# 122 - 228 Introduction to Parasitic Infections

### 228 Introduction to Parasitic Infections

appear to be particularly susceptible to PCP. The glucocorticoid 
exposure threshold that warrants chemoprophylaxis is ill-defined, 
but such preventive therapy should be strongly considered for any 
patient who is receiving more than the equivalent of 20 mg of pred­
nisone daily for 30 days or who is receiving glucocorticoids in con­
junction with other immunosuppressive agents. Clinical experience 
also suggests that chemoprophylaxis is useful for patients receiving 
certain immunosuppressive agents (e.g., tumor necrosis factor inhibi­
tors, antithymocyte globulin, rituximab, and alemtuzumab). The 
duration of such chemoprophylaxis is empirically estimated based on 
prior clinical experience and immunologic factors that would plausi­
bly relate to immunity, such as CD4+ T-cell counts, recognizing that 
such estimates are not precise.
TMP-SMX is the most effective prophylactic drug; few patients 
experience a PCP breakthrough when they are reliably taking a recom­
mended TMP-SMX chemoprophylactic regimen. Several TMP-SMX 
regimens have been used successfully. Regimens of one single-strength 
or double-strength tablet daily are the regimens with which there is 
the most experience, but one double-strength tablet two or three times 
weekly also has been recommended for various PLWH and non-HIVinfected populations of patients.
For patients who cannot tolerate TMP-SMX (usually because 
of hypersensitivity or bone marrow suppression), alternative drugs 
include daily dapsone, weekly dapsone-pyrimethamine, atovaquone, 
and monthly aerosol pentamidine. Patients who develop hypersensi­
tivity to TMP-SMX can sometimes tolerate the drug if a gradual doseescalation protocol is used. Atovaquone is effective and well tolerated; 
however, this drug is available only as an oral preparation, and gastro­
intestinal absorption is unpredictable in patients with abnormal gas­
trointestinal motility or function. Aerosolized pentamidine is effective, 
but it is not as effective as TMP-SMX and may not provide protection 
in areas of the lung that are not well-ventilated. Dapsone cross-reacts 
with sulfonamides in a substantial fraction of patients and is rarely use­
ful in patients with a history of life-threatening reactions to TMP-SMX.
■
■FURTHER READING
Buchacz K et al: Incidence of AIDS-defining opportunistic infections 
in a multicohort analysis of HIV-infected persons in the United States 
and Canada, 2000–2010. J Infect Dis 214:862, 2016.
Del Corpo O et al: Diagnostic accuracy of serum (1-3)-β-D-glucan 
for Pneumocystis jirovecii pneumonia: A systematic review and metaanalysis. Clin Microbiol Infect 26:1137, 2020.
Lécuyer R et al: Characteristics and prognosis factors of Pneumocystis 
jirovecii pneumonia according to underlying disease. Chest 165:1319, 
2024.
Le Gal S et al: Pneumocystis infection outbreaks in organ trans­
plantation units in France: A nation-wide survey. Clin Infect Dis 
70:2216, 2020.
Ma L et al: Genome analysis of three Pneumocystis species reveals 
adaptation mechanisms to life exclusively in mammalian hosts. Nat 
Commun 7:10740, 2016.
Panel on Opportunistic Infections in HIV-Infected Adults 
and Adolescents: Guidelines for the prevention and treatment 
of opportunistic infections in HIV-infected adults and adoles­
cents: Recommendations from the Centers for Disease Control and 
Prevention, the National Institutes of Health, and the HIV Medi­
cine Association of the Infectious Diseases Society of America. 
Available at https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinicalguidelines-adult-and-adolescent-opportunistic-infections/pneumocystis0?view=full.  Accessed December 21, 2024.
Wills NK et al: The prevalence of laboratory-confirmed Pneumocystis 
jirovecii in HIV-infected adults in Africa: A systematic review and 
meta-analysis. Med Mycol 59:802, 2021.
Zolopa A et al: Early antiretroviral therapy reduces AIDS progression/
death in individuals with acute opportunistic infections: A multicenter 
randomized strategy trial. PLoS One 4:e5575, 2009.

