Anisakis Simplex: Life Cycle, Morphology, Symptoms

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Anisakis Simplex: Life Cycle, Morphology, Symptoms
Anisakis Simplex: Life Cycle, Morphology, Symptoms

Video: Anisakis Simplex: Life Cycle, Morphology, Symptoms

Video: Anisakis Simplex: Life Cycle, Morphology, Symptoms
Video: Anisakiasis | Anisakis | Life cycle, symptoms, treatment | By phanindra gupta 2024, March
Anonim

Page content

  • Epidemiology
  • Discovery history
  • Causes of anisakidosis
  • Pathogenesis
  • Classification
  • Symptoms of anisacidosis
  • Complications
  • Diagnostics
  • Differential diagnosis
  • Complications of anisakidosis
  • Diagnosis of anisacidosis
  • Treatment of anisakidosis
  • Prevention of anisacidosis
  • You can defeat parasites!

Anisakidosis is a human parasitic infection of the gastrointestinal tract that develops after eating raw or poorly cooked seafood containing Anisakis simplex nematode larvae. Fish, squid and crustaceans most often act as carriers in which the larvae of these parasites grow, but do not mature into adults.

When large marine mammals such as seals, sea lions, dolphins and whales consume these crustaceans and fish, the larvae of the parasites will already develop into adult worms. As for humans, the larvae in it will not be able to fully complete their development and cause infection. Symptoms of this disease include severe abdominal pain, nausea, and vomiting. In some cases, the antigens present in Anisakis simplex may cause allergic reactions and hypersensitivity.

What to do in such a situation? To get started, we recommend reading this article. This article details the methods of dealing with parasites. We also recommend contacting a specialist. Read the article >>>

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Epidemiology

Anisakidosis occurs worldwide, with a higher incidence in countries where raw fish is frequently eaten, such as Japan, the Netherlands, France, Spain, Germany and the United States (California). Approximately 14,000 cases have been reported since 2000. Given the widespread consumption of raw fish in the form of sushi and sashimi, Japan is the country with the highest prevalence of gastric anisakidosis.

Discovery history

The first case of human infection with Anisakis simplex was reported in the Netherlands, by Van Thiel, who described the presence of a marine nematode in a patient suffering from acute abdominal pain. The nematoda was later revealed to be Anisakis spp. And soon, this human infection was called anisakidosis. Since their first description, most of the other cases have been reported by Japanese researchers, although other cases have also been reported in Korea, the Netherlands, Germany, Spain, Italy, the United States, and other countries.

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Causes of anisakidosis

The causative agent of the disease is the larva of the roundworm of the Anisakis simplex family. The source and final owner of anisakidosis is marine life - seals, dolphins, whales, stingrays, waterfowl. The intermediate reservoirs can be fish, molluscs, crustaceans. The route of transmission is alimentary, associated with the use of raw or poorly cooked seafood. Infestation of squid in the world ocean reaches 28%, populations of herring, flounder, greenling, cod - up to 100%. Anisakid larvae are in the digestive tract of fish and only after their death migrate into the muscle tissue.

The main risk factors are considered to be living in coastal marine areas; work in the fishing industry related to cutting and processing carcasses; professions related to the preparation of dishes from little-processed or raw fish and seafood (cooks and kitchen workers). It is believed that the risk of infection with anisacidosis increases with the use of cod, squid and mackerel for culinary purposes. Persons with sensitization to the antigens of pathogens are at risk of developing symptoms of anaphylaxis, according to various sources, their number ranges from 0.4 to 22% of residents of endemic areas.

Pathogenesis

Mature individuals of anisakida lay eggs, which fall into the water and are swallowed by intermediate reservoirs - sea fish or molluscs, where helminths live in the digestive system, less often in the muscles. When eaten by the final hosts, larvae reach sexual maturity in the intestines of the latter and, with feces, release eggs onto environmental objects.

