African Trypanosomiasis and Acute Pulmonary Schistosomiasis in Travelers
abstracts & commentaries
Synopsis: Two recent articles remind us that African trypanosomiasis and acute pulmonary schistosomiasis occur in travelers from developed countries.
Sources: Sinha A, et al. African trypanosomiasis in two travelers from the United States. Clin Infect Dis 1999;29:840-844; Cooke GS, et al. Acute pulmonary schistosomiasis in travelers returning from Lake Malawi, sub-Saharan Africa. Clin Infect Dis 1999;29:836-839.
Sinha and colleagues reported two travelers from the United States who contracted African trypanosomiasis during a recent safari trip in Tanzania. Both patients presented with fevers, sweats, chills, and myalgias. One patient recalled a painful fly bite six days prior to onset of her symptoms. The second patient recalled numerous tsetse fly bites and noted an expanding erythematous lesion on his right flank as well as an edematous swelling below the left lower lip. Both patients had been on malaria chemoprophylaxis. The first patient was diagnosed when the Giemsa-stained thin and thick malaria blood smears revealed trypomastigotes. The second patient was diagnosed by Wright’s staining of a peripheral blood smear, which revealed trypomastigotes. The organisms were identified as Trypanosoma brucei rhodesiense, or the East African form of African trypanosomiasis. Cerebrospinal fluid (CSF) from both patients was examined and showed no parasites. Both patients were successfully treated with suramin.
Comment by Lin H. Chen, MD
Human African trypanosomiasis (HAT), or sleeping sickness, is endemic in sub-Saharan Africa and is caused by two subspecies of trypanosomes—T.b. gambiense and T.b. rhodesiense. Gambian HAT, also referred to as the West African form, occurs in western and central Africa, whereas Rhodesian HAT, the East African form, is endemic in eastern and southern Africa. Rhodesian HAT presents more acutely and progresses more rapidly. Sinha et al reported that since 1967, all cases of HAT occurring in U.S. travelers have been Rhodesian HAT, and most patients contracted the disease during visits to game parks.
This disease is transmitted by tsetse flies. Acute presentations may include an inoculation chancre as well as nonspecific symptoms such as fevers, headaches, myalgia, malaise, and transient edema. The patients may develop weight loss, lymphadenopathy, and splenomegaly. Late-stage manifestations include somnolence, behavior change, stupor, and coma. Convulsions are more common in children. Left untreated, the disease is fatal.
The diagnosis of Rhodesian HAT is made by demonstration of trypanosomes in blood, chancre, or CSF. Because the degree of parasitemia is higher in Rhodesian HAT than in Gambian HAT, trypanosomes are easier to detect in blood; lymph node aspirates are rarely necessary. A CSF analysis should be done whenever HAT is established or suspected, and CSF should be examined for trypanosomes with "double centrifugation." The presence of parasites, CSF pleocytosis (WBC > 5/mm3), or Mott cells (large globular inclusion-containing plasma cells) indicates late-stage disease. Treatment of early-stage Rhodesian HAT is with suramin, and with melarsoprol when there is central nervous system (CNS) involvement.
Acute Pulmonary Schistosomiasis
Cooke and colleagues reported four patients with acute schistosomiasis presenting to John Radcliffe Hospital in Oxford, England, in 1997. All four patients had been swimming in Lake Malawi. All four patients developed symptoms from two to eight weeks after swimming, including fevers, headaches, lethargy, cough, and urticarial rash. Laboratory evaluations were notable for eosinophilia with or without leukopenia, mild thrombocytopenia, and mild liver function abnormalities. Chest radiography and computerized tomography (CT) revealed pulmonary nodules. Only one patient was found to have Schistosoma haematobium in a stool sample, but all four patients had positive schistosomal serology. Although the enzyme-linked immunoassay (ELISA) did not identify the species specifically, the infections were acquired in the same area and were assumed to be S. haematobium. All were treated with a single dose of praziquantel 40 mg/kg. Three of the patients experienced transient exacerbation of symptoms, but all recovered.
Comment by Lin H. Chen, MD
Schistosomiasis occurs in tropical and subtropical areas of Africa, South America, the Middle East, and East Asia. S. haematobium is endemic in Lake Malawi in sub-Saharan Africa, where the four travelers from the United Kingdom acquired their infection. Acute schistosomiasis is associated more frequently with S. japonicum and S. mansoni infection, and is rarely observed during S. haematobium infection. The article by Cooke et al indicates that acute pulmonary schistosomiasis can occur with S. haematobium infections, and it will be interesting to see if similar presentations continue to appear.
Schistosomiasis is acquired in fresh water, through intact skin, when the human host comes into contact with the infectious cercarial larvae. The initial contact sometimes leads to a localized dermatitis. Acute schistosomiasis (Katayama fever) may develop 4-8 weeks after exposure, with symptoms of fever, sweats, chills, cough, and headaches. The pulmonary manifestation is speculated to be an immune response to the schistosomulae. Physical signs include lymphadenopathy, hepatosplenomegaly, and rash. Eosinophilia is a significant laboratory finding.
Detection of parasite eggs in stool or urine establishes the diagnosis, but may not be present early in the course. Biopsies of the rectum, intestine, liver, prostate, or bladder can make the diagnosis if parasite ova can be demonstrated. Serologic conversion can also establish the diagnosis of acute schistosomiasis. Praziquantel is the treatment of choice for schistosomiasis, and is well tolerated.
These two articles demonstrate that travelers from developed countries can contract African trypanosomiasis and acute pulmonary schistosomiasis during travel within endemic areas. Many of the patients reported in these two articles presented with nonspecific symptoms, but the patients’ history of fly bite or swimming in Lake Malawi helped a great deal in determining the diagnoses. With increased tourism to Africa, travel medicine specialists need to consider these diagnoses in febrile travelers returning from endemic areas. (Dr. Chen is Clinical Instructor, Harvard Medical School and Travel/Tropical Medicine Clinic, Lahey Clinic Medical Center, Cambridge, MA.)
1. Pepin J, Donelson JE. African trypanosomiasis (sleeping sickness). In: Guerrant RL, Walker DH, Weller PF, eds. Tropical Infectious Diseases. Philadelphia, Pa: Churchill Livingstone; 1999:774-784.
2. King CH, Mahmoud AAF. Schistosomiasis. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical Infectious Diseases. Philadelphia, Pa: Churchill Livingstone; 1999:1031-1038.
Which of the following statements is false?
a. Infection with Trypanosoma brucei rhodesiense occurs in eastern Africa and causes a more acute disease than Trypanosoma brucei gambiense.
b. Acute schistosomiasis is usually associated with infection from S. mansoni and S. japonicum rather than S. haematobium.
c. When the diagnosis of African trypanosomiasis is being considered, one should perform a lumbar puncture to examine the CSF for parasites and WBCs.
d. Acute schistosomiasis should be considered in febrile patients with eosinophilia who report exposure to fresh water in Africa.
e. The history of a chancre from a tsetse fly bite should raise suspicion for possible schistosomiasis.