Section 17	Protozoal and Helminthic 
Infections: General Considerations
Sharon L. Reed, Charles E. Davis

Introduction to 

Parasitic Infections
The word parasite comes originally from the Greek parasitos (para, 
alongside of; and sitos, food), meaning someone who eats at another’s 
table or lives at another’s expense. Although the same is true of many 
bacteria and viruses, the designation parasite is reserved, by conven­
tion, for helminths and protozoa. These organisms are larger and more 
complex than bacteria, with a eukaryotic cell structure similar to that 
of human host cells. Historically, this similarity has made it difficult to find 
effective antiparasitic agents that do not cause unacceptable toxicity to 
human cells. Fortunately, intensive research and modern techniques 
have now provided suitable agents for safe and effective treatment of 
most parasitic infections. See Chap. S12 for details on diagnostic 
procedures and Chap. 229 for details on treatment.
Internal parasites of human beings are divided into two types: hel­
minths (worms) and protozoa. Helminths are multicellular organisms 
that can often be seen with the naked eye (Chap. 237). There are two 
phyla: Platyhelminthes (flat worms) and Nemathelminthes (round­
worms). Both phyla include some genera that mature in the gastroin­
testinal tract and others that migrate through the tissue after ingestion 
or skin penetration. Tables S12-1 and S12-2 present the helminthic 
genera, their definitive and intermediate hosts, their geographic distri­
butions, and the parasitic stages in the human body.
CHAPTER 228
Introduction to Parasitic Infections 
The key to understanding which helminths use humans as defini­
tive hosts is to remember that helminth ova develop into larvae, and 
larval stages develop into adults. Humans serve as the definitive host 
when they ingest helminth larvae, which develop into adults in the 
intestine and usually cause mild disease, often without any symptoms. 
(The exception is ingestion of the late-stage larvae of the somatic or 
tissue flukes, as shown in Table S12-1.) In contrast, if humans ingest 
helminth ova and serve as the intermediate host, the ova develop into 
larvae, which penetrate the intestine, migrate through the tissue, and 
invade organs where they mature into adults. Intermediate hosts with 
parasitic invasion of organs may experience severe disease.
Protozoa are microscopic single-celled organisms. Among the many 
differences between helminths and protozoans, the most important 
is the ability of protozoa (like bacteria) to multiply within the human 
body and cause overwhelming infections. A major mechanism pro­
moting unrestrained growth is evasion of the host immune response 
either by antigenic variation (Trypanosoma brucei) or by survival inside 
host cells (e.g., Plasmodium, Babesia, Cryptosporidium, Leishmania, 
and Toxoplasma). In contrast, almost all helminths require stages 
in other hosts to complete their life cycles and multiply. As a result, 
except for Strongyloides and Capillaria, which can complete their life 
cycle in humans, increases in the burden of infection with helminths 
require repeated exogenous reinfections. Thus, permanent residents of 
endemic countries, who are exposed repeatedly, may have heavy severe 
infections, while most travelers with one or two exposures are unlikely 
to experience the full spectrum of chronic helminthic infections.
In contrast to helminthic infections, naïve patients with their first 
protozoal infection usually are the most severely affected because 
partial immunity often limits the number of parasites during recurrent 
infections. Protozoan replication to large numbers in the host also pro­
motes the development of drug-resistant forms, especially in malaria 
(Chap. 229). Because protozoa belong to many different phyla, it is 
easier to understand the pathogenesis and management of protozoal 
infections when they are classified by the site of infection (intestinal 
protozoans, free-living amebae, and blood and tissue protozoans)

(Table S12-3). Immunocompromised hosts are at risk of disseminated 
infection with several protozoa, including Leishmania, Toxoplasma, 
Cryptosporidium, and Trypanosoma cruzi, which are AIDS-defining 
illnesses. Among the helminths, Strongyloides can disseminate in 
immunocompromised individuals.

