# 135 - 239 Intestinal Nematode Infections

### 239 Intestinal Nematode Infections

fish or poultry. Raw fish dishes, such as som fak in Thailand and 
sashimi in Japan, account for many cases of human gnathostomiasis. 
Some cases in Thailand result from the local practice of applying frog 
or snake flesh as a poultice.

Pathogenesis and Clinical Features 
Clinical symptoms are due 
to the aberrant migration of a single larva into cutaneous, visceral, 
neural, or ocular tissues. After invasion, larval migration may cause 
local inflammation, with pain, cough, or hematuria accompanied by 
fever and eosinophilia. Painful, itchy, migratory swellings may develop 
in the skin, particularly in the distal extremities or periorbital area. 
Cutaneous swellings usually last ~1 week but often recur intermit­
tently over many years. Larval invasion of the eye can provoke a sightthreatening inflammatory response. Invasion of the CNS results in 
eosinophilic meningitis with myeloencephalitis, a serious complication 
due to ascending larval migration along a large nerve tract. Patients 
characteristically present with agonizing radicular pain and paresthe­
sias in the trunk or a limb, which are followed shortly by paraplegia. 
Cerebral involvement, with focal hemorrhages and tissue destruction, 
is often fatal.
Diagnosis and Treatment 
Cutaneous migratory swellings with 
marked peripheral eosinophilia, supported by an appropriate geo­
graphic and dietary history, generally constitute an adequate basis 
for a clinical diagnosis of gnathostomiasis. However, patients may 
present with ocular or cerebrospinal involvement without anteced­
ent cutaneous swellings. In the latter case, eosinophilic pleocytosis 
is demonstrable (usually along with hemorrhagic or xanthochromic 
CSF), but worms are almost never recovered from CSF. Computed 
tomography or magnetic resonance imaging of the brain during neu­
ronal gnathostomiasis often demonstrates cerebral hemorrhage from 
the destructive migration of the parasite. Surgical removal of the 
parasite from subcutaneous or ocular tissue, though rarely feasible, 
is both diagnostic and therapeutic. Albendazole or ivermectin may 
be helpful, especially for cutaneous gnathostomiasis (Table 238-1). 
At present, cerebrospinal involvement is managed with supportive 
measures and generally with a course of glucocorticoids; the role 
of albendazole or ivermectin is uncertain and could be detrimental. 
Gnathostomiasis can be prevented by adequate cooking of fish and 
poultry in endemic areas.
PART 5
Infectious Diseases
■
■FURTHER READING
Auer H, Walochnik J: Toxocariasis and the clinical spectrum. Adv 
Parasitol 109:111, 2020.
Centers for Disease Control and Prevention: Surveillance for 
trichinellosis—United States, 2015, Annual Summary. Atlanta, GA: 
U.S. Department of Health and Human Services, CDC, 2017.
Clinical Subcommittee of the Hawaii Governor’s Joint 
Task Force on Rat Lungworm Disease. Preliminary guidelines 
for the diagnosis and treatment of human neuroangiostrongyli­
asis (rat lungworm disease) in Hawaii. https://health.hawaii.gov/docd/
files/2018/08/RLWD_Preliminary_Clinical_Guidelines_FINAL_082918.
pdf.  Accessed December 1, 2023.
Diaz JH et al: The disease ecology, epidemiology, clinical manifestations, 
and management of trichinellosis linked to consumption of wild animal 
meat. Wilderness Environ Med 31:235, 2020.
Lupi O et al: Mucocutaneous manifestations of helminth infections. 
Nematodes. J Am Acad Dermatol 73:929, 2015.
Martins YC et al: Central nervous system manifestations of 
Angiostrongylus cantonensis infection. Acta Trop 141:46, 2015.
Rostami A et al: Meat sources of infection for outbreaks of human 
trichinellosis. Food Microbiol 64:65, 2017.
Sitcar AD et al: Raccoon roundworm infection associated with cen­
tral nervous system disease and ocular disease—six states, 2013–2015. 
Morbid Mortal Wkly Rep 65:930, 2016.

