Hookworms

Author: MBLOGSTU

Introduction

Most cases of classic hookworm disease are caused by Ancylostoma duodenale or Necator americanus, species typically found only in humans. On rare occasions, these species have been reported in other mammals. Less often, classic hookworm disease is caused by the zoonotic species A. ceylanicum; rare human intestinal infections with A. malayanum, A. japonica, Necator suillis and N. argentinus have also been reported.

In humans, certain zoonotic hookworms can cause cutaneous larva migrans. Ancylostoma braziliense—a hookworm of cats and dogs—is responsible for most cases of cutaneous larva migrans, while A. caninum, Uncinaria stenocephala (hookworms of dogs and cats), and Bunostomum phlebotomum (a hookworm of cattle) are less often involved.

The hookworms Necator americanus, Ancylostoma duodenale and Ancylostoma ceylanicum infect approximately 576–740 million persons worldwide, predominantly in impoverished rural and tropical regions. Together, they cause one of the world’s most debilitating neglected tropical diseases. Chronic hookworm infection results predominantly in continuous intestinal blood loss, which is the major pathologic consequence.

Epidemiology

Since hookworm transmission involves contamination of the environment by hookworm eggs, risk factors include poor personal hygiene and inadequate household sanitation, which are often influenced by socioeconomic status. Studies have found associations with the absence of latrines and low socioeconomic conditions.

Heterogeneity in worm burdens may result from differences in both exposure (household, socioeconomic, climatic, environmental, and occupational factors) and susceptibility (genetic and nutritional factors). Age and sex also affect infection rates.

Geographical Distribution

Ancylostoma: Found in Europe around the Mediterranean, on the West coast of South America, and in parts of China, India, and Nepal.

Necator: Distributed throughout much of the western hemisphere, Africa, and Southeast Asia.

Morphological Differences Between Hookworm Species

The table below summarizes the morphological differences between Ancylostoma duodenale and Necator americanus:

Characteristic	Ancylostoma duodenale	Necator americanus
Size	Larger	Smaller
Shape	Single curve (C-shaped)	Double curves (S-shaped)
Mouth	2 pairs of ventral teeth	1 pair of ventral cutting plates
Copulatory Circle	Oval in shape	Oval in shape
Bursa (Top view)	Present	Present
Copulatory Spicule Endings	1 pair with separate spicule endings	1 pair that unite to form a terminal hooklet
Caudal Spine	Present	Absent
Vulva Position	Post-equatorial	Pre-equatorial

Habitat and Morphology

Habitat: The adult hookworm lives in the small intestine of humans, primarily in the jejunum, less often in the duodenum, and rarely in the ileum.

Adult Worm: Hookworms are small, greyish white, cylindrical worms. When freshly passed, they may appear reddish brown due to ingested blood. The anterior end is slightly bent dorsally. The adult male is about 8 mm in length while the female is approximately 12.5 mm.

Eggs: The eggs are oval or elliptical, measuring about 65 μm in length and 40 μm in breadth. They are colorless (non–bile stained) and are surrounded by a transparent hyaline shell membrane. Each egg typically contains a segmented ovum with four blastomeres and floats in a saturated saline solution.

Life Cycle

The hookworm life cycle includes several key stages:

• Larval Stage (L3): Infective larvae penetrate human skin—a primarily chemical process mediated by proteolytic enzymes (e.g., those secreted by N. americanus larvae capable of degrading collagen, fibronectin, laminin, and elastin). Ancylostoma larvae also secrete hyaluronidase to facilitate dermal migration.
• Once the L3 larvae penetrate the skin, they migrate and eventually reach the gut. There, they form a brief buccal capsule as fourth-stage larvae before transitioning to fifth-stage larvae and then adulthood.
• Adult hookworms attach to the intestinal mucosa using either teeth (Ancylostoma) or cutting plates (Necator). They feed on human blood, causing chronic intestinal blood loss.

Pathogenesis

Hookworm pathogenesis is driven by multiple mechanisms:

• Larval Activation & Migration: The release of a range of proteolytic enzymes from larval glands facilitates skin penetration and migration by degrading connective tissue substrates. For example, Necator americanus secretes proteases active against collagen, fibronectin, laminin, and elastin; while Ancylostoma species produce hyaluronidase to disrupt cellular adhesion.
• Blood Feeding: Upon entering the gut, the larvae form a buccal capsule and transition to adulthood. The initial step in blood feeding involves attachment to the intestinal mucosa using teeth or cutting plates. This is followed by mechanical disruption of a mucosal plug and aided by metalloproteases. To help ingest blood, hookworms also secrete anticoagulant peptides (NAPs) that facilitate blood flow from ruptured capillaries.
• Immune Evasion & Long-Term Survival: Hookworms deploy broad spectrum Kunitz-type protease inhibitors that neutralize host proteases. They may also induce T lymphocyte apoptosis and locally modulate inflammatory responses to minimize host pathology, thereby ensuring long-term survival in the small intestine.

Clinical Manifestations

The clinical features of hookworm infection are largely a result of chronic blood loss:

Skin Manifestations

Hookworm-Related Cutaneous Larva Migrans (HrCLM): This parasitic skin disease is caused by animal hookworm larvae—commonly Ancylostoma caninum, Ancylostoma braziliense, or Uncinaria stenocephala—migrating within the epidermis. It presents as a linear or serpiginous, slightly elevated, erythematous track.

Ground Itch: An early sign during L3 larval penetration of the skin, likely caused by allergic components secreted by the larvae. Secondary bacterial infections are common during this stage.

Pulmonary Manifestations

Pulmonary involvement may mimic the syndrome seen with Ascaris lumbricoides, presenting as low-grade fever, mild cough, dyspnea, and hemoptysis. In severe infection, pneumonia with consolidation or bronchitis may develop.

Intestinal Manifestations

Acute intestinal symptoms include abdominal pain, nausea, anorexia, vomiting, and hemorrhagic diarrhea (or melena). In chronic hookworm disease, continuous blood loss leads to iron-deficiency anemia with symptoms such as fatigue, pallor, tachycardia, and exertional dyspnea. Hypoproteinemia may result in edema, and malabsorption can contribute to malnutrition. In children, chronic infection may adversely affect physical and intellectual growth. Severe infections can be life-threatening, particularly in infants.

Eosinophilic Enteritis

Eosinophilic enteritis, caused by zoonotic hookworms such as A. caninum, is characterized by recurrent episodes of severe abdominal pain accompanied by peripheral eosinophilia—though without significant blood loss. In some cases, the clinical picture may mimic appendicitis or intestinal perforation.

Laboratory Diagnosis

Diagnosis of hookworm infection is primarily made by stool examination.

• Stool Microscopy: Characteristic hookworm eggs are demonstrated by direct microscopy. Because eggs are typically unembryonated when passed, concentration techniques (sedimentation or flotation) are used to detect infections—particularly light or asymptomatic cases.
• Occult Blood Test: May detect low levels of blood loss in mild infections.
• Harada-Mori Culture: This technique is recommended to differentiate hookworm species since their eggs are morphologically indistinguishable.
• Kato-Katz Method: Employed to quantify eggs per gram of stool.
• Imaging Techniques: Sometimes used to investigate pulmonary complications.
• Detection of Charcot-Leyden crystals may also support the diagnosis.
• Serodiagnosis is generally of little value due to a high false-positive rate.

Key Points:

• Hookworm eggs are typically passed in the stool in an unembryonated state with a thin shell and a clear space between the developing embryo and the shell.
• If stool samples are left unpreserved for over 24 hours, eggs may continue developing and larvae may hatch; these larvae must be differentiated from those of <