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Chagas' Disease or American trypanosomiais: See full discussion (Most of Latin America): Chagas' disease is a protozoan infection with Trypanosoma cruzi transmitted by insect bite. Patients may be asymptomatic or have a lesion at the site of the bite; and symptoms of prolonged fever, tachycardia, fatigue, weakness, splenomegaly, and lymphadenopathy. Myocarditis or meningoencephalitis may also occur. Most patients experience spontaneous remission of symptoms, followed by a lifelong low-grade parasitemia. There is not currently a satisfactory treatment for any stage of Chagas' disease. Current treatment includes nifurtimox 8-10 mg/kg/day po qid for 90-120 days or benznidazole 5 mg/kg/day po for 60 days. These long-term therapies are toxic to some patients. In the United States, nifurtimox is available only from the Centers for Disease Control and benznidazole is not available in the U.S.
Filariasis (O. volvulus): See full discussion (Distribution given below). The filarial parasites are tissue-dwelling roundworms whose microfilarial (mf) larvae are transmitted by several species of mosquitos or flies. The most problematic forms of filariasis are (1) Bancroftian filariasis and Malayan filariasis (much of the tropical and subtropical world between the Tropics of Cancer and Capricorn) which involve the lymphatic system and result in elephantiasisis; (2) loiasis or loa loa (tropical Africa) in which worms live in subcutaneous tissue; and (3) Onchocerciasis (tropical Africa and to a lesser extent Central and South America) which causes river blindness and skin disorders. Treatment in most cases is effective only against the mf, hence the infection continues and repeated treatment (with ivermectin and/or DEC) may be necessary.
Hemorrhagic fevers (HFs): See full discussion of HFs. The major HFs include hemorrhagic fever with renal syndrome, hantavirus pulmonary syndrome, South American HFs, Lassa HF, Marburg and Ebola HFs, Kyasanur Forest HF, Omsk HF, Crimean-Congo HF, Chikungunya fever, dengue fever and HF, and Rift Valley fever (distribution is noted in the full discussion). The viral hemorrhagic syndrome (VHS) results from widespread increased permeability of microvasculature. Depending on the severity of vascular instability and decrease in platelet function, presentation may range from mild to severe illness; and hemorrhagic manifestations are not always apparent. A common course of illness begins with an abrupt onset of fever, myalgia, cutaneous flushing, and conjunctival suffusion. Within several days, the patient's condition worsens to include syncope, photophobia, headache, hyperesthesia, abdominal pain, nausea/vomiting, anorexia, and prostration. Treatment is primarily supportive, except that Lassa fever, South American HFs, and possibly Crimean-Congo HF and Rift Valley HF may be treated with a slow infusion of IV ribavirin.
Hemorrhagic fever with renal syndrome: See full discussion of HFs (Europe, Russia, East China, and Korea): Hemorrhagic fever with renal syndrome is caused by hantavirus. Incubation ranges from 9-35 days. Severity of the illness varies, mild or subclinical infections common. More severe cases are characterized by a febrile stage lasting 3-5 days with abrupt onset of fever, headache, photophobia, blurred vision, facial flushing extending to neck and shoulders, conjunctival petechiae, periorbital edema, pharyngeal injection and/or petechiae, axillary petechiae, lumbar back pain and CVA tenderness lasting 3-5 days. The illness may gradually resolve after this febrile stage or a hypotensive stage may begin as the temperature falls. The hypotensive stage is characterized by decreased blood pressure, tachycardia, and sometimes shock. Proteinuria, thrombocytopenia, leukocytosis, oliguria occur, as does renal failure in some cases. Renal function returns as the oliguric phase resolves and the polyuric phase ensues. Electrolyte imbalances and dehydration may occur in the polyuric phase. Disseminated intravascular coagulation may occur relatively early in the course of illness. Treatment is supportive as discussed in Hemorrhagic Fevers.
Leprosy: See full discussion (Tropical and sub-tropical Africa, Asia, Pacific Islands, South America, Central America, and Mexico): Leprosy is caused by the acid-fast rod Mycobacterium leprae which is transmitted probably via the respiratory route through prolonged exposure in childhood. Incubation is usually 2-5 years; and up to 20 years. There are two basic types of leprosy: lepromatous leprosy (LL) and tuberculoid leprosy (TL) and either of these may be classified as borderline or indeterminate. Most initial infections involve few symptoms and spontaneous recovery is common with a minority of patients developing clinical disease. LL is a progressive malignant process including skin lesions/changes; as well as nerve damage and disability. TL is not as disabling as LL and includes skin lesions and nerve damage. Borderline leprosy may have features of both LL and TL, and may evolve into either form. Indeterminate leprosy is manifested by one or several macules or poorly defined skin lesions, that may heal spontaneously, remain stable, or progress to forms described above. Multi-drug therapy is the current accepted standard for all types of leprosy, and for LL generally includes dapsone, clofazamine, and rifampin daily for at least 2-3 years until all biopsies are negative for acid-fast bacilli. Patients with indeterminate or tuberculoid leprosy may be treated with dapsone and rifampin as above for 6-12 months, followed by dapsone alone for a total of at least two years of therapy. Antigen-antibody complex reactions (to therapy) are common and are treated with prednisone or thalidomide.
