under review, amebae were demonstrated in the first five, and also

shown microscopically in the sections of the

large intestines in Cases 1, 2, 5, and 6. In Case 7 E. histolytica were present in the peritoneal fluid which was aspirated after death.

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possibly due to a greater awareness of the

condition as a result of the postmortem

con-firmation of the diagnosis in the first case. \Ve now believe that this is a more frequent

complication of amebiasis in children than liver abscess.

We have little doubt that the amebae were responsible for tile perforations,

pos-sibiy aided by bacteria and helminths. We

have silown the amebae infiltrating the mus-cular coats of the intestine and peritoneum

(Figs. 3-6 & 8-10). This is not likely to be a

postmortem invasion, because there is as-sociated round cell infiltration. Furthermore, we store tile bodies under refrigeration com-mencing an hour after death, and amebae

would soon become inactive and die at

those temperatures. In Case 7 amebae were

silOwn in the peritoneal fluid which was

aspirated immediately after death.

The cytolytic propetries of amebae are

well documented. PauP#{176}has shown massive amebic infiltration of the muscles of the

anterior abdominal wall with illustrations.

Therefore it is not surprising that with the

extensive destruction of the mucosa and

submucosa associated with the teeming

bil-lions of amebae, that tile exposed deeper coats of the intestine should be invaded by the amebae. That the extensive tissue

ne-crosis is not a postmortem phenomenon is

shown by the fact that in Case 3 it was seen

at operation.

We are not aware of any other organism or agency capable of such destruction of

the large intestine, whereas there are flu-merous reports, especially from workers in South Africa, of such lesions said to be caused by amebae. All perforations due to

the Ascaris have occurred in the small

in-testine or appendix, never in our experience

in the large intestine.

Balantidum coli is known to cause ulcer-ation of tile mucosa and submucosa of the

large intestine. We did not detect this

or-ganism in our cases, and it is very rare in

Ceylon.

In Case 1 it may be argued that the round worm found in the peritoneum

caused tile perforations of an already

ul-cerated intestine, as was thought to be pos-sible by Oschner et al.h1 But there were three perforations, which are unlikely to have been caused by one round worm which had already escaped into the

pen-toneal cavity. Some of the perforations seen especially in Figure 7 are probably anti-facts; if so, they were produced in spite of

the gentlest handling of an intestine ne-crosed to the consistency of wet blotting paper. This particular postmortem

exami-nation was done only 3 hours after death. In our case there were some conflicting clinical signs. In the first, fifth, and seventh

cases there was a misleading absence or rigidity of tile abdomen until very late, so much so that the diagnosis of perforation

was in doubt in the first two cases. In Case 2 there was only very slight resistance of the abdomen. The features that appeared

early were abdominal distension and oblit-eration of the liver dullness, but there was generalized tenderness and absence of

per-istaltic sounds. In Cases 2 and 4 penistaltic

sounds were heard until late. It is more

than possible that the diagnosis may often be missed with this misleading

symptoma-tology because many cases of acute diarrhea due to other causes may manifest abdomi-nal distension with tenderness. Since

pen-mission for autopsies is still difficult to

ob-tam, many deaths due to amebic

penfora-tions may be diagnosed as being due to

“acute gastnoenteritis.” Furthermore, dysp-nea due to an associated

bronchopneumo-nia or abdominal distension may also dis-tract the attention of an overworked medi-cal officer from the abdomen to the chest,

as happened in a case where there was a

perforation at postmortem, but which we have omitted from this discussion because

there was no confirmatory evidence that it was amebic in origin.

The utter impotence of the usual

amebi-cidal drugs was brought home to us fond-bly during the treatment of our cases. We

watched with despair while the marauders destroyed the host. In all the cases where

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devour-948

ing erythrocytes with their pouting

pseu-dopodia, and this in spite of 4 days of

oxy-tetracycline and iodochlorhydroxquinoline by mouth in Case 1; 2 days of oxytetra-cycline in Case 2; five days of

oxytetracy-clime and emetine in high dosage in Case 3; and 5 days of emetine, oxytetracycline, and

1 day of emetine in Case 7. Emetine has the

serious disadvantage of causing nausea and

vomiting, so that we did not use it in Cases

1 and 2 in view of the toxic state of the

patients. However, since these cases

dem-onstrated that the amebae were a greater hazard than the possible toxicity of the

drug, we used large doses of emetine in Cases 3 and 4 but without any better sue-cess (0.75 mg/lb body weight in Case 3).

Other workers have shared similar expeni-ences regarding amebicidal drugs. Paulbo described a case where the amebae were

attacking the abdominal wall (amebiasis cutis) uninfluenced by the drugs. Arm-strong et 12, 13 stated that no regimen

of treatment has been followed with sue-cess in eliminating E. histolytica from all their patients. Scragg9 mentioned that in all hen 8 years of experience no patient with amebic perforation recovered. Barker1 is to our knowledge the only one who has

claimed 5 recoveries in 19 cases of amebic colonic perforation; of these five, two only were proved to be perforations by x-ray

examination, the remaining three being

din-ical diagnoses. He concludes his excellent paper by saying that “operative treatment has rarely if ever any place in the manage-ment of colonic perforations occurring dur-ing the course of fulminating amebic

dys-enteny. Emphasis is laid on the possibility

of saving a greater number of these cases by means of treatment with intravenous fluid and electrolyte therapy, blood replace-ment, and antiobiotic and anti-amebic

then-apy. This form of treatment, to achieve success, demands great care and attention to detail.”

