- Top charities
Published: December 2012
This page discusses the general case for mass deworming. In general, we focus our discussion on work similar to that of the Schistosomiasis Control Initiative.
Mass deworming means treating large numbers of people with parasite-killing drugs: praziquantel kills schistosomiasis, while albendazole kills soil-transmitted helminths. Treatment takes place in areas where these parasites are believed to be extremely common, and side effects of the drugs are believed to be minor; thus, everyone in a given population (sometimes schoolchildren; sometimes the community at large) is treated, without being individually tested for the presence of infections.
Mass deworming is generally very inexpensive on a per-person-treated basis (in the range of $0.50). The benefits are potentially major, but also debatable: because parasitic infections rarely cause mortality or other acute effects, the evidence on their impact on quality of life is thin. In brief:
Previous versions of this page:
"Schistosomiasis" and "soil-transmitted helminths (STH)" both describe chronic parasitic infections. We discuss each below.
Schistosomiasis involves infection with parasites released by snails and transmitted through the skin when it is exposed to infested water.1 The most common species of schistosoma infections in humans are S. mansoni, S. haematobium, and S. japonicum.2
While S. japonicum is present primarily in Asia and the Pacific, S. mansoni and S. haematobium are found in much of the tropics, including Sub-Saharan Africa.3 There is disagreement about how common schistosomiasis infections are; estimates range from 200 million to more than 600 million people infected.4 Because the Schistosomiasis Control Initiative, the charity for which we have undertaken this review, works only in Africa, we focus here on the morbidity caused by S. mansoni and S. haematobium. S. japonicum is believed by some scholars to be more dangerous than the other strains of schistosomiasis.5
The pathology of schistosomiasis varies by species and infection intensity. S. mansoni tends to infect the intestines, liver, and spleen,6 while S. haematobium typically infects blood vessels near the bladder.7
People can be infected by many of the worms at once, but schistosomes cannot reproduce inside the body.8 The burden of infections is typically highest in children and gradually declines as people age (even without treatment).9
In general, the morbidity caused by schistosomiasis arises from the eggs that the parasite lays while it inhabits the human host.10 Symptoms can include:
Some, but not all, symptoms of schistosomiasis are reversible with treatment.16
Soil-transmitted helminths (STHs) include trichuriasis (or whipworm), hookworm, and ascariasis (or roundworm). Each is estimated to affect the following number of people worldwide:17
The ascariasis and trichuriasis worms feed on the contents of the intestines, while hookworms feed on host blood in the small intestine, moving frequently and leaving small bleeding sores behind.18
People can be, and often are, infected by multiple worms (and multiple species of worms) at once, but worms cannot reproduce in the body.19
The prevailing understanding of soil-transmitted helminths is that many cases are asymptomatic and that morbidity depends on the intensity of infection.20 Symptoms can include:
Mass deworming is intended for areas with high prevalence of the infections discussed here; people are treated without being individually tested.
Distributions sometimes target school-age children and sometimes target the population at large (for example, see our review of the Schistosomiasis Control Initiative). The Disease Control Priorities Report states that schools provide a strong infrastructure and that teachers can be trained to deliver drugs safely.27
A fuller picture of the process can be gained from our notes on our visit to a stakeholders meeting for a national deworming program and a demonstration deworming, as guests of the Schistosomiasis Control Initiative.
Strong evidence suggests that mass deworming reduces the prevalence of the infections discussed here.
As discussed above, the consequences of schistosomiasis/STHs fall into three categories:
We address each of these separately below, and then discuss other possible effects about which less is known.
In this section, we first discuss the effect of deworming on haemoglobin levels (low haemoglobin indicates anemia).30 This is because anemia is the symptom for which we have, by far, the most and highest-quality evidence, and a discussion of this symptom is illustrative of some general problems with assessing the evidence regarding the benefits of deworming.
We then discuss the other evidence we have seen on the immediate impacts of deworming; this evidence is very limited.
We have examined several literature reviews discussing the impact of deworming on changes in haemoglobin levels. We focus below on three reviews, two of them Cochrane reviews and one of them an especially transparent non-Cochrane review:
We have looked up each of these four studies and determined that each of them was pre-screened: each examined the impact of treatment on infected individuals as opposed to the impact of treatment on the general population.35
found a statistically significant 3.7 g/L increase in haemoglobin levels in two small screened trials (i.e. treating only people known to have soil-transmitted helminths).36 However, no effect on haemoglobin status was observed in the 11 (typically larger) trials that treated the entire population.37 We believe that Taylor-Robinson et al. 2012 should have included the haemoglobin results from Miguel and Kremer 2004, a large and well-known cluster-randomized unscreened trial of deworming, but that would be unlikely to change the overall picture, since it also failed to find a statistically significant increase in haemoglobin.38
Smith and Brooker 2010 investigates the question of whether haemoglobin effects are stronger in populations with higher prevalence of hookworm, and thus focuses on studies that can be used to help address this question.39 It does not appear to support its hypothesis that hookworm prevalence can predict the size of haemoglobin effects, but it does find a +1.89 g/L effect for STH-only deworming and a +2.37 g/L effect for combination deworming.40 The review provides some detail on the four studies going into the 2.37 g/L estimate: one or two are pre-screened,41 and all involved baseline hookworm prevalence of > 50% (weighted average 64%).42
We exclude results from Gulani 2007, King, Dickman, and Tisch 2005, and older Cochrane reviews on the grounds that the newer Cochrane reviews present a more exhaustive and transparent picture of the evidence.43
From these reviews, we conclude:
What is the significance of a +2.37 g/L effect? Of the above reviews, Smith and Brooker 2010 is most useful for getting context on the significance of this effect, because it gives means, standard deviations, and the percentage of people found to be under various thresholds for anemia for each of the relevant studies.44 Average concentrations range from ~100-130 g/L; standard deviations from 5-15 g/L; the absolute reduction in moderate anemia (threshold is 110 g/L)45 is ~9% in one study and ~14% in another (note that this is in line with the observed effects on anemia in the panel studies done by the Schistosomiasis Control Initiative). For another point of comparison, experimental evidence on insecticide-treated nets (ITNs) implies that children sleeping under ITNs experience +5.7 g/L compared to children sleeping under no nets.46
The evidence is quite thin regarding other immediate symptoms of these infections.
