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Sherris Medical Microbiology, 7e
Chapter 55: Tissue Nematodes
TRICHINELLA
TRICHINELLA SPIRALIS: PARASITOLOGY AND LIFE CYCLE
Adult Trichinella live in the duodenal and jejunal mucosa of carnivores throughout the world, particularly swine, rodents, bears, canines, felines, and
marine mammals. Originally thought to be members of a single species, it is now clear that arctic, temperate, and tropical strains of Trichinella
demonstrate significant epidemiologic and biologic differences, and they have been reclassified into eight distinct species. Only two species, T spiralis
and the arctic species T nativa, display a high level of pathogenicity for humans. This discussion focuses on the former, while highlighting the unique
epidemiologic and clinical characteristics of the latter.
Intestinal parasites of many flesh­eating mammals
Within the host intestinal tissue, the tiny (1.5 mm) male copulates with his larger (3.5 mm) mate and, apparently spent by the effort, dies. Within 1 week,
the inseminated female begins to discharge offspring. Unlike those of most nematodes, these progeny undergo intrauterine embryonation and are
released as second­stage larvae. The birthing continues for the next 4 to 16 weeks, resulting in the generation of some 1500 larvae, each measuring 6
by 100 μm.
From their submucosal position, the larvae find their way into the vascular system and pass from the right side of the heart through the pulmonary
capillary bed to the systemic circulation, where they are distributed throughout the body. Larvae penetrating tissue other than skeletal muscle
disintegrate and die. Those finding their way to striated muscle continue to grow, molt, and gradually encapsulate over a period of several weeks.
Calcification of the cyst wall begins 6 to 18 months later, but the contained larvae may remain viable for 5 to 10 years (Figure 55–2). The muscles
invaded most frequently are the extraocular muscles of the eye, the tongue, the deltoid, pectoral, and intercostal muscles, the diaphragm, and the
gastrocnemius. If a second animal feeds on the infected flesh of the original host, the encysted larvae are freed by gastric digestion, penetrate the
columnar epithelium of the intestine, and mature just above the lamina propria. This cycle is summarized in Figure 55–3.
✺ Larvae reach striated muscle and encapsulate but are still viable
✺ Eating infected flesh spreads the disease
FIGURE 55–2.
Trichinella spiralis larvae. A. Coiled larvae in a “squash prep” of deltoid muscle biopsy, in which a small sliver of muscle is squashed under the
cover slip and examined without further fixation (image by Paul Pottinger MD). B . Coiled larva from a muscle digest. (Reproduced with permission from
Connor DH, Chandler FW, Schwartz DQ, et al: Pathology of Infectious Diseases. Stamford, CT: Appleton & Lange, 1997.)
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FIGURE 55–2.
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Trichinella spiralis larvae. A. Coiled larvae in a “squash prep” of deltoid muscle biopsy, in which a small sliver of muscle is squashed under the
cover slip and examined without further fixation (image by Paul Pottinger MD). B . Coiled larva from a muscle digest. (Reproduced with permission from
Connor DH, Chandler FW, Schwartz DQ, et al: Pathology of Infectious Diseases. Stamford, CT: Appleton & Lange, 1997.)
FIGURE 55–3.
Trichinosis. Trichinella spiralis larvae ingested by pig (1) eventually end up as human cysts (6).
TRICHINOSIS
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Trichinosis, also called trichinellosis, is widespread in carnivores worldwide. Among domestic animals, swine are most frequently involved. They
acquire the infection by eating dead rats or garbage containing cyst­laden scraps of uncooked meat. Human infection, in turn, results largely from the
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TRICHINOSIS
EPIDEMIOLOGY
Trichinosis, also called trichinellosis, is widespread in carnivores worldwide. Among domestic animals, swine are most frequently involved. They
acquire the infection by eating dead rats or garbage containing cyst­laden scraps of uncooked meat. Human infection, in turn, results largely from the
consumption of improperly prepared pork products. In the United States, agricultural regulations have greatly reduced the incidence of trichinosis,
and most pig­associated outbreaks have been traced to pork sausage prepared in the home or in small, unlicensed butcheries. Clusters have also
followed feasts on wild pig in California and Hawaii. At present, however, the majority of human cases in the United States, particularly those in Alaska
and other western states, have been attributed to consumption of wild animal meat, especially bear meat. Outbreaks among Alaskan and Canadian
Inuit populations have followed the ingestion of raw T nativa­infected walrus meat. Outbreaks in Europe have involved horse meat or wild boar flesh.
In other areas of the world, infection is commonly acquired from wild animals (“sylvatic sources”), including wild boar, bush pigs, and warthogs.
Swine infected by eating rats or meat in garbage
✺ Human infection most often from undercooked pork or wild animals
Human infections occur worldwide. In the United States, the prevalence of cysts found in the diaphragms of patients at autopsy has declined
substantially. This decline has been attributed to decreased consumption of pork and pork products; federal guidelines for the commercial
preparation of such foodstuffs; the widespread practice of freezing pork, which kills all but arctic strains of T nativa; and legislation requiring the
thorough cooking of any meat scraps to be used as hog feed. Nevertheless, it is estimated that many Americans carry live Trichinella in their
musculature and that more acquire it annually. Fortunately, the overwhelming majority has a small number of larvae and are asymptomatic. Only 5 to
15 clinically recognized cases are reported annually to federal officials.