David J. Diemert, Thomas B. Nutman

Intestinal Nematode 

Infections
More than one billion individuals worldwide are infected with one or 
more species of intestinal nematode. Table 239-1 summarizes biologic 
and common clinical features of infections due to the major intestinal 
parasitic nematodes. These parasites are most common in regions 
with inadequate sanitation and disposal of fecal waste, particularly in 
resource-limited countries in the tropics and subtropics, although they 
have also been seen with increasing frequency among immigrants and 
refugees to developed countries. Although intestinal nematode infec­
tions are not usually fatal, they contribute to malnutrition, impaired 
physical and cognitive development, and diminished work capacity. 
It is interesting that these helminth infections may protect some indi­
viduals from allergic diseases. Humans may on occasion be infected 
with nematode parasites that ordinarily infect animals; these zoonotic 
infections produce diseases such as trichostrongyliasis, anisakiasis, 
capillariasis, and abdominal angiostrongyliasis.
Intestinal nematodes are roundworms that range in length from 1 mm 
to many centimeters when mature (Table 239-1). Their life cycles are 
complex and highly varied; some species, including Strongyloides 
stercoralis and Enterobius vermicularis, can be transmitted directly 
from person to person, while others, such as Ascaris lumbricoides, 
Trichuris trichiura, and the hookworms, require a soil phase for devel­
opment. Because most helminth parasites cannot fully complete their 
life cycle within the same human host, heavy burdens of adult worms 
require repeated exposure to the parasite in its infectious stage, whether 
larva or egg. Hence, clinical disease, as opposed to asymptomatic (or 
subclinical) infection, generally develops only with repeated exposure 
and is typically related to infection intensity. In children with marginal 
nutritional status, intestinal helminth infections may impair growth 
and development. Eosinophilia and elevated serum IgE antibody levels 
are features of many helminth infections, the latter particularly when 
the helminth life cycle involves tissue migration such as A. lumbricoides, 
S. stercoralis, or the hookworms. Significant protective immunity to 
intestinal nematodes appears not to develop in humans.
■
■ASCARIASIS
A. lumbricoides is the largest intestinal nematode parasite of humans, 
reaching up to 40 cm in length. Most infected individuals have low worm 
burdens and are asymptomatic. Clinical disease arises from larval migra­
tion in the lungs or the effects of adult worms in the intestines.
Life Cycle 
Adult worms live in the lumen of the small intestine. 
Mature female Ascaris worms are extraordinarily fecund, each pro­
ducing over 200,000 eggs a day that are expelled within feces. Ascarid 
eggs, which are remarkably resistant to environmental stresses, become 
infective after several weeks of maturation in warm, moist soil and can 
remain infective for years. After infective eggs are swallowed, gastric 
acid dissolves their protective outer layer, releasing larvae into the 
intestine that invade the mucosa, migrate through the circulation to the 
lungs, penetrate into the alveoli, ascend the bronchial tree, and return—
through swallowing—to the small intestine, where they develop into 
adult worms. The time between initial infection and egg detection in the 
feces is typically between 2 and 3 months. Adult worms live for 1–2 years.
Epidemiology 
Ascaris is widely distributed in tropical and sub­
tropical regions as well as in other humid areas in more temperate 
regions of the world. Transmission typically occurs through fecally 
contaminated soil and is due either to inadequate treatment of sewage 
or to the use of human feces as fertilizer. With their propensity for 
poorer oral hygiene, younger children are most often affected. Infec­
tion outside endemic areas, though uncommon, can occur when eggs 
on transported produce are ingested.

TABLE 239-1  Major Human Intestinal Parasitic Nematodes
NECATOR AMERICANUS, 
ANCYLOSTOMA DUODENALE, 
ANCYLOSTOMA CEYLANICUM 
(HOOKWORM)
ASCARIS LUMBRICOIDES 
(ROUNDWORM)
FEATURE
Global prevalence in 
humans (millions)

