Anisakiasis

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Anisakiasis

 

Historical aspect

 

Anisakiasis was first recognized in the Netherlands (Van Thiel et al., 1960).

The patient was diagnosed as acute localized entritis of terminal ileum.

Surgical operation revealed that a small nematode was penetrating the mucus

membrane. The larva was identifed as 3rd-stage larva of Anisakis simplex.

Epidemiology

 

Nationwide surveys of anisakiasis in Japan have been compiled are mainly

evaluations of cases with eosinophilic granuloma from pathological labaratories

at various universities. Since 1955 Ishikura has kept a record of acute

localized enteritis, and in 1965 determined the need for a separate pathological

entity for the majority of such cases. They were evaluated as intestinal

anisakiasis, and show that this disorder is common in the north, with the

chronic granuloma and phlegmonous acute intestinal type especially common, since

many of the marine organisms that act as paratenic hosts are caught in large

volumes in that area. Marine fishes, especially mackel and squids are most

important paratenic hosts in Japan. Anisakis larvae are always found on the

surface of internal organs and muscle. The location of larvae were as follows:

 

 

Distribution of Anisakis simplex larvae in muscle of common mackerel caaught

in coastal waters off Shizuoka Prefecture, Chiba Prefecture (B), sardines ©

and squids. Diagnosis of the acute form of intestinal anisakiasis has been

increasing rapidly, beginning with the use of the endoscope to establish the

presence of larvae in cases of peritonitis displaying acute symptoms. With the

increasing use of this method in Hokkaido and across the rest of the nation, the

incidence of intestinal anisakiasis has changed. There are still problems in

separating cases with intestinal anisakiasis; the impossibility of determining

lar-vae in the intestinal cavity when the wall is perforated; the increase in

cases recovering without surgery; and the decrease in parasitologically

established cases, Ieaving the ratio of gastric to intestinal cases at less than

1 to 22 (Table 1), where only 567 of 12,586 are cases intestinal anisakiasis.

Intestinal anisakiasis is different from cancer,

where a histopathological diagnosis is possible even when the pathogenic agent

has not been established. Acute intestinal anisakiasis may be

histopathologically determined without a trace of the larvae, making an

epidemiological diagnosis difficult to establish. Diagnosis of probable

intestinal anisakiasis is based on rapid advances in clinical experience, X-ray,

ultrasonography, and immuno-serodiagnosis. Discussion of the suitability of such

a diagnosis is still going on, and if agreement among re-searchers can be

achieved, the number of cases of intestinal anisakiasis will increase

dramatically with the ratio of intestinal to gastric anisakiasis consequently

changing. The main problems with epidemiological statistics for anisakiasis

relate to the sources of infection. In the last ten years the incidence in

Hokkaido and Kyushu has been reversed, with changes in the cycle of parasites in

the host marine organisms. These changes have been most remarkable in Alaska

pollack, mackerel, and sardines.

Pathological Aspect

1. The Fate of Orally Infected Larvae (Animal Experiments) It has been noted

that some orally administered larvae are expelled through the anus, verified by

Ruitenberg, who considered it important that such larvae were dead and digested

at evacuation, with no reports of living evacuated larvae. Ruitenberg did

extensive experiments with oral infection, and related them to larval

penetration of the walls of the abdominal and intestinal cavities, and also

noted experiments on histopathological determinations of infecting larvae

migrating into the digestive tract wall. Myers (1963) reported orally

administered larvae in the abdomen, small intestine, large intestine, pancreas,

and liver, while Young (1969) found coiled larvae that had penetraed into the

mesentry.

2. Intraperitoneal infection with Anisakis larvae.

There is considerable difficulty in comparing experimental results due to

the complexity of determining fish species, the freshness of the raw fish, and

differences in experimental animals and experimental procedures. However, the

number of larvae penetrating the intestinal tract wall and entering the

abdominal cavity is similar to the number that stop in the wall of the

intestinal tract and die there. Larvae are found in practically all organ

tissue, the caul, mesentery, abdominal wall, Liver, pancreas, spleen, uterus,

urinary bladder, testicles, ovaries, sperm duct, thyroid gland, muscle, fat, and

other tissue. Yoshimura (1979) reported on 13 cases from Honshu with what he

termed extragastro intestinal anisakiasis in which larvae were found in the

digestive wall, and the author (1989) has recognized 45 such cases as well.

These larvae had penetrated the gastric and intestinal walls and reached the

abdominal cavity. Where the digestive tract wall is perforated,

experiments have shown that larvae disappear into the gastric wall within 10

minutes, and from endoscopic examinations perforation has been reported within

seconds. Penetration takes place within a very short time with the physical

stimulation resulting in subjective symptoms which soon subside and may not be

paid attention to explaining the frequently found asymptomatic cases where

larvae are identified of autopsy.

