|
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.
N. americanus
is the most common hookworm worldwide, whereas A. duodenale
is more geographically restricted. In contrast to these
major anthropophilic species, three species of zoonotic
hookworm are minor causes of disease in humans. A.
ceylanicum infects dogs and cats and can also infect humans
but is not considered an important pathogen. The dog
hookworm A. caninum causes human eosinophilic enteritis in
northeastern Australia , and A. 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 N. americanus or
A. duodenale results in a local pruritic, erythematous, papular
rash known as "ground itch."
Image Link
;
Image Link ;
ImageLink.
[ 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:
Image Link
Humans acquire hookworm when third-stage infective larvae in soil
either penetrate the skin ( both N. americanus and A. duodenale) or
when they are ingested (A. duodenale only).
The larvae are
each approximately 600 µm 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 areas |
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.
|
