Ascariasis

Ascariasis
Classification and external resources
Ascaris lumbricoides
ICD-10	B77
ICD-9	127.0
OMIM	604291
DiseasesDB	934
MedlinePlus	000628
eMedicine	article/212510
MeSH	D001196

Ascariasis is a disease of humans caused by the parasitic roundworm Ascaris lumbricoides. Perhaps as many as one quarter of the world's population are infected, with a prevalence of 45% in Latin America and 95% in parts of Africa. Ascariasis is particularly prevalent in tropical and sub-tropical regions where hygiene is poor. Other species of the genus Ascaris can cause disease in domestic animals, such as Ascaris suum which infects pigs. Some genes have been identified in humans that may increase susceptibility to infection.

Infection occurs by swallowing food contaminated with Ascaris eggs from feces. The larvae hatch in the intestine, burrow through the gut wall, and migrate to the lungs through the blood system. There they break into the alveoli and pass up the trachea and oesophagus where they are coughed up and swallowed. The larvae pass through the stomach for a second time into the intestine where they mature into adult worms. They maintain their position by swimming against the intestinal flow caused by peristalsis. Adult worms have a life-span of 1-2 years which means that individuals may be infected all their lives as worms die and new worms are acquired.

Infections are usually asymptomatic, especially if the number of worms is small, because the degree of disease is related to the number of worms in the intestine as well as to the size and health of the human host. It is typical to find that most individuals harbour a small number of worms, while a small proportion are heavily infected, something that is characteristic of many worm infections. The distribution of A.lumbricoides among human hosts is best described empirically by the negative binomial distribution.

Signs and symptoms

As larval stages travel through the body, they may cause visceral damage, peritonitis and inflammation, enlargement of the liver or spleen, and a verminous pneumonitis. The worms in the intestine may cause malabsorption and anorexia which contribute to malnutrition. The malabsorption may be due to a loss of brush border enzymes, erosion and flattening of the villi, and inflammation of the lamina propria. The worms can occasionally cause intestinal blockage when large numbers get tangled into a bolus or they may migrate from the small intestine, which may require surgery. More than 796 Ascaris lumbricoides worms weighing up to 550 g [19 ounces] were recovered at autopsy from a 2-year-old South African girl. The worms had caused torsion and gangrene of the ileum, which was interpreted as the cause of death.

In many parts of the world ascariasis is a pandemic. Many patients are diagnosed accidentally. Sometimes the worm blocks the Ampulla of Vater or goes into the Main Pancreatic Duct resulting in acute pancreatitis with raised serum levels of Amylase and Lipase. Occassionally they can travel through the Billiary tree and even into the gallbladder causing Acute Cholangitis or Acute Cholecystitis. Ascaris takes most of its nutrients from the partially digested host food in the intestine. There is some evidence that it can secrete anti-enzymes, presumably to protect itself from digestion by the hosts' enzymes.

In Canada in 1970, a postgraduate student tainted his roommates' food with Ascaris lumbricoides. Four of the victims became seriously ill; two of these suffered acute respiratory failure.

Ascariasis may result in allergies to shrimp and dustmites due to the shared antigen, tropomyosin, though this has not been confirmed in the laboratory. Ascaris have an aversion to some general anesthetics and may exit the body, sometimes through the mouth.

Mechanism

Life cycle

Adult worms (1) live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces (2). Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks (3), depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed (4), the larvae hatch (5), invade the intestinal mucosa, and are carried via the portal, then systemic circulation and/or lymphatics to the lungs . The larvae mature further in the lungs (6) (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon reaching the small intestine, they develop into adult worms (8). Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.

First appearance of eggs in stools is 60–70 days. In larval ascariasis, symptoms occur 4–16 days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting, fever, and observation of live worms in stools. Some patients may have pulmonary symptoms or neurological disorders during migration of the larvae. However there are generally few or no symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause pneumonitis and eosinophilia.

Source

The source of transmission is from soil and vegetation on which fecal matter containing eggs has been deposited. Ingestion of infective eggs from soil contaminated with human feces or transmission and contaminated vegetables and water is the primary route of infection. Intimate contact with pets which have been in contact with contaminated soil may result in infection, while pets which are infested themselves by a different type of roundworm can cause infection with that type of worm (Toxocara canis, etc.) as occasionally occurs with groomers.

