Determinants of Willingness to Pay for Fecal Sludge Management Services and Knowledge Gaps: A Scoping Review

Achieving universal access to safely managed sanitation services is one of the Sustainable Development Goal 6 targets (SDG6.2). The cost and availability of services to ensure the safe management of on-site sanitation, such as pit latrines and septic tanks, can be major barriers for poor households. Particularly, fecal sludge emptying services have become increasingly important due to the growing urban population. This review aims to scope the literature on stated and revealed willingness to pay (WTP) for emptying on-site sanitation systems and to identify determinants of WTP and gaps in knowledge. We performed electronic searches of six databases. After deduplication, 1846 records were identified, of which 14 were included in the review. In these studies, we identified 26 distinct scenarios that reported mean or median WTP values for emptying services and their market price (i.e., price at which the services were provided). Among the 26 scenarios, 77% (n = 20) reported that WTP was lower than the market price. We identified 20 statistically significant determinants of WTP, which can be leveraged when developing or improving manual and mechanical emptying services to attract more customers. Future research should consider services that adopt flexible pricing or mobile money payment and optimize their emptying operations to increase WTP. Validating the effectiveness of such services in solving the WTP–market price imbalance is a significant knowledge gap

<i>Schistosoma mansoni</i> infection suppresses the growth of <i>Plasmodium yoelii</i> parasites in the liver and reduces gametocyte infectivity to mosquitoes

<div><p>Malaria and schistosomiasis are major parasitic diseases causing morbidity and mortality in the tropics. Epidemiological surveys have revealed coinfection rates of up to 30% among children in Sub-Saharan Africa. To investigate the impact of coinfection of these two parasites on disease epidemiology and pathology, we carried out coinfection studies using <i>Plasmodium yoelii</i> and <i>Schistosoma mansoni</i> in mice. Malaria parasite growth in the liver following sporozoite inoculation is significantly inhibited in mice infected with <i>S</i>. <i>mansoni</i>, so that when low numbers of sporozoites are inoculated, there is a large reduction in the percentage of mice that go on to develop blood stage malaria. Furthermore, gametocyte infectivity is much reduced in mice with <i>S</i>. <i>mansoni</i> infections. These results have profound implications for understanding the interactions between <i>Plasmodium</i> and <i>Schistosoma</i> species, and have implications for the control of malaria in schistosome endemic areas.</p></div

Gametocyte infectivity.

<p>(A) Parasitemia. Female BALB/c mice were each inoculated with 1 x 10⁶ <i>Plasmodium yoelii</i> parasitized erythrocytes intravenously with (n = 4 mice) or without (n = 5) pre-existing <i>Schistosoma mansoni</i> infection. Parasitaemia was determined by microscopic examination on days 3, 4, and 5 post-inoculation; day 3: Student’s two-tailed t-test; **P<0.01, t = -4.906, df = 7; Day5: *P<0.05, t = -2.922, df = 5 (<b>B</b>) Gametocyte density. Gametocyte density was determined on days 3 and 4 post-inoculation of 1 x 10⁶ <i>P</i>. <i>yoelii</i>-parasitized erythrocytes intravenously. Day 3: Student’s two-tailed t-test; **P<0.01, t = 3.813, df = 5; Day 4: **P<0.01, t = 3.608, df = 5. Error bars show the geometric mean with 95% confidence intervals. (C) Percentage of mosquitoes with one or more oocysts present on the midgut eight days post-feeding on infected mice. A minimum of eight mosquitoes were allowed to feed on each individual mouse in the group per day **P = 0.0003, (2-way ANOVA, F = 22.23, DFn = 1, DFd = 14). Error bars mar the standard error of the mean per mouse group. (D) Oocyst numbers per mosquito. The numbers of oocysts present on mosquito midguts were determined eight days post-mosquito feeding; day 3: Student’s two-tailed t-test, **P<0.01, t = 3.077, df = 25. Error bars show the geometric mean with 95% confidence intervals. Data is representative of three independent experiments.</p

Information for PCR primers.

<p>Information for PCR primers.</p

Malaria parasite liver burden in BALB/c, C57BL/6, and CBA/J mice.

<p>(A) Copy number of <i>Plasmodium yoelii</i> 18s RNA gene per 1×10⁶ mouse G3PDH gene measured at 42 h post sporozoite inoculation. Female BALB/c, B6, and CBA/J mice (N = 5) infected with 50 <i>Schistosoma mansoni</i>-cercaria 10 weeks previously were challenged with 1,500 SPZ of <i>P</i>. <i>yoelii</i> along with <i>S</i>. <i>mansoni-</i>non-infected controls. BALB/c: ***P<0.001, t = 6.283, df = 8; B6: *P<0.05, t = 2.511, df = 8; CBA: **P<0.01, t = 4.220, df = 7. (B) Copy number of <i>Plasmodium berghei</i> 18s RNA gene per 1×10⁶ mouse G3PDH gene measured at 42 h post sporozoite inoculation. Female BALB/c, B6, and CBA/J mice (N = 5) infected with 50 <i>S</i>. <i>mansoni</i>-cercaria 10 weeks previously were challenged with 1,500 SPZ of <i>P</i>. <i>berghei</i> along with <i>S</i>. <i>mansoni-</i>non-infected controls. BALB/c: *P<0.05, t = 2.306, df = 8; B6: ***P<0.001, t = 5.336, df = 8; CBA: *P<0.05, t = 2.846, df = 7. All data were statistically examined using Student’s two-tailed t-test.</p

Liver immunopathology in <i>Schistosoma mansoni</i>-cercariae infection and intraportal infusion of frozen <i>S</i>. <i>mansoni</i>-eggs.

