We report schistosomiasis in 8 of the 16 persons returning from the Tanzanian shore of Lake Tanganyika, an area for which data regarding this disease are virtually absent. Studies on schistosomiasis in Tanzania have focused mainly on regions around Lake Victoria, widely ignoring Lake Tanganyika.[4, 5] These cases illustrate the risk of acquiring schistosomiasis not only for travelers to this area but also for the resident population considering their more intense and life-long exposure. Also, this outbreak underlines the usefulness of detecting disease activity by using travelers as sentinels.[9, 13, 14] Lake Tanganyika has erroneously been mentioned as a high-risk area for travelers for acquiring schistosomiasis. We assume, however, that rather Lake Malawi was meant in that report since there is no “Lake Tanganyika in Malawi.” Lake Malawi, in fact, is well known as a high-risk area for schistosomiasis in travelers and has been the most important source of acute schistosomiasis in travelers seen at the Hospital of Tropical Diseases, London, within a period of 14 years. There is only one report on S mansoni in the Kigoma area, which focuses on the baboon population in Gombe National Park. Although S mansoni infection is believed to be mainly restricted to humans, these primates might possess a potential role as a reservoir for S mansoni in this area. Further research including genomic analyses is warranted to answer that question. Our patients had repeatedly been exposed to freshwater over several weeks, so date of first infection and time frames, eg, from first infection to symptoms and seroconversion could not be exactly specified. In acute schistosomiasis, the suspicion of the diagnosis is mainly a clinical one after freshwater exposure, but the confirmation is often based on serological testing. However, this causes a diagnostic gap: seroconversion occurs in most cases around 6 weeks post infection and 4 weeks after first symptoms, respectively, or even later.[16, 17] Since eggs are deposited usually within 5–10 weeks post infection, assays for the detection of eggs usually yield negative results in acute schistosomiasis.[16-18] Therefore, Schistosoma egg excretion is not a reliable marker during the early, acute phase of the disease for which PCR may become increasingly important as a diagnostic tool.[3, 11] As observed in our patients, acute infection may be asymptomatic, and may evolve without abnormal laboratory parameters. This offers strong arguments to perform at least a schistosome antibody test at about 3 months after freshwater contact. Misdiagnosis in travelers may translate into increased risks of chronic infection and neuroschistosomiasis. Praziquantel, the treatment of choice in schistosomiasis, acts primarily on adult worms. Praziquantel should not be administered in acute schistosomiasis because it does not kill schistosomula and may even be deleterious when given during the acute phase by inducing an allergic type of response to parasitic destruction. Corticosteroids may alleviate the symptoms but may also reduce the plasma concentration of praziquantel if given at the same time. Therefore, it is recommended to use praziquantel approximately 3 months after the last freshwater exposure. Interestingly, eight persons remained uninfected although having been repeatedly exposed to freshwater in the same sites as the eight infected individuals. No obvious differences in exposure habits were found, ie, they had been exposed to freshwater at the same locations, and the amount and duration of freshwater contacts were comparable. This infection rate of 50% may indicate a rather low density of cercariae in the water of that area. Our study also emphasizes the need for professional pre-travel advice, particularly for long-term travelers in schistosomiasis-endemic areas. Although repellents have been suggested to prevent penetration of the skin by the cercariae,[20, 21] this only reduces the risk but does not provide full protection. Thus, the avoidance of freshwater contact remains the only effective preventive measure for travelers to disease-endemic areas. For the resident population, this is hardly a feasible option. In conclusion, this outbreak in returning travelers illustrates that S mansoni poses a thus far underestimated hazard for the local population living on the Tanzanian shore of Lake Tanganyika. Systematic investigations into the actual disease burden and the implementation or review of control measures are warranted.