Complications
Considered the most serious complication of trichinellosis.
Occurs in up to 20% of cases, usually during the third or fourth week of infection.[78]
It is mediated by an inflammatory response rather than being the consequence of direct parasitic invasion.
The clinical manifestations include chest pain, palpitations, dyspnea, and lower extremity edema secondary to congestive cardiac failure.[79]
Measurement of serum troponin level is a simple and reliable method to screen for trichinella myocarditis.[66]
The most common abnormalities on ECG include nonspecific alteration of ventricular repolarization represented by ST-T wave abnormalities and arrhythmias (bundle-branch block or sinus tachycardia). Less commonly, other bradyarrhythmias and tachyarrhythmias, and low-voltage QRS complexes in the limb leads, are seen.[62]
Two-dimensional echocardiography may show global or segmental ventricular hypokinesis, ventricular dilation, and pericardial effusions.[67]
The treatment of trichinella myocarditis is with anthelmintics, corticosteroids, and antiarrhythmics.
Thrombophilia can lead to the development of deep vein thrombosis, pulmonary embolism, and disseminated intravascular coagulation.[32]
Dyspnea, cough, and pneumonitis occur as a result of parasitic invasion of the diaphragm and respiratory muscles, myocarditis with congestive heart failure, pulmonary Loffler-like infiltrates, or secondary bacterial infection leading to pneumonia.[65]
Chest x-ray may show pulmonary infiltrates.
Pneumonia and sepsis may complicate severe cases of trichinellosis. Treatment is with appropriate antibiotics.
A small percentage of patients with severe disease may develop glomerular or tubular kidney damage. The most common manifestations include oliguria, proteinuria, hematuria, and presence of casts. In some cases there is progression to acute renal failure. Different types of glomerulonephritis have been documented from human pathology samples.[63]
This is a rare manifestation of trichinellosis described among the Inuit, associated with repeated consumption of raw walrus meat.[82]
Neurologic involvement in trichinellosis seems to be rare and may occur in <1% of patients.[61]
Severe headache and muscular weakness are extremely common neurologic manifestations in trichinellosis.[6] Other neurologic features include tinnitus, vertigo, deafness, aphasia, seizures, apathy, insomnia, and a paralysis-like state.[6][7]
More serious involvement of the central nervous system in neurotrichinellosis includes meningitis, encephalitis, polyradiculoneuritis, myasthenia gravis, paresis, and sinus thrombosis.[7] Mydriasis, a marker of severe neurologic disease and death, can be present.[47] Decreased tendon reflex is a moderate risk factor for severe neurologic disease and death.[47]
Neurologic complications usually occur within 3-4 weeks of the initial infection and tend to coincide with cardiac manifestations.[80]
Although usually transient, asthenia, myalgia, and weakness may persist for months to years after diagnosis.[81]
EEG may show diffuse electrical slowing in cases of encephalitis. Analysis of cerebrospinal fluid may reveal marginal elevation of lymphocytes, eosinophils, and/or protein.[61] CT or MRI of the brain may show small hypodensities in the brain parenchyma, most probably representing infarctions secondary to parasite-induced vasculitis.[6]
The treatment of neurotrichinellosis is with anthelmintics and corticosteroids.
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