Endemic areas
Hot, humid regions
Hot, humid regions
Hot and warm, humid regions
Hot, humid regions
Worldwide
Infective stage
Egg
Filariform larva
Filariform larva
Egg
Egg
Route of infection
Oral
Percutaneous
Percutaneous or 
autoinfective
Gastrointestinal location 
of worms
Small intestine
Jejunal mucosa
Small intestinal, mucosa
Cecum, colonic 
mucosa
Adult worm size
15–40 cm
7–13 mm
1–2 mm
30–50 mm
2–13 mm
Pulmonary passage of 
larvae
Yes
Yes
Yes
No
No
Incubation perioda (days)
60–75
40–100
25–30
70–90
35–45
Longevity
1 year
N. americanus: 2–5 years
A. duodenale: 6–8 years
A. ceylanicum: 6–8 yearsb
Fecundity (eggs/day/
worm)
240,000
N. americanus: 9000–10,000
A. duodenale: 10,000–28,000
A. ceylanicum: 5,000–15,000
Principal symptoms
Gastrointestinal symptoms; 
rarely, biliary obstruction 
or, in heavy infections, 
gastrointestinal obstruction
Iron-deficiency anemia in 
moderate and heavy infections
Diagnosis
Eggs in stool
Eggs in fresh stool, larvae in 
old stool
Treatment
Mebendazole
Albendazole
Ivermectin
Moxidectin
Pyrantel pamoate
Mebendazole
Albendazole
aTime from infection to egg production by mature female worm. bAssumed but no evidence base in humans.
Clinical Features 
During the lung phase of larval migration, 
~9–12 days after egg ingestion, patients may develop an irritating 
nonproductive cough and burning substernal discomfort that is 
aggravated by coughing or deep inspiration. Dyspnea and bloodtinged sputum are less common. Fever can occur. Eosinophilia 
develops during this symptomatic phase and subsides slowly over 
weeks. Chest imaging may reveal rounded infiltrates a few millime­
ters to several centimeters in size that are hallmarks of eosinophilic 
pneumonitis (Löffler’s syndrome). These infiltrates may be transient 
and intermittent, clearing after several weeks. Where there is sea­
sonal transmission of the parasite such as on the Arabian peninsula, 
seasonal pneumonitis with eosinophilia may develop in previously 
infected and sensitized hosts.
In light infections, adult worms in the small intestine usually cause 
no symptoms. In heavier infections, a large bolus of entangled worms 
can cause pain and small-bowel obstruction, sometimes complicated 
by perforation, intussusception, or volvulus. Obstruction is more com­
mon in children due to their having intestinal lumens of narrow diam­
eter. Single worms may cause disease when they migrate into aberrant 
sites. A large worm can enter and occlude the biliary tree, causing bili­
ary colic, cholecystitis, cholangitis, pancreatitis, or (rarely) intrahepatic 
abscesses. Migration of an adult worm up the esophagus can provoke 
coughing or vomiting up the worm. In highly endemic areas, intestinal 
and biliary ascariasis can rival acute appendicitis as a cause of surgical 
acute abdomen.
Laboratory Findings 
Most cases of ascariasis can be diagnosed 
by microscopic detection of characteristic Ascaris eggs (65 × 45 μm) in 

PARASITIC NEMATODE
TRICHURIS 
TRICHIURA 
(WHIPWORM)
ENTEROBIUS 
VERMICULARIS 
(PINWORM)
STRONGYLOIDES 
STERCORALIS
Oral
Oral
Cecum, appendix
Decades (due to 
autoinfection)
5 years
2 months
5000–10,000
3000–7000
2000–10,000
Gastrointestinal symptoms; 
malabsorption or sepsis in 
hyperinfection
Gastrointestinal 
symptoms, rectal 
prolapse, or anemia 
in heavy infection
Perianal pruritus
CHAPTER 239
Larvae in stool or duodenal 
aspirate; sputum in 
hyperinfection; serology
Eggs in stool
Eggs from perianal 
skin on cellulose 
acetate tape
Ivermectin
Albendazole
Mebendazole
Albendazole
Ivermectin 
Mebendazole
Albendazole
Pyrantel pamoate
Intestinal Nematode Infections 
fecal samples, although increasingly, polymerase chain reaction (PCR) 
of worm DNA extracted from stool is being used in research and some 
clinical settings. Occasionally, patients present after passing an adult 
worm—identifiable by its large size and smooth cream-colored surface—
in the stool or, much less commonly, through the mouth or nose. 
During the early transpulmonary migratory phase, when eosinophilic 
pneumonitis occurs, larvae can be found in sputum or gastric aspirates 
before diagnostic eggs appear in the stool. The eosinophilia that is 
prominent during this early stage usually decreases to minimal levels 
in established infection. Adult worms may be visualized, occasionally 
serendipitously, on contrast radiographic studies of the gastrointestinal 
tract. A plain abdominal film may reveal masses of worms in gas-filled 
loops of bowel in patients with intestinal obstruction. Pancreaticobili­
ary worms can be detected by ultrasound and endoscopic retrograde 
cholangiopancreatography; the latter method has been used to extract 
biliary Ascaris worms.
TREATMENT
Ascariasis
Ascariasis should always be treated to prevent potentially serious 
complications. Albendazole (400 mg once), mebendazole (100 mg 
twice daily for 3 days or 500 mg once), pyrantel pamoate (11 mg/kg 
once with a maximum dose not to exceed 1 g), ivermectin (150–200 
μg/kg once), and moxidectin (8 mg once) are effective. These medi­
cations are contraindicated in pregnancy, however. Mild diarrhea 
and abdominal pain are uncommon side effects of these agents.