Prevalence declining as a result of meat inspection and cooking and freezing pork
Human infections are usually subclinical
PATHOGENESIS AND IMMUNITY
The pathologic lesions of trichinosis are related almost exclusively to the presence of larvae in striated muscle, heart, and CNS. Invaded muscle cells
enlarge, lose their cross­striations, and undergo basophilic degeneration. Intense inflammation surrounds the involved area, consisting of
neutrophils, lymphocytes, and eosinophils. With the development of specific IgG and IgM antibodies, eosinophil­mediated destruction of circulating
larvae begins, production of new larvae is slowed, and the expulsion of adult worms is hastened. A vasculitis demonstrated in some patients has been
attributed to deposition of circulating immune complexes in the walls of the vessels.
✺ Larvae in striated muscle, heart, and CNS
Acute inflammation with eosinophil­mediated destruction of larvae
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MANIFESTATIONS
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One or two days after the host ingests tainted meat, the newly matured adults penetrate the intestinal mucosa, producing nausea, abdominal pain, and
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Acute inflammation with eosinophil­mediated destruction of larvae
TRICHINOSIS: CLINICAL ASPECTS
MANIFESTATIONS
One or two days after the host ingests tainted meat, the newly matured adults penetrate the intestinal mucosa, producing nausea, abdominal pain, and
diarrhea. In mild infections, these symptoms may be overlooked, except in a careful retrospective analysis; in more serious infections, they may persist
for several days and render the patient prostrate. Diarrhea persisting for a period of weeks has been characteristic of T nativa outbreaks after
ingestion of walrus meat by the Inuit population of northern Canada. Larval invasion of striated muscle begins approximately 1 week later and initiates
the more characteristic phase of the disease, which may last for about 6 weeks. Patients in whom 10 or fewer larvae are deposited per gram of tissue
are usually asymptomatic; those with 100 or more generally develop significant disease; and those with 1000 to 5000 have a very stormy course that
occasionally ends in death. Fever, muscle pain, muscle tenderness, and weakness are the most prominent manifestations of trichinosis. Patients may
also display eyelid swelling, a maculopapular skin rash, and small hemorrhages beneath the conjunctiva of the eye and the nails of the digits.
Hemoptysis and pulmonary consolidation are common in severe infections. If there is myocardial involvement, electrocardiographic abnormalities,
tachycardia, or congestive heart failure may be seen. Central nervous system invasion is marked by encephalitis, meningitis, and polyneuritis. Delirium,
psychosis, paresis, and coma can follow.
Initial abdominal pain and diarrhea as adults penetrate gut wall
✺ Symptoms depend on number and extent of larval muscle invasion
Severe complications include hemoptysis, heart failure, coma, and death
DIAGNOSIS
Trichinosis presents in a protean fashion, which can delay diagnosis and impact clinical outcomes. The most consistent laboratory abnormality is an
eosinophilic leukocytosis during the second week of illness, which persists for the remainder of the clinical course. Eosinophils typically range from
15% to 50% of the white cell count, and in some patients, this may induce extensive damage to the cardiac endothelium. In severe or terminal cases, the
eosinophilia may disappear altogether. Serum levels of IgE and muscle enzymes are elevated in most clinically ill patients.
✺ Eosinophilia up to 50% starting in second week
There are a number of valuable serologic tests, including indirect fluorescent antibody and enzyme­linked immunosorbent assay. Significant antibody
titers are generally absent before the third week of illness, but may then persist indefinitely.
Biopsy of the deltoid or gastrocnemius muscles during the third week of illness often reveals encysted larvae (Figure 55–2B).
Antibody usually appears after 2 weeks and then persists
✺ Muscle biopsy
reveals
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TREATMENT
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Antibody usually appears after 2 weeks and then persists
✺ Muscle biopsy reveals larvae
TREATMENT
Patients with severe edema, pulmonary manifestations, myocardial involvement, or CNS disease are treated with corticosteroids. The value of specific
anthelmintic therapy remains controversial. The mortality rate of symptomatic patients is 1%, rising to 10% if the CNS is involved. Mebendazole and
albendazole halt the production of new larvae, but in severe infection, the destruction of tissue larvae may provoke a hazardous hypersensitivity
response in the host. This may be moderated by initiating corticosteroids before treating with antihelminthics.
✺ Corticosteroids used in severe cases
✺ Antihelminthic therapy used with caution
PREVENTION
Control of trichinosis requires adherence to feeding regulations for pigs, and limiting contact between domestic pigs and wild animals, particularly
rodents, who might be carrying Trichinella larvae in their tissues. Domestically, care should be taken to cook pork to an internal temperature of at least
76.6°C, or freeze it at −15°C for 3 weeks before cooking. Trichinella nativa in the flesh of arctic animals may survive freezing for a year or more. All
strains may survive apparently adequate cooking in microwave ovens due to the variability in the internal temperatures achieved.
✺ Prevention via thorough cooking
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