HELMINTHIC INFECTIONS
The Platyhelminthes (flatworms) are categorized as tapeworms (ces­
todes) and flukes (trematodes). Tapeworms are composed of a head or 
scolex bearing the holdfast organs and segments, which become gravid 
as they mature. Some tapeworms can reach lengths of many yards; the 
longest tapeworms develop in the intestine, where they rarely cause 
serious disease. In contrast, flukes are small leaf-shaped organisms 
whose size is not a measure of disease severity.
■
■FLATWORMS
Cestodes 
Tapeworms cause either intestinal or somatic infection, 
depending on the species. Intestinal infections occur when the human 
host ingests larvae in the tissue of the intermediate host, whereas 
somatic infections occur when humans accidentally ingest ova excreted 
from the wild or domesticated definitive animal host.
INTESTINAL TAPEWORMS  As shown in Table S12-1, humans acquire 
most intestinal tapeworms by eating the insufficiently cooked flesh of 
the intermediate host. Thus, Taenia saginata is commonly called the 
beef tapeworm, Taenia solium the pork tapeworm, and Diphylloboth­
rium latum the fish tapeworm. Hymenolepis nana is capable of com­
pleting its life cycle in the human intestine and is acquired by ingestion 
of infected grain beetles or of ova from infected humans or mice. None 
of these parasites causes significant damage, and infection is usually 
asymptomatic. There are two occasional exceptions. When people 
ingest T. solium ova from their own intestine or from another infected 
individual, it can cause somatic infection. D. latum avidly absorbs 
vitamin B12 in the intestine and can cause pernicious anemia in 1–2% 
of infected Scandinavians with a genetic predisposition.
PART 5
Infectious Diseases
SOMATIC TAPEWORMS  There are three major causes of somatic tape­
worm infections. Two species of Echinococcus cause echinococcosis. 

E. granulosus is acquired by accidental ingestion of ova from dogs 
infected when fed the infected tissues of sheep or other animals by 
sheepherders or hunters. E. multilocularis is transmitted primarily in 
sub-Arctic areas when humans ingest ova from foxes, dogs, or cats 
that have been infected through consumption of the tissues of infected 
rodents. Both species cause hydatid cysts when the eggs hatch into lar­
vae, penetrate the intestine, and migrate into the liver or lung. Ingested 
T. solium ova cause somatic disease (cysticercosis) when the larvae 
penetrate the intestine, migrate into tissue, and form cysts (cysterci), 
usually in the muscles or central nervous system (CNS).
Trematodes 
Flukes also cause both intestinal and somatic infections 
(Chap. 241 and Table S12-1). Most fluke infections are localized to Asia, 
Africa, Southeast Asia, or the Pacific islands. Infection with intestinal 
flukes is usually asymptomatic, although heavy infections sometimes 
cause abdominal discomfort and mucous diarrhea. Liver flukes and 
lung flukes cause somatic infections when humans ingest a larval form 
from an intermediate host. Adults develop in the intestine, migrate into 
adjacent tissues, and cause disease. The major liver flukes (Clonorchis 
sinensis, Opisthorchis spp., and Fasciola hepatica) are causes of recurrent 
bacterial cholangitis (due to obstruction) or portal hypertension and cir­
rhosis. Only F. hepatica can be acquired worldwide; it is especially com­
mon in sheep-raising areas, where the animals ingest water plants (e.g., 
watercress). The lung flukes (Paragonimus spp.) occur globally except 
in Europe; most lesions occur as pulmonary cysts, although occasional 
lesions develop in the CNS or the abdominal cavity.
The blood flukes cause schistosomiasis, one of the most common 
and serious parasitic infections (Chap. 241 and Table S12-1). The 
major species are Schistosoma mansoni, S. haematobium, and S. japonicum. 
All are transmitted to humans when free-swimming larvae exit an 
infected snail in freshwater and penetrate the skin. Swimmer’s itch 
sometimes follows skin penetration but is usually of short duration. 