Partial intestinal obstruction should be managed with nasogastric 
suction, IV fluid administration, and instillation of piperazine 
through the nasogastric tube, although complete obstruction and 
its severe complications require immediate surgical intervention.

■
■HOOKWORM
Three species (Necator americanus, Ancylostoma duodenale, and 
Ancylostoma ceylanicum) are responsible for most human hookworm 
infections. Most infected individuals are asymptomatic. Hookworm 
disease develops from a combination of factors—heavy worm burden, 
prolonged duration of infection, and inadequate iron intake—and 
results in iron-deficiency anemia and, on occasion, hypoproteinemia.
Life Cycle 
Adult hookworms, which are ~1 cm long, use buccal 
teeth (Ancylostoma) or cutting plates (Necator) to attach to the smallbowel mucosa where they secrete enzymes that enable them to invade 
submucosal tissues and ingest blood and villous tissue. Female adult 
hookworms produce thousands of eggs daily. The eggs are deposited 
with feces in soil, where rhabditiform larvae hatch and develop over 
a 1-week period into infectious filariform larvae. Infective larvae pen­
etrate the skin and reach the lungs by way of the bloodstream. There 
they invade alveoli and ascend the airways to the larynx before being 
swallowed and reaching the small intestine. The prepatent period from 
skin penetration to appearance of eggs in the feces is ~6–8 weeks, but 
it may be longer with Ancylostoma spp. Less commonly, larvae of Ancy­
lostoma spp., if swallowed orally, can survive and develop directly into 
adult worms that parasitize the intestinal mucosa. Adult hookworms 
may survive over a decade but usually live ~6–8 years for A. duodenale 
and 2–5 years for N. americanus.
PART 5
Infectious Diseases
Epidemiology 
Over 400 million people are infected with hook­
worms worldwide. Whereas N. americanus is the predominant spe­
cies throughout the tropics and subtropics, A. duodenale is more 
geographically restricted to areas of North Africa and northern Asia. 
A. ceylanicum is much less common than the other two species and is 
mainly found in Southeast Asia. Age prevalence studies have shown 
a constant increase in hookworm prevalence throughout childhood 
and into adulthood. Older children have the greatest intensity of 
hookworm infection; however, in rural areas where fields are fertil­
ized with human feces, older working adults also may be heavily 
infected.
Clinical Features 
Most hookworm infections are of light intensity 
and therefore are clinically asymptomatic. Infective larvae may pro­
voke a pruritic maculopapular rash (“ground itch”) at the site of skin 
penetration as well as serpiginous tracks of subcutaneous migration 
(similar to those of cutaneous larva migrans; Chap. 238) in previously 
sensitized hosts. Larvae migrating through the lungs occasionally 
cause mild transient pneumonitis, but this condition develops less 
frequently in hookworm infection than in ascariasis. In the early intes­
tinal phase, infected persons may develop epigastric pain, abdominal 
bloating, and other abdominal symptoms accompanied by eosino­
philia. The major consequence of chronic hookworm infection is iron 
deficiency. Symptoms are minimal if iron stores are adequate, but 
undernourished individuals develop symptoms of progressive irondeficiency anemia and hypoproteinemia, including fatigue, weakness, 
and shortness of breath.
Laboratory Findings 
The diagnosis is established by the finding 
of characteristic 40 × 60 μm oval hookworm eggs in the feces. Stool 
concentration techniques may be required to detect light infections. 
Eggs of the three species are indistinguishable by light microscopy, 
whereas PCR provides significant improvement in species-specific 
diagnosis, although this remains a research tool that is not available in 
commercial laboratories. In a stool sample that is not fresh, hookworm 
eggs may have hatched to release rhabditiform larvae, which must be 
differentiated from those of S. stercoralis. Hypochromic microcytic 
anemia, occasionally with eosinophilia or hypoalbuminemia, is char­
acteristic of hookworm disease.

