Paediatrics and International Child Health

ISSN: 2046-9047 (Print) 2046-9055 (Online) Journal homepage: http://www.tandfonline.com/loi/ypch20

Parasitic infections of the gut in children

Kapula Chifunda & Paul Kelly

To cite this article: Kapula Chifunda & Paul Kelly (2018): Parasitic infections of the gut in children,
Paediatrics and International Child Health, DOI: 10.1080/20469047.2018.1479055

To link to this article: https://doi.org/10.1080/20469047.2018.1479055

Published online: 22 Aug 2018.

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PAEDIATRICS AND INTERNATIONAL CHILD HEALTH
https://doi.org/10.1080/20469047.2018.1479055

Parasitic infections of the gut in children

Kapula Chifundaa and Paul Kelly a,b

a
Tropical Gastroenterology and Nutrition group, University of Zambia School of Medicine, Lusaka, Zambia; bBlizard Institute, Barts and
The London School of Medicine, Queen Mary University of London, London, UK

ABSTRACT ARTICLE HISTORY

Parasitic infections of the gut have major implications for child health, but many questions Received 4 April 2018
remain unanswered. Protozoal parasites, especially cryptosporidiosis and giardiasis, cause Accepted 16 May 2018
diarrhoea and contribute to impaired growth, neurocognitive development and mortality. KEYWORDS
Entamoeba histolytica causes dysentery and may have more subtle effects on child growth. Parasites; child health;
Helminth infections are mostly asymptomatic, and untargeted mass deworming has not been diarrhoeal disease;
shown to be beneficial. However, children with heavy infections certainly benefit from cryptosporidiosis; helminths;
antihelminthic treatment. Hepatosplenic schistosomiasis is a neglected problem on a massive giardiasis
scale, which causes portal hypertension and lifelong morbidity in individuals who get infected
in childhood. Neurocysticercosis causes epilepsy and is a significant consequence of taeniasis
solium, another neglected disease which is entirely preventable. Parasitic infections of the gut
contribute to child health problems on a large scale. Fresh approaches are needed to
prevention and treatment.

Introduction surface of the small intestinal mucosa, and the cyst

Parasitic infections of the gut are responsible for a
very large burden of morbidity and mortality in tropi-
cal and low- and middle-income countries (LMIC).
These infectious diseases, however, are not confined
to LMIC. Cryptosporidiosis, for example, has caused
massive outbreaks in the USA, and giardiasis is also
globally distributed. Strictly speaking, a parasite is
merely an organism which lives on or in another
organism without conferring any benefit to the host,
and usually to its disadvantage. In common medical
usage, however, the term ‘parasite’ refers to protozoa,
helminths or insects rather than bacteria or viruses.
This article also includes some recognised fungal
infections of the gut. Only the most important para-
sites are described, and for less prevalent pathogens
more detailed articles should be consulted [1–3]. Life
cycles and detailed parasitological descriptions will
not be given here.
Infectious agents
Protozoa
Giardia intestinalis (syn. G. lamblia). Giardia was the
first parasite to be recognised under the microscope
by van Leeuwenhoek (in his own stool sample) in
1681. Its flagellated trophozoite is instantly recogni-
sable in a view of the ventral surface, but may be
harder to recognise when cut tangentially in a histo-
logical section (Figure 1). There are two forms of
giardia: the motile trophozoite which lives on the
which is the infective form passed out into the faeces.
Transmission is faeco-oral, from person-to-person and
in drinking water or food. This is possible because the
infectious dose is low, perhaps only 10 or 100 cysts. G.
intestinalis isolates can be divided into seven assem-
blages, A–H. Only assemblages A and B, which can be
subdivided into AI-III and an ever-increasing number
of sub-types of the B assemblage [4,5], infect humans.
Assemblages A and B can infect a wide range of
animals and there is evidence that giardiasis is fre-
quently a zoonosis, though probably not through
direct contact with animals [6]. Giardia is common in
many diverse populations [7,8] but its association with
diarrhoea is controversial [9]. Giardia carries with it an
associated risk of polyparasitism [10].
The pathogenesis of giardiasis is unclear, but it is
known that the trophozoite adheres to the entero-
cyte brush border and disturbs brush border hydro-
lytic and absorptive capacity. There is some evidence
for immune participation in the development of a
mild enteropathy which contributes to symptoms
[11]. Individuals with hypogammaglobulinaemia or
agammaglobulinaemia are at risk of chronic giardia-
sis, as are people with IgA deficiency, but individuals
with HIV and AIDS do not have increased risk. This
supports the view that secretory immunity in the
intestinal lumen is more important for clearance
than cell-mediated responses within the intestinal
mucosa.
Diagnosis is by stool microscopy, but stool antigen
tests are now in widespread use [12]. Treatment is