The larvae then wander in the skin until they find a blood vessel and 
migrate to the target organ. S. mansoni and S. japonicum migrate 
to the mesentery vessels and eventually make their way to the liver, 
while S. haematobium targets the veins around the ureter and blad­
der. Extensive egg deposition by S. mansoni and S. japonicum and the 
immune reactions to the ova cause granuloma formation and, with 
many repeated exposures, portal vein obstruction and cirrhosis. The 
same process in the ureters and bladders during infection with S. hae­
matobium eventually interferes with urine flow and leads to repeated 
urinary tract infections and kidney damage.
■
■ROUNDWORMS
Nematodes 
Roundworms are nonsegmented bisexual organisms. 
The species that infect humans include intestinal and tissue groups. 
Humans may also acquire certain nonhuman mammalian round­
worms that either can be limited to the skin or can migrate to tissues 
and cause serious disease (the larva migrans syndromes).
INTESTINAL ROUNDWORMS  The major intestinal roundworms are 
Ascaris lumbricoides, Necator americanus (New World hookworms), 
Ancylostoma duodenale (Old World hookworms), Trichuris trichiura 
(whipworms), Enterobius vermicularis (pinworms), and Strongyloides 
stercoralis. Taken together, infections caused by intestinal roundworms 
are the most common infections in the world. Ascaris, hookworms, 
and Trichuris infect about 900 million individuals, and at least 100–370 
million have strongyloidiasis. These infections are most common in 
resource-poor developing countries, especially where people defecate 
outside and/or human feces is used as fertilizer (“night soil”). Infection 
is transmitted either by ingestion of ova (A. lumbricoides, T. trichiura, 
and E. vermicularis) or by active penetration of the skin by larvae 
(hookworms and S. stercoralis) (Table S12-2).
Intestinal roundworms cause serious health problems in residents 
of endemic regions with poor sanitation, but travelers are at low risk of 
developing significant disease from most of these parasites. Intestinal 
blockage and malnutrition from heavy Ascaris infections and anemia 
from heavy hookworm infections are now restricted to areas of heavy 
endemicity. Except in the case of Strongyloides and Capillaria, which 
can reproduce in the body, multiple exposures over time are neces­
sary for the development of severe disease. Strongyloides infection 
persists over decades and can disseminate when the immune system is 
compromised. Although Capillaria remains localized to the intestine, 
infections can become so heavy that protein-losing enteropathy and 
malnutrition cause serious disease.
The life cycles of Ascaris and the hookworms involve migration 
through the heart and lungs before development into adults in the 
intestine. In particular, Ascaris occasionally causes eosinophilic pneu­
monia (Loeffler’s syndrome) during heavy infections. Pinworms are 
the most common causes of intestinal roundworm infection persisting 
in the United States and other developed countries. The anal and peri­
neal itching caused by pinworm migration out of the anus and subse­
quent egg deposition is well known to families throughout the world.
TISSUE ROUNDWORMS  The major diseases caused by tissue round­
worms are filariasis, angiostrongyliasis, gnathostomiasis, and trichinel­
losis. By far, the most important globally is filariasis; the thread-like 
filarial worms infect an estimated 80 million individuals in tropical 
and subtropical areas of the world. Four filarial species cause three 
distinct diseases: lymphatic filariasis (Wuchereria bancrofti and Brugia 
malayi), river blindness (Onchocercus volvulus), and loiasis (Loa loa, 
the African eye worm). Humans, the major reservoir, acquire these 
infections from bites of infected arthropods (Table S12-2). The larvae 
develop into adults, which remain static in tissue: the lymphatics for 
lymphatic filariasis and subcutaneous tissue for O. volvulus and L. loa. 
After adults mate, next-stage larvae are produced, and their migration 
causes additional damage.
Repeated bouts of migrating larvae and blocking of the lymphatics 
by adults are necessary to establish the syndrome of lymphatic filaria­
sis; thus, it is unusual for the short-term traveler (<3 months’ residence 
in an endemic region) to develop significant disease. In river blindness, 
the larvae produced by adult O. volvulus migrate through the skin and