What does it mean if smaller programs with screened participants show effects, while larger programs of mass deworming do not? One possibility is that STH deworming does have some impact on nutrition in infected individuals, but that the effect is too small to pick up in unscreened population studies. Another possibility is that the effects seen in smaller programs are spurious. The Cochrane review highlights the latter possibility, stating that “the data on targeted deworming is limited (three small trials, n = 149); the quality of the evidence is ’moderate’ for weight and ’low’ for haemoglobin.” (The Cochrane review also points to a third possibility: “the intervention itself is different … having been screened, and then told they have worms, children are more likely to comply with treatment, and alter their behaviour.” We find this possibility least likely.)
Miguel and Kremer 2004 involved combination deworming, without prescreening, for some children and STH-only treatment for others (depending on the prevalence of schistosomiasis in the area).48 It found a ~25% reduction in school absenteeism, though no effect on test scores.49 It also found statistically significant impacts on self-reported sickness (both for "last week" and "often"), but not for height or weight.50 Followup studies implied potential developmental effects and externalities, discussed in later sections (along with our reservations about the study's representativeness).
King, Dickman, and Tisch 2005 also summarizes observational studies that examine people who are vs. aren't infected with schistosomiasis. It reports non-statistically significant differences in aerobic performance and unspecified measures of school performance and obstetric history, mixed differences (statistical significance depending on just how the comparison is made) in unspecified measures of pain history and exercise intolerance, and statistically significant effects in unspecified measures of exercise duration and diarrhea history.52 These observational studies could overstate the effects of infections (if infection is correlated with other things such as hygienic, economic or biological factors53) or understate the effects of infections (if "uninfected" people are infected after all, as King has argued elsewhere).54
Unfortunately, this review does not allow us to link individual studies from the bibliography to the particular meta-analysis outcomes reported. We do not consider it to meet our criteria for a high-quality literature review and cannot be confident in its claims.
Overall, evidence for the impact of deworming on short-term general health is thin.
Most of the effects discussed above are relatively small, and there is little consistency across different reviews and approaches. We would guess that combination deworming does have some small impacts on general health, but are fairly confident that it does not have large such impacts.
In addition to subtle general health impacts, deworming may avert more severe symptoms. Schistosomiasis can cause organ damage, particularly to the bladder, liver and kidneys, sometimes resulting in death, though these deaths appear highly infrequent and we have little information about the extent of non-fatal organ damage. Severe symptoms of STHs appear infrequent and short in duration.
In this section, we discuss schistosomiasis and STHs separately.
We have only identified one review55 (referred to here as "van der Werf et al.") that systematically attempts to attribute severe symptoms (organ damage/malfunction, death) to schistosomiasis. This review discusses symptoms such as the presence of abnormal amounts of blood in the urine, self-reported painful urination, enlarged liver/spleen, and various signs of kidney stress or malfunction.56 However, this review is problematic for several reasons:
Outside of this review, the only quantified information we have found on severe consequences of schistosomiasis involves deaths. It appears to us that even attributing deaths to schistosomiasis is very difficult, and estimates vary widely.62 Nonetheless, we regard the World Health Organization's 2004 estimate (published in 2008) of 41,000 deaths as the most credible.63 By comparison, the same source estimates that malaria results in roughly 890,000 deaths a year, more than twenty times as many, the vast majority of which are in children under 5.64
We can also get a sense of how bad the non-death burden of schistosomiasis is estimated to be, using the World Health Organization's Disability-adjusted life-year (DALY) estimates. For each age group, we tabulated the ratio of DALYs (a measure of all manifestations of disease burden) to YLLs (comparable to DALYs but only addressing mortality).65 These figures estimate that death accounts for about 80-90% of the burden of disease in people age 15-29; 90%-94% in people age 30-44; 95%+ in people age 45+; and only 10-20% in people under 14. This picture is consistent with the idea that older people are more likely to die due to schistosomiasis, while younger people are more likely to suffer other consequences such as subtle general health impacts and developmental effects.
The serious effects of soil-transmitted helminth infections vary by species.66 Because these severe symptoms are quite rare, we have found characterizing their frequency and severity to be difficult. The most thorough and up-to-date overview that we are aware of is the chapter on intestinal nematode infections (another name for soil-transmitted helminths) in the World Health Organization's The Global Epidemiology of Infectious Disease publication. That chapter is the published version of the working paper that was used to generate the Disease Control Priorities report's cost-effectiveness estimate for soil-transmitted helminth treatment.
For ascariasis, the most serious complication is short-term intestinal obstruction, sometimes resulting in death.67 We estimate that, each year, intestinal obstruction (which may require hospitalization and surgery and has an estimated duration of ~4 weeks) would occur in .026% of the school-age population of Sub-Saharan Africa (1 in ~3800 children per year) without treatment,68 resulting in about 3 deaths per million children per year of the school-age population.69
For trichuriasis, heavy infections can result in a "dysenteric form" involving a bleeding/inflamed colon, discomfort and bloody stools, with a duration of 12 months or more70; this is estimated to occur about once a year per ~700 children school-aged children in Sub-Saharan Africa each year.71 It is unclear whether trichuriasis continues to cause mortality, but if it does, this is quite rare.72
Hookworm's most serious symptom is believed to be anemia.73 We discuss this symptom above and conclude that there is not strong evidence for an impact of deworming treatment on anemia; any such impact is likely to be small.
It appears that death estimates for STHs in general have recently been revised downward, substantially. The World Health Organization's Global Burden of Disease report for 2001 (published in 2006) listed 1,000 deaths per year in sub-Saharan Africa for each of ascariasis and trichuriasis and 2,000 for hookworm, for a total of 4,000;74 but the Global Burden of Disease report for 2004 (published in 2008) lists a total of 412 deaths in sub-Saharan Africa (for the 3 infections combined).75
In our view, the most compelling case for deworming as a cost-effective intervention comes not from its subtle general health impacts (which appear relatively minor and nonspecific) nor from its potential reduction in severe symptoms of disease effects (which we believe to be rare), but from the possibility that deworming children has a subtle, lasting impact on their development, and thus on their ability to be productive and successful throughout life.
Empirical evidence on this matter is very limited,
resting on two relatively well-known and well-executed studies.
