Tropical Medicine 6: Muscular Manifestations
(Including Myocardium)
Myalgia
Trichinosis
This is a disease resulting from the consumption of undercooked meats,
particularly pork. The parasitic roundworm, Trichinella spiralis,
exists in a larval
form within nurse cells, from which they emerge and penetrate the
gut wall
following ingestion. There, they mature and
reproduce, shedding larvae which
migrate via the lymphatic system into blood circulation and ultimately
into the
muscles to form new nurse cells. As humans, we are dead-end hosts
(unless we
are eaten, in which case the predator may become infected).
Symptoms consist of nonspecific abdominal and flu-like complaints (GI phase), followed about 10 days later by fever, myalgia, pruritis, periorbital edema, and eosinophilia (acute phase), which may last from 1 week to 2 months. Subsequently, these symptoms will slowly diminish in most individuals (chronic phase). Larval invasion of the myocardium and CNS comprise the rare (2%) fatal cases of trichinosis.
The best means of diagnosis is via muscle biopsy, with the demonstration of the nurse cells (which may be grossly visible as small, pale, almost-papillary lesions at the time of biopsy). Serological tests are also available.
Treatment during the GI phase consists of mebendazole 200 mg 4 times daily for 5 days or albendazole 400 mg 4 times daily for 3 days. In the acute phase, the anthelmintics are used until symptoms recede, and prednisolone 40 mg 4 times daily is added. No treatment other than physical therapy is generally necessary in the chronic phase.
Cysticercosis
Similar to trichinosis, this disease develops following ingestion of
undercooked
beef or pork which contains the parasite larvae, in this case,
tapeworms. Recalling the lifecycle
of
Taenia
presented in TM4 (Vol III—TM4 Gastrointestinal and Abdominal Manifestations), ingestion of
the tapeworm eggs (via fecal-oral contamination) results in larvae-establishing
cysticerci in the tissues of the new host.
Most patients with cysticercosis are entirely asymptomatic, although some may develop transient local pain as the cysticerci develop. Occasionally, pea-sized nodules may be palpable in the subcutaneous tissues. Cysticerci may also develop in the CNS causing significant morbidity, which is discussed in Vol III—TM7 Neurological Manifestations.
Most cysticercosis of the muscles and subcutaneous tissues diagnosed in the United States are found coincidentally on x-ray. Over time, the cysticerci are calcified, and the multiple, cigar-shaped calcifications are quite distinctive. (See figure.)
Treatment of muscular cysticercosis, beyond symptomatic with antiinflammatory medication, is not necessary; however, perform brain imaging to rule out the potentially more serious neurocysticercosis.
Tropical Pyomyositis
Pyomyositis is a painful, seemingly spontaneous bacterial infection of the muscles; although rare in temperate zones, it is relatively common in the tropics. Pyomyositis may remain isolated in a single muscle or group of muscles, but is also associated with sepsis. Large muscles of the lower extremity are usually affected. Although Staphlyococcus aureus (S aureus) is the most commonly responsible organism, other pyogenic bacteria may occur in 5% of cases.1 The infection may spread to include osteomyelitis, endocarditis, meningitis, and neumonia.
Treatment includes incision and drainage, and requires debridement of any necrotic tissues. Aggressive broad-spectrum antibiotic therapy is needed; spread to heart or bone may require more than a month of high-dose IV therapy.
Hypertonicity
Tetanus
Tetanus is most commonly associated with acute injury. Tetanus symptoms
are caused by two toxins released from the
Clostridium tetani,
an anaerobic bacterium
whose spores germinate following introduction at the wound site.
Clinically, the earliest symptom of generalized tetanus intoxication is often trismus (lockjaw). This may progress to spastic paroxysms involving the face, trunk, and extremities. Occasionally, uncontrollable fever, tachycardia and other arrhythmias, and hypertension may develop as well. The disease may progress for 10 days, and mortality may reach 60% due to respiratory muscle involvement or the autonomic dysfunction.2 Recovery may take 4 weeks in survivors. A more mild localized form may be seen; if untreated, progression to generalized tetanus may occur.
Diagnosis is clinical; laboratory evaluation is not generally helpful. The working diagnosis of strychnine poisoning, dystonic reactions, hypocalcemia, and seizure must be considered.
Treatment consists of tetanus immunoglobulin (human Ig 500 to 5000 IU IM or equine tetanus 10 000 to 1 000 000 IU IM) and supportive care, being careful to avoid stimulation. Metronidazole 500 mg PO twice daily may slow multiplication of the bacteria, but does not speed clearing of the toxin. Benzodiazepines or baclofen may help diminish the spasms, and occasional paralysis and intubation may be necessary.
Seizures – Refer to Vol III—TM7 Neurological Manifestations.
Hypotonicity (Weakness, Paralysis) – Refer to Vol III—TM7 Neurological Manifestations.
Myocardial Diseases (typically present as congestive heart failure)
Chagas Disease (American Trypanosomiasis)
Chagas disease is acquired through the feces (scratched into the bite
site) from the reduvid bug, Trypanosoma
cruzi. Endemic to economically disadvantaged
regions of tropical Central and South America, it may also be acquired
via blood transfusions.
Following an acute phase, which may be asymptomatic or flu-like, the infection becomes latent for an extended period of time. After decades, evidence of infection may re-emerge in the form of cardiomyopathy (Chagas was once the leading cause of CHF in Latin America) and megasyndromes (megaesophagus and megacolon). The pathophysiology is immunological destruction of the myocytes and the myoenteric plexus rather than direct damage by the parasites.
Diagnosis may be made in the acute phase by the identification of the parasites in thin blood smears on microscopy. Immunological techniques are also available; though sensitive, they lack specificity.
Use of nifurtimox and benznidazole in the acute phase may shorten the course of the acute symptoms and prevent the neurological and myocardial complications in 50% to 70% of cases. These agents are not commercially available in the United States, but may be available through the CDC.
References
- Strickland GT, editor. Hunter’s tropical medicine and emerging infectious diseases, 8th ed. Philadelphia, Pa: WB Saunders, 2000.
- Gill GV, Beeching NJ. Lecture notes in tropical medicine, 5th ed. Malden, MA: Blackwell Science, 2004