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Hookworm infection
Authors: Peter F Weller, MD, MACP, Karin Leder, MBBS, FRACP, PhD, MPH, DTMH
Section Editor: Edward T Ryan, MD, DTMH
Deputy Editor: Elinor L Baron, MD, DTMH

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan 2021. | This topic last updated: Sep 20, 2019.

INTRODUCTION

Hookworm infections are common in the tropics and subtropics [1-3]. The prevalence of hookworm
infection is highest in sub-Saharan Africa, followed by Asia, Latin America, and the Caribbean. Infection
is rare in regions with less than 40 inches of rainfall annually.

There are two major species of hookworm that cause human infection: Ancylostoma duodenale (in
Mediterranean countries, Iran, India, Pakistan, and the Far East) and Necator americanus (in North and
South America, Central Africa, Indonesia, islands of the South Pacific, and parts of India).

In addition, a hookworm of dogs and cats, Ancylostoma ceylanicum, has been recognized as a widely
prevalent cause of human zoonotic infections in India, Southeast Asia, tropical Australia, and some
Melanesian Pacific Islands [4-6].

EPIDEMIOLOGY AND LIFE CYCLE

It is estimated that approximately 500 million people are infected with hookworms worldwide [1,2].
Globally, hookworm infections have their major impact not by causing death but rather by contributing
to morbidity especially due to anemia, including about 4 million disability-adjusted life years in 2010 [2].
The prevalence of hookworm infection in rural areas of the southeastern United States in the early 20th
century was high [7]. Extensive control efforts diminished the prevalence within the United States;
regions in the southeastern United States that have poor sanitation still are sites of hookworm
infection [7,8]. (See 'Prevention and control' below.)

Three conditions are important for transmission of hookworm infection: human fecal contamination of
soil, favorable soil conditions for larval survival (moisture, warmth, shade), and contact of human skin
with contaminated soil. Individuals who walk barefoot or with open footwear in fecally contaminated
soil are at risk for infection; risk groups include native residents of endemic areas, tourists, and infantry
troops [9,10].

The hookworm life cycle begins with passage of eggs from an adult host into the stool ( figure 1).
Hookworm eggs hatch in the soil to release rhabditiform larvae that mature into infective filariform

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larvae. Infection is transmitted by larval penetration into human skin; as few as three larvae are
sufficient to produce infection [11]. From the skin, larvae migrate into the blood vessels and are carried
to the lungs. Approximately 8 to 21 days following infection, larvae penetrate into the pulmonary
alveoli, ascend the bronchial tree to the pharynx, and are swallowed. In addition to percutaneous larval
penetration (the principal mode of transmission), A. duodenale infection may also be transmitted by the
oral route.

In the small intestine, the larvae mature into adult worms and attach to the intestinal wall with
resultant blood loss. A. duodenale larvae may persist within tissues before returning to the intestine,
with delay in egg laying [12]. Following fertilization by adult male worms, gravid female adults lay eggs
within the bowel. Eggs become detectable in feces about six to eight weeks following infection with N.
americanus. Most adult worms are eliminated in one to two years, though infection can persist for
many years [13].

Issues related to the relationship between hookworm infection and allergic and autoimmune diseases
are discussed separately. (See "Increasing prevalence of asthma and allergic rhinitis and the role of
environmental factors".)

CLINICAL MANIFESTATIONS

The potential manifestations reflect the four phases of hookworm infection [10]:

● Dermal penetration by infecting larvae

● Transpulmonary passage
● Acute gastrointestinal symptoms
● Chronic nutritional impairment

Cutaneous manifestations — Dermal penetration of the skin frequently produces a focal pruritic

maculopapular eruption at the site of larval penetration (termed "ground itch"). Less often, serpiginous
tracks of intracutaneous larval migration can be seen; this is similar to cutaneous larva migrans, which
is typically caused by the infective larvae of the animal hookworms. Ground itch generally occurs
between the toes and usually resolves within a few days. (See "Hookworm-related cutaneous larva
migrans" and "Skin lesions in the returning traveler".)

Transpulmonary passage — Transpulmonary passage is usually asymptomatic. A mild cough and

pharyngeal irritation may occur during larval migration in the airways, though eosinophilic pulmonary
infiltrates (such as those seen in the setting of Ascaris pulmonary involvement) are rare. (See
"Ascariasis".)

Pulmonary symptoms attributable to hookworm have not been observed in experimentally infected
volunteers [12]. Furthermore, bronchoalveolar lavage in these individuals has demonstrated only
erythema of the bronchial mucosa without prominent eosinophilia in lavage fluids.