Bleakley 2007 analyzes the Rockefeller Sanitary Commission's campaign to eradicate hookworm in the American South in the early 20th century, and concludes:
Areas with higher levels of hookworm infection prior to the RSC experienced greater increases in school enrollment, attendance, and literacy after the intervention. No significant contemporaneous results are found for literacy or occupational shifts among adults, who had negligible prior infection rates. A long-term follow-up indicates a substantial gain in income that coincided with exposure to hookworm eradication.76
There are good reasons to be cautious in using this study as evidence relevant to deworming:
That said, we believe the paper merits some weight on the question of developmental benefits, because
This paper hypothesizes that the fall in hookworm prevalence led to benefits primarily by improving people's ability to become literate and otherwise benefit from school.81
Baird et al. 2011 and Baird 2007 are followups to Miguel and Kremer 2004, discussed in the above sections, which involved combination deworming, without prescreening, for some children and STH-only treatment for others (depending on the prevalence of schistosomiasis in the area).82 The program was not technically randomized, but used a method we consider similar to randomization to determine who was treated.83 These studies analyzed data on young adults who had been involved in the deworming program in grade school, comparing children who started receiving deworming treatment earlier to those who started receiving it later.
Baird et al. 2011 compared the first two groups of schools to receive deworming (as treatment group) to the final group (as control); the treatment group received 2.41 extra years of treatment on average.84 The study's headline effect is that those in the treatment group worked, and earned, substantially more,85 driven largely by a shift into the manufacturing sector.86 It also found a positive impact on meals consumed though not on overall consumption,87 small but non-statistically significant gains in school performance (though not on IQ),88 and gains on self-reported health though not on height or weight-for-height (and the treatment group had higher health expenditures).89 More at our 2012 blog post and full writeup on this paper.
Baird 2007 analyzes a similar, early dataset from the same program, though using a different definition of "treatment group" from the later paper: while Baird et al. 2011 uses the first two groups of schools to receive treatment as its treatment group and the last as its control, Baird 2007 simply looks at the number of years of deworming assigned to each child.90 It finds contrasting, though also encouraging, results: some statistically significant impacts on height and weight91 but no such impacts on education and labor market outcomes,92 and small negative impacts on cognitive performance.93
There are reasons to be cautious in interpreting these studies:
In 2012, the authors behind these studies shared their data and code so that we could thoroughly examine them. Our examination resulted in an overall higher level of confidence in the studies than we had had previously, though the above concerns remain. More at our 2012 blog post and full writeup on the topic.
We find it highly plausible that deworming has subtle but significant developmental effects that improve quality of later life. The two studies we know of on this topic each have substantial issues, and we do not consider them conclusive evidence for the presence (much less for the size) of these effects, but we do consider them suggestive evidence, enough to take the possibility of developmental effects seriously.
We further discuss how strong we find the case for developmental effects of deworming to be, in comparison with the case for long-term effects of other interventions, in a 2012 blog post.
It is possible that deworming benefits people who do not receive treatment, by reducing overall prevalence of worm infections in a community. The only evidence we have seen for this idea comes from the same Kenya program discussed above. Miguel and Kremer 2004 found significant impacts on children in nearby but untreated schools.95 In addition, Ozier 2011 reviewed later data on younger children, and concluded:
community deworming before a child’s first birthday brings about a 0.2-standard-deviation improvement in performance on Raven’s Matrices, a decade after the intervention. Estimated effects on vocabulary measures are similar in magnitude, but not always as significant; effects on memory are not statistically distinguishable from zero. A summary measure, the first principal component of all six cognitive measurements, also shows a roughly 0.2-standard-deviation effect. These effects are equivalent to between 0.5 and 0.8 additional grades in school … the effect of community deworming spillovers on height, height-for-age, and stunting all appear statistically indistinguishable from zero.96
For reasons discussed above, we believe these studies are likely to overstate the impact of deworming, and that this overstatement is particularly likely to be an issue for externalities due to the unusual flooding and elevated level of infections. In addition, we note that the unusual design of Miguel and Kremer 2004 (in which nearby schools were assigned to be dewormed earlier or later in an essentially arbitrary way) is unlikely to be representative of large-scale school-based deworming campaigns such as those of the Schistosomiasis Control Initiative.
That said, we think it is worth noting the possibility of externalities, as this could both (a) increase the cost-effectiveness of deworming beyond what we estimate below; (b) imply that some of the research on deworming reviewed above may understate the impact of deworming.
We have not identified many possible negative/offsetting impacts of deworming.
The World Health Organizations recommends annual treatment for schistosomiasis and twice-annual treatment for soil-transmitted helminths for school-aged children in areas with prevalence above 50%.100 In areas with lower prevalence, the World Health Organization recommends less frequent deworming.101 We have not been able to fully understand the rationale for the World Health Organization recommendations. The underlying principle is that reinfection rates are higher in areas with greater prevalence, so more frequent deworming will be necessary to avoid morbidity in those areas, but we have not found evidence that shows the superiority of annual treatment (as compared with, e.g., semi-annual or bi-annual treatment).
The World Health Organization's recommendations about which groups of people to treat also vary with prevalence; in low-prevalence areas, treatment is restricted to school-aged children and certain categories of adults.102 We do not know how the cost-effectiveness of treating adults in high-prevalence areas compares with the cost-effectiveness of treating children.
The main reason for focusing deworming treatment on children is that, with the exception of hookworm, the prevalence of the helminths and schistosomes is highest in childhood.103 Although deworming in childhood does not prevent adults from being reinfected with new worms, the theory underlying mass treatment is that it does prevent the developmental effects of having worms in childhood and the serious organ damage that can result from long-term high-intensity infections.104
The cost-effectiveness of deworming is very difficult to summarize, because (a) mortality and other clear, major life impacts are rare; (b) the benefits (particularly subtle general health impacts and developmental benefits) appear subtle and hard to quantify.
In addition, the cost-effectiveness of deworming may vary substantially depending on:
We have attempted to quantify short-term health impacts using information from the Disease Control Priorities Report. Doing so has raised substantial challenges. We have found significant errors in this report's analysis that stood uncorrected in the several years between the report's publication and our 2011 investigation, and estimates of the frequency and severity of symptoms are difficult to interpret and appear to be grounded in very little in the way of empirical data. Details on how we have used this information to estimate short-term health impacts are available at our 2011 deworming report.