3. The invasive course of larvae into the abdominal cavity Larvae

administered orally pass through the wall of the digestive tract and enter the

abdominal cavity, where they reach the serous membranes of organs and often

produce numerous eosinophilic cell granuloma. Compared with other fish and

squid, a large proportion of larvae from the blood of Trachurus japonica

penetrate into the abdominal cavity, while Somber japonica larvae were found to

enter the abdominal cavity after 10 hours, and in order of incidence

concentrated in the omentum, momentary, and various organs. No penetration of

the small intestine was found with larvae from Theragra chalcogramma, only

perforation of the gastric wall; Larvae were found in omentum, muscle, and fat

tissue. Reports of Todarodes pacificus state that the parasitic larvae behave in

much the same manner, entering the abdominal cavity via the gastric wall, but

rather than concentrating in the omentum and mesentery, many were found

in muscle and fat tissue or scattered in the serous membrane of organs. There

was no clear indication that the seriousness of the infection in different

experimental animals was dependent upon the host species, however, this may be

due to differences in the time from infection until examination. The

experimental results indicate that the number of larvae penetrating the

abdominal cavity are between 1/3 and 1/4 of the total. Extra-gastrointestinal

anisakiasis cases are those where the ailment was diagnosed outside the gastric

and intestinal canal, although recently there have been more discoveries of

larvae penetrating into the abdominal cavity, with larvae being found just after

perforation of the small intestine membrane, or in the abdominal cavity after

penetration of the small intestine. Yoshimura et al.(1979) reported one case

with stomach penetration and eosinophilic cell granuloma in the caul, and

another with perforation in the end section of the illus, and there

are more reports of such cases. Many physicians have verified the perforation

of the mucous membrane from bleeding observed endoscopically while, Mizugaki et

al. (1970) has shown histological experimental results with a strong cell

reaction at second infection and perforation outside the stomach and intestine

with extensive bleeding and internal bleeding in the mucous membrane. This is

considered to be a result of localized reactions to secretion and excrement (ES

antigen).

4. The first infection, re-infection and double infection of larvae.

Experimental studies on rabbits have been conducted, where they were subjected

to a subcutaneous first infection with Anisakis larvae, which stayed alive for

seven days and caused a foreign body reaction in the tissue. At re-inflection

dead larvae appeared from the second day, the surrounding edema and flare was

clearly histologically acute exudative inflammation with infiltration of immune

cell neutrocytes and eosinophilic cells. The exudative inflammation quickly

subsided and there was abscess and granuloma formation around the dead larvae.

When the re-infection used soluble fraction fluid instead of live larvae,

supernatant fluid generally produced an instantaneous allergic reaction, and

caused a delayed allergic reaction with sedimented antigen. This brought antigen

directly to the stomach and intestinal walls, and even when live larvae were

buried there, the stomach reaction was weaker than in

the intestine. The proportion of larvae entering the stomach and intestinal

walls at the first and later infections were determined in separate experiments,

with more larvae found to penetrate the walls of immunized animals. This

experiment did not study larvae that had penetrated into the abdominal cavity an

aspect which requires further investigation. In the Netherlands, attention has

been drawn to the " double hit " theory, which is that acute exudative

inflammation caused by intestinal anisakiasis results from penetration by a

single larvae offering immunization for only about 4 months. This local

hypersensitivity was quickly questioned by Ruitenberg who considered it to be

acute allergic reaction at re-infection. Together with anisakiasis, so-called

skip lesions occur in great numbers. To study this phenomena we orally

administered larvae to rabbits which then showed abscess and granuloma morbidity

(symptoms of the first infection) in their digestive tracts. After 3

weeks Anisakis larval antigens were injected in the ear vein of the rabbits,

causing acute exudation in the vicinity of the reinfection, showing that the

inflammation in the area of the first infection has became infected again. With

skip lesions there is a simultaneous elective outbreak of the ailment similar to

the localized morbidity, however, when the site of the first infection and the

re-infection are different, it is differentiated from a skip lesion. The

experiments also showed that tissue morbidity at re-infection was most severe

where the greatest penetration had taken place, indicating that the strongest

changes occurred in the earliest affected parts. Changes in the vicinity of the

remains of intrusions into the abdominal cavity were weak (light bleeding and

edema), and although clinical observation of repeated Anisakis infections have

been reported, more details will be established when a thorough survey of the

abdominal cavity is made at surgery.