eye, causing skin damage and eventual blindness. Loiasis is a milder 
disease restricted to central and western Africa. Although both the 
adults and the larvae of L. loa migrate through the skin and eye, many 
infected individuals are asymptomatic, and the infection is often diag­
nosed only when an adult worm migrates across the subconjunctival 
tissue and is visible to the patient and the physician. Red lumps in the 
skin from heavy cutaneous migration are called Calabar swellings.
The other four major roundworm tissue infections are acquired by 
ingestion of larvae in undercooked food. The sources for trichinellosis 
are swine and other large mammals; for gnathostomiasis, freshwater 
fish and chicken; for ancylostomiasis, snails, fish, prawns, and crabs; 
and for Guinea worm, infected water fleas. Guinea worm infection 
(dracunculiasis, caused by Dracunculus medinensis) has been almost 
eradicated. Trichinella spiralis larvae penetrate the intestine and migrate 
widely, with a preference for skeletal tissue; the release of eosinophils 
and IgE causes muscle soreness and may cause palpebral swelling and 
other manifestations of generalized allergic reactions. Angiostrongylus 
cantonensis is the most common parasitic cause of eosinophilic men­
ingitis. Ingested larvae penetrate the intestine and migrate to the brain 
and meninges, where they quickly die and attract massive numbers 
of eosinophils. Although complications can occur, most individuals 
recover spontaneously. Gnathostoma spinigerum larvae also penetrate 
the intestine and migrate, showing a preference for the skin, eyes, and 
meninges. Mechanical damage from the migration and inflammation 
produced by the resultant immune reaction can cause boil-like lesions 
on the skin, painful eye damage, and eosinophilic meningitis. Although 
eosinophilic meningitis caused by G. spinigerum is less common than 
that caused by A. cantonensis, it is often more severe and can result in 
paralysis or brain hemorrhage.
PROTOZOAL INFECTIONS
■
■INTESTINAL PROTOZOA
Entamoeba histolytica is the one intestinal protozoan that causes inva­
sive disease. This disease consists of dysentery or bloody diarrhea that 
must be differentiated from that due to bacteria such as Salmonella, 
Campylobacter, and Shigella. Although amebiasis usually has a slower 
onset with lower fever than these bacterial infections, E. histolytica can 
disseminate from the bloodstream to cause distant abscesses, particu­
larly of the liver. The diagnosis cannot be made by identification of the 
characteristic cyst or trophozoites (Chap. 230), as they are identical to 
those of the noninvasive E. dispar, which is more common globally.
Cryptosporidium and Giardia are the most common water-borne pro­
tozoal infections. Cryptosporidium can cause major outbreaks because it 
is highly infectious and resistant to high levels of chlorine (Chap. 236). 
Without immune reconstitution, immunosuppressed patients, particu­
larly those with AIDS, can develop severe, even fatal watery diarrhea. 
Infections caused by the remaining intestinal protozoans—Giardia, Isos­
pora, Cyclospora, and microsporidia (Chap. 236)—have a much more 
indolent course, with intermittent diarrhea. Microsporidia, unique 
intracellular protozoa that form infectious spores, may cause limited 
gastrointestinal infection in immunocompetent hosts, but patients with 
AIDS can develop chronic diarrhea and wasting or disseminated infec­
tion to the biliary or respiratory tract.
■
■FREE-LIVING AMOEBAS
The free-living amoebas Acanthamoeba and Naegleria are found world­
wide in freshwater and brackish water (Chap. 230 and Table S12-3). 
Organisms of these two genera cause very different syndromes. In 
immunocompromised individuals, Acanthamoeba may cause invasive 
infection, with brain masses and skin lesions. However, all humans are 
susceptible to Acanthamoeba keratitis after trauma to the eye and expo­
sure to contaminated water. In contrast, naeglerial meningitis, acquired 
in warm lakes or hot springs, causes sudden pyogenic and usually fatal 
meningitis. Balamuthia, reported only from the Americas, causes indo­
lent meningoencephalitis, with both cerebrospinal fluid pleocytosis 
and a space-occupying lesion, in immunocompetent patients. Despite 
the availability of miltefosine, which is active in vitro against Naegleria, 
infection of the CNS is almost universally fatal.

■
■BLOOD AND TISSUE PROTOZOANS

Plasmodium and Babesia 
Malaria, caused by six species of Plasmo­
dium, carries higher mortality rates than any other parasitic infection 
(Chap. 231). All species are transmitted in tropical and subtropical 
areas by female Anopheles mosquitoes. Plasmodium falciparum is 
most common in sub-Saharan Africa, where it causes more than 
80% of malaria infections and 90% of malarial deaths. Infection with 