We have attempted to quantify longer-term developmental impacts by working off of the effects found in the Kenya studies discussed above, and making adjustments for what we perceive as unrepresentativeness or other questions around these studies.
Details of our cost-effectiveness analysis, which incorporates both of these, are discussed in a 2012 blog post. In a nutshell:
More, including links to our spreadsheets, at our 2012 discusssion of cost-effectiveness for deworming and other interventions
We believe there is substantial room to do more deworming in suitable countries. Details at our review of the Schistosomiasis Control Initiative.
"People become infected when larval forms of the parasite – released by freshwater snails – penetrate their skin during contact with infested water.... There are two major forms of schistosomiasis – intestinal and urogenital – caused by five main species of blood fluke (see table)." World Health Organization, "Schistosomiasis Fact Sheet."
King and Dangerfield-Cha 2008, Pg 67.
“I do think that the same effects [as with S. japonicum, the strain in the Coutinho et al. 2006 study,] obtain with S. mansoni and S. haematobium. It is possible that their effect size will be smaller than that seen with S. japonicum—there is a school of thought which suggests that anti-S. japonicum inflammation is more intense because of its higher egg output and its more recent switch to parasitism of the human host. I don’t know if this is true.” Charles King, email to GiveWell, November 10, 2011.
Saconato and Atallah 2009, Pg 2.
Danso-Appiah et al. 2009, Pg 2.
"Each worm’s establishment in a host is the result of a separate infection event, and the number of infective stages shed (the infectiousness of the host) is a function of the number of worms present. In population dynamic terms this implies that the individual worm is the unit of transmission for helminths, while the individual host is the unit for microparasites (Anderson & May 1982)... Since the size of the worm burden varies considerably between individuals, and infection implies only that worms are present, a population of "infected" people will exhibit considerable variation in the severity of disease manifestations." Bundy et al. 2004, Pgs 245-46.
“The age-dependent patterns of infection prevalence are generally similar among the major helminth species, exhibiting a rise in childhood to a relatively stable asymptote in adulthood (figure 24.1). Maximum prevalence of A. lumbricoides and T. trichiura is usually attained before five years of age, and the maximum prevalence of hookworm and schistosome infections is usually attained in adolescence or in early adulthood. The nonlinear relationship between prevalence and intensity has the consequence that the observed age-prevalence profiles provide little indication of the underlying profiles of age intensity (age in relation to worm burden). Because intensity is linked to morbidity, the age-intensity profiles provide a clearer understanding of which populations are vulnerable to the different helminths (figure 24.1). For A. lumbricoides and T. trichiura infections, the age-intensity profiles are typically convex in form, with the highest intensities in children 5 to 15 years of age (Bundy 1995). For schistosomiasis, a convex pattern is also observed, with a similar peak but with a plateau in adolescents and young adults 15 to 29 years of age (Kabatereine and others 1999). In contrast, the age-intensity profile for hookworm exhibits considerable variation, although intensity typically increases with age until adulthood and then plateaus (Brooker, Bethony, and Hotez 2004). In East Asia it is also common to find the highest intensities among the elderly. However, more generally, children and young adults are at higher risk of both harboring higher levels of infection (thus greater levels of morbidity) and becoming reinfected more quickly. Both may occur at vital stages in a child’s intellectual and physical development.” Hotez et al. 2006, Pgs 469-470.
“The eggs of S. haematobium have a terminal spine and must traverse the bladder tissues towards the lumen of the bladder and urinary tract for elimination via urine. In the process, a considerable number become trapped in the bladder walls and surrounding tissues to initiate immune- induced inflammatory reactions, which subsequently lead to morbidity. It is important to note that eggs trapped in the tissues cause disease rather than the worms themselves.” Danso-Appiah et al. 2008, Pg 3.
"Sustained heavy infection leads to iron deficiency anaemia and other nutritional deficiencies, especially in children (Awasthi 2003; King 2005). The disease often results in retarded growth, reduced physical activity, and impaired cognitive function in children (Stephenson 1993; Nokes 1999; PCD 1999; Jukes 2002; WHO 2002)." Danso-Appiah et al. 2008, Pg 3.
"Late-stage complications are insidious and include calcification of the bladder wall, bladder stones, and secondary bacterial infection (Jordan 1993). Tissue damage caused by trapped eggs can lead to diffuse or localized wall thickening of the bladder and the distal ureter hydronephrosis orhydroureter, which may eventually lead to kidney failure (Kardorff 2001; WHO 2002; van der Werf 2003). Elevated urine albumin levels and reported pain upon micturition by children have a strong correlation with S. haematobium infection (Rollinson 2005). An important long-term consequence of infection is squamous cell carcinoma of the bladder (Jordan 1993; King 2005; Shiff 2006). A recent review points out that bladder carcinoma is the seventh most common cancer worldwide in men and that the highest incidence rate among men is found in Egypt (37.1 per 100,000 person-years) (Murta-Nascimento 2007), which might be related to S. haematobium infection and morbidity (Jordan 2000)." Danso-Appiah et al. 2008, Pg 3.
"Schistosomiasis infects the intestine, liver, and spleen. It can cause bloody diarrhoea, bloody stools, and abdominal pain (Gryseels 1992; WHO 1993). Infection of the liver and spleen causes liver fibrosis and portal hypertension that are generally irreversible in the late stages and kill patients, sometimes as a result of haemorrhage from varices (WHO 1993). Liver failure may also occur, especially when S. mansoni infection is associated with viral hepatitis (Pereira 1994)." Saconato and Atallah 2009, Pg 2.
There is substantial disagreement about the number of annual fatalities due to schistosomiasis-caused non-functioning kidneys and hematemesis (estimates range from under 27,000 to 280,000).
"WHO (2002) estimates that 27,000 people die annually from STH infections and schistosomiasis (case fatality rate of 0.0014 percent). Many investigators, however, believe that this figure is an underestimate. Crompton (1999) estimated that 155,000 deaths annually occur from these infections (case fatality rate of 0.08 percent), whereas Van der Werf and others (2003), using the limited data available from Africa, estimated the schistosomiasis mortality alone at 280,000 per year (case fatality rate of 0.014 percent) because of nonfunctioning kidneys (from S. haematobium) and hematemesis (from S. mansoni). Therefore, the difference between estimates for helminth-associated mortality is more than 10-fold." Hotez et al. 2006, Pg 470.
