Parasitology - Nematodes

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Nematodes

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Non-segmented round worms

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Cestodes

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Segmented flat worms

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Trematodes

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Non-segmented flat worms

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Nematodes

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- All are eukaryotes
- Most nematodes are non-parasitic

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Geohelminths

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Enterobius vermicularis (Pinworm)
Trichuris trichiura (Whipworm)
Ascaris lumbricoides (Giant intestinal worm)
Toxocara canis and T. cati (Visceral larva migrans)
Hookworms (Ancylostoma duodenale, Necator americanus)
Strongyloides stercoralis

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Immune reaction to worms

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Worm infections elicit Th2 protective immune responses.

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Most important cytokines in the immune expulsion of protozoa and worms

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IFN-gamma, IL-4, IL-5

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Immune reaction to protozoa

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Protozoan infections elicit Th1 protective immune responses.

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Enterobius vermicularis
(Pinworm)

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Helminths:
Nematoda
- Affects nearly all children under the age of 12
-

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Enterobius vermicularis
(Pinworm)

Location

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Lumen of the transverse and descending colon, and in the rectum

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Enterobius vermicularis
(Pinworm)

Food

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Adult pinworms feed on E. coli and other bacteria found in the formed stool

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Enterobius vermicularis
(Pinworm)

Life Cycle

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- Embryonated eggs are swallowed and hatch into the 2nd stage larvae once they reach the small intestine. Development to the 3rd and 4th stages also occur there
- Adult worms take up residence in the large intestine
-Entire cycle is completed in 4-6 weeks after ingestion of the infected egg.
-Alternatively, eggs can hatch on the skin at the site of deposition, and the 2nd stage larvae can crawl back through the anus into the rectum and eventually the colon, where they develop into producing adults (retro-infection)
-Adult worms mate, and w/in 6 weeks, each female contains approximately 10k fertilized , non-embryonated eggs. Males die shortly after copulation
-Gravid females migrate out the anus onto the peri-anal skin at night (stimulated by the drop in body temp), and releases her eggs and dies.
- Eggs rapidly embryonate and become infective within 6 hours of being laid (the child picks up eggs by scratching his/her anus and sucking his/her thumb)

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Enterobius vermicularis
(Pinworm)

Infection

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Infection occurs with the ingestion of embryonated eggs

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Enterobius vermicularis
(Pinworm)

Adult parasites

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The male is smaller with a curved tail. Males and females do not actively migrate out of the intestine and are rarely seen in the stool

Adults can be readily identified when tehy are seen in histologic sections because of bilateral cuticular projections known as alae.

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Enterobius vermicularis
(Pinworm)

Pathology

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Pinworms have not been shown to cause disease in the GI tract. However, they are often associated with pathological changes in the appendix, even though they do not induce such changes. Therefore, it is important to recognize them in surgical specimens

Can cause hypersensitization in perianal region and can cause itching

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Enterobius vermicularis
(Pinworm)

Diagnosis

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Eggs are usually not found in feces, but are located on the perianal region of the skin. Therefore, a sticky tape swab is used to collect the eggs (right after the patient wakes up before washing) for microscopic examination

Low grade eosinophilia can be seen at times, but is not helpful for diagnosis

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Enterobius vermicularis
(Pinworm)

Treatment

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Mebendazole or albendazole

MOA: depolymerizes invertebrate tubulins, only.

Will only get rid of adult worms, not eggs and larvae, so retreatment is required in 3 weeks.

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Enterobius vermicularis
(Pinworm)

Prevention and control

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Prevention is impossible among
school-aged children, especially
those attending day care facilities
and lower grades. We “out-grow”
our pinworm infections once we
reach puberty. The change in gut physiology at that time will expel worms.

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Trichuris trichiura
(Whipworm)

Infection

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Parasite is acquired through the ingestion of embryonated eggs of Trichuris, which are found in fecally contaminated soil but are mostly found on fresh produce in regions of the world where human feces is routinely used as fertilizer.