P. falciparum may be particularly severe because the organism can 
invade any erythrocyte, reaches very high parasite loads, damages 
organs by adhering to vascular epithelium, and is the most likely 
Plasmodium species to be resistant to antimalarial drugs. Plasmodium 
vivax, the dominant cause of malaria outside sub-Saharan Africa, 
reaches lower levels of parasitemia and exhibits less drug resistance 
because it invades only reticulocytes with Duffy antigen. Many Africans, 
especially in the western part of the continent, lack the Duffy blood 
group; consequently, Plasmodium ovale, another cause of milder malaria, 
can compete successfully with P. vivax. Both P. vivax and P. ovale pro­
duce persistent liver forms, which must be treated with primaquine 
(Chap. 229). Because malaria can cause a variety of symptoms ranging 
from acute fever to coma, this diagnosis must be considered in any 
traveler or immigrant from a malarial area. Recently, locally acquired 
P. vivax malaria has been detected in Florida and Texas and P. falci­
parum in Maryland; thus, malaria should be included in the differential 
diagnoses of unexplained fever even in patients who have never left 
the United States. Babesia also infects erythrocytes and may cause a 
nonspecific febrile illness or, in asplenic patients, severe infection. This 
parasite is carried by ixodid ticks and is geographically limited to the 
northeastern and midwestern United States, with only sporadic cases 
in Europe and other temperate areas.
CHAPTER 228
Trypanosomes 
The three species of trypanosomes all have flagel­
lated bloodstream forms, but they cause very different diseases. T. cruzi, 
the cause of Chagas disease, is transmitted in South and Central 
America in the feces of blood-sucking reduviid bugs (Chap. 234). After 
initial parasitemia, patients are often asymptomatic for years while 
the parasite multiplies intracellularly in muscle and ganglion cells. 
Although only a minority of patients go on to develop organ damage 
(megaesophagus and cardiomyopathy), all infected patients can spread 
the disease through transfusions, mother-to-child transmission, and 
organ transplants.
Introduction to Parasitic Infections 
African trypanosomiasis is limited to sub-Saharan Africa, where it is 
transmitted by the bite of a tsetse fly. A history of a tsetse bite and the 
presence of a painful chancre are strong diagnostic clues (Chap. 234). 
Although the parasites causing this disease in western Africa (Trypano­
soma brucei gambiense) and eastern Africa (T. brucei rhodesiense) look 
identical, they are genetically and clinically distinct. T. b. gambiense 
causes low-level parasitemia with cyclical fevers over months or years 
before CNS invasion, whereas T. b. rhodesiense causes high-level para­
sitemia, invades the CNS early on, and can lead to death within weeks 
of onset.
Leishmania 
Leishmaniasis is caused by more than 20 species of obligate 
intracellular protozoa transmitted by sandflies, which are present in 
almost 100 countries in tropical and temperate zones (Chap. 233). A 
wide spectrum of clinical symptoms result, ranging from self-healing, 
painless skin ulcers to mucocutaneous disease with destruction of the 
nose and palate to disseminated visceral leishmaniasis with hepatic 
and splenic involvement. The resulting disease depends on the infect­
ing strain and the host immune response. Visceral leishmaniasis 
can present as an acute febrile illness, with the later development of 
hepatosplenomegaly, and is an AIDS-defining illness in HIV-infected 
patients. More than 90% of cases of visceral leishmaniasis occur in 
India, Bangladesh, Ethiopia, Sudan, and Brazil.
Toxoplasma 
Toxoplasma gondii is an obligate intracellular parasite 
that is found worldwide. Infection follows ingestion of oocysts in food 
or water contaminated by cat feces, ingestion of tissue cysts in under­
cooked meat, or transplacental transmission. After gastrointestinal 
invasion, tachyzoites can invade any nucleated cell and cause lifelong 
infection in most patients (Chap. 235). Clinical manifestations depend

on the host’s age and immune status at the time of infection. Congeni­
tal toxoplasmosis results from primary maternal infection; outcomes 
are most severe early in pregnancy and include visual, hearing, and 
cognitive impairments. Babies infected later in pregnancy may appear 
normal but can develop chorioretinitis decades later. Primary infection 
in immunocompetent hosts may be asymptomatic, may present as an 
infectious mononucleosis–like syndrome, or may manifest as chorio­
retinitis during outbreaks. During immunosuppression by AIDS or 
organ transplantation, reactivation of latent cerebral infection can be 
fatal unless diagnosed and treated early.

APPROACH TO THE PATIENT
Parasitic Infection
A thorough history and physical examination are the keys to diag­
nosis of any disease and particularly of parasitic infections. Because 
many of the more serious parasitic infections are uncommon in the 
United States, a travel history, particularly to developing nations, 
is a critical component. The longer the stay in an area endemic for 
significant parasitic infections, the greater the risk, even for healthy 
travelers. In addition, other factors increase the chance of acquiring 
these infections. Notably, immunocompromise greatly increases the 
likelihood of developing some of the more serious parasitic infec­
tions. Even healthy travelers with adventure itineraries, extensive 
travel to rural areas, or involvement in war zones or refugee camps 
are at increased risk. Immigrants from developing countries may 
seek care for symptoms or signs associated with parasitic infections.
Information on the patient’s immunization history and adher­
ence to appropriate malarial chemoprophylaxis is critical. The 
recent approval of the first parasitic vaccines against P. falciparum 
is very exciting, but it will be targeted initially only for children in 
high prevalence areas. Typhoid fever is much less likely to be the 
cause of prolonged fever in an immunized individual. Similarly, 
PART 5
Infectious Diseases
TABLE 228-1  Parasitic Infections, by Organ System and Signs/Symptomsa
ORGAN SYSTEM, MAJOR 
SIGN(S)/SYMPTOM(S)
PARASITE(S)
GEOGRAPHIC DISTRIBUTION
COMMENTS
Skin
Serpentine rash
Hookworm
Worldwide
Can cause anemia in heavy infections
 