CONTACT Paul Kelly

© 2018 Informa UK Limited, trading as Taylor & Francis Group
2 K. CHIFUNDA AND P. KELLY
Figure 1. Trophozoites of Giardia intestinalis occupying a
luminal position adjacent to the epithelium in a small intest-
inal biopsy.
with nitroimidazoles [13]:tinidazole (50–75 mg/kg sin-
gle dose is a simple regimen) or metronidazole.
Mepacrine, furazolidone and nitazoxanide are also
effective.
Entamoeba histolytica. Entamoeba histolytica is the
cause of amoebic dysentery (bloody diarrhoea, with
or without fever) and amoebic abscess. Its diagnosis,
and therefore epidemiological description, is compli-
cated by the fact that there is an amoeba, Entamoeba
dispar, which is identical microscopically, but abso-
lutely non-pathogenic [14]. It can only be distin-
guished from E. histolytica by molecular tests such as
the polymerase chain reaction (PCR) or genomic
sequencing. There are other species of Entamoeba
(Entamoeba coli, E. moshkovskii, E. polecki, E. hart-
manni, Iodamoeba butschlii and Endolimax nana)
which require considerable expertise to distinguish
from E. histolytica. As E. dispar is absolutely indistin-
guishable from E. histolytica except by molecular tech-
niques, much of the older epidemiology requires
revision and many older estimates of prevalence are
probably too high [15].
The infective form of the pathogen is the cyst,
which has a predilection for invasion of the distal
gut. Trophozoites of E. histolytica exert their patho-
genic effects through a remarkable capacity for tissue
destruction which involves the secretion of proteases,
phospholipases and molecules called amoebapores
[16]. The clinical features of amoebic dysentery are
due to the destruction of the colonic wall by amoebae
which undermine the mucosa leading to ulceration
and bleeding into the liquid stool which is induced by
neutrophil-mediated inflammation. In severe cases
this can lead to perforation of the colon.
As with giardiasis, there is no increase in incidence or
severity in HIV infection. Immunity to amoebiasis is only
partial and probably mediated by antibody responses to
lectins on the surface of the trophozoites [17].
Diagnosis relies on stool microscopy, but requires
great care and expertise as noted above. Serological
diagnosis is very useful in severe cases and can be
performed as an emergency. Stool antigen testing is
increasingly used [18]. Treatment is with nitroimida-
zoles, e.g. tinidazole 60 mg/kg for 3 days, ideally
followed by diloxanide furoate to eradicate cyst car-
riage. Nitazoxanide and paromomycin are also useful.
Cryptosporidium spp. There are over 25 species of
Cryptosporidium, but only two frequently infect
humans, C. parvum and C. hominis. C. parvum is a
zoonosis and has reservoirs in farm animals, but C.
hominis has only anthroponotic transmission and has
to be transmitted from one person to another. The life
cycle is complex, including sexual and asexual cycles
of replication. The infective form is the oocyst, which
excysts in the intestine to initiate infection of enter-
ocytes. The pathophysiology is debated, but is clearly
different to giardiasis or amoebiasis in that the tro-
phozoite occupies an intracellular location but does
not cause cell lysis. Transmission is faeco-oral.
The distribution of cryptosporidiosis is worldwide.
Massive waterborne outbreaks have been reported
due to contamination of drinking water [19] and swim-
ming pools. However, there is strong evidence that the
most important adverse impact of cryptosporidiosis is in
young children in LMIC. It causes growth failure, neuro-
cognitive impairment, and makes a major contribution
to malnutrition. In community studies [20,21] and in
hospitalised patients [22], cryptosporidiosis is associated
with substantially increased mortality. Cryptosporidiosis
first came to prominence in the first years of the HIV
epidemic because its incidence and disease severity are
strongly influenced by concurrent HIV infection. This is a
reflection of the dependence of the immune response
on T helper (CD4) cells, with an additional contribution
from natural killer cells secreting additional interferon-
γ [23].
Diagnosis is based on stool microscopy using mod-
ified Ziehl–Neelsen or auramine stains, but increas-
ingly stool antigen and PCR-based tests are being
used. The only licensed treatment for cryptosporidio-
sis (Figure 2) is nitazoxanide [24], but new agents are
being evaluated in clinical trials [25].
Isospora (syn. cryptisospora) belli. As with cryptos-
poridiosis, isosporiasis was described as a rarity before
the HIV pandemic, but it was then recognised as a
major opportunistic pathogen. It is one of the most
common pathogens in patients with AIDS-related