Loiasis (filariasis): See full discussion (Distribution given below). The filarial parasites are tissue-dwelling roundworms whose microfilarial (mf) larvae are transmitted by several species of mosquitos or flies. The most problematic forms of filariasis are (1) Bancroftian filariasis and Malayan filariasis (much of the tropical and subtropical world between the Tropics of Cancer and Capricorn) which involve the lymphatic system and result in elephantiasisis; (2) loiasis or loa loa (tropical Africa) in which worms live in subcutaneous tissue; and (3) Onchocerciasis (tropical Africa and to a lesser extent Central and South America) which causes river blindness and skin disorders. Treatment in most cases is effective only against the mf, hence the infection continues and repeated treatment (with ivermectin and/or DEC) may be necessary.
Malnutrition: Though not a communicable disease, malnutrition bears mention here as a common problem among refugees and, to a lesser extent, immigrants. We expect at some time to have a full discussion of malnutrition. Malnutrition may be the result of decreased intake of one or all food groups or to decreased absorption. Metabolic disorders, diarrheal illnesses, or the indirect effects of chronic illnesses are common causes of decreased absorption. Malnutrition has long-term deleterious effects on the person suffering from decreased intake or absorption; or on the fetus or on the children of the person with malnutrition. Loss of intellectual potential, incomplete physical or mental development, and vulnerability to illness are among the long-term effects of malnutrition. Basic types of malnutrition include marasmus, protein malnutrition (Kwashiorkor), and cachexia. Though not often a problem among refugees, obesity may also be viewed as malnutrition. Marasmus is due to inadequate caloric intake and is characterized by failure to gain weight, then weight loss with resultant emaciation. Loss of subcutaneous fat causes poor turgor and wrinkling of skin. With advanced marasmus, the basal metabolic rate slows with resulting decreased vital signs and profound weakness. Children with marasmus often are the subject of the most dramatic photographs of Somali, Ethiopian, and other children of famine. Kwashiorkor or protein-calorie malnutrition (PCM) may be due to inadequate intake or absorption (or loss) of protein. Kwashiorkor is more common and the clinical picture is less dramatic than the emaciation of marasmus. Initially, inadequate protein causes lethargy or irritability. As the condition progresses, anorexia develops, weakness increases, muscle tissue decreases, and growth is retarded. Hepatomegaly occurs, kidney function decreases, and cardiac function is impaired. Edema is common and may mask other aspects of the disorder. Skin changes include dermatitis, changes in pigmentation, and changes in hair. Typically, hair is sparse, thin, and often streaked with red or gray color. Immune function is decreased and infection is common and often is the cause of death. Treatment of marasmus and Kwashiorkor includes fluid replacement, gradual protein and calorie replacement (fats are poorly tolerated in Kwashiorkor), and correction of vitamin and other deficiencies. A concern in both refugee camps and countries of second asylum, is the tendency of parents to overfeed when food becomes available. Cachexia is a metabolic disorder marked by general ill health and malnutrition, with weakness and emaciation; and is common in cancer, AIDS and other severe illnesses. In contradistinction to anorexia or starvation, in cachexia, there is approximately equal loss of fat and muscle, significant loss of bone mineral content, and cachexia does not respond to nutritional supplements or increased intake.
Onchoceriasis (filariasis): See full discussion (Distribution given below). The filarial parasites are tissue-dwelling roundworms whose microfilarial (mf) larvae are transmitted by several species of mosquitos or flies. The most problematic forms of filariasis are (1) Bancroftian filariasis and Malayan filariasis (much of the tropical and subtropical world between the Tropics of Cancer and Capricorn) which involve the lymphatic system and result in elephantiasisis; (2) loiasis or loa loa (tropical Africa) in which worms live in subcutaneous tissue; and (3) Onchocerciasis (tropical Africa and to a lesser extent Central and South America) which causes river blindness and skin disorders. Treatment in most cases is effective only against the mf, hence the infection continues and repeated treatment (with ivermectin and/or DEC) may be necessary.
Rift Valley fever: See full discussion of HFs (Africa, especially Central, Egypt): The Rift Valley fever (RVF) virus is transmitted by mosquito or perhaps other blood-sucking insect bite; and by exposure to body fluids or meat of infected animals. The incubation period is 3-5 days. Most people with RVF have no symptoms or a mild febrile illness with liver abnormalities. Others, however, develop a classic HF with weakness, fatigue, back pain, dizziness, and rapid weight loss. Retinal vasculitis occurs in about 10% of cases, and encephalitis occurs in a few patients. Though definitive research on treatment is lacking, treatment of severe cases may include the use of IV ribavirin as described in the full discussion of hemorrhagic fevers.
River blindness: See filariasis summary or full discussion.