Strongyloides
Moist tropics and subtropics
Disseminated infection in immunocompromise
 
Toxocara (animal roundworm)
Tropical and temperate zones
Cutaneous or visceral larva migrans
Itchy skin rash
Onchocerca
Mexico, Central/South America, 
Africa
Painless ulcers
Leishmania
Tropics and subtropics
Amastigotes detectable in biopsies; may cause destructive 
mucocutaneous infection; AIDS-defining infection
Skin nodules
Onchocerca
Mexico, South America, Africa
Large nodules of adult worms
 
Loa loa (African eye worm)
Western and central Africa
Migratory nodules
 
Gnathostoma
Southeast Asia and China
Migratory nodules with eosinophilia
Painful nodules, especially 
involving feet
Dracunculus (Guinea worm)
Africa
Nearly eradicated
Central Nervous System
Somnolence, seizures, coma
Plasmodium falciparum
Subtropics and tropics
Cerebral malaria, especially in children
 
Trypanosoma brucei 
rhodesiense
Sub-Saharan eastern Africa
Painful chancre from tsetse fly bite; death in weeks to months
Space-occupying lesions, 
seizures
Acanthamoeba
Worldwide
Immunocompromised individuals
 
Balamuthia
Americas
Indolent meningoencephalitis with brain mass
 
Toxoplasma
Worldwide
Reactivation disease in immunocompromise; ring-enhancing 
lesions; AIDS-defining infection
 
Taenia solium
Mexico, Central/South America, 
Africa
 
Schistosoma japonicum
Far East
Aberrant eggs can form brain or spinal cord masses.
 
Schistosoma mansoni
Africa, Central/South America
Aberrant eggs can form brain or spinal cord masses.

hepatitis A or B is unlikely to be the cause of jaundice and fever in 
fully immunized patients. In this era of increasing drug resistance, 
even adherence to appropriate malarial chemoprophylaxis does 
not guarantee that fever is not malarial. Nevertheless, most travel­
ers who acquire malaria have taken inadequate or no prophylaxis. 
Although these considerations do not prove that the symptoms are 
caused by parasites, they narrow the differential diagnosis.
There are many other important aspects of the history, includ­
ing when symptoms began. Was the individual still in the endemic 
area at the time, or did the symptoms commence after return to 
the United States? If they started during travel, was any treatment 
received? Malaria must be the first consideration in a febrile patient 
returning from an endemic area. If the patient was well upon return 
from travel, the timing of symptom onset is a critical point. For 
example, if the chief manifestation is fever that began >10–14 days 
after departure from the endemic region, many tropical diseases 
can be ruled out, including dengue fever, chikungunya fever, and 
Zika virus infection. On the other hand, fever beginning several 
months or later after return makes malaria a likely diagnosis. Trav­
elers’ diarrhea, the most common complaint of travelers, is usually 
caused by bacteria or viruses and resolves in a short time with or 
without treatment. Travelers’ diarrhea that persists for weeks is 
much more likely to be parasitic in origin.
Most patients who consult physicians after international travel 
either have troublesome symptoms or have been referred for symp­
toms or signs whose source was unclear to a referring caregiver. 
After a careful travel history including the individual’s symptoms 
and the exact geographic zones visited, a thorough physical exami­
nation must be conducted. The symptoms, signs, and physical 
findings should help to establish possible diagnoses. Table 228-1 
breaks down the symptoms of major parasitic infections by organ 
system and geographic distribution, with comments on clinical and 
epidemiologic associations.
Larvae detectable in skin snips and nodules
Cysticercosis; variable sized or calcified larval cysts on CT
(Continued)

TABLE 228-1  Parasitic Infections, by Organ System and Signs/Symptomsa
ORGAN SYSTEM, MAJOR 
SIGN(S)/SYMPTOM(S)
PARASITE(S)
GEOGRAPHIC DISTRIBUTION
COMMENTS
Pyogenic meningitis
Naegleria
Worldwide
Motile trophozoites in fresh cerebrospinal fluid; pyogenic; rapid 
death
Eosinophilic meningitis
Angiostrongylus (rat lung 
worm)
Southeast Asia, Pacific, 
Caribbean
 
