Intestinal infection is caused by parasites, mainly in tropical areas.
Human Hookworm is caused predominantly by parasitic nematodes: Necator americanus and Ancylostoma duodenale; organisms that play a minor role include Ancylostoma ceylonicum, Ancylostoma braziliense, and Ancylostoma caninum.
Hookworm infection is acquired through the exposure of the skin to larvae in soil contaminated by human feces.
The soil becomes infectious about nine days after contamination and remains for weeks, depending on the conditions.
Around the world, hookworms infect approximately 440 million people. Although most of those affected are asymptomatic, about 10% experience anemia.
Hookworms can persist for many years in the host and damage children’s physical and intellectual development and the economic development of communities.
Historically, hookworm infection has disproportionately affected the poorest of the less developed nations, primarily due to inadequate access to safe drinking water, sanitation, and health education.
Despite the frequent absence of symptoms, Hookworm contributes substantially to the incidence of anemia and malnutrition in developing nations.
It occurs most commonly in tropical and subtropical rural areas of Asia, sub-Saharan Africa, and Latin America.
The individual treatment for Hookworm consists of iron replacement and anthelmintic therapy. Even with intensive, annual, school-based programs, community eradication has proved difficult.
Despite this, hookworms’ successful control and eradication is a worthwhile goal for new methods that would offer enormous economic and social benefits for much of Africa and Asia.
Hookworm Life Cycle
The life cycle of hookworms begins with the passage of hookworm eggs in human feces and their deposition in the soil.
Each day in the intestine, a mature female worm of Anquilostoma duodenale produces about 10,000-30,000 eggs, and an adult female worm of N americanus has 5000-10,000 eggs.
After deposition in the soil and under appropriate conditions, each egg develops into an infective larva. These larvae are stopped and not nursed during development.
If they can not infect a new host, they die when their metabolic reserves are depleted, usually in about six weeks.
Larval growth is more proliferative in favorable, sandy, and humid soils, with an optimum 20-30 ° C temperature.
Under these conditions, the larvae hatch in 1 or 2 days to become Rabditiformes, also known as L1.
The larvae Rabditiformes feed on the feces and are subjected to 2 successive molts; after 5-10 days, they become infective filariform larvae or L3. These L3 undergo development arrest and can survive in wet soils for up to 2 years.
However, they dry quickly if exposed to direct sunlight, drying, or saltwater. L3 lives in the top 2.5 cm of the soil and moves vertically towards moisture and oxygen.
The larvae L3 have a length of 500-700 μm (barely visible to the naked eye) and can penetrate quickly into normal skin, most often in the hands or feet.
Transmission occurs after five or more minutes of skin contact with the soil containing viable larvae. Penetration of the skin can cause local pruritic dermatitis, also known as itching on the floor.
Itching on the floor at the penetration site is more familiar with Ancylostoma than with Necator.
The larvae migrate through the dermis, enter the bloodstream and move to the lungs in 10 days. Once in the lungs, they rupture in the alveoli, causing mild and usually asymptomatic alveolitis with eosinophilia.
Hookworms are among the causes of pulmonary infiltrates and Eosinophilia syndrome.
Having penetrated the alveoli, the larvae are taken to the glottis using the ciliary action of the respiratory tract.
The host may develop a mild reactive cough, sore throat, and fever that resolve after the worm migrates to the intestines during lung migration.
The larvae are swallowed and taken to their final destination in the glottis, the small intestine.
During this part of the migration, the larvae experience two more molts, developing a buccal capsule and reaching their adult form.
The adult buccal capsule A duodenal has teeth to facilitate attachment to the mucosa, while an adult Americanus N has cutting plates in place. A muscular esophagus creates suction in the buccal capsule.
Using their buccal capsule, the adult worms adhere to the mucosal layer of the proximal small intestine, including the lower part of the duodenum, jejunum, and proximal ileum.
In doing so, they break the arterioles and venules along the luminal surface of the intestine.
Adult worms release hyaluronidase, which degrades the mucosa and erodes blood vessels, resulting in the extravasation of blood. They also ingest a little blood.
Adult worms also elaborate factors (e.g., neutrophil inhibiting factor) that protect them from host defenses.
In 3 to 5 weeks, the adults become sexually mature, and the females begin to produce eggs that appear in the host’s feces.
Although N americanus only infects percutaneously, A duodenal can also infect through ingestion; however, in your Ancylostoma, you can also remain inactive in the tissues and then be transmitted through breast milk.
This ability to enter latency in the human host may be an adaptive response developed to increase the chances of spread.
If all the larvae matured promptly during the dry seasons of the year, the females would release the eggs in barren soil.
Eggs produced and released during the wet season are more likely to meet optimal soil conditions for further development.
Neither the Necator nor the Ancylostoma multiplies within the host. If the host does not expose itself again, the infection disappears after the worm dies. The lifespan of an adult A duodenal is about one year, and that of an adult Americanus is 3-5 years.
Types of Hookworm
Stomach worm infection results in the following three clinical entities in humans:
- Classical hookworm disease is a gastrointestinal (GI) infection characterized by chronic blood loss leading to iron deficiency, anemia, and protein malnutrition; it is caused mainly by N americanus and A duodenal and less commonly by the Zoonotic species A ceylonicum.
- Cutaneous larva migrans: This is an infection whose manifestations are limited to the skin; It is usually caused by A braziliense, whose definitive hosts include dogs and cats.
- Eosinophilic enteritis is a gastrointestinal (GI) infection characterized by abdominal pain but not loss of blood; The Hookworm of dog A caninum causes it.
In the cutaneous larva migrants, the infective larvae of Zoonotic species such as A braziliense do not elaborate sufficient concentrations of hydrolytic enzymes to penetrate the junction of the dermis and the epidermis.
Therefore, the larvae remain trapped on the surface of this layer, where they migrate laterally at a rate of 1-2 cm/day and create the pathognomonic serpiginous tunnels associated with this condition.
The larvae can survive on the skin for approximately ten days before dying. In eosinophilic enteritis, larvae of A caninum generally enter a human host when they penetrate the skin, although infection by oral ingestion is also possible.
These larvae probably remain dormant in the skeletal muscles and do not create symptoms. The larvae can reach the intestine and mature into adult worms in some individuals.
It is unknown why some people experience caninum development and then respond with a severe localized allergic reaction.
Adult worms secrete several potential allergens in the intestinal mucosa.
It has been reported that some patients experience increasingly severe recurrent abdominal pain, which may be analogous to a response to repeated insect bites.
Secondary intestinal blood loss is the primary clinical manifestation of Hookworm infection.
Hookworm historically refers to childhood syndrome of iron deficiency anemia, protein malnutrition, growth, and mental retardation with lethargy due to chronic intestinal blood loss secondary to Hookworm infection in the face of an iron-deficient diet.
Each Necator worm ingests 0.03 mL of blood daily, while each Ancylostoma worm ingests 0.15-0.2 mL of blood daily.
The amount of blood loss and the degree of anemia is positively correlated with the load of the worm. In contrast, hemoglobin, serum ferritin, and Protoporphyrin levels correlate significantly and negatively with the number of worms.
The threshold for anemia caused by the worm differs nationally, with only 40 worms that produce anemia in countries with low iron consumption.
In general, the degree of hookworm infection can be classified as follows:
- Light (<100 worms).
- Moderate (100 -500 worms).
- Heavy (500-1000 worms).
People who develop a severe initial infection seem to return to acquire an intense illness, and people who are slightly infected again reach light conditions.
Since each adult worm is the molt of a single infective larva, this suggests a continuous exposure to highly contaminated environments with little amnesic immunity in the host.
People with mild infections have minimal blood loss and may have an infection but not a disease, especially if iron intake or stores are adequate to compensate for blood loss.
In addition, as A duodenal consumes more blood per worm than N American, the severity of the anemia may differ as a factor of the hookworm species that is causing the infection.
Severe anemia affects intellectual and physical development in children and cardiovascular performance in adults.
Due to the clinically significant loss of blood and the ingestion of serum proteins by the worm, hypoproteinemia can also develop, which manifests clinically as weight loss, anasarca, and edema.
It results from enteropathy with loss of proteins, with immunoglobulins among the proteins lost due to the worm’s digestion.
This results in a delay in growth and increased susceptibility to infections such as malaria and gastrointestinal infections with enteric bacteria, viruses, and protozoa.
This protein-losing enteropathy may also contribute to a faster progression of an HIV infection.
Enteropathy can occur independently of anemia in patients with a sufficiently high iron intake.
It seems that the worms dodge or inhibit the effective human immune response.
The persistence of hookworm infection supports the theory that worms have developed adaptive molecular mechanisms to achieve a homeostatic balance with the host immune response.
Little is known about the innate immune response to metazoan in general and hookworms in particular.
Since 1989, with David Strachan’s observation of a correlation between the incidence of hay fever in children and family size, the hygiene hypothesis has excited researchers about a possible inverse relationship between helminth infections and allergic diseases and autoimmune.
The increased prevalence of atopy, asthma, and food allergy in areas free from worms has been cited as support for the hygiene hypothesis. It has even led to the investigation of worms or worm products as therapy for such diseases.
Similarly, areas of high hookworm endemicity have low reaction rates to antigens from dust mites.
Poor sanitation, limited access to clean water, and low income are well-documented risk factors for hookworm infection.
High-risk populations include international travelers, refugees, and internationally adopted and recent immigrants.
Favorable environmental conditions lead to the development of hookworm disease.
Optimal conditions for eggs include ambient temperatures of 20-30 ° C and warm, moist, and well-aerated soil protected from sunlight.
These conditions occur during the cultivation of numerous agricultural products; therefore, hookworm infections occur mainly in rural areas.
Larvae do not develop at temperatures below 13 ° C and are destroyed by temperatures below 0 ° C and above 45 ° C.
They are also killed by drying and direct sunlight.
Patient education focuses on preventive measures. In general, barefoot walking outdoors in endemic areas should be discouraged.
However, the effect of use is likely to overestimate the proper footwear in hookworm transmission.
Inadequate sanitation remains a primary risk factor for hookworm infection.