“Schistosomiasis is, in its very essence, a chronic inflammatory disease. This is because parasite eggs must pass through host tissues from the circulation to the lumen of bowel or bladder in order to leave the human body. However, this is an inefficient process — during the course of infection, over half of the eggs produced by female schistosomes never leave the human body and remain trapped in host tissues. There, the eggs induce a granulomatous response that progresses to focal areas of fibrosis within the affected organ. Over many years, the cumulative impact of tissue damage can lead to organ failure and consequent severe clinical morbidity and mortality. Early in infection, some of the tissue damage is reversible, but as fibrosis progresses, the cumulative damage caused by infection becomes irreversible. Even when infection is over, which may occur as adults reach their 30s and 40s, irreversible parasite-mediated organ damage may continue to affect patient health status.” King and Dangerfield-Cha 2008, Pg 67.
Mathers, Ezzati, and Lopez 2007, Pg 8.
"A. lumbricoides is the large roundworm (15 cm) and lies free in the human duodenum where it feeds on lumenal contents (see Crompton, Nesheim & Pawlowski (1989) for further details of the biology of this parasite). Like all the other nematodes considered here, the worms are dioecious, which is to say that they exist as male and female. The female produces some 100 000 eggs per day which pass out in the faeces of the host and embryonate externally at a rate determined by local environmental factors. The eggs hatch on ingestion, releasing a larva that undergoes a tissue migration involving the cardiovascular and pulmonary systems. The larva moults as it migrates and ultimately is coughed up from the lungs, swallowed, and becomes established as the adult in the small intestine. The cycle from egg deposition to female patency, when the female is able to produce eggs, has a duration of some 50 days.
T. trichiura, the human whipworm, is a much smaller worm (25 mm) and inhabits the colon (Bundy & Cooper 1989). The anterior two-thirds of the worm is thin and thread-like and is laced through the mucosal epithelium, upon which the worm is believed to feed, leaving the blunt posterior projecting into the colonic lumen for excretion and oviposition. The female produces some 2000 eggs per day which pass out in the host faeces and embryonate externally. The infectious eggs hatch on ingestion and undergo a specifically local migration, via the crypts of Lieberkühn to the mucosal surface. The development cycle takes some 60 days.
The two major hookworm species, which are of similar magnitude to the whipworm, inhabit the small intestine, where they attach to villi with biting mouthparts (Schad & Warren 1990). The worms feed on host blood and move frequently to new sites, leaving multiple, bleeding petechial haemorrhages on the mucosal surface." Bundy et al. 2004, Pgs 244-45.
"Each worm’s establishment in a host is the result of a separate infection event, and the number of infective stages shed (the infectious- ness of the host) is a function of the number of worms present. In population dynamic terms this implies that the individual worm is the unit of transmission for helminths, while the individual host is the unit for microparasites (Anderson & May 1982)... Since the size of the worm burden varies considerably between individuals, and infection implies only that worms are present, a population of "infected" people will exhibit considerable variation in the severity of disease manifestations." Bundy et al. 2004, Pgs 245-46.
"The size of the worm burden (the intensity of infection) is therefore a central determinant of helminth transmission dynamics, and is also the major determinant of morbidity since the pathology is related to the size of the worm burden, usually in a non-linear fashion (Stephenson 1987, Cooper & Bundy 1987, 1988). Since the size of the worm burden varies considerably between individuals, and infection implies only that worms are present, a population of “infected” people will exhibit considerable variation in the severity of disease manifestations. The intuitive assumption that all infections are equal may help to explain the historical confusion over the pathogenicity and public health significance of helminth infection (Bundy 1988, Cooper and Bundy 1989). From these considerations it is apparent that an under- standing of helminth epidemiology centres around an understanding of the patterns of infection intensity." Bundy et al. 2004, Pgs 245-46.
Gulani et al. 2007.
"There is a general acceptance of the simple view that very intense infection results in illness, a view that reflects both clinical experience of overwhelming infection and, perhaps equally importantly, an atavistic repugnance at the insidious invasion of the body by large numbers of worms. Such extremes of infection result in the severe anaemia of necatoriasis and the intestinal obstruction of ascariasis (Stephenson 1987), and the chronic colitis of classical trichuris dysentery syndrome (Cooper & Bundy 1988)." Bundy et al. 2004, Pg 248.
"There is a general acceptance of the simple view that very intense infection results in illness, a view that reflects both clinical experience of overwhelming infection and, perhaps equally importantly, an atavistic repugnance at the insidious invasion of the body by large numbers of worms. Such extremes of infection result in the severe anaemia of necatoriasis and the intestinal obstruction of ascariasis (Stephenson 1987), and the chronic colitis of classical trichuris dysentery syndrome (Cooper & Bundy 1988)." Bundy et al. 2004, Pg 248.
"Ascariasis is the best documented helminthiasis in terms of mortality. There are numerous studies of case fatality rates in hospitals (reviewed by Pawlowski & Davies 1989). These indicate that the outcome of acute complications of ascariasis is modified by the general health status of the patient, the intensity of infection and the medical procedure (see Pawlowski & Davies 1989). In one hospital in Sao Paulo, for example, the case fatality rate was 1.35 per cent for conditions which could be managed conservatively, and 26.1 per cent in patients undergoing surgery (Okumura et al. 1974). These studies confirm that death is a not infrequent outcome of complications of ascariasis, but provide little insight into mortality rates in the community. An extrapolation from central hospital data in Myanmar suggests there are 0.008 deaths per 1000 infections per year (Thein-Hliang 1987), but this is considered to be a considerable underestimate since only a small proportion of children with severe complications are likely to have access to the hospital (Pawlowski & Davies 1989). Only two population based estimates are available: one for the Darmstadt epidemic (0.1 deaths per 1000 infected per year) (Krey 1949) and one for Japan prior to national control efforts (0.061 deaths per 1000 infected per year) (Yokogawa 1976). Based on the present estimate of global infection, these rates suggest that between 8 000 and 14 000 children die each year.