diarrhoea in many parts of sub-Saharan Africa [26],
but it affects children much less frequently [22]. Its
life cycle is similar to that of Cryptosporidium, and
transmission is probably also similar although much
less thoroughly investigated. It is treated with co-
trimoxazole at double the dose used for antibacterial
effects for 10 days [27]. In HIV-infected individuals,
prophylaxis with co-trimoxazole will be required
thereafter until CD4 counts are restored. The number
of CD4 cells required to permit discontinuation of
secondary prophylaxis is not established, but in adults
this is probably about half the lower limit of normal
and this may be a useful rule of thumb in children.
Fungi
Microsporidia. Two species of microsporidia (phylum
Microspora [28]) infect the human intestine:
Enterocytozoon bieneusi and Encephalitozoon intestina-
lis (formerly Septata intestinalis). The microsporidia
were originally classified as protozoa but are now
recognised to be fungi [28]. Human intestinal micro-
sporidiosis was also recognised in the wake of the HIV
pandemic [29,30]. It has also been recognised to be
an important cause of persistent diarrhoea in
Ugandan children, strongly associated with HIV but
also found in HIV-uninfected children [31]. Much more
work is required to define the epidemiology of human
intestinal microsporidiosis in LMICs, about which
there is very scanty information. The problem is com-
pounded by the difficulty of microscopic diagnosis,
which requires a very high degree of skill as the
spores are difficult to distinguish from bacteria. PCR
Figure 2. Trophozoites of Cryptosporidium in the brush border
of intestinal epithelial cells in a patient with HIV-related
diarrhoea.
PAEDIATRICS AND INTERNATIONAL CHILD HEALTH 3
diagnosis is a good alternative but only available in
specialised centres. Treatment is unsatisfactory.
Zygomycetes. Zygomycetes are ubiquitous agents
found in organic debris, on fruit, and in soil. The
terms ‘mucormycosis’ and ‘phycomatosis’ have
been used in the past for these infections. These
agents can infect the subcutaneous and submucosal
tissues in an immunocompetent host, but in the
debilitated host, they can cause acute fulminant
invasive infection [32]. Intestinal zygomycosis is,
rarely, encountered in severely malnourished chil-
dren and sometimes as a complication of severe
chronic intestinal disease, such as amoebic colitis.
On occasion, the infection can occur without appar-
ent predisposition. Treatment is with amphotericin B
in doses escalating to 1–1.5 mg/kg if possible; surgi-
cal debridement is also often necessary.
Nematodes
Nematodes are roundworms. Prevalence is very high
in LMIC. There is a group of nematodes known as soil
transmitted helminths: Ascaris lumbricoides, the
hookworms, Trichuris trichiura and (although often
omitted from this list) Strongyloides stercoralis. The
soil-transmitted helminths infect the human host in
one of two ways. The first group includes Ascaris and
Trichuris; the ova are spread onto vegetables and
hands in human faeces and are then ingested.
Ascaris larvae hatch in the intestine and penetrate
into the systemic circulation, whereas Trichuris larvae
develop only in the gut and migrate distally to colo-
nise the colon as adults. The second group (hook-
worm, Strongyloides) penetrate the skin of the foot
as their portal of entry. Ova excreted onto the soil by
open defaecation hatch, followed by penetration of
the bare skin of the foot by the larvae, leading to
dissemination to other tissues. Children are often
affected by soil-transmitted helminths because of
their propensity to play bare-footed and to shed
faeces on the ground while outside and unattended.
Children with intense infections with these hel-
minths can develop severe symptoms; however, the
great majority of infections are lighter and
asymptomatic.
The great majority of these infections can be trea-
ted with benzimidazole drugs such as albendazole,
which are highly effective even after a single dose.
The exception is S. stercoralis which is best treated
with ivermectin.
Ascaris lumbricoides. Adult ascaris worms are up to