The predominant localization of the parasite is the stomach and small intestine, the larvae are able to migrate into the gallbladder, hepatic and pancreatic ducts, mesenteric lymph nodes, and peri-uterine tissue. By penetrating deep into the mucous membrane, the pathogen causes symptoms of local inflammation with ulcerative-necrotic, hemorrhagic changes, and the formation of granulomas. Granulomas are an accumulation of leukocytes, mainly eosinophils, which causes toxic-allergic local and general symptoms, dysfunction of visceral nerve endings.

Classification

The clinical manifestations of anisacidosis are varied, but this helminthiasis can be systematized according to the degree of invasion into the body and localization of the parasite. Most often, the disease is mild, moderate and severe requires immediate treatment due to the threat or the presence of complications. An acute, subacute, chronic form of infection is also distinguished.

The classification includes:

  1. Gastric helminthiasis. It is more common in individuals with normal non-atrophic gastrointestinal mucosa, the parasite is localized mainly in the greater curvature of the organ. This form accounts for up to 95% of cases of anisacidosis.
  2. Intestinal helminthiasis. Manifestations are nonspecific, 50.7% of patients develop intestinal obstruction, 8% of patients - perforation or peritonitis, 2% - intestinal bleeding. In 7% of cases of the disease, laparotomy is performed.
  3. Toxic-allergic helminthiasis. In the foreground are the symptoms of body sensitization, which occur in 3.5% of persons with symptoms of parasitosis, clinically manifesting from skin rashes to Quincke's edema, urticaria, and anaphylactic shock.
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Symptoms of anisacidosis

The incubation period varies from 12 hours to 7-14 days. With gastric localization, the disease begins acutely with sharp pains in the epigastric region, nausea, and vomiting. Fever is uncommon, on the contrary, there are indications of a decrease in body temperature. With concomitant gastric ulcer, blood streaks are often detected in the vomit. Skin manifestations - rashes on the body like urticaria, blisters with itching. Intestinal symptoms rarely occur before the 5th day after eating contaminated foods, manifest with diffuse widespread abdominal pain.

Discomfort is usually limited to the umbilical, right iliac regions, there is bloating, flatulence, nausea, and vomiting. A short-term stool rupture is possible, in which mucus, blood are found, then persistent constipation associated with partial paralysis of the intestines. Intoxication is determined in the form of weakness, dizziness, decreased performance, fever more than 37.5 ° C. Disorders of consciousness, a sharp increase in abdominal pain, a rapid drop in blood pressure, a rapid (over 1-2 hours) increase in temperature are considered life-threatening.

Complications

The most common complications of Anisakis simplex infection are perforation, intussusception, intestinal perforation with the development of symptoms of peritonitis, bleeding. Due to excessive swelling of the mucous membrane of the digestive tract, intestinal obstruction may occur; when the parasite is localized in the biliary and pancreatic ducts, obstructive jaundice, cholecystitis, cholangitis, pancreatitis and pancreatic necrosis are possible, respectively. Potentially fatal consequences of the presence of pathogens in the body without proper treatment are angioedema, anaphylactic shock.

Diagnostics

Confirmation of the diagnosis is carried out by an infectious disease specialist, a parasitologist, sometimes doctors of other specialties are involved. It is important to carefully collect an epidemiological history with a clarification of the nature of food intake, stay in endemic areas. The main diagnostic laboratory and instrumental signs of a parasitic infection are:

  • Physical data. With an objective examination in the case of an asymptomatic course, there are no pathological changes. On the skin there may be urticaria rashes, urticaria, and scratching marks. Palpation of the abdomen reveals soreness in the epigastrium, characteristic of gastric localization, rumbling, diffuse sensitivity with signs of an intestinal form. Symptoms of an acute abdomen are sometimes determined. A visual assessment of vomit and feces is mandatory.
  • Laboratory research. In a general clinical blood test, leukocytosis and eosinophilia are found in 30% of patients (more often with symptoms of stomach damage). There is an increase in the level of total Ig E, a transient increase in the activity of ALT and AST. With inflammation of the gallbladder, the level of alkaline phosphatase, total and direct bilirubin increases, with pancreatitis, there are high numbers of amylase, the level of urine diastase. In the coprogram - creatorrhea, steatorrhea, leukocytes, erythrocytes.
  • Identification of infectious agents. Microscopy of feces, vomiting to confirm anisacidosis is not very informative. The diagnostic level of sIgE in plasma reaches only 4-6 weeks of infection. Basophil transformation test with A. simplex extract is highly specific; skin prick tests are used. With histological materials, a PCR study is carried out, the possibility of using immune blotting is being studied.
  • Instrumental methods. Chest x-ray is essential for differential diagnosis of allergic symptoms; a study with barium reveals filamentous filling defects, edema of the mucous membrane of the stomach, and narrowing of the intestinal lumen. CT: segmental edema of the intestinal wall with proximal dilatation without complete intraluminal occlusion, ascites; according to EFGDS - point erosion, manifestations, infiltration, edema of the mucous membrane, larva anisakid.