Gastrointestinal symptoms — Patients may experience gastrointestinal symptoms at the time of

larval migration to the small intestine. Nausea, diarrhea, vomiting, midepigastric pain (usually with
postprandial accentuation), and increased flatulence have been observed in individuals with naturally
acquired infections [9] and in experimentally infected volunteers [14,15].
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Initial infections may be associated with gastrointestinal symptoms more frequently than subsequent
infections. In one individual who was experimentally infected on four occasions, gastrointestinal
symptoms and diarrhea were marked with the first infection, mild after the second, and absent after
the third and fourth infections [14].

In those with heavy infections, especially in endemic regions, hookworm infections may cause overt
gastrointestinal bleeding [16,17].

Gastrointestinal symptoms improve following treatment of hookworm infection [18].

Chronic nutritional impairment — The major impact of hookworm infection is on nutritional status

[1,2]. This is particularly important in endemic areas where children and pregnant women may have
limited access to adequate nourishment. In addition, maternal hookworm infection is associated with
low birthweight.

Hookworms cause blood loss during attachment to the intestinal mucosa by lacerating capillaries and
ingesting extravasated blood. This process is facilitated by the production of anticoagulant peptides
that inhibit activated factor X and factor VIIa/tissue factor complex [19] and inhibit platelet activation
[20]. Each N. americanus and A. duodenale worm consumes about 0.3 mL and 0.5 mL of blood per day,
respectively. The daily losses of blood, iron, and albumin can lead to anemia and contribute to impaired
nutrition, especially in patients with heavy infection [10].

DIAGNOSIS

Clues to the presence of hookworm infection include clinical manifestations as described above,
together with history of skin exposure to potentially contaminated soil and/or otherwise unexplained
blood eosinophilia.

The diagnosis may be established by stool examination. Molecular diagnostic tests can differentially
speciate infecting hookworm species. There are no reliable serologic tests available.

In some cases hookworms may be detected endoscopically, attached to the gastric and small intestinal
mucosal [3,17].

Stool examination — Stool examination for the eggs of N. americanus, A. duodenale, or A. ceylanicum is

useful for detection of clinically significant hookworm infection ( picture 1). Fecal egg excretion
becomes detectable about eight weeks after dermal penetration of N. americanus infection and up to
38 weeks after dermal penetration of A. duodenale [12]. Stool examination is not helpful prior to
established intestinal tract disease, including during early stages of dermal, pulmonary, or intestinal
involvement.

The standard method of diagnosis is with the Kato Katz technique. Other techniques used include the
simple sodium nitrate flotation technique (SNF), FLOTAC, and mini-FLOTAC. Microscopic methods of
stool examination for detection of hookworm infection vary, but are relatively insensitive especially
with low-intensity infections [21], so serial examinations are needed.

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Polymerase chain reaction (PCR) tests (including multiplex PCR assays, which can simultaneously detect
hookworm, Ascaris lumbricoides, and Trichuris trichiura) have been developed. PCR has superior
sensitivity compared with microscopy and has increasing commercial accessibility [22-24]. A PCR assay
of human stool can specifically detect A. ceylanicum [25].

The eggs of N. americanus and A. duodenale are morphologically indistinguishable. Speciation is not
necessary for clinical purposes and is only possible if adult worms are detected in stool or at endoscopy
[26,27].

Eosinophilia — Otherwise unexplained eosinophilia may be a major clue to the presence of a parasitic

infection. Eosinophilia has been attributed to persistent attachment of adult worms to the intestinal
mucosa. Among 128 Indochinese refugees with eosinophilia, a diagnosis of intestinal parasitism was
made in 95 percent of cases; hookworm and Strongyloides were the most common organisms (55 and
38 percent, respectively) [28]. In one study of immigrants and travelers with eosinophilia in Spain, the
most commonly identified parasites were Strongyloides (34 percent), Schistosoma (11 percent), and
hookworm (9 percent) [29].

The degree of eosinophilia with hookworm infection is usually mild and varies during the course of the
disease. Among experimentally infected volunteers, blood eosinophilia increased progressively after
two to three weeks and peaked at five to nine weeks. Peak eosinophil counts ranged from 1350 to 3828
cells/microL [30].

In untreated infections, eosinophilia slowly diminishes in magnitude but can remain elevated for
several years [13].

