Hookworms

Another significant group of parasitic worm causing STH are hookworms. This comprise
of two main species which are known to infect humans, namely Ancylostoma
duodenale and Necator americanus [1]. However some species are also known for their
lesser role in hookworm-related diseases. Ancylostoma ceylanicum and A. caninum which
are primarily a canine hookworm is known for its capability to cause zoonotic disease
leading to enteritis and ileitis. And lastly, A. braziliense, A. caninum, and Uncinaria stenoce
are considerably known to cause cutaneous larva migrans among hookworms [2][3].

Epidemiology
Approximately 470 million individuals are known to have hookworm infections
globally. Its distribution is widely spread particularly in warm and moist regions including
Asia, Africa, Central and South America, and the South Pacific. N. americanus serves as the
leading cause of hookworm infections worldwide, whereas A. duodenale is more prevalent in
the Mediterranean region and South-western Asia [2].
Common factors that increases the risk for hookworm infection include warm and
moist environment, low socioeconomic status, poor sanitation and hygiene, and high
exposure to soil particularly in agricultural jobs which can all be deemed in the community
of Kaunlaran [1][4].

Pathophysiology and Life Cycle

Hookworm eggs are initially passed in the stool of an infected individual. During
favorable conditions including warm, moist and shaded setting, first-stage larvae or
rhabditiform larvae hatch in 1 to 2 days and become free-living in soil. They eventually molt
twice to become infective filariform (third-stage) which can survive 3 to 4 weeks in suitable
environmental conditions. Infection starts once it comes into contact with the human skin
which is typically on bare feet. The larvae penetrate the skin through their buccal mucosa,
invading the host which sometimes presented as ground itch. In N. americanus, cutaneous
penetration occurs through production of proteases to break down collagen and elastin
which are components of connective tissues; whereas in Ancylostoma larvae, hyaluronidase
enzyme is produce to penetrate the dermal integrity of the host. The larvae will eventually
make their way to the blood vessels to the right side of the heart and then to the lungs.
Their migration to the pulmonary vasculature causes a type-1 hypersensitivity reaction
causing Loeffler syndrome. As they migrate into the pulmonary alveoli, they eventually
ascend through the bronchial tree then into the pharynx, and are swallowed into the
intestinal tract. As they reach the duodenum, they actually molt twice to become immature
worms that have cutting plates to attach on the intestinal mucosa of the host. They reside
in the small intestine to become mature which may take several years. Hookworm
maturation and sexual differentiation for mating usually occurs in 4 to 6 weeks; a mature
female usually lays 3000 eggs per day in the intestinal lumen which exits the host through
the feces. The chronic consumption of the parasite and leakage of blood from their
attachment in the intestinal wall causes significant blood loss especially in heavily infected
hosts that could reach up to 9.0 mL/day. Accompanying factors such as deprived nutrition
of the hosts may lead to iron-deficiency anemia. In addition to this, concurrent protein loss
may result to hypoproteinemia and hypoalbuminemia, which can cause anasarca and
aggravate host malnutrition [5].

Signs and symptoms

Hookworm infections predominantly present asymptomatically, although clinical
features and symptoms are usually nonspecific and relate to agent stage and site of agent
invasion.
Upon cutaneous penetration, infection typically presents as ground itch
characterized by localized erythematous reaction. As the hookworm infection progresses to
the lungs, it usually demonstrates as coughing episodes, sneezing, bronchitis, hemoptysis,
and even eoisinophilic pneumonia known as Loeffler syndrome. Rare cases might also
present Wakana syndrome which is distinguished by peroral infection, nausea accompanied
by vomiting, throat itchiness and irritation, as well as dyspnea and cough. And finally, once
infection reaches the small intestine, abdominal symptoms arise which include pain,
distension, diarrhea, occult fecal blood, and, even melena [1][5].
However, hookworm infection is known for its nutritional burden mainly through iron
deficiency anemia due to blood loss via mechanisms of direct parasitic consumption and/or
leakage caused by attachment of parasites on the intestinal mucosa. Concurrent
hypoalbuminemia caused by the chronic protein loss, may even lead to symptoms of edema
and anasarca[6]. There are rare instances that individuals with severe infection may also
present with geophagia wherein they crave soil and even ingest dirt [1][7].

what can be deduced in the community of Kaunlaran based from their poorly managed
nutritional program puts them in a greater risk for iron deficiency anemia.

[1] Albonico M, Savioli L. Hookworm: a neglected resurgent infection. BMJ. 2017 Oct 24;359:j4813
[2] Ghodeif AO, Jain H. Hookworm. [Updated 2021 Jan 27]. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK546648/
[3] Cdc.gov. 2021. CDC - Hookworm - Biology. [online] Available at:
<https://www.cdc.gov/parasites/hookworm/biology.html> [Accessed 24 April 2021].
[4] Parija SC, Chidambaram M, Mandal J. Epidemiology and clinical features of soil-transmitted
helminths. Trop Parasitol. 2017 Jul-Dec;7(2):81-85. [PMC free article] [PubMed] [Reference list]
[5] Jourdan PM, Lamberton PHL, Fenwick A, Addiss DG. Soil-transmitted helminth infections. Lancet.
2018 Jan 20;391(10117):252-265.
[6] Loukas A, Prociv P. Immune responses in hookworm infections. Clin Microbiol Rev. 2001
Oct;14(4):689-703, table of contents.
[7] Hotez PJ, Brooker S, Bethony JM, Bottazzi ME, Loukas A, Xiao S. Hookworm infection. N Engl J Med.
2004 Aug 19;351(8):799-807.