TREATMENT
Hookworm Infection
Hookworm infection can be treated with several safe and effective 
anthelmintic drugs, including albendazole (400 mg once daily for 

3 days) and mebendazole (500 mg once daily or 100 mg twice daily 
for 3 days). Mild iron-deficiency anemia can often be treated with 
oral iron supplementation alone. Severe hookworm disease with 
protein loss and malabsorption necessitates nutritional support and 
oral iron replacement along with deworming. There is significant 
concern that the benzimidazoles (mebendazole and albendazole) 
are becoming much less effective against human hookworms.
Ancylostoma caninum and Ancylostoma braziliense 
A. caninum, 
the canine hookworm, has been identified as a cause of human eosino­
philic enteritis, especially in northeastern Australia. In this rare zoo­
notic infection, adult hookworms attach to the small intestine (where 
they may be visualized by endoscopy) and elicit abdominal pain and 
intense local eosinophilia. Treatment with mebendazole (100 mg twice 
daily for 3 days) or albendazole (400 mg once) or endoscopic removal 
is effective. Both of these animal hookworm species can cause cutane­
ous larva migrans (“creeping eruption”; Chap. 238).
■
■STRONGYLOIDIASIS
S. stercoralis is distinguished by its ability—unique among helminths 
(except for Capillaria; see below)—to complete its life cycle and repli­
cate within a human host. This capacity permits ongoing cycles of auto­
infection as infective larvae are internally produced that can develop 
into egg-producing adult worms without exiting the host. Infection 
with S. stercoralis can thus persist for decades without further exposure 
to exogenous infective larvae. In immunocompromised hosts, large 
numbers of invasive Strongyloides larvae can disseminate widely and 
can be fatal.
Life Cycle 
In addition to a parasitic life cycle in the human host, 
Strongyloides can undergo a free-living cycle of development in the 
soil (Fig. 239-1). This adaptability facilitates the parasite’s survival in 
the absence of mammalian hosts. Rhabditiform larvae passed in feces 
can transform into infectious filariform larvae either directly or after a 
free-living phase of development. Humans acquire S. stercoralis when 
filariform larvae in fecally contaminated soil penetrate the skin or 
mucous membranes. The larvae then travel through the bloodstream 
to the lungs, where they break into the alveolar spaces, ascend the 
bronchial tree, are swallowed, and thereby reach the small intestine. 
There the larvae mature into adult worms that embed in the mucosa 
of the proximal small bowel. The minute (1- to 2-mm long) parasitic 
adult female worms reproduce by parthenogenesis; adult males do not 
exist in the human host. Eggs hatch in the intestinal mucosa, releasing 
rhabditiform larvae that migrate to the lumen and pass with the feces 
into soil. Alternatively, rhabditiform larvae in the bowel can develop 
directly into filariform larvae that penetrate the colonic wall or perianal 
skin and enter the circulation to repeat the migration that establishes 
ongoing internal reinfection.
Epidemiology 
S. stercoralis is spottily distributed in tropical areas 
and other warm, humid regions and is common in Southeast Asia, subSaharan Africa, and Brazil. In the United States, the parasite is endemic 
in parts of the Southeast and is found in immigrants, refugees, travel­
ers, and military personnel who have lived in endemic areas.
Clinical Features 
In uncomplicated strongyloidiasis, many 
patients are asymptomatic or have mild cutaneous and/or abdominal 
symptoms. Recurrent urticaria, often involving the buttocks, is the 
most common cutaneous manifestation. Larvae migrating in the skin 
can elicit a pathognomonic serpiginous eruption known as larva cur­
rens. This pruritic, raised, erythematous lesion advances as rapidly as 
10 cm/h along the course of larval migration. Adult parasites burrow 
into the duodenojejunal mucosa and can cause abdominal (usually 
midepigastric) pain, which resembles peptic ulcer disease except that

Larvae migrate via
bloodstream or lymphatics
to lungs, ascend airway 
to trachea and pharynx,
and are swallowed.
Hyperinfection:
With immunosuppression, larger
numbers of filariform larvae develop,
penetrate bowel, and disseminate,
causing:
Filariform
larvae (450 µm)
Rhabditiform larvae
in soil
FIGURE 239-1  Life cycle of Strongyloides stercoralis. (Reproduced with permission from RL Guerrant et al [eds]: Tropical Infectious Diseases: Principles, Pathogens and 
Practice, 2nd ed. Elsevier, 2006.)
it is aggravated by food ingestion. Nausea, watery diarrhea, abdominal 
bloating, occult gastrointestinal bleeding, and weight loss can occur. 
Small-bowel obstruction may develop with early, heavy infection. Pul­
monary symptoms are rare in uncomplicated strongyloidiasis. Eosino­
philia is common, with levels fluctuating over time.
The ongoing autoinfection cycle of S. stercoralis is normally con­
strained by the host’s immune system. Impairment of host cellmediated immunity, especially with high-dose glucocorticoid therapy 
and less commonly with other immunosuppressive medications, or 
associated with infection with human T-cell lymphotropic virus type 1 
(HTLV-1), may lead to hyperinfection and the generation of large 
numbers of filariform larvae. Colitis, enteritis, or malabsorption may 
develop. Hyperinfection can also lead to disseminated strongyloidiasis, 
characterized by larvae invading not only gastrointestinal tissues and 
the lungs but also the central nervous system, skin, peritoneum, liver, 
and kidneys. Moreover, bacteremia may develop because of the spread 
of enteric flora through disrupted mucosal barriers. Gram-negative sepsis, 
pneumonia, or meningitis may complicate or dominate the clinical 
course. Eosinophilia is often absent in severely infected patients. Dis­
seminated strongyloidiasis, particularly in patients with unsuspected 
infection who are taking glucocorticoids, has a high mortality rate.
Diagnosis 
In uncomplicated strongyloidiasis, visualizing rhab­
ditiform larvae by light microscopic examination of a fecal sample is 
diagnostic. Rhabditiform larvae are ~250 μm long, with a short buccal 
cavity that distinguishes them from hookworm larvae. In uncom­
plicated infections, few larvae are passed and single stool examina­
tions detect only about one-third of cases. Serial examinations and 
the use of the agar plate detection method improve the sensitivity of 
stool diagnosis. Again, PCR has begun to be used more widely and 
provides increased diagnostic sensitivity. In hyperinfection, a single 

2-mm hermaphroditic
adult    s
penetrate small-bowel
mucosa and release eggs,
which hatch to
rhabditiform larvae.
Lung or intestinal stage may cause:
Eosinophilia and
intermittent
epigastric pain
Autoinfection:
Transform within the intestine
into filariform larvae, which
penetrate perianal skin
or bowel mucosa,
causing:
Rhabditiform
larvae (250 µm)
Pruritic larva currens
Eosinophilia
Larvae shed in stool
Colitis, polymicrobial sepsis,
pneumonitis, or meningitis
Free-living
1-mm adults
in soil
CHAPTER 239
Direct development
Eggs in soil
Indirect development
(heterogonic)
(can multiply outside host
for several generations) in soil
Intestinal Nematode Infections 
microscopy-based stool examination is usually positive given the large 
number of larvae being produced. Strongyloides larvae may also be 
found by sampling of the duodenojejunal contents by aspiration or 
biopsy. An enzyme-linked immunosorbent assay for serum antibod­
ies to antigens of Strongyloides is a sensitive method for diagnosing 
uncomplicated infections. Such serologic testing should be performed 
for patients with prior potential exposure, especially those with eosino­
philia and/or those who may be starting glucocorticoid therapy or 
undergoing solid organ transplantation. In disseminated strongyloi­
diasis, filariform larvae are easily detected in stool as well as in samples 
obtained from sites of potential larval migration, including sputum, 
bronchoalveolar lavage fluid, or surgical drainage fluid.
TREATMENT
Strongyloidiasis
Even in the asymptomatic state, strongyloidiasis must be treated 
because of the potential for subsequent hyperinfection and fatal 
dissemination. Ivermectin (200 μg/kg daily for 2 days) is more 
effective than albendazole (400 mg daily for 3 days). Decreases in 
eosinophil count and antibody titer indicate a response to treat­
ment. For disseminated strongyloidiasis, treatment with ivermectin 
should be extended for at least 14 days after fecal examinations 
have become negative. In potentially immunocompromised hosts, 
the course of ivermectin should be repeated 2 weeks after initial 
treatment. Ivermectin has been successfully given per rectum in 
those unable to take ivermectin orally and can be given parenterally 
(using veterinary preparations) through single-patient expanded 
access protocols.

