Approximately 779 million people are at great risk (85% in Africa) in 78 countries of which 42 are in Africa, and 207 million (97% in sub-Saharan Africa) are estimated to be affected by schistosomiasis [1]. Out of estimated 201.5 million people infected in sub-Saharan Africa (both Schistosoma mansoni and Schistosoma haematobium) [1], more than a half experience substantial morbidity [2]. It was estimated that about 54 millions are infected with S. mansoni in sub-Saharan Africa, and about 0.93 millions are with hematemesis, likely having severe hepatosplenic morbidity due to intestinal schistosomiasis [2]. This corresponds with the annual incidence of 180,000 with hematemesis, of whom 83.3% die annually and also with liver failure being responsible for extra-substantial proportion of death.

Morbidity in intestinal schistosomiasis related to S. mansoni involves the intestinal tract, manifesting with diarrhea, abdominal pain, and blood in the stools. Also infection with S. mansoni may present as hepatosplenic schistosomiasis, characterized by enlargement of the liver and spleen and accompanied by increased firmness of the organs [3]. Many of the eggs (about a half) excreted by S. mansoni enter the systemic circulation via the portal vein and lodge in the liver [4], where they give rise to vascular and inflammatory granulomatous changes that can lead to periportal fibrosis, portal hypertension with development of esophageal varices, and the risk of life-threatening hematemesis.

Tanzania is among the 7 countries (Burkina Faso, Mali, Sierra Leon, Ghana, Mozambique, Tanzania, and Madagascar) most severely affected with schistosomiasis, classified as high prevalence setting [5]. Intestinal schistosomiasis, due to S. mansoni, is a serious public health problem which is endemic in many parts of Tanzania [6]. About 19% of the population in Tanzania is constantly exposed to S. mansoni infection especially in rural and peri-urban areas [7]. In Tanzania, extensive transmission of S. mansoni occurs along the shores of the Great Lakes [6] and areas of Lake Victoria basin including the lake shores and its associated islands are the most affected areas in Tanzania. For instance among adults from randomly selected villages in Ukerewe islands, Kardoff et al. [8] and Malenganisho et al. [9] found a prevalence of 86% in Galu and Muriti villages and 78% in Musozi village, respectively. Of those examined adults, about 41.5% in Musozi village and 30.0% in Miriti and Galu villages had periportal fibrosis [8,9]. There is also evidence that the level of S. mansoni transmission is increasing also in the northeastern and western parts of Lake Victoria shore that previously was regarded as low level or free of transmission areas [10].

Although it is quite clear that, in S. mansoni endemic areas, children and young adolescents exhibit the highest prevalence and intensity of infection [11]; however, severe late-stage consequences are likely during the adulthood, despite generally lower intensities of infection. In order to determine the S. mansoni-related hepatosplenic morbidity, the present study targeted on the adult community for collecting morbidity baseline data as mass drug administration (MDA) and other interventions in this control programme targeting all community members of 4 year and above.

A total of 388 participants were recruited for ultrasonography and parasitological examinations. Due to a logistical problem, 32 individuals in Buhama village were not measured for the left liver lobe size, right liver lobe size, and main portal vein size, including 5 individuals in Kabaganga village in whom their heights were not taken. These cases were therefore excluded from the analysis of organometric data. Of 388 included, 28 (7.2%) individuals had other abnormalities and hence were excluded in scoring and assessing PPF using the pattern image.

Of the 360 total individuals examined by ultrasonography, 152 (42.2%) had evidence of periportal fibrosis (PPF) (by LIP); 30.6% had mild PPF (pattern B, C, and D) and 10.8% had severe PPF (pattern E and F). Of 36 with severe PPF, 29 (8.8%) had pattern E and 7 (2.0%) had pattern F. Of 152 with PPF, 87.2% (136/152) of them had evidence of SBWT; thus being confirmed by quantitative method of assessing PPF. The prevalence of PPF was higher in male (47.0%) than in female (34.4%; P=0.007). The prevalence of severe PPF was also remarkably higher in male (15%) than in female (5%; P= 0.001). The prevalence of PPF increases with age and then almost remained constant throughout the adulthood. The prevalence of PPF was consistently high in all 8 villages; Isenyi village leading with 56.4% prevalence while Buhama village was the lowest with 30.0%. The prevalence of S. mansoni was also higher in male (35.6%) than in female (26.0%; P=0.043) but the prevalence decreased with increase in age (Table 1).

Fecal egg excretion in positive cases was between 24 and 984 (median 48). There was no difference of median or mean egg excretion by sex (median, male 48 epg vs female 48 epg; mean, male 113.0 epg vs female 88.2 epg, P=0.3708). The quantitative fecal egg excretion (mean epg) was the highest in the older age group (156.0 and 128.0 epg in the 50-59 and 60 and over age groups, respectively), and in Izindabo (159.7 epg) and Nyakasasa (126.8 epg) villages. However, the differences from the rest age groups and villages were not significant by Pearson chi-square or t-test.

Hepatosplenomegaly assessed as non-specific findings related to S. mansoni infection was also common in Kome Island; 55.2% had splenomegaly and 68.1% had left lobe hepatomegaly. The prevalence of the right liver lobe shrinkage was 14.8%, and the right liver lobe enlargement was 6.7%. The shrinkage of the right liver lobe was higher in male (19.0%) than in female (9.6%; P=0.014) (Table 2).

