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 Pathology of Hookworm Infection (Ancylostomiasis)

 

Dr Sampurna Roy MD           April 2016

 

 

Hookworm infection in humans is caused by an infection with the helminth nematode parasites Necator americanus and Ancylostoma duodenale.

Mode of infection: Hookworms (Necator and Ancylostoma) are generally contracted by walking barefoot on soil contaminated by feces from infected animals or persons, or by swimming or wading in contaminated water.

Hookworm infection is among the most important tropical diseases in humans.

The greatest number of hookworm cases occur in Asia, followed by sub-Saharan Africa.

Necator americanus is the most common hookworm worldwide, whereas Ancylostoma duodenale is more geographically restricted.

In contrast to these major anthropophilic species, three species of zoonotic hookworm are minor causes of disease in humans.

Ancylostoma ceylanicum infects dogs and cats and can also infect humans but is not considered an important pathogen.

The dog hookworm Ancylostoma caninum causes human eosinophilic enteritis in northeastern Australia ,and Ancylostoma braziliense causes cutaneous larva migrans.

Some of the highest rates of hookworm transmission occur in the world's coastal regions, where infective third-stage larvae can migrate freely in sandy soils and where temperatures and moisture are optimal for viability of larvae. 

In these areas, repeated exposure to third-stage larvae of Necator americanus or Ancylostoma duodenale results in a local pruritic, erythematous, papular rash known as "ground itch."

[ Note:  The three main soil-transmitted helminth infections, Ascariasis , Trichuriasis, and hookworm, are common clinical disorders in man.

The gastrointestinal tract of a child living in poverty in a less developed country is likely to be parasitised with at least one, and in many cases all three soil-transmitted helminths, with resultant impairments in physical, intellectual, and cognitive development.]

Life Cycle: 

Humans acquire hookworm when third-stage infective  larvae in soil either penetrate the skin (both Necator americanus and Ancylostoma duodenale) or when they are ingested (Ancylostoma duodenale only).

The larvae are each approximately 600 m long.

After entering the host, the larvae receive a host-derived signal that causes them to resume development.

The larvae then migrate through the vasculature and are swept by the afferent circulation to the right side of the heart and then to the pulmonary vasculature.

From the lung capillaries, the larvae rupture and enter the parenchyma, where they ascend the alveoli, bronchioles, bronchi, and trachea.

After being coughed up and swallowed, the larvae enter the gastrointestinal tract, where they molt twice and develop to the adult stage.

Approximately six to eight weeks pass from the time the larvae first infect humans until they reach sexual maturity and mate.

Each female hookworm produces thousands of eggs daily.

Intestinal blood loss in the host begins just before egg production and release and continues for the life of the hookworm.

Hookworm eggs exit the body in faeces.

When deposited in soil, with adequate warmth, shade, and moisture, the eggs hatch within 24 to 48 hours and develop into first-stage larvae.

These larvae molt twice as they develop to the third stage.

The larvae are nonfeeding organisms that can live for several weeks in the soil, until they exhaust their lipid metabolic reserves.

Transmission of hookworm is most prevalent in areas  where there is high moisture and appropriate soil conditions.

Sandy soils containing silt are most favored and account for the high prevalence of hookworm infection in coastal area.

 

The term "hookworm disease" refers primarily to the iron-deficiency anemia that results from moderate or heavy infection.

In the passage through lungs, petecheal hemorrhages and areas of transient bronchopneumonia are produced.

Blood loss occurs when the worms use the well developed buccal capsule to attach themselves to the intestinal  mucosa and submucosa (specially the duodenum and first portion of the jejunum) and contract the muscular esophagus to  create negative pressure, which sucks a plug of tissue into their buccal capsules.

There is damage of small areas of the mucosa producing punctate hemorrhages and at the same time they draw blood from the mucosa.

Capillaries and arterioles are ruptured not only mechanically but also chemically, through the action of hydrolytic enzymes.

To ensure blood flow, the adult hookworms release anticlotting agents.

Some red cells undergo lysis, thereby releasing hemoglobin, which is digested by a cascade of hemoglobinases that line the gut of the parasite.

The major clinical manifestations of hookworm disease are the consequences of chronic intestinal blood loss.

Iron-deficiency anemia occurs and hypoalbuminemia develops when blood loss exceeds the intake and reserves of host iron and protein.

Morphological changes in the small intestine in hookworm disease include villous atrophy and crypt hyperplasia. 

These changes and the malabsorptive state that is commonly present are probably unrelated to the infection.

When severe anaemia occurs in young children, it retards growth as well as well as sexual and mental development.

The presence of characteristic ova in stools, establishes the diagnosis.

Serologic tests are available but play little role in clinical diagnosis.

The term "hookworm disease" refers primarily to the iron-deficiency anemia that results from moderate or heavy infection.

In the passage through lungs, petecheal hemorrhages and areas of transient bronchopneumonia are produced.

Blood loss occurs when the worms use the well developed buccal capsule to attach themselves to the intestinal  mucosa and submucosa (specially the duodenum and first portion of the jejunum) and contract the muscular esophagus to  create negative pressure, which sucks a plug of tissue into their buccal capsules.

There is damage of small areas of the mucosa producing punctate hemorrhages and at the same time they draw blood from the mucosa.

Capillaries and arterioles are ruptured not only mechanically but also chemically, through the action of hydrolytic enzymes.

To ensure blood flow, the adult hookworms release anticlotting agents.

Some red cells undergo lysis, thereby releasing hemoglobin, which is digested by a cascade of hemoglobinases that line the gut of the parasite.

The major clinical manifestations of hookworm disease are the consequences of chronic intestinal blood loss.

Iron-deficiency anemia occurs and hypoalbuminemia develops when blood loss exceeds the intake and reserves of host iron and protein.

Morphological changes in the small intestine in hookworm disease include villous atrophy and crypt hyperplasia. 

These changes and the malabsorptive state that is commonly present are probably unrelated to the infection.

When severe anaemia occurs in young children, it retards growth as well as well as sexual and mental development.

The presence of characteristic ova in stools, establishes the diagnosis.

Serologic tests are available but play little role in clinical diagnosis.

 

Further reading:

A study of risk factors for intestinal helminth infections using epidemiological and anthropological approaches

A history of hookworm vaccine development.

Nine cases of hookworm infection in the small intestine detected by capsule endoscopy.

Human Hookworm Infection in the21st century

Hookworm infections in human and laboratory animals--differences and similarities in immune responses.

Soil-transmitted helminth infections: ascariasis, trichuriasis, and hookworm.

New technologies for the control of human hookworm infection.

Hookworm infection.

 

 

Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)

 

 

 


 

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