Transmission also comes through municipal recycling of wastewater into crop fields. This is quite common in emerging industrial economies, and poses serious risks for not only local crop sales but also exports of contaminated vegetables. A 1986 outbreak of ascariasis in Italy was traced to irresponsible wastewater recycling used to grow Balkan vegetable exports.

Transmission from human to human by direct contact is impossible.

Diagnosis

The diagnosis is usually incidental when the host passes a worm in the stool or vomit. The eggs can be seen in smear of fresh feces examined on a glass slide under a microscope and there are various techniques to concentrate them first or increase their visibility, such as the ether sedimentation method or the Kato technique. The eggs have a characteristic shape. During pulmonary disease larvae may be found in fluids aspirated from the lungs. White blood cells counts may demonstrate peripheral eosinophilia, but this is common in many parasitic infections and is not specific to ascariasis. On X-ray, 15–35 cm long filling defects, sometimes with whirled appearance (bolus of worms).

Prevention

Prevention includes: use of toilet facilities; safe excreta disposal; protection of food from dirt and soil; thorough washing of produce; and hand washing.

Food dropped on the floor should never be eaten without washing or cooking, particularly in endemic areas. Fruits and vegetables should always be washed thoroughly before consumption.

Treatment

Main article: Ascaricide

Pharmaceutical drugs that are used to kill roundworms are called ascaricides and include:

• Mebendazole (Vermox) (C₁₆H₁₃N₃O₂). Causes slow immobilization and death of the worms by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell. Oral dosage is 100 mg 12 hourly for 3 days.
• Piperazine (C₄H₁₀N₂.C₆H₁₀O₄). A flaccid paralyzing agent that causes a blocking response of ascaris muscle to acetylcholine. The narcotizing effect immobilizes the worm, which prevents migration when treatment is accomplished with weak drugs such as thiabendazole. If used by itself it causes the worm to be passed out in the feces. Dosage is 75 mg/kg (max 3.5 g) as a single oral dose.
• Pyrantel pamoate (Antiminth, Pin-Rid, Pin-X) (C₁₁H₁₄N₂S.C₂₃H₁₆O₆) Depolarizes ganglionic block of nicotinic neuromuscular transmission, resulting in spastic paralysis of the worm. Spastic (tetanic) paralyzing agents, in particular pyrantel pamoate, may induce complete intestinal obstruction in a heavy worm load. Dosage is 11 mg/kg not to exceed 1 g as a single dose.
• Albendazole (C₁₂H₁₅N₃O₂S) A broad-spectrum antihelminthic agent that decreases ATP production in the worm, causing energy depletion, immobilization, and finally death. Dosage is 400 mg given as single oral dose (contraindicated during pregnancy and children under 2 years).
• Thiabendazole. This may cause migration of the worm into the esophagus, so it is usually combined with piperazine.
• Hexylresorcinol effective in single dose, mentioned in : Holt, Jr Emmett L, McIntosh Rustin: Holt's Diseases of Infancy and Childhood: A Textbook for the Use of Students and Practitioners. Appleton and Co, New York,11th edition
• Santonin, more toxic than hexylresorcinol, mentioned in : Holt, Jr Emmett L, McIntosh Rustin: Holt's Diseases of Infancy and Childhood: A Textbook for the Use of Students and Practitioners. Appleton and Co, New York, 11th edition
• Oil of chenopodium, more toxic than hexylresorcinol, mentioned in : Holt, Jr Emmett L, McIntosh Rustin: Holt's Diseases of Infancy and Childhood: A Textbook for the Use of Students and Practitioners. Appleton and Co, New York, 11th edition

Also, corticosteroids can treat some of the symptoms, such as inflammation. In some cases with severe infestation, the sudden death of the worms may cause bowel obstruction, requiring surgical intervention.

