PART III Etiologic Agents of Infectious Diseases
Sarcocystis Species
SECTION D Human Parasites and Vectors
FIGURE 272.4. Human as aberrant intermediate host for Humans as aberrant intermediate hosts for Sarcocystis species
Sarcocystis species. (From Fayer R, Esposito DH, Dubey JP.
Human infections with Sarcocystis species. Clin Microbiol
Rev 2015;28:295–311. Copyright by the American Society Sporocyst
for Microbiology.) excreted
Definitive host
(reptiles?)
Presumed:
Snake eats intermediate host
species infected with mature
sarcocysts of Sarcocystis nesbitti
diagnoses such as influenza, dengue, or malaria, serial clinical and labora-
tory investigations for evidence of developing myositis and eosinophilia
should be considered.1,5 In patients with myositis, trichinellosis should
be excluded. Confirmation of muscular sarcocystosis requires histologic
observation of sarcocysts in muscle. Polymerase chain reaction is not
widely available, and standardized serologic assays validated for use in
humans do not currently exist.1
TREATMENT AND PREVENTION
Human intestinal sarcocystosis is largely self-limited, and no specific
treatment is available. No proven treatment exists for human muscular
273 Toxoplasma gondii (Toxoplasmosis)
Despina G. Contopoulos-Ioannidis and Jose G. Montoya
Toxoplasma gondii, a parasite with worldwide distribution, is responsi-
ble for a significant disease burden in humans.1 Primary infection can
be asymptomatic, mildly symptomatic with a mononucleosis like illness
and/or lymphadenopathy, or it can cause severe ocular disease, even
in immunocompetent people.2,3 It also can result in substantial neuro-
logic and ocular sequelae in congenitally infected children.3–7 Atypical
and more virulent T. gondii strains can be associated with community-
acquired pneumonia, disseminated disease,8 and even death among oth-
erwise healthy individuals in certain tropical areas.9 High attack rates
and an unusual presentation, with a tickborne-disease-like illness with
leukopenia, lymhopenia, thrombocytopenia, and transaminitis, has been
reported after exposure to infected game-meat.10 Reactivation of chronic
infection can occur in severely immunosuppressed individuals and cause
life-threatening disease.11–15 Patients with profound T-lymphocyte-medi-
ated immune compromise are at high risk of reactivation, if not receiv-
ing anti-Toxoplasma prophylaxis. At-risk groups include those with the
acquired immunodeficiency syndrome (AIDS),16,17 hematopoietic stem
cell transplants recipients,11–13 and patients receiving high doses of corti-
costeroids and other biologic agents such as monoclonal antibodies (e.g.,
alemtuzumab, adalimumab, infliximab, rituximab, natalizumab).18–28
Studies addressing the possible link of latent Toxoplasma infection with
psychiatric disorders and cancer have been inconclusive.29–31
PATHOGEN AND LIFE CYCLE
T. gondii is an obligate intracellular parasite with the capacity to infect
almost any warm-blooded animal. The parasite has three infectious stages:
1384
Sporocysts are ingested in
contaminated food or water Sporozoites
excyst
Schizonts develop
in blood vessels
Human are
aberrant
intermediate Merozoites
hosts invade muscle
Sarcocysts develop in
skeletal and cardiac muscle
sarcocystosis. One patient treated with albendazole was reported to have
improved, but it was not clear if this improvement was related to treat-
ment or the natural course of infection.18 Co-trimoxazole, a drug with
known antiprotozoal activity, may have activity against schizonts in
the early phase of infection.1,19 Glucocorticoids and nonsteroidal anti-
inflammatory medications may improve symptoms associated with
myositis.5,11,12
Thorough cooking or freezing of meat kills bradyzoites and prevents
intestinal sarcocystosis.1,2 To prevent muscular sarcocystosis, ingestion of
sporocysts must be avoided.1
All references are available online at Elsevier eBooks for Practicing Clinicians.
tachyzoites, which are responsible for rapid spread of the parasite between
cells and tissues and the clinical manifestations of toxoplasmosis; brady-
zoites, which are contained within tissue cysts, maintain chronic infec-
tion, and stay dormant for the life of the host unless the immune system
is severely compromised (with the exception of local reactivations in the
eye that can occur in immunocompetent patients); and sporozoites, which
are contained within oocysts, are shed by members of the felid family, and
widely disseminate the agent in the environment.32 A sexual cycle only
takes place in the small intestine of felids, allowing for the exchange of
genetic material between strains and potentially generating variant strains
in geographic areas where wild and large cats can travel long distances.33,34
Genotyping studies have identified several clonal lineages of T. gondii
in Europe, North America, and South America.35,36 Toxoplasma genetic
studies have grouped the parasite worldwide into sixteen haplogroups.
Haplogroup 2 is predominantly seen in Europe, whereas in North America
haplogroups 1, 2, 3, and atypical strains are more common.37 Haplogroup
12 has also been seen in North America and has been associated with more
aggressive clinical presentations.10 In South America, haplogroup 2 is rarely
seen, and predominance of 1, 3, and atypical have been reported.8,38–42
Investigators have suggested that differences in T. gondii strains may
partially explain the observed differences in the clinical spectrum of
infection in different parts of the world, particularly between Europe,
North America, and South America. Atypical T. gondii strains have been
reported from several areas of the world, including North America and
Mexico,43,44 Central and South America, Australia and Africa.33,37,44–47
This finding should be taken into consideration when clinical syndromes
consistent with severe toxoplasmosis are encountered in individuals