5. Complications with bacillus infection. It is estimated that one-third

of the Anisakis larvae eaten with marine organisms are evacuated through the

anus, onethird die in the walls of the stomach and intestine, and one-third die

forming granuloma or after penetrating the abdominal cavity. To enter the

abdominal cavity, the wall of the digestive tract must be penetrated, and this

is more common in the intestinal than the gastric form studies in which

laparotomy was performed because of acute stomach ailments report abdominal

fluid present in about 70010 of cases. In early stages the abdominal fluid is

lemon yellow and clear, becoming opaque then yellow and turbid as the illness

worsens. This leads experienced physicians to suspect secondary infection, but

microscopic observations do not show bacteria in the sediment of the abdominal

fluid. Ishikura (1970) described 2 cases out of 132 subjects with bacteria in

the histopathological samples, a further 5 cases with

accumulation of neutrocyies or necrotic areas between the mucous and serous

membranes which were also considered to show bacterial infection. Agglomeration

of bacteria in the tissue of one of 6 cases was reported by Saito (1966), though

these cases did not show ulcerated necrosis of the mucous membrane and the

bacterial infection must have taken place from the intestine via larval

perforations. Naka (1969) reported on bacterial cultivation revealing mucous in

the abdominal fluid and intestinal serous membrane and found 7 cases out of 65

with coli baccillus and staphylococcus, and of 23 cases with fibrous fur 4 had

bacteria in the mesentary. We injected 30 Anisakis larvae into the abdominal

cavity of rabbits, and injected antigen into the ear vein three months later.

The immunized rabbits had antigen injected in the lymphatic cavity under the

serous membrane of the ileum by Fisher's method and simultaneously nonpathogenic

coli baccilla were injected at the same site

before closing off the abdomen. These rabbits were later subjected to repeated

laparotomy and tissue from the intestinal wall was observed under the

microscope. The observations were conducted for 40 days and revealed ulceration

of the mucous membrane, necrosis, and necrotic abcesses with numerous

neutrocytes under the mucous membrane; the appearance of giant cells was

accelerated and necrotic perforations were apparent. This coincides with

observations of acute anisakiasis in humans, but more comprehensive observations

are necessary to determine whether the pathogenic changes appear as Crohn's

disease when it becomes chronic.

6. The immune mechanisms in Anisakis larvae infections in humans. Based

on immune response experiments with animals, infections of the abdominal cavity

were found to create immunity and led to speculation that the immunity created

by larvae that had penetrated into the abdominal cavity was stronger than that

created by larvae that had entered the digestive tract wall and died there, and

that this may be the situation wih human cases of anisakiasis. This hypothesis

is supported by the increasing number of laparotomies performed as a result ,of

acute symptoms of the primary infection in which intestinal anisakiasis has been

determined. The increase appears to be due to more thorough examinations of the

stomach by surgeons performing laparotomies on intestinal anisakiasis cases.

Primary infections of the digestive tract walls are rarely diagnosed since they

are often assymptomatic but may be discovered during laparotomies performed for

other ailments or at post

mortems. Re-infection with anisakiasis larvae cause violent immune reactions

leading to acute symptoms (mainly ileus) that result in laparotomy which then

leads to the discovery of signs of the primary infection. As described in

another section (with the pathology of the mild form of intestinal anisakiasis)

, this activation of the first infection may mistakenly be interpreted as the

appearance of a wave-like phenomenon or a relapse change.

Endoscopical findings

Care should be taken not to mistake the worm penetrating the gastric wall for

the stringlike mucus. As seen on closer observation, as Anisaks simplex larva

shows a thin, strinlike appearence and its color is milk-white, while a

Pseudoterranova decipience larva is broder and yellow or yellowish-brown in

color. The endoscopic features of acute gastric anisakiasis were as follows:

(a) Existence of Anisakis larvae; (b) edematous hypertrophic gastric folds; ©

increase of gastric secretion and gastric peristalsis; (d) the findings of

mucosal lesions through which Anisakis larvae penetrated were as follows: 120

cases (46%) of edema, 64 cases (25%) of redness, 48 cases (19%) of coagulation,

16 cases (6%) of hemorrhage, and ten (4%) cases of ulceration; (e) erosions in

the other gastric mucosa were seen at a smaller incidence than erosive gastrtis.

Edematous hypertrophic gastric folds were observed along the long axis of the

stomach, primarily occurring on the side of

greater curvature. The folds numbered one in 69 cases (27%), two in 116 cases

(45%), and three in 52 cases (20%). Thus, in the largest number of cases there

were two folds. With regard to the site of parasitic penetration in connection

with edematous hypertrophic gastric folds, there were as many as 196 cases (76%)

with penetration on the oral side, 32 cases (12%) in the middle portion, 25

cases (10%) on the anal side , and five cases (2%) having local swelling.

 

http://www.tmd.ac.jp/med/mzoo/vlm/anisakiasis.html

 

 

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