Gnathostoma
Southeast Asia and China
Migratory nodules
Eyes
Painful corneal ulcers
Acanthamoeba
Worldwide
Freshwater and brackish water; corneal trauma; long-wear contact 
lenses
Corneal opacification
Onchocerca
Mexico, Central/South America, 
Africa
Congenital or adult visual loss Toxoplasma
Worldwide
Primary infection in pregnancy and normal hosts; reactivation 
infection in immunocompromised
Retinal mass
Toxocara
Worldwide
Ocular larva migrans
Visible roundworm in eye
Onchocerca
Mexico, Central/South America, 
Africa
 
L. loa
Western and central Africa
Worms may cross eye during migration.
Pain, possible vision loss
Gnathostoma
Southeast Asia and China
Migratory skin nodules, eosinophilia
Lungs
Pulmonary nodule/abscess
Paragonimus
Far East, Africa, Americas
Ectopic migration to abdomen or central nervous system
Cough, transient infiltrates, 
eosinophilia
Migrating helminths
Worldwide
Loeffler’s syndrome from migrating Ascaris, hookworm, 
Strongyloides
Heart
Pulmonary edema
P. falciparum (complication)
Tropics and subtropics
End-organ damage from severe malaria
Cardiomegaly, arrhythmias
Trypanosoma cruzi
Mexico, Central/South America
Late amastigote infection of myocardium; AIDS-defining infection
Gastrointestinal Tract
Hepatosplenomegaly
Malaria (multiple episodes)
Tropics and subtropics
Splenomegaly with anemia and recurrent fever are hallmarks of 
malaria.
 
S. mansoni
Africa, Central/South America
Portal obstruction with cirrhosis and late varices
 
Leishmania donovani complex
Tropics and subtropics
Visceral leishmaniasis; AIDS-defining infection
Hepatomegaly
Entamoeba histolytica
Tropics
Acute with fever, right-upper-quadrant pain; or chronic with 
enlarged liver; hypoechoic abscess(es) on ultrasound or CT
 
Echinococcus
Sheep-raising areas
Characteristic cysts of liver > lung
 
Fasciola
Sheep-raising areas
Eosinophilia
Cholangitis
Clonorchis
China, Southeast Asia
Recurrent cholangitis and late cholangiocarcinoma
 
Microsporidia
Worldwide
AIDS
 
Cryptosporidium
Worldwide
AIDS-defining infection
Bloody diarrhea
E. histolytica
Tropics
Less fever than in diarrhea of bacterial etiology
 
S. mansoni
Africa, Central/South America
Only in heavy, acute infection with fever and eosinophilia
 
S. japonicum
Far East
Only in heavy, acute infection
Watery diarrhea
Cryptosporidium
Worldwide
Severe in immunocompromised patients
 
Giardia
Worldwide
Foul-smelling stool with steatorrhea
 
Isospora belli
Worldwide
Fever, abdominal pain, chronic diarrhea
 
Microsporidia
Worldwide
Chronic diarrhea with AIDS
 
Capillaria
Southeast Asia, Egypt
Malabsorption, wasting
Passage of large roundworm 
(>6 cm)
Ascaris
Worldwide
Patients may confuse the roundworm with an earthworm.
Small roundworms visible 
around anus
Pinworm
Worldwide
Anal itching; eggs rarely detected by ova and parasite (O&P) exam
 
Trichuris
Worldwide
Rectal prolapse with heavy infection in children
Passage of tapeworm 
segments
T. solium or Taenia saginata
Worldwide
Usual reason for seeking medical care
 
Diphyllobothrium latum
Worldwide
Pernicious anemia in genetically predisposed Scandinavians
Genitourinary System
Itchy discharge
Trichomonas vaginalis
Worldwide
Common sexually transmitted disease of both sexes
Hematuria
Schistosoma haematobium
Africa
Hematuria with negative cultures, urinary tract infections, and late 
bladder cancer

(Continued)
Most common cause globally of eosinophilic meningitis; 
spontaneous resolution
Immune response to microfilaria in cornea
Worms may cross eye during migration.
CHAPTER 228
Introduction to Parasitic Infections 
(Continued)