Native Americans have traditionally used epazote (Chenopodium ambrisioides) for treatment, which was not as powerful as pharmaceutical compounds, but spontaneous passage of Ascarids provided some proof of efficacy.^{[citation needed]}

Epidemiology

Disability-adjusted life year for ascariasis per 100,000 inhabitants in 2002.

  no data

  less than 10

  10-20

  20-30

  30-40

  40-50

  50-60

  60-80

  80-100

  100-120

  120-140

  140-150

  more than 150

Roughly 1.5 billion individuals are infected with this worm, primarily in Africa and Asia. Ascariasis is endemic in the United States including Gulf Coast; in Nigeria and in Southeast Asia. One study indicated that the prevalence of ascariasis in the United States at about 4 million (2%) [8]. In a survey of a rural Nova Scotia (Canada) community, 28.1% of 431 individuals tested were positive for Ascaris, all of them being under age 20, while all 276 tested in metropolitan Halifax were negative.

Deposition of ova (eggs) in sewage hints at the degree of ascariasis incidence. A 1978 study showed about 75% of all sewage sludge samples sampled in United States urban catchments contained Ascaris ova, with rates as high as 5 to 100 eggs per litre^{[citation needed]}. In Frankfort, Indiana, 87.5% of the sludge samples were positive with Ascaris, Toxocara, Trichuris, and hookworm^{[citation needed]}. In Macon, Georgia, one of the 13 soil samples tested positive for Ascaris^{[citation needed]}. Municipal wastewater in Riyadh, Saudi Arabia detected over 100 eggs per litre of wastewater and in Czechoslovakia was as high as 240–1050 eggs per litre.

Ascariasis can often be measured by examining food for ova. In one field study in Marrakech, Morocco, where raw sewage is used to fertilize crop fields, Ascaris eggs were detected at the rate of 0.18 eggs/kg in potatoes, 0.27 eggs/kg in turnip, 4.63 eggs/kg in mint, 0.7 eggs/kg in carrots, and 1.64 eggs/kg in radish. A similar study in the same area showed that 73% of children working on these farms were infected with helminths, particularly Ascaris, probably as a result of exposure to the raw sewage.

Genus and Species	Ascaris lumbricoides
Common Name	Large Intestinal Roundworm
Etiologic Agent of:	Ascariasis
Infective stage	Embryonated Egg
Definitive Host	Human
Point of Entry	Mouth
Mode of Transmission	Ingestion of Embryonated egg through contaminated food or water
Habitat	Small Intestine
Pathogenic Stage	Adult, Larva
Mode of Attachment	Retention in the mucosal folds using pressure
Mode of Nutrition	Feeding of Chyme
Pathogenesis	Larva – pneumonitis, Loeffler’s Syndrome; Adult – Obstruction, Liver abscess, Appendicitis. With Blood-Lung Phase along with Hookworms and Strongyloides stercoralis.
Laboratory diagnosis	Concentration methods and Direct Fecal Smear: Kato-Katz
Treatment	Albendazole, Mebendazole, or Pyrantel pamoate
Diagnostic Feature – Adult	Female – prominent genital girdle
Diagnostic Feature – Egg	Coarse mammilated albuminous coating

Research

There are two animal models for studying Ascaris infection:

• Howes HL (June 1971). "Anthelmintic studies with pyrantel. II. Prophylactic activity in a mouse-ascaris suum test model". J. Parasitol. (The Journal of Parasitology, Vol. 57, No. 3) 57 (3): 487–93. doi:10.2307/3277899. JSTOR 3277899. PMID 5090955. 

• Lichtensteiger CA, DiPietro JA, Paul AJ, Neumann EJ, Thompson L (April 1999). "Persistent activity of doramectin and ivermectin against Ascaris suum in experimentally infected pigs". Vet. Parasitol. 82 (3): 235–41. doi:10.1016/S0304-4017(99)00018-7. PMID 10348103. 

See also

• Tapeworm infection
• Toxocariasis
• 1970 ascariasis poisoning incident

External links

• Video of removal of Ascari lumbricoides with an endoscope
• Images (warning, very graphic): [2], [3]
• CDC DPDx Parasitology Diagnostic Web Site

• Ascariasis: Radiology and color pathology pictures from MedPix
• Discussion of Ascaris on the "This week in Parasitism" Podcast