Of 152 patients with PPF, 24 (15.8%) had irregular or nodular liver surface, 10 (5.9%) showed that their liver edge was abnormally round, and 27 (17.1%) showed distorted or convexed liver shape. The gall bladder wall thickness as an evidence of involvement by periportal fibrosis was present in 67 patients (44.1%). In all of these 67 cases, gallbladder wall thickening was associated with central portal fibrosis. Collateral vessels were detected in 42 patients (27.6%) and ascites in 4 patients (2.6%).

Twenty-eight had other specified pathological abnormalities of the liver not to be related to S. mansoni infection; their majority had fatty liver (24.4%), hemangioma (17.9%), and gallstone (10.7%).

The baseline finding clearly shows that there is high prevalence of PPF (42.2%) and other S. mansoni-related hepatosplenic morbidity in the communities of Kome Island. The left lobe hepatomegaly that was found in 68.1%, the right liver lobe shrinkage in 14.8%, and splenomegaly in 55.2% indicated a high morbidity in Kome community caused by S. mansoni infection. The prevalence of PPF in this community was similar to 41.5% observed by Malenganisho et al. [9] in Musozi village which is believed to be most highly affected with intestinal schistosomiasis in Ukerewe District. However, our figure was comparatively higher than 30.0% and 24.4% in a study done in the same areas of Ukerewe Islands among randomly selected adult community members as were observed by Kardoff et al. [8] and Kaatano et al. [15], respectively. The morbidity related to S. mansoni was also much higher in the villages on proximity with the lake shore, agreeing to a similar observation by Kaatano and others in 1993 (unpublished observations) in Ukerewe (PPF 30.7% in onshore vs 18.7% in inland villages) as was expected. S. mansoni normally is highly prevalent along the lake shore [16]. Since living on or near the lakeshore is ecological proxy for risky water-contact behavior because those individuals in these areas are more likely to undertake risky water-contact behavior in comparison with the ones who are distant from the lake.

However, on the other hand, the prevalence of PPF of 42.2% as observed in our study area was comparatively higher than other studies in the rest other East Africa along Lake Victoria shore using the Niamey protocol. King et al. [17] in Kenya revealed a prevalence of PPF of 3% while Booth et al. [18] recorded the prevalence of PPF of 31.5% and 6.1% in 2 villages of Uganda along the shores of Lake Albert. Geographical variation in levels of morbidity and infection rate is a common phenomenon, in part mainly being attributed in part to the focal nature of transmission [19], which has been observed in even very close in adjacent communities [20].

The finding of the prevalence of PPF being significantly higher in male than female is as expected as and was also confirmed by other workers [8,9]. Water contact activities such as swimming and fishing which are normally commoner for males than females; in most cases of the male water contact (swimming, fishing, etc) takes long and usually involves most part of the body in contact with lake water. However, one of the important and striking observations in this study was the occurrence of the high prevalence of PPF (37%) in the teenage group of 10-20 years. Similar trends of observation were recorded by Malenganisho et al. [9] in Musozi village, Ukerewe Islands District and by Gabone et al. [21] in Kome Island, Sengerema District, Lake Victoria. This result contrasts with that of Vennervald et al. [3] from an endemic area of Kenya where a similar age group did not show significant PPF despite high rates of splenomegaly and hepatomegaly. In another study in Ukerewe [15] which were rather more representative of all community members, its prevalence in same age group was 12.5% while 5.4% of PPF was detected by El-Scheich et al. [22] among school age children in Ukerewe. This finding probably supports the ideas that intensive exposure to heavy infection during early childhood in high transmission areas is responsible for such rapid progression of morbidity. Earlier studies [23] estimated the time lapse between infection with S. mansoni and evolution of PPF in humans to be at least 5 years. However, the evolution of PPF in our setting of Lake Victoria region as compared with Sudan [23] and other part of northern Africa might be longer where Kardoff et al. [8] classified it as intermediate. Although our study did not include children less than 14 years, it can be inferred that in an established stable transmission area, such as the shores of Lake Victoria, PPF starts to develop in childhood. Such assumption is also supported by PPF (4.7%) detected in Ukerewe [15] among 5-10 years age group.

Observation of the lower egg excretion detection rate (i.e., low S. mansoni infection prevalence) might be attributed to methodology of collection of stool samples. Due to logistic reason, in our case only 1 stool sample was collected instead of 2 samples in 2 consecutive days that might underestimate the infection rate due to the fact that by examination of a single stool sample, particularly in low intensity, cases are frequently missed as a result of less sensitive when only 1 stool sample is examined [24]. However, the procedures of sample collection and parasitological testing were ensured to be the same throughout the baseline survey. This fact is also supported by relatively higher rate of periportal fibrosis and also by degree of discordance between hepatic fibrosis and demonstration of eggs in stools noted in our study; 65.1% (99/152) of those individuals with detectable hepatic fibrosis at the baseline survey had no demonstrable eggs in their stools.

Conclusively, a high S. mansoni-related morbidity justifies the implementation of mass drug administration and other intervention such as provision of alternative sources of water supply (pumped wells) that has already started in the study area.