30 cm in length and 10–15 cm is common. They live
in the gut lumen (Figure 3). They are much larger than
any other nematodes which infect humans and their
effects are mechanical – obstruction of the gut lumen
4 K. CHIFUNDA AND P. KELLY
Figure 3. Ascaris lumbricoides in the duodenum detected
during routine endoscopy.
or the biliary or pancreatic ducts. As noted above, the
vast majority of individuals with ascariasis have no
symptoms.
Hookworms. Two species of hookworm infect man:
Necator americanus and Ankylostoma duodenalis.
Adult worms of N. americanus are about 1 cm long
and those of A. duodenalis are slightly larger (espe-
cially the female). Hookworms are so called because
of the barbs with which the adult worms bury into
and draw blood from the intestinal mucosa. It is this
blood loss which causes the most common clinical
manifestation of intense hookworm infection: iron
deficiency (Figure 4).
Trichuris trichiura
T. trichiura is predominantly found in LMIC, but is also
present in south-eastern USA. The vast majority of
infections are asymptomatic, but in some endemic
areas heavy infections can cause the trichuris dysentery
syndrome which is characterised by bloody diarrhoea.
Heavy infections can also lead to rectal prolapse.
Figure 4. Hookworm in the duodenum detected during
routine endoscopy.
Strongyloides stercoralis. Strongyloides poses a much
more difficult problem than other intestinal nematode
infections. It is difficult to diagnose and to treat, and
infections can persist for many years. Consequently, the
epidemiology is not clear [33].
Diagnosis depends on finding larvae in stool, but this
is insensitive. Serological tests are more sensitive than
stool tests. The Baermann stool test is the most sensitive
for coprodiagnosis, but PCR may be better still. Optimal
treatment is ivermectin (200 µg/kg in adults; the pae-
diatric dose is not established). Strongyloides has the
potential to cause a hyperinfection syndrome [33] which
is precipitated by intercurrent infections (e.g. human
t-lymphotropic virus I) or immunosuppressive medica-
tion, but not (curiously) HIV. It can also cause malabsorp-
tion and skin rash (larva currens) many years after
infection. While interesting phenomena, these are prob-
ably not relevant to paediatric practice.
Enterobius vermicularis. Enterobius has a truly global
distribution and is common in children all over the
world. Adult worms live in the right colon of the
human host, migrating onto the perianal skin at
night to lay eggs. This causes itching: pruritus ani is
the characteristic symptom and the mode of transmis-
sion as the ova then stick to the children’s fingers and
can pass to other children through digital–oral con-
tact. It causes no major clinical disease.
Trichinella spiralis. Trichinella spiralis occurs world-
wide in communities that eat pork. It is an important
infection of man in Europe and the USA; it is less
important in the tropics but occurs in both east and
west sub-Saharan Africa. It has been reported to cause
disease and death in the Arctic, where polar explorers
have died due to trichinosis from eating walrus meat. It
is not a geohelminth. Unlike other nematodes, T. spiralis
requires two hosts to complete its life cycle, most com-
monly pigs but a variety of other domestic and wild
hosts can support its life cycle. Human infection is
acquired from eating undercooked meat, usually from
infected pigs. The small intestine harbours the adult
only during the ‘enteric’ phase of infection (up to
7 days after ingestion of meat containing larvae), during
which the human host will have nausea, vomiting and
abdominal pain. During the migratory phase, symp-
toms include fever, myalgia, periorbital oedema and
eosinophilia. The third stage of infection may be
accompanied by cachexia, oedema, myocardial or neu-
rological features, including heart failure or convulsions.
Treatment is with mebendazole (200 mg) or thiabenda-
zole (25 mg/kg) twice daily for 10 days.
Cestodes
Taenia saginata. Taenia saginata, the beef tape-
worm, is the largest parasitic organism which infects