The final estimate of global mortality due to ascariasis in the Global Burden of Disease project was 11,000 concentrated in the age group 5–14 years (Murray and Lopez 1996). Mortality was distributed by region in proportion to the region-specific population at risk (above higher thresh- old) and to the region-specific probability of dying between birth and 4 years (World Bank 1993). This last quantity was added to take account of regional variations in access to acute medical services.
No population-based mortality estimates have been published for T. trichiura infection. Prior to the advent of safe and effective therapy for T. trichiura infection in the late 1970s a number of reports described paedi- atric inpatients with Trichuris Dysentery Syndrome who, despite clinical efforts, died as a result of profuse haemorrhage and secondary anaemia (Wong and Tan 1961, Fisher and Cremin 1970) or of intussusception (Reeder, Astacio & Theros 1968). Although there continue to be reports of the syndrome, a fatal outcome in a clinical setting today would suggest inappropriate management. The picture in the community, however, may be rather different since, in the absence of specific diagnosis, the aetiology of chronic bloody dysentery may be unrecognized. Nevertheless, mortality is undoubtedly a rare consequence of trichuriasis.
The profound anaemia of hookworm infection is life-threatening and has been estimated, although the means of estimation are not described, to result in 65 000 deaths per year (World Health Organization 1992). Again there is a lack of empirical data, presumably in this case because of the difficulty in identifying the etiology of anaemia-related deaths. A figure of 4 300 deaths was used by Murray and Lopez (1996) and was distributed to ascribe the highest proportion of mortality to women of childbearing age (15–44 years) and to older age groups. The distribution of deaths between regions was divided in the same way as for the other infections.
In including these estimates of mortality we recognize that they are unsupported by vital registration statistics. But it should also be recognized that intense infection is most prevalent in the poorest regions of the poorest countries. In such areas mortality may be most likely because of limited access to appropriate management, while both the diagnosis of cause of death and its registration may be least reliable. There is clear evidence that deaths do occur. What is unclear is the extent of this mortality." Bundy et al. 2004, Pgs 281-82.
World Health Organization 2006, Pg 10.
World Health Organization 2006, Pg 10.
"Schools offer a readily available, extensive, and sustained infrastructure with a skilled workforce that is in close contact with the community. With support from the local health system, teachers can deliver the drugs safely. Teachers need only a few hours of training to understand the rationale for deworming and to learn how to give out the pills and keep a record of their distribution." Hotez 2006, Pg 473.
“The CRs [cure rates] and ERRs [egg reduction rates] for the recommended doses of albendazole and mebendazole in treating A. lumbricoides, T. trichiura and hookworm are shown in Fig. 1. For A. lumbricoides, all drug regimens are highly effective, with median CRs of 95–97% and median ERRs of 99–100%. More importantly, there is little variation in the drug efficacies between the individual studies for any given drug regimen. In contrast, the patterns for T. trichiura and hookworm are more variable. For both of these parasites, there is marked heterogeneity both in the drug efficacy between drug regimens and the drug efficacy between individual studies administering a given regimen. This is particularly evident for T. trichiura, for which both single-dose albendazole and mebendazole show poor levels of drug efficacy, particularly in terms of CR. For example, the median CR for a single dose of 400 mg albendazole is only 38%, with individual studies reporting CRs ranging from 4.9% to 99.3%.” Bennett and Guyatt 2000, Pg 72.
World Health Organization 2008(a). See Table 2 (page 4) for haemoglobin thresholds by age.
Danso-Appiah et al. 2008, Analysis 5.2 (Pg 60).
Danso-Appiah et al. 2008, Analysis 2.2 (Pg 58).
Danso-Appiah et al. 2008, Analysis 1.2 (Pg 57).
"Metrifonate is partially effective against hookworm infection (Kurz et al. 1986), and therefore, inclusion of studies using metrifonate would potentially overestimate the impact of praziquantel treatment." Smith and Brooker 2010, Pg 791.
“[Only infected children included, Single dose (comparison 1):] For haemoglobin, the mean value was slightly higher at the end of the study with deworming (mean difference 0.37 g/dL, 95% CI 0.10 to 0.64; 108 participants, two trials; Analysis 1.7).” Taylor-Robinson et al. 2012. Pg 19.
Taylor-Robinson et al. 2012. Pgs 19-20:
Examining the three separate analyses leads us to believe that combining the underlying studies together into a single meta-analysis would not lead to a statistically significant effect, but we have not carried out such a calculation.
However, further exposition from the authors has specified that haemoglobin data was collected from a random subsample of trial participants: “The reason for the smaller Hb sample is that it was only collected for a random subsample, information that is readily available from the authors.” Duflo et al. 2012.
"In 2007, a systematic review of randomised controlled trials (RCTs) investigating the impact of anthelmintic treatment reported an increase in haemoglobin concentration (Hb) of 1.71 g ⁄ l after treatment (Gulani et al. 2007). But this review did not distinguish between different helminth species or account for intensity of infection, which may have underestimated the true treatment effect (Awasthi & Bundy 2007); the effect of treatment is likely to be greatest where hookworm is most prevalent and intense … The present work aims to quantify the impact of hookworm infection and anthelmintic treatment using benzimidazoles, albendazole and mebendazole, among non-pregnant populations in hookworm-endemic areas. Speciﬁcally, we review available data from cross-sectional
studies that investigated the relationship between intensity of hookworm infection and Hb. We also summarise available data from RCTs and pre- and post-intervention
observational studies that compared the effects of benzimidazole treatment, either alone or in combination with the anti-schistosomal drug praziquantel, on Hb and anaemia levels. Finally, based on the value of combining deworming with micronutrient supplementation in children, we evaluate the impact of treatment in combination with iron supplementation (Hall 2007)." Smith and Brooker 2010, Pg 777.
"Among RCTs using albendazole, impact of treatment corresponded to a 1.89 g ⁄ l increase (95%CI: 0.13–3.63) in mean Hb while mebendazole had no impact. There was a positive impact of 2.37 g ⁄ l (95%CI: 1.33–3.50) on mean Hb when albendazole was co-administered with praziquantel, but no apparent additional beneﬁt of treatment with benzimidazoles combined with iron supplementation. " Smith and Brooker 2010, abstract.
Smith and Brooker 2010. Table 2, pg 784.
Smith and Brooker 2010. Table 2, pg 784. (92.9+59.4+51.9+51.4)/4 = 63.9.