■
■TRICHURIASIS
Most infections with Trichuris trichiura are asymptomatic, but heavy 
infections may cause gastrointestinal symptoms. Like the other soiltransmitted helminths, whipworm is distributed globally in the trop­
ics and subtropics and is most common among poor children from 
resource-limited regions of the world.

Life Cycle 
Adult Trichuris worms reside in the colon and cecum, 
their thin anterior portions embedded in the superficial mucosa. 
Thousands of eggs laid daily by adult female worms pass with the 
feces and mature in the soil. After ingestion, infective eggs hatch in the 
duodenum, releasing larvae that mature before migrating to the large 
bowel. The entire cycle takes ~3 months, and adult worms may live for 
several years.
Clinical Features 
Most individuals infected with T. trichiura have 
no symptoms or eosinophilia. Heavy infections may result in anemia, 
abdominal pain, anorexia, and bloody or mucoid diarrhea resembling 
inflammatory bowel disease. Rectal prolapse can result from massive 
infections in children due to protracted tenesmus. Moderately heavy T. 
trichiura burdens also contribute to impaired physical growth.
Diagnosis and Treatment 
The characteristic 50 × 20 μm lemonshaped T. trichiura eggs are readily detected on microscopic examina­
tion of stool. Adult worms, which are 3–5 cm long, are occasionally 
seen on proctoscopy. PCR is being used increasingly in settings where 
it is available. Albendazole (400 mg daily for 3 days) or mebendazole 
(100 mg twice daily for 3 days) is safe and moderately effective for 
treatment. The addition of ivermectin (200 μg/kg daily for 3 doses) to 
either benzimidazole drug increases cure rates significantly.
PART 5
Infectious Diseases
■
■ENTEROBIASIS (PINWORM)
E. vermicularis is more common in temperate climates than in the 
tropics. In the United States, ~40 million persons are infected with 
pinworms, with most cases occurring in children.
Life Cycle and Epidemiology 
Adult Enterobius worms are 
~5–10 mm long and dwell in the cecum. Gravid female worms migrate 
nocturnally out of the anus to the perianal region where they release up 
to 10,000 immature eggs each. The eggs become infective within hours 
and are transmitted by hand-to-mouth passage. From ingested eggs, 
larvae hatch and mature into adults. This life cycle takes ~1 month, 
and adult worms survive for ~2 months. Autoinfection results from 
perianal scratching and transport of infective eggs on the fingers or 
under the nails to the mouth. Retroinfection can also occur by larvae 
released from embryonated eggs on the perianal skin migrating back 
into the rectum. Because of the ease of person-to-person spread, pin­
worm infections are common among family members.
Clinical Features 
Most pinworm infections are asymptomatic. 
Perianal pruritus is the cardinal symptom. The itching, which is often 
worse at night as a result of the nocturnal emergence of female worms, 
may lead to excoriation and bacterial superinfection. Heavy infections 
have been associated with abdominal pain, weight loss, and rarely acute 
appendicitis. Uncommonly, pinworms may migrate into the female 
genital tract, causing vulvovaginitis and pelvic or peritoneal granulo­
mas. Eosinophilia is uncommon.
Diagnosis 
Since pinworm eggs are not released in feces, the diagno­
sis cannot be made by conventional fecal ova and parasite microscopy. 
Instead, eggs are detected by the application of clear cellulose acetate 
tape to the perianal region in the morning. After the tape is transferred 
to a slide, microscopic examination can detect pinworm eggs, which 
are oval, measure 55 × 25 μm, and are flattened along one side.
TREATMENT
Enterobiasis
Infected children and adults should be treated with mebendazole 
(100 mg once), albendazole (400 mg once), or pyrantel pamoate 