A feature common to six of these cases

was whipworm infestation of the large

in-testine. Could this have been a factor in the pathogenesis of the ulceration of the

mu-cosa and subsequent perforation of the

in-testine? Westpha1’ showed that certain bacteria were necessary for E. histolytica

to establish itself as a pathogen in the gut. It is well known that in Europeans in Africa

and elsewhere amebiasis is a mild disease which is very rarely fatal. Is this possibly

due to the fact that helminthiasis is less likely to be associated with amebae in

peo-pie with a higher standard of nutrition,

sani-tation, and hygiene? Others have noticed the

association of helminths in general with in-testinal amebiasis. Hence it could be postu-lated that the injury caused by the head of

the whipworm threading through the

mu-cous membrane might open a passage for the amebae to invade it. It has also been the observation of another physician working

in the same hospital as the present authors,

Mirando, that whipworm infestation is

often associated with intestinal amebiasis. If this relationship is considered of

signifi-cance, elimination of the whipworm would

also be necessary in the treatment and pro-phylaxis of amebiasis. However, whipworm infestation is so common in Ceylon that its association with amebic ulceration may well be a fortuitious one without any pathogenic significance. A more extensive clinical study

and possibly animal experimentation would be necessary to verify this. The difficulty, according to the Professor of Parasitology,

University of Ceylon, is to find an animal

host that is susceptible to the pathogenic effects of both the E. and the

Tnichocepha-lus dispar.

Cellular response of tissues to amebic

in-vasion is poor. Tile usual one is a lympho-cytic infiltration, as was seen in the sections of the intestine in these cases. When tissue damage is severe, a polymorphonuclean re-sponse is also said to occur.16 However in

all our cases, though the tissue damage was

very severe, no polymorphonuclear response was seen.

SUMMARY

Seven cases of amebic perforation of the

large intestine in children are presented.

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ARTICLES

misleading symptomatology, (b) the rela-tive ineffectiveness of oxytetracycline, the

hydroxyquinoline group of drugs, and eme-tine as amebicidal agents, and (c) the

fail-tire of surgical treatment. Attention is also drawn to the association of whipworm in-festation, with a suggestion that this may

possibly be aiding the amebic invasion of

tile large gut. Neither an operative nor a

conservative regimen has met with any

sue-cess at our hands in saving a single life so fan.

REFERENCES

1. Barker, E. M. : Colonic perforations in amoebia-sis. S. Afr. Med. J., 32:634, 1958.

2. Manson-Bahr, P. G. : Dysenteric Disorders. London, Cassell, 1939, p. 173.

3. Anderson, H. H., Bostic, W. L., and John-ston, I-I. G. : Amebiasis. Springfield, liii-nois, Thomas, 1953, p. 177.

4. Herrera, R. C., et at.: Presentaci#{243}n de un caso de perforaciones multiples de intestino un

ni#{241}o con amibiasis. Bol. Med. Hosp. Inf., 10:423, 1953.

5. Cordoba, P. B., et at.: Perforacion intestinal amibiana en Ia infancia commentario sobre II casos. Anot. Pediat., 21 :239, 1959. 6. Ravinna, A., Joseph, A., and Cohen, W. :

Hare-fuah, 58: 155, 1960.

7. Faust, E. C. : Amebiasis. Springfield, Illinois,

Thomas, 1954, p. 45.

8. Armstrong, T. G., Wilmot, A. J., and Elsdon-Dew, R. : Treatment of amoebic dysentery in Bantu African. Trans. Roy. Soc. Trop. Med. Hyg., 42:597, 1949.

9. Scragg, J.: Personal communication.

10. Paul, M.: New concepts on amoebic abscess of the liver. Brit. J. Surg., 47:512, 1960.

11. Oschner, A., DeBakey, E. G., and Dixon, J. L.: Complications of ascariasis requiring

surgi-cal treatment. Amer. J. Dis. Child., 77:389, 1949.

12. Armstrong, T. G., Wilmot, A. J., and Elsdon-Dew, R. : Aureomycin and amoebic dysen-tery. Lancet, 2: 10, 1950.

13. Armstrong, T. G., \Vilmot, A. J., and

Elsdon-Dew, R.: Terramycin in amoebic dysentery.

S. Afr. Med. J., 26:766, 1952.

14. \Vestphal, A. : Betrachtungen zur Arbeit von

Koller #{252}berAmobiasis in Neu-Guinea. Arch.

Schiffs- Tropen-Hyg., 41 :262, 1937. 15. Mirando, E. H. : Personal communication.

16. Anderson, H. H., Bostic, W. L., and Johnston,

11. C. : Amebiasis. Springfield, Illinois,

Thomas, 1953, pp. 107-116.

17. Silva, E. E. M.: Periodic acid Schiff staining combined with iron haematoxylin and light

green for amoebae in sections. S. Afr. Med.

J., 26:766, 1952.

Acknowledgment

Our thanks are due to Dr. Stella de Silva for permitting us to publish one of her cases (Case No. 6); to Mr. Justin de Silva and Mr. Irugal

Ban-dara of the Department of Pathology, University of Ceylon, for the preparation of the microscopic slides; to Professor Cooray and his staff of the De-partment of Pathology of the University of Ceylon for reports; and to Mr. Amarasekera and Mr.

Jaya-weera of the Department of Photography, Faculty

of Medicine, University of Ceylon.

Some of the sections were stained by a special technique, to show the Entameba histolytica,

per-fected by Silva” of the Department of Pathology,

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1962;30;937

Pediatrics

C. de S. Wijesundera and C. C. de Silva