humans, growing up to 20 m in length. It is acquired
by eating beef in which the cysticerci of the parasite
have been deposited. Consequently, human infection
can largely be prevented by inspection of beef in
abattoirs to ensure that contaminated beef does not
get to market. Symptoms are minimal and may
include vague abdominal discomfort, but occasionally
patients complain of proglottids (segments) of the
tapeworm appearing on the perianal skin. Treatment
is with praziquantel 10 mg/kg.
Taenia solium. This is similar to T. saginata but is
acquired from pigs. Its importance is that auto-infection
can occur which leads to dissemination of cysticerci
throughout the tissues of the host. The most feared
outcome is neurocysticercosis, characterised by cysti-
cerci in the brain, which leads to epilepsy and other
focal neurological signs. Treatment is very difficult and
may require surgery following prolonged courses of
praziquantel.
Hydatid disease. Hydatid disease is caused by
Echinococcus granularis or E. multilocularis. The defini-
tive host is a dog or cat, and the human is an acci-
dental host. Transmission occurs by ingestion of an
egg which has been passed in the faeces of the
definitive host. Cysts have a characteristic appearance
on ultrasound examination, with a deeply hypo-
echoic fluid-filled centre and ‘daughter’ cysts around
the edges [34]. Suspected hydatid cysts should not be
investigated using needle aspiration, lest the contents
escape into surrounding tissues or body cavities and
set up widespread infection. Anaphylaxis can also
occur. The diagnosis should be confirmed serologi-
cally. Treatment options include surgery or aspiration
and injection of sterilising agents, but these proce-
dures are always preceded by at least 2 weeks of
albendazole and/or praziquantel to kill the protosco-
lices [35]. Treatment is best undertaken by experts.
Surprisingly, hydatid disease does not cause fever,
leucocytosis or eosinophilia, unless rupture has
occurred in which case treatment must be instituted
urgently, beginning with albendazole and broad-
spectrum antibiotics.
Hymenolepis nana. H. nana is the dwarf tapeworm,
transmitted by the faeco-oral route. It causes minimal
effects and is not usually treated. In heavy infections,
praziquantel (at least 20 mg/kg) is given as a single dose,
divided over the course of one day.
Trematodes
Schistosomiasis. The most important trematode infec-
tion of man, by far, is schistosomiasis. Of the
eight species which infect man, Schistosoma haemato-
bium causes urinary disease, and hepatosplenic
PAEDIATRICS AND INTERNATIONAL CHILD HEALTH 5
schistosomiasis is most frequently owing to
Schistosoma mansoni. Transmission begins with ova
passed into water in excreta, from which miracidia
infect susceptible fresh-water snails such as
Biomphalaria spp. Cercariae hatch from these snails
by the thousand and penetrate the skin of people
while bathing, swimming or fishing. In endemic areas,
infections begin during the early years of life and may
continue for decades. The ova released from pairs of
adult worms living in the mesenteric veins pass up the
portal vein to the liver, where they induce inflamma-
tory and fibrotic responses which lead ultimately to
portal hypertension. This leads to oesophageal varices
and ascites, which may be found in children from
5 years of age upwards in endemic areas.
Characteristic ova of each species can be detected
in faeces or in intestinal biopsy specimens. Specific
antibodies can be detected by immune assay in more
than 95% of patients during the first few weeks of
infection. Calprotectin rapid assays have been found
to correlate positively and strongly with egg patent S.
mansoni infection [36]. Praziquantel given as a single
dose (40 mg/kg for S. mansoni; 60 mg/kg in divided
doses is also used by many physicians) is probably the
drug of choice. Oxamniquine (20 mg/kg divided into
two doses in a single day) is also effective for S. man-
soni. Where it occurs, S. mansoni in children has devas-
tating long-term outcomes, and, in the authors’
opinion, the neglect of this childhood infection is a
major failure of global health in the 21st century as it
is currently highly treatable [37].
Bile duct flukes. Clonorchis sinensis and Opisthorchis
viverrini are important bile duct flukes in South-east
Asia which are associated with eating uncooked fish.
They cause jaundice and cholangiocarcinoma. Adult
flukes settle in the small intrahepatic bile ducts, and
then they live there for 20–30 years. The long-lived
flukes cause chronic inflammation of the bile ducts,
and this produces epithelial hyperplasia, periductal
fibrosis and bile duct dilation. These flukes should
be suspected in a patient from an endemic area and
may be detected by imaging [38]. Treatment is with
praziquantel 10 mg/kg three times daily for 2 days.
Fasciola hepatica. Fasciola hepatica, also known as
‘the common liver fluke’ or ‘the sheep liver fluke’,
causes fascioliasis. A related parasite, Fasciola gigan-
tica, can also infect humans. Fascioliasis is found in
over 50 countries in all five continents, especially
where sheep or cattle are reared. Humans are infected
by eating aquatic plants contaminated by animal
faeces. The immature larval flukes migrate through
the intestinal wall, the abdominal cavity, and the
liver tissue, into the bile ducts, where they develop
into mature adult flukes, which produce eggs. The
pathology typically is most pronounced in the bile
6 K. CHIFUNDA AND P. KELLY
ducts and liver. In the early (acute) phase, symptoms
can occur as a result of the parasite’s migration from
the intestine to and through the liver. Symptoms can
include gastro-intestinal symptoms such as nausea,
vomiting and abdominal pain/tenderness. Fever, rash
and difficulty with breathing may occur. During the
chronic phase (after the parasite settles in the bile
ducts), the clinical manifestations may be similar or
more discrete, reflecting inflammation and blockage
of bile ducts, which can be intermittent. Inflammation
of the liver, gallbladder and pancreas also can occur.
Treatment is with triclabendazole, two doses of
10 mg/kg separated by 12–24 h.
Major clinical syndromes
Diarrhoea. Diarrhoea is one of the most prominent
illnesses of childhood, which still causes millions of
deaths and loss of life years each year [39,40]. There
are multiple causes of diarrhoea in children in LMIC,
including viral, bacterial and protozoal infections
[7,8,41]. Among the parasitic infections in children,
cryptosporidiosis has been associated with the most
adverse outcomes, including persistent diarrhoea,
malnutrition and death [25]. While a great deal of
research on how best to diagnose and treat diarrhoeal
disease in children is currently ongoing, the mainstay
of treatment is oral rehydration therapy with zinc
using WHO protocols.
Failure to thrive. Any of the infections described in
this article may cause failure to thrive. This non-specific
clinical description encompasses a range of clinical
presentations from poor appetite to frank malnutrition.
Stunting (poor linear growth) is the most common
manifestation of poor nutrition around the world.
Recent estimates suggest that 30% of the world’s chil-
dren, some 170 million children, are stunted [42].
Stunting is associated with increased mortality in the
long term. Wasting (loss of weight) is seen in severe
acute malnutrition, which is less common but has a
higher mortality rate. Of the infections described in this
article, cryptosporidiosis is the most strongly asso-
ciated, and evidence from Guinea Bissau indicates
that cryptosporidiosis precedes malnutrition [21].
These relationships, however, are complex, with infec-
tion and malnutrition interacting in a vicious cycle [43].
Much work is currently ongoing to tease out the path-
ways of this interaction.
Anaemia. Anaemia may be caused by heavy hook-
worm infections. The impact of lighter infections is
controversial. Enthusiasts contend that mass deworm-
ing will have a major impact on the global prevalence
of anaemia in children, but the scientific evidence for
this appealing idea is not compelling [44,45]. A mas-
sive trial of mass deworming in India included in the
Cochrane review did not support this hypothesis and
the case for mass deworming remains unproven [44].
Haemorrhage from oesophageal varices. Bleeding
from oesophageal varices in children is unusual, but
it may occur in children living in areas where schisto-
somiasis with S. mansoni or S. japonicum is very com-
mon; S. mekongi and S. intercalatum can also cause
hepatosplenic schistosomiasis. The clinical picture of
schistosomiasis-related portal hypertension is charac-
teristic. Unlike oesophageal variceal bleeding owing
to cirrhosis, patients with schistosomiasis do not have
hepatocellular dysfunction: jaundice, encephalopathy
and coagulopathy are very unusual and transaminase
concentrations in blood are usually normal. The clin-
ical imperative is to replace blood volume loss and
stop the haemorrhage using endoscopic band ligation
if necessary. Treatment with β-adrenoceptor blockers
is very effective at preventing bleeding in the long
term. In LMIC, this is the most important therapeutic
measure and will usually be required lifelong unless
porto-systemic shunting therapies are available.
Neurocognitive impairment. The association between
gut infections and neurocognitive impairment has only
recently been recognised, and its strength is still
unclear as are the pathways which may mediate it. It
is likely, although not yet proven, that infection and
enteropathy drive inflammatory responses which lead
to anorexia and reduced nutrient intake, as well as
malabsorption and abnormal partitioning of nutrients
into different tissues. The next decade will see a clearer
understanding emerge of this important consequence
of intestinal parasitic infection.
Disclosure statement
No potential conflict of interest was reported by the
authors.
ORCID
Paul Kelly http://orcid.org/0000-0003-0844-6448
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