(11 mg/kg once), with the same treatment repeated after 2 weeks 
because the drugs do not kill eggs or early-stage larvae. Treatment 
of household members is recommended to eliminate asymptomatic 
reservoirs of potential reinfection. Linens and clothing should be 
washed in hot water followed by a hot dryer to kill deposited eggs.
■
■TRICHOSTRONGYLIASIS
Trichostrongylus species, which are normally parasites of herbivorous 
animals, occasionally infect humans, particularly in Asia, Africa, and 
Australia. Humans acquire the infection by accidentally ingesting 
Trichostrongylus larvae on contaminated leafy vegetables. The larvae 
do not migrate in humans but mature directly into adult worms in 
the small bowel. The pathology caused by these worms is similar to 
hookworm, although they ingest far less blood. Most infected persons 
are asymptomatic, but heavy infections may give rise to mild anemia 
and eosinophilia. In stool examinations, Trichostrongylus eggs resemble 
hookworm eggs but are larger (85 × 115 μm). Treatment consists of 
mebendazole, albendazole, or pyrantel pamoate (Chap. 229).
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■ANISAKIASIS
Anisakiasis is a gastrointestinal infection caused by the accidental 
ingestion in uncooked saltwater fish of nematode larvae belonging 
to the family Anisakidae. The incidence of anisakiasis in the United 
States has increased as a result of the growing popularity of raw fish 
dishes. Most cases occur in Japan, the Netherlands, and Chile, where 
raw fish—sashimi, pickled green herring, and ceviche, respectively—
are national culinary staples. Anisakid nematodes parasitize large sea 
mammals such as whales, dolphins, and seals. As part of a complex 
parasitic life cycle involving marine food chains, infectious larvae 
migrate to the musculature of a variety of fish species that serve as 
intermediate hosts. Both Anisakis simplex and Pseudoterranova 
decipiens have been implicated in human anisakiasis, but an identi­
cal gastric syndrome may be caused by the red larvae of eustrongylid 
parasites of fish-eating birds.
When humans consume infected raw or undercooked fish, live 
larvae may be coughed up within 48 h. Alternatively, larvae may 
immediately penetrate the mucosa of the stomach. Within hours, vio­
lent upper abdominal pain accompanied by nausea and occasionally 
vomiting ensues, mimicking an acute abdomen. The diagnosis can be 
established by direct visualization on upper endoscopy, outlining of 
the worm by contrast radiographic studies, or histopathologic exami­
nation of extracted tissue. Extraction of the burrowing larvae during 
endoscopy is curative. In addition, larvae may pass to the small bowel, 
where they penetrate the mucosa and provoke a vigorous eosinophilic 
granulomatous response. Symptoms may appear 1–2 weeks after the 
infective meal, with intermittent abdominal pain, diarrhea, nausea, 
and fever resembling the manifestations of Crohn’s disease. Ingestion 
of Anisakis-derived proteins through consumption of fish meat con­
taining Anisakis parasites can elicit allergic gastrointestinal and even 
anaphylactic responses.
Anisakid eggs are not found in the stool since the larvae do not 
mature in humans. Serologic tests have been developed but are not 
widely available.
Anisakid larvae in saltwater fish are killed by cooking to 60°C, freez­
ing at –20°C for 3 days, or commercial blast freezing, but usually not by 
salting, marinating, or cold smoking. No medical treatment is available; 
surgical or endoscopic removal should be undertaken.
■
■CAPILLARIASIS
Intestinal capillariasis is caused by ingestion of raw fish infected 
with Capillaria philippinensis. Subsequent autoinfection can lead to 
a severe wasting syndrome. The disease occurs in the Philippines 
and Thailand and, on occasion, elsewhere in Asia. The natural life 
cycle of C. philippinensis involves fish from fresh and brackish water. 
When humans eat infected raw fish, the larvae mature in the intestine 
into adult worms, which produce invasive larvae that cause intestinal 
inflammation and villus loss and can develop into new adult worms 
without leaving the human host. Capillariasis has an insidious onset