See Smith and Brooker 2010, Table 2 (Pgs 784-785).
Mathers, Lopez, and Murray 2006, Pg 113.
Overall, the packed cell volume of children in the ITN group was higher by 1.7 absolute packed cell volume per cent compared to children not using nets. When the control group used untreated nets, the difference was 0.4 absolute packed cell volume per cent." Lengeler 2004, Pg 4.
See our 2012 blog post on this review.
"Following World Health Organization recommendations (WHO (1992)), schools with geohelminth prevalence over 50 percent were mass treated with albendazole every six months, and schools with schistosomiasis prevalence over 30 percent were mass treated with praziquantel annually. All treatment schools met the geohelminth cut-off in both 1998 and 1999. Six of twenty-ﬁve treatment schools met the schistosomiasis cut-off in 1998 and sixteen of ﬁfty treatment schools met the cut-off in 1999." Miguel and Kremer 2004, Pgs 168-169.
" Intestinal helminths—including hookworm, roundworm, whipworm, and schistoso- miasis—infect more than one-quarter of the world’s population. Studies in which med- ical treatment is randomized at the individual level potentially doubly underestimate the beneﬁts of treatment,missing externality beneﬁts to the comparison group from re- duced disease transmission, and therefore also underestimating beneﬁts for the treat- ment group. We evaluate a Kenyan project in which school-based mass treatment with deworming drugs was randomly phased into schools, rather than to individuals, allow- ing estimation of overall program effects. The program reduced school absenteeism in treatment schools by one-quarter, and was far cheaper than alternative ways of boost- ing school participation. Deworming substantially improved health and school partic- ipation among untreated children in both treatment schools and neighboring schools, and these externalities are large enough to justify fully subsidizing treatment. Yet we do not ﬁnd evidence that deworming improved academic test scores." Miguel and Kremer 2004, abstract.
Miguel and Kremer 2004, Table V, Pg 173.
King, Dickman, and Tisch 2005, Table 1, Pg 1565.
King, Dickman, and Tisch 2005, Table 1 and Table 2, Pg 1565.
"The use of observational studies and the inclusion of select subpopulation surveys (eg, school-age children) allows possible confounding effects on the observed results, thus obscuring the assessment of attributable risk due to schistosomiasis. Schistosomiasis is inevitably associated with other potential causes for morbidity and disease, especially with restricted access to safe water supplies and with co-infection by other parasites. Several studies have reported that age, sex, socioeconomic status, and diet can signiﬁcantly modify the risk for schistosomiasis-associated morbidity. In nine of ten individual surveys that adjusted for some or all of these cofactors, the effect of schistosomiasis on measured disability outcomes has remained signiﬁcant. However, details of these potentially modifying factors were not available in most of the studies included in our analysis, and so adjustment was not attempted in the estimation of our summary statistics." King, Dickman, and Tisch 2005, Pg 1566-1567.
“Many of our `gold-standard' field diagnostic tests are too insensitive for such research. That is, the standard tests routinely misdiagnose as `uninfected' those individuals who actually carry light infections (Wilson et al., 2006). In the case of schistosomiasis, the Kato-Katz stool test used to detect and quantify intensity of intestinal schistosome infections is only 40% – 60% sensitive when performed on a single stool specimen (de Vlas et al., 1993, Carabin et al., 2005). While this microscopic exam may variously detect eggs of hookworm, Ascaris, Trichuris, and other intestinal worms, it is not particularly sensitive for detection of hookworm, and will often miss the other STH species if their infection intensities happen to be light. As a result, this standard field screening approach will significantly misclassify (by underdiagnosis) the clinical burden of single and mixed parasite infection.
Inadequate testing for Schistosoma or STH results in misclassification bias that substantially reduces our power to detect numerically small, but clinically relevant infection-related differences in health outcomes, including anaemia (reductions in haemoglobin level), or stunting and chronic undernutrition (age-related height and weight deficits). Misdiagnosis, when combined with co-morbid conditions that are competing causes of disease (e.g., hookworm or malaria), effectively limits our appreciation of both the individual and the combined health impacts of common human parasitic infections.” King 2010, Pg 2.
We primarily refer here to Van der Werf 2001, the working paper version (with more detail) than Van der Werf 2003.
Van der Werf 2001, Pgs 3-5.
Van der Werf and de Vlas 2001, Pgs 13-15 discusses the method of generating estimates of the relationship between schistosomiasis prevalence and the prevalence of the various sequelae discussed. Charts throughout the remainder of the review show the curve that is fitted to the data points provided by the studies reviewed. We find that the attribution method (a) ignores the possibility of confounders, i.e., the possibility that non-schistosomiasis factors (such as poverty and general hygiene) are correlated both with schistosomiasis and with the sequelae discussed; (b) is prone to exaggerate the strength of any given relationship (as we believe can be seen by examining the charts).
Van der Werf et al. 2003, Pg 132.
World Health Organization 2008b, Pg 110.
" van der Werf MJ, de Vlas SJ. Morbidity and infection with schistosomes or
soil-transmitted helminths. Rotterdam, Erasmus University, 2001." World Health Organization 2008b, Pg 139.
One of the most severe symptoms discussed is severe hematemesis (vomiting blood). But Van der Werf et al. rely on self-reported survey data of hematemesis, (Van der Werf and de Vlas 2001, Pgs 62-63) which is problematic because vomiting blood can easily be confused with coughing blood or even a nosebleed (National Institutes of Health, 2011).
World Health Organization 2008b, Pg 110.
“Estimated total malaria deaths for 2004 were 0.89 million, of which 771 000 were in children aged under five years. These estimates are lower than those in the GBD 2002 (1.27 million deaths, of which 1.15 million deaths were of children aged under five years).” World Health Organization 2008b, Pg 109.
GiveWell, "Schistosomiasis Mortality Analysis," "YLL per DALY" rows on "From GBD" sheet. For more on these terms, see our discussion of DALYs.
Bundy et al. 2004, Pgs 269-273.
Unfortunately, the published version (Bundy et al. 2004) does not contain regionally disambiguated mortality estimates, so we use the figure from the unpublished working paper that was used to generate the DCP's cost-effectiveness estimate, of .3 per 100,000 population. Bundy et al. undated, Table 9, Pg 72.