First-stage larvae hatches in the small intestine, penetrates the columnar epithelium, and comes to lie just above the lamina propria. Four molts later, the immature adult emerges and is passively acrried to the large intestine, where it re-embeds itself in the columnar cells and induces its essential niche. Adult Trichuris live in the transverse and descending colon. The anterior, narrow, elongate esophagus is embedded within a syncytium (worm forces columnar host cells to form synctium and supply nutrients) of host cells created by the worm, probably as the result of exposure of the host to worm secretions emanating from its stichosome. The posterior abdomen protrudes into the lumen allowing eggs to escape. The worms do not ingest blood. The parasites grow and mature in the large intestine, where mating also occurs.
Patency (the first time eggs are detectable in feces) is about 90 days following the time of ingestion of embryonated eggs. Females can produce 3-5k eggs per day and are long-lived. Fertilized eggs are deposited in soil with feces and must embryonate there before becoming infectious. Environmental factors, including high humidity, sandy or loamy soild and a warm temperature, favor rapid development of the embryo. Under optimal conditions, embryonic development takes place over an 18-22 day period.

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Trichuris trichiura
(Whipworm)

Pathology

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Cycle is direct and in severe infection many adult males and female worms are embedded in the caecum and colon

Trichuris adults secrete a pore-forming protein that may play a role in diarrhea. Adult worms do not feed directly on blood or other host tissues. Mechanism of anemia still unknown. Usually no blood in stool, though heavy infection may lead to blood in stool. Also causes weight loss and cognitive deficit, possibly due to malnutrition.

Crohn's disease disappears during Trichuris infection thus, the worm may be the true target during infection.

Clincal disease may present as dysentery or as chronic colitis. May also caused prolapsed rectum.

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Trichuris trichiura
(Whipworm)

Diagnosis

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The eggs of Trichuris trichiura are readily identified in the stool.

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Trichuris trichiura
(Whipworm)

Overview

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Soil-transmitted helminths that cause serious morbidity in school aged children in developing countries.

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Trichuris trichiura
(Whipworm)

Adult worm

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Size of chalk. Has head and tail. Head is embedded in a row of cells, and tail hangs out in the lumen.

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Trichuris trichiura
(Whipworm)

Egg

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Football shaped with thick outer layer. Has entrance and exit at both ends.

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Trichuris trichiura
(Whipworm)

Treatment

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Mebendazole or Abendazole

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Trichuris trichiura
(Whipworm)

Prevention and Control

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Sanitary disposal of feces

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Ascaris lumbricoides
(Giant intestinal worm)

Infection

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Survive in soil. Acquired by the ingestion of embryonated eggs, usually through fecally contaminated food such as salad greens and other fresh, uncooked produce. Embryonated egg contain fully developed second stage larva. This is an infective egg taht took four weeks to develop in the soil

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Ascaris lumbricoides
(Giant intestinal worm)

Adult parasites

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The adult worms are large (size of pen) and live free in the lumen of the small intestine

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Ascaris lumbricoides
(Giant intestinal worm)

Pathology

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The larvae hatch from the eggs, penetrate the small intestine and migrate by way of the blood stream to the lungs causing a transitory "verminous" pneumonia-like syndrome. Leads to lung tissue damage due to migratory larvae.

Bowel obstruction may occur due to too many worms

Parasite secretes trypsin inhibitor, prevents host from digesting proteins, causes malnutrition

The adult worms may also migrate (e.g., during bouts of high fever not related to Ascaris, or irritating drugs), ending up in such abnormal sites as the liver, gall bladder, pancreas (ampula of vater or commond duct), peritoneal cavity, appendix and pharynx. Severe damage is the usual result of this migration.

Also, in heavy infections, a bolus of worms may cause intestinal blockage resulting in intestinal stasis. Death can rapidly ensue and thus this situation is considered a pediatric emergency.

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Ascaris lumbricoides
(Giant intestinal worm)

Diagnosis

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Unfertilized eggs, as well as fertilized eggs may be present in the stool. Light infections in which only females are present are characterized by unfertilized eggs only. In unfertilized eggs, note variations in size and shape, thin shell, interior completely filled with refractile granules.

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Ascaris lumbricoides
(Giant intestinal worm)

Overview

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One of the largest nematodes to infect humans. Adults live in the small intestine and tend to occur most severely in children.

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Ascaris lumbricoides
(Giant intestinal worm)

Eggs

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Ascaris eggs thrive in warm, moist soil, and are highly resistant to a variety of harsh environmental conditions. The eggs can survive in sub-arctic conditions and are ubiquitous.

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Ascaris lumbricoides
(Giant intestinal worm)

Life cycle

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Adult worms occupy the lumen of the upper small intestine, where they live on predigetsed food as well as host cellular debris. The worms maintain themselves in the lumen of the small intestine by assuming an S-shaped configuration, pressing their cuticular surfaces against the columnar epithelium of the intestine, and continually moving against the peristalsis. The worms are covered with a tough, thick cuticle composed of collagens and unusual lipids, thus enabling them to successfully resist being digested by hydrolases. In addition, the adult worms produce a battery of protease inhibitors, some of which may also interfere with host digestion.
Adult females are prolific laying 200k eggs/day. The eggs pass out of the adult fertilized but non-embryonated. They become incorporated into the fecal mass and exit the host in feces. Embryonation takes place outside the host in soil, and is completed 2-4 weeks after being deposited there. Eggs not reaching soil immediately can survive in moist environments for up to 2 months.
The embryonated egg must be swallowed for the lifecycle to continue. The first stage larva develops into the 2nd stage inside the egg, but retains the second stage cuticle around its body.
In the host, the 2nd stage larva is stimulated to hatch by a combination of the alkaline conditions in the small intestine and the solubilization of certain outer layers of the eggshell, facilitated by bile salts. These conditions induce the larva to produce a proteolytic enzyme facilitating its exit from the egg. The egg protease is activated by alkaline conditions, thus insuring that it will hatch in the right place inside the host. In the intestinal lumen, the immature parasite penetrates the intestinal wall, enters the lamina propia, penetrates a capillary and is carried by the portal circulation to the liver. In the liver, the worm feeds on parenchymal tissue and grows. It then migrates via the bloodstream to the heart, and into the pulmonary circulation. As it grows, it becomes stuck in the alveolar capillary, and it thus breaks out into the alveolar space. The larva migrates up the bronchi into the trachea and across the epiglottis to be swallowed so it can reach the small intestine.

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Ascaris lumbricoides
(Giant intestinal worm)

Immune reaction

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The most intense host reaction is during the migratory phase of infection. Ascaris antigens released during the molting process have allergenic properties that cause inflammation associated with eosinophilic infiltration of the tissues, peripheral eosinophilia and an antibody response leading to an increase in IgE levels.

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Ascaris lumbricoides
(Giant intestinal worm)

Clinical Disease

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Light infections are asymptomatic as long as the adult worms do not migrate

Heavy infections lead to protein calorie malnutrition - failure to thrive syndrome, bowel obstruction, aberrant migratory events.

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Ascaris lumbricoides
(Giant intestinal worm)

Treatment

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Mebendazole or Abendazole

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Ascaris lumbricoides
(Giant intestinal worm)

Medical Ecology

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Few people carry a lot of worms, so these people are supplying lots of eggs to infect other people. These people have a genetic propensity to carrying worms and developing appropriate immune response

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Ascaris lumbricoides
(Giant intestinal worm)

Prevention and Control

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Sanitary Disposal of feces

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Toxocara canis
Toxocara cati

Overview

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Helminths, nematoda that infect cats and dogs

Ascaris of the dog, but when human mistakenly gets infected, worm realizes that it is not in a dog, and tries to find its way out. It wanders aimlessly and causes damage, especially in the eyes and brains. Typically in small children.

In dogs it can cross placenta and enter pups, thus they can be born with it.

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Toxocara canis
Toxocara cati

Pathology

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Tissue damage (systemic) due to migratory 3rd stage larvae

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Toxocara canis
Toxocara cati

Clinical disease

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Fever, loss of visual acuity, blindness, learning disabilities

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Toxocara canis
Toxocara cati

Diagnosis

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Serological tests (ELISA-based)

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Toxocara canis
Toxocara cati

Treatment

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Mebendazole and Prednisone (to keep down inflammation until worms die)

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Toxocara canis
Toxocara cati

Prevention and Control

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Sanitary disposal of dog and cat feces, cover sand boxes at night, regular treatment of pets