<p>(A) Malaria parasite liver burden with/without intraportal infusion of frozen <i>S</i>. <i>mansoni</i>-eggs. Female B6 mice were intraportally inoculated 3,000/10,000 frozen <i>S</i>. <i>mansoni</i>-eggs and challenged with 1,500 sporozoites of <i>Plasmodium yoelii</i> along with controls inoculated with PBS (control: N = 3; 3,000 frozen eggs: N = 5, ***P<0.001, t = 1.943, df = 6; 10,000 frozen eggs: N = 3, *P<0.05, Student’s two-tailed t-test, t = 4.072, df = 4). (B) Macroscopic and microscopic images of liver pathology. The black lines indicate 250 micro meters. (C) The number of granulomas in the liver. Female BALB/c mice and B6 mice were inoculated with 50 <i>S</i>. <i>mansoni</i>-cercariae subcutaneously (naive: N = 5; 50 cercariae: N = 3) or inoculated with 3,000 frozen <i>S</i>. <i>mansoni</i>-eggs along with controls inoculated with PBS intraportaly (PBS: N = 5; 3,000 frozen eggs: N = 5). The numbers of granuloma were counted in 20 microscopic fields at 100 x magnification. *P<0.05, ***P<0.001. All data were statistically examined using Student’s two-tailed t-test. (D) The numbers of immune cells induced by intraportal infusion of 3,000 frozen <i>S</i>. <i>mansoni</i>-eggs. Female B6 mice (N = 4/group) were intraportaly inoculated 3,000 <i>S</i>. <i>mansoni</i>-eggs. (E) The numbers of immune cells induced by 50 <i>S</i>. <i>mansoni</i>-cercaria infection. Female BALB/c mice (naive: N = 9, 8 weeks: N = 9, 10 weeks N = 6) were infected with 50 <i>S</i>. <i>mansoni</i>-cercariae. *P<0.05, **P<0.01, ***P<0.001. All data were statistically examined using Student’s two-tailed t-test.</p

Growth of malaria parasites in the liver and blood of mice following SPZ inoculation of <i>Plasmodium yoelii</i> with and without <i>Schistosoma mansoni</i> infection.

<p>(A) Copy number of <i>P</i>. <i>yoelii</i> 18s RNA gene per 1×10⁶mouse G3PDH gene measured at 42 h post SPZ inoculation. Female BALB/c mice (N = 6) infected with 50 <i>S</i>. <i>mansoni</i>-cercariae 10 weeks previously were challenged with 1,500 <i>P</i>. <i>yoelii</i> SPZ along with <i>S</i>. <i>mansoni</i>-non-infected controls. **P<0.01, Student’s two-tailed t-test, t = 4.362, df = 10. (B) Parasitaemia. Blood stage malaria parasites were monitored daily from day 2 to 8 post i.v. inoculation of 500 <i>P</i>. <i>yoelii</i> SPZ. (C) Percentage survival. Data from one representative experiment of three independent repeats are shown.</p

<i>Plasmodium yoelii</i> parasite density in the blood and liver.

<p>Copy number of <i>P</i>. <i>yoelii</i> 18s RNA gene per 1×10⁶ mouse G3PDH gene measured at 42 h post sporozoite inoculation. Female BALB/c mice (N = 5) infected with 50 <i>Schistosoma mansoni</i>-cercaria 10 weeks previously were challenged with 1,500 SPZ of <i>P</i>. <i>yoelii</i> along with <i>S</i>. <i>mansoni</i>-non-infected controls. (A) <i>P</i>. <i>yoelii</i> parasitaemia in the blood. (B) <i>P</i>. <i>yoelii</i> parasite density and proliferation in the liver. ***P<0.001, Student’s two-tailed t-test, t = -6.316, df = 8.</p

Malaria outcomes with low dose SPZ challenge.

<p>Female BALB/c mice (N = 16) infected with 50 <i>Schistosoma mansoni</i>-cercariae 10 weeks previously were challenged with 50 sporozoites of <i>Plasmodium yoelii</i> along with <i>S</i>. <i>mansoni</i>-non-infected controls. (A) The percentage of mice that did not develop blood stage infection following inoculation of low does SPZ. Data were statistically examined using the log-rank test. ***P<0.001, x2 = 29.8, df = 1. (B) Parasitaemia. Mean parasitaemia in <i>S</i>. <i>mansoni</i> infected group was calculated only among blood stage malaria positive mice.</p

Malaria parasite liver burden in wild-type B6, IFN-gamma-deficient, and Interleukin-4-deficient mice.

<p>Copy number of <i>Plasmodium yoelii</i> 18s RNA gene per 1×10⁶ mouse G3PDH gene measured at 42 h post sporozoite inoculation. Female IFN-γ^-/- mice (N = 8), IL-4^-/- mice (N = 8), and B6 WT mice (N = 4) were intraportally inoculated with 3,000 frozen <i>S</i>. <i>mansoni</i>-eggs and challenged with 1,500 SPZ of <i>P</i>. <i>yoelii</i> along with each control groups inoculated 100 μL PBS (N = 4). B6 WT mice: *P<0.05, t = 3.017, df = 5; IFN-γ^-/- mice: Not significant (NS), t = -1.303, df = 10; IL-4-/- mice: NS, t = -0.016, df = 10.</p