Tapeworms and cysticercosis (Worldwide, but endemic in certain areas): Tapeworm or cestode infections result from the ingestion of Taeniasis sp. eggs, often found in undercooked meat or excreted proglottids (segments) of the adult tapeworm. Depending on the species, adult tapeworms reach a length of eight meters and live as long as 25 years. The beef tapeworm (Taeniasis saginata) usually causes gastrointestinal discomfort and weight loss. Awareness of infection often is through discovery of proglottids in the stool. Manifestations of intestinal infection with the pork tapeworm (Taeniasis solium) are similar to those of the beef tapeworm. However, ingestion of food that is fecally contaminated with T. solium eggs results in cysticercosis. The symptoms of cysticercosis are caused by the presence of cysticeri (encapsulated larvae) and the resulting inflammatory reaction or space-occupying lesions. The incubation period is as long as five years. Manifestions are most commonly varied neurologic problems, including fever, headache, CVA, hydrocephalus, seizures, and other symptoms of increased intracranial pressure. Visual manifestations may be from increased intracranial pressure or a cyst in the eye. Cysts are also found in subcutaneous and muscle tissue. Treatment of intestinal tapeworms is with a single dose of praziquantel 5-10 mg/kg. Treatment of cysticercosis is with albendazole 5 mg/kg po tid for 8-30 days or praziquantel 20 mg/kg po tid for 14 days. Therapy may increase symptoms, in which case dexamethasone helps reduce distress. Also see echinococcosis and hymenolepiasis.
Toxocariasis (Worldwide): Toxocariasis is the most common visceral larva migrans and is due to infection with the tissue nematode (roundworm) toxocara canis or T. cati. Toxocariasis is most common among children who eat feces-contaminated dirt. Most infections are small load and asymptomatic except for mild eosinophilia. Heavy worm loads, decreased immune competence, and other factors may lead to malaise, fever, cough and wheezing, hepatomegaly, anorexia, and weight loss. Ocular toxocariasis also occurs and usually leads to decreased vision. For symptomatic infections, the treatment of choice is diethylcarbamazine 6 mg/kg/day po tid for 10 days. Asymptomatic infections are not necessary to treat.
Trachoma (Worldwide; more commonly endemic in poor rural communities in developing countries and common among nomadic and semi-nomadic cattle-herder): Trachoma is a recurrent conjunctivitis beginning in childhood and caused by Chlamydia trachomatis. Trachoma is a major cause of blindness in developing countries. Childhood infections and reinfections result in bilateral follicular conjunctivitis, epithelial keratitis, and corneal vascularization. Conjunctival scarring results in ingrown/in-turned eyelashes and lid deformities that, in turn, cause corneal scarring. Secondary bacterial infections are common, resulting in further complications. Treatment is with po tetracycline or erythromycin, both 250 mg 6 times daily for 3-5 weeks. Doxycycline 100 mg po bid for 3-5 weeks is also a common treatment. A single dose of azithromycin 20 mg/kg po is also used.
Trichinosis (trichinella) (Worldwide): Trichinosis is a nematode (roundworm) infection with Trichinella sp. from ingestion of meat that contains cysts, especially undercooked pork or meat from a carnivore. Infection ranges from light and asymptomatic to heavy and life-threatening. Manifestations vary according to the life cycle of the worms: Initially there is malaise, nausea, cramping abdominal pain, and diarrhea. Gastrointestinal symptoms are followed in 1-6 weeks by fever, eosinophilia, periorbital and facial edema, conjunctivitis, dysphagia, dyspnea, cough, myalgia, and muscle spasms. Complications include meningitis and other neurological disorders, myocarditis, pneumonia, and nephritis. The current treatment of choice is mebendazole 300 mg po tid for 10 days (sometimes with prednisone to control symptoms).
Trypanosomiasis (African) or African sleeping sickness (Tropical Africa): Trypanosomiasis is caused by protozoal parasites, Trypanosoma brucei rhodesiene or T b gambiense, transmitted by bite of the tsetse fly. T b rhodesiene infections are more virulent than T b gambiense; and in the former, patients experience three stages of illness (trypanosomal chancre, hemolymphatic, and meningoencephalitic) as opposed to two stages in the latter (trypanosomal chancre and meningoencephalitic) with significantly milder symptoms. The painful trypanosomal chancre (3-10 cm) appears about two days after the bite and lasts 2-4 weeks. The hemolymphatic stage is characterized by high fevers lasting several days, with symptom-free periods of days to weeks. Less common manifestations of this stage are severe headache, malaise, arthralgia, lymphadenopathy, circinate rash, pruritis, and hepatosplenomegaly. Weight loss and debilitation also occur, and myocarditis may develop. The meningoencephalitic stage is characterized by progressive apathy, nighttime insomnia and daytime somnolence, anorexia, retarded speech, extrapyramidal signs (tremors, fasciculations, choreiform movements, and Parkinsonian-like appearance), and finally, coma and death. Treatment is complex and toxic, and depends on the infecting organism and stage of illness. Among the medications currently in use are suramin, melarsoprol, pentamidine, eflornithine, and corticosteroids.