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of hookworm depends on the stage of infection:

● Dermal penetration – Cutaneous manifestations of hookworm infection can resemble cutaneous

larva migrans (infection with the dog or cat hookworm, Ancylostoma braziliense or Ancylostoma
caninum). Hookworm causes focal skin lesions at the site of larval dermal penetration. In rare
cases, migration of hookworm larvae elicits a serpiginous migratory track; if so, this occurs shortly
after dermal penetration. In contrast, larvae causing cutaneous larva migrans elicit more extensive
migratory serpiginous lesions, which last more than a few days and may appear weeks to months
following exposure. (See "Hookworm-related cutaneous larva migrans".)

● Transpulmonary passage – Pulmonary manifestations due to hookworm infection can resemble

pulmonary infection due to A. lumbricoides or Strongyloides. In some cases, sputum examination
may demonstrate diagnostic larvae; otherwise, stool microscopy may be performed, although
Ascaris stool eggs may not be detected until three to four weeks following infection. (See
"Strongyloidiasis" and "Ascariasis".)

● Acute gastrointestinal symptoms – Gastrointestinal symptoms due to hookworm infections are

nonspecific so may be difficult to differentiate from other causes of abdominal pain and flatulence.
Infectious etiologies causing similar symptoms include giardiasis, strongyloidiasis, and

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Dientamoeba fragilis. (See "Giardiasis: Epidemiology, clinical manifestations, and diagnosis" and
"Strongyloidiasis" and "Dientamoeba fragilis".)

● Chronic nutritional impairment – The soil-transmitted helminths A. lumbricoides and T. trichiura can
also cause growth retardation and malnutrition. In general, iron-deficiency anemia is most strongly
associated with hookworm infection. The soil-transmitted helminths may be distinguished based
on stool microscopy. (See "Ascariasis" and "Enterobiasis (pinworm) and trichuriasis (whipworm)".)

● Eosinophilia – Consideration of other parasitic and nonparasitic causes of eosinophilia may be

warranted. (See "Approach to the patient with unexplained eosinophilia".)

THERAPY

Anthelminthic treatment of hookworm infection consists of albendazole (400 mg once on empty

stomach) [31,32]. Mebendazole (100 mg twice daily for three days is more effective than a single dose
of 500 mg) and pyrantel pamoate (11 mg/kg per day for three days, not to exceed 1 g/day) are
acceptable alternative therapies [31]. Tribendimidine, a broadspectrum anthelmintic agent, also has
efficacy against hookworm [33]. Ivermectin has poor efficacy against hookworm.

The above approach is supported by the following studies:

● In a randomized trial in China including more than 300 patients aged ≥5 years, single-dose
albendazole had greater efficacy than single-dose mebendazole (69 and 29 percent cure rates,
respectively) [34,35]. Triple-dose therapy had greater efficacy, with cure rates of 92 and 54 percent,
respectively.

● In a meta-analysis including 38 studies and more than 7000 individuals, cure rates for albendazole,
pyrantel pamoate, and mebendazole were 80, 50, and 32 percent; egg reduction rates were 90, 72,
and 61 percent, respectively [32].

● In a randomized trial in Laos including more than 400 children aged 6 to 15 years with hookworm
infection treated with either (i) triple therapy with albendazole (400 mg), pyrantel pamoate (20
mg/kg), and oxantel pamoate (20 mg/kg), (ii) albendazole plus oxantel pamoate, or (iii) pyrantel
pamoate plus oxantel pamoate. The cure rates were 84, 52, and 53 percent, respectively, and the
egg reduction rates were comparable (99 percent) [36].

Treatment of hookworm infections in patients with marginal nutrition status has beneficial effects on
growth, exercise tolerance, and cognitive function [3]. Even in those without impaired nutrition,
anthelminthic therapies can improve hemoglobin levels [37]. Iron replacement alone can lead to
restoration of a normal hemoglobin level in individuals with hookworm infection, but anemia recurs
unless anthelminthic therapy is given.

PREVENTION AND CONTROL

Preventive measures consist of hygiene measures including drinking safe water, properly cleaning and
cooking food, hand washing, and wearing shoes.

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Regular deworming of groups at risk, including children, pregnant women, and women of childbearing
age, may prevent and reverse malnutrition, iron-deficiency anemia, impaired growth, and poor school
performance; uncertainties of the population-level benefits of such approaches remain [3,38,39]. (See
"Mass drug administration for control of parasitic infections".)

Development of an effective human vaccine is possible; studies are underway [40].

SUMMARY AND RECOMMENDATIONS

● There are three species of hookworm that cause human infection: Ancylostoma duodenale (in
Mediterranean countries, Iran, India, Pakistan, and the Far East), Necator americanus (in North and
South America, Central Africa, Indonesia, islands of the South Pacific, and parts of India), and
Ancylostoma ceylanicum (in India, Southeast Asia, tropical Australia, and some Pacific Islands).
Infection is rare in regions with less than 40 inches of rainfall annually. (See 'Introduction' above.)

● The hookworm life cycle begins with passage of eggs from an adult host into the stool ( figure 1).
Hookworm eggs hatch in the soil to release larvae that mature into infective larvae. Infection is
usually transmitted by larval penetration into human skin (A. duodenale infection may also be
transmitted by the oral route). From the skin, larvae migrate into the blood vessels and are carried
to the lungs, where they penetrate into the pulmonary alveoli, ascend the bronchial tree to the
pharynx, and are swallowed. (See 'Epidemiology and life cycle' above.)

● Clinical manifestations include dermal penetration by infecting larvae, transpulmonary passage

(usually asymptomatic), acute gastrointestinal symptoms, and chronic nutritional impairment.
Hookworms cause blood loss during attachment to the intestinal mucosa by lacerating capillaries
and ingesting extravasated blood. The daily losses of blood, iron, and albumin can lead to anemia
and contribute to impaired nutrition, especially in patients with heavy infection. (See 'Clinical
manifestations' above.)

● The diagnosis is established by stool examination via microscopy or polymerase chain reaction for
the eggs of N. americanus or A. duodenale; there are no reliable serologic tests available. Stool
examination for detection of hookworm infection is insensitive; serial examinations may be
required to make the diagnosis. (See 'Stool examination' above.)

● Otherwise unexplained eosinophilia may be a major clue to the presence of a parasitic infection.
Eosinophilia has been attributed to persistent attachment of adult worms to the intestinal mucosa.
(See 'Eosinophilia' above.)

● We suggest albendazole (400 mg once on empty stomach) for treatment of hookworm infection
(Grade 2B). Mebendazole and pyrantel pamoate are acceptable but less effective alternative
therapies. Iron replacement alone can lead to restoration of a normal hemoglobin level in
individuals with hookworm infection, but anemia recurs unless anthelminthic therapy is given. (See
'Therapy' above.)

● Preventive measures consist of hygiene measures including drinking safe water, properly cleaning
and cooking food, hand washing, and wearing shoes. Anthelminthic drugs may be administered to

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populations at risk with the intention of maintaining low individual worm burdens. (See 'Prevention
and control' above.)

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34. Steinmann P, Utzinger J, Du ZW, et al. Efficacy of single-dose and triple-dose albendazole and
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GRAPHICS

Intestinal hookworm infection life cycle

Eggs are passed in the stool (1), and under favorable conditions (moisture, warmth, shade) larvae hatch in one
to two days. The released rhabditiform larvae grow in the feces and/or the soil (2), and after 5 to 10 days (and two
molts) they become filariform (third-stage) larvae that are infective (3). These infective larvae can survive three
to four weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the
skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the
pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed (4). The larvae reach the small
intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where
they attach to the intestinal wall with resultant blood loss by the host (5). Most adult worms are eliminated in one
to two years, but the longevity may reach several years. Some Ancylostoma duodenale larvae, following penetration
of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A. duodenale may
probably also occur by the oral and transmammary route. Necator americanus, however, requires a transpulmonary
migration phase.

Reproduced from: Centers for Disease Control and Prevention. DPDx: Hookworm. http://www.cdc.gov/dpdx/hookworm/index.html.

Graphic 61675 Version 6.0

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Hookworm ovum in stool

A wet mount of stool (x400) shows an ovum of hookworm. The eggs of the two species
of hookworm, Necator americanus and Ancylostoma duodenale, are indistinguishable in
wet mounts.

Courtesy of Harriet Provine.

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Contributor Disclosures
Peter F Weller, MD, MACP Grant/Research/Clinical Trial Support: GlaxoSmithKline [Anti-IL5 mAb for EGPA].
Consultant/Advisory Boards: Knopp Biosciences [Hypereosinophilic syndrome treatment]; GlaxoSmithKline
[Eosinophilic diseases]; Genzyme [Eosinophilia]. Other Financial Interest: AstraZeneca [Hypereosinophilic
syndrome]. Karin Leder, MBBS, FRACP, PhD, MPH, DTMH Nothing to disclose Edward T Ryan, MD,
DTMH Grant/Research/Clinical Trial Support: Sanofi [Yellow fever]. Elinor L Baron, MD, DTMH Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.

Conflict of interest policy

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