Differential diagnosis

The differential diagnosis is carried out with other helminthic invasions, especially nematodes, but since their symptoms are similar, the main role is assigned to laboratory and instrumental research. Salmonellosis always proceeds with fever, characterized by copious swamp stools.

Foodborne toxicoinfection has a violent onset with repeated vomiting, loose stools, temperature reaction of the body, and rapid dehydration. With cholera, stool breakdown occurs first, then symptoms of stomach dysfunction, bowel movements resemble rice water.

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Complications of anisakidosis

Intestinal obstruction, perforation of the intestinal wall with the development of peritonitis, and in the absence of timely assistance and death.

Diagnosis of anisacidosis

The diagnosis is made based on a set of data:

  • Epidemiological history - the presence of the fact of eating sea fish (herring, cod and others) and seafood (squid, crustaceans) insufficiently thermally processed or in a raw and half-baked form, staying in a geographically endemic territory for anisacidosis and consuming seafood there.
  • Clinical data - symptoms characteristic of a gastric or intestinal form of the disease in combination with an allergic reaction in the past or present. In view of the nonspecificity of the symptoms of the disease, differential diagnosis will need to be carried out with a variety of diseases of the digestive system: gastritis, gastric ulcer and duodenal ulcer, gastroenteritis, Crohn's disease, oncological processes, pancreatitis, cholecystitis, appendicitis, diverticulitis and others.

Laboratory research:

  • The detection of anisakid larvae in the vomit and feces of patients is a rather rare method of detection, most often neither larvae nor helminth eggs are detected by microscopy;
  • Instrumental diagnostics: FGDS (fibrogastroduodenoscopy) reveals edema and erosion of the mucous membrane in the places where the larvae are introduced, and sometimes remove the larvae themselves; contrast fluoroscopy.
  • Surgical intervention for resection of the stomach or part of the intestine allows you to identify the embedded anisakids;
  • A general blood test can reveal leukocytosis, eosinophilia.
  • Serological methods have no practical application.

Treatment of anisakidosis

Therapeutic measures for anisacidosis are reduced to:

  • Surgical intervention using minimally invasive methods or conventional techniques, which is possible with suspicion of appendicitis, intestinal obstruction, bowel perforation, that is, with complications that have arisen. During surgery, larvae are often removed using an endoscope, but care should be taken to completely remove them, since the remaining head end can lead to the appearance of new granulomas.
  • Drug therapy is carried out with antiparasitic drugs (mebendazole, albendazole) in short courses, in which a positive therapeutic effect is noted.

The prognosis of the disease is difficult in the event of complications and the absence of timely resuscitation assistance.

Prevention of anisacidosis

  • Compliance with food culture (eating only proven heat-treated fish and seafood, avoiding the consumption of raw or lightly salted fish).
  • Compliance with the rules for handling suspicious marine fish and seafood. The rules include gutting the fish quickly after catch to prevent the early introduction of anisakid larvae into the fish muscles, freezing fish at a temperature of –20º for at least 120 hours (5 days), and at -18º for 14 days; heat treatment of fish (at a temperature of + 80º and more, 20 minutes is enough for the death of larvae); sufficient salting of fish - salt concentration of 14% within 10-12 days.
  • Compliance with the rules for cutting fish (separate knife, board and dishes).
  • Helminthological examination of sea fish and seafood.

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