“Particularly large burdens of T. trichiura may result in the “classical” dysenteric form of trichuriasis, synonymous with Trichuris Dysentery Syndrome (Ramsey 1962) and Massive Infantile Trichuriasis (Kouri & Valdes Diaz 1952). This typically occurs in children between 3 and 10 years of age and is associated with burdens involving at least several hundreds of worms carpeting the colonic mucosa from ileum to rectum. The colon is inflamed, oedematous and friable, and often bleeds freely (Venugopal et al. 1987). Reviews of case histories suggest that the mean duration of disease at the time of presentation is typically in excess of 12 months and that relapse after treatment frequently occurs (Gilman et al. 1983, Cooper et al. 1990, Callender et al. 1994). The probability of relapse, and of a child experiencing multiple episodes, is greatly enhanced because a proportion of heavily infected children are predisposed to reacquire heavy infection even after successful treatment (Bundy et al. 1987a, 1987b). The typical signs of the syndrome (see Bundy & Cooper 1989a for a review of 13 studies involving 697 patients) are rectal prolapse, tenesmus, bloody mucoid stools (over months or years), growth stunting, and a profound anaemia, which may lead to a secondary anaemia. The complete spectrum of clinical features associated with the syndrome occurs in some 30 per cent of children with intense trichuriasis. Many of the major clinical effects are reversible by appropriate therapy (Cooper, Bundy & Henry 1986, Gilman et al. 1983), hence the disability is considered here to be a contemporaneous consequence of infection.” Bundy et al. 2004, Pgs 271-273.
“No population-based mortality estimates have been published for T. trichiura infection. Prior to the advent of safe and effective therapy for T. trichiura infection in the late 1970s a number of reports described paedi- atric inpatients with Trichuris Dysentery Syndrome who, despite clinical efforts, died as a result of profuse haemorrhage and secondary anaemia (Wong and Tan 1961, Fisher and Cremin 1970) or of intussusception (Reeder, Astacio & Theros 1968). Although there continue to be reports of the syndrome, a fatal outcome in a clinical setting today would suggest inappropriate management. The picture in the community, however, may be rather different since, in the absence of specific diagnosis, the aetiology of chronic bloody dysentery may be unrecognized. Nevertheless, mortality is undoubtedly a rare consequence of trichuriasis.” Bundy et al. 2004, Pg 282.
Mathers, Lopez, and Murray 2006, Pg 162.
World Health Organization 2008(c). Sheet 'AFR', cells G39+G40+G41.
"This study evaluates the economic consequences of the successful eradication of hookworm disease from the American South, which started circa 1910. The Rockefeller Sanitary Commission (RSC) surveyed infection rates and found that 40 percent of school-aged children in the South were infected with hookworm. The RSC then sponsored treatment and education campaigns across the region. Follow-up studies indicate that this campaign substantially reduced hookworm disease almost immediately. Areas with higher levels of hookworm infection prior to the RSC experienced greater increases in school enrollment, attendance, and literacy after the intervention. No significant contemporaneous results are found for literacy or occupational shifts among adults, who had negligible prior infection rates. A long-term follow-up indicates a substantial gain in income that coincided with exposure to hookworm eradication. I also find evidence that the return to schooling increased with eradication." Bleakley 2007, abstract.
"First, the RSC sent teams of health-care workers to counties to administer and dispense deworming treatments free of charge. RSC dispensaries visited a large and mostly contiguous fraction of the South and the campaign treated over 400,000 individuals with deworming medication.1 Second, the RSC sought to educate doctors, teach- ers, and the general public on how to recognize the symptoms of . hookworm disease so that fewer cases would go untreated. An- other part of this publicity campaign included education about the importance of hygiene, especially with regard to the use of sanitary privies. In this period, oftentimes even public buildings such as schools and churches did not have such hygienic facilities. Follow-up surveys conducted afterward showed a substantial de- cline in hookworm infection [RSC 19151. Although the stated goal of eradication was not achieved, the hookworm-infection rate of the region did drop by more than half, and fewer extreme cases of the disease went unnoticed and untreated." Bleakley 2007, Pg 77.
"the anti-hookworm campaign achieved considerable progress against the disease in less than a decade. This is a sudden change on historical time scales. Moreover, I examine outcomes over a fifty-year time span, which is unquestionably long relative to the five-year RSC intervention … How realistic is the assumption that areas with high infec- tion rates benefited more from the eradication campaign? Re- surveys found a decrease in hookworm infection of 30 percentage points across the infected areas of the South. Such a dramatic drop in the region's average infection rate, barring a drastic reversal in the pattern of hookworm incidence across the region, would have had the supposed effect of reducing infection rates more in highly infected areas than in areas with moderate infec- tion rates. Figure I presents data on this issue.6 The basic as- sumption of this section that areas where hookworm was highly endemic saw a greater drop in infection than areas with low infection rates is born out across states and across counties." Bleakley 2007, 80-81.
See Bleakley 2007, Figure III, Pg 100. A similar approach is taken for school attendance - see Figure II, Pg 88.
"The finding that highly infected counties experienced surges in school attendance is not sensitive to controlling for a variety of alternative hypotheses. I contrast these hypotheses with the effect of hookworm and the RSC by starting with (1) and (2) and adding plausible proxies for the supposed con- founds. The control variables enter into the specification inter- acted with Postt . These results are found in Panel B of Table III. In every case, the added control variables are jointly sig- nificant at conventional confidence levels. The new controls include variables for health and health policy, educational resources, race and race relations, urbanization and land use, and parental background. (See the Appendix for a complete list of controls and their sources.)" Bleakley 2007, Pg 90.
"I also consider the role played by the quantity of and returns to schooling in the wage results. Controlling directly for education does not significantly change the estimated effect of hookworm treatment. Additionally, I can easily reject, for conventional re- turns to schooling, the hypothesis that the wage effect is due entirely to a rise in education.2o However, the fact that I estimate increases in literacy without concomitant rises in the quantity of schooling suggests an alternative hypothesis: changes in quality. In particular, it may be that students spend the same number of years in school, but the time is better spent. For example, there might be less absenteeism, or students might be better equipped to absorb the material while in school. As was shown above, students were less likely to work while in school and were more more likely to be literate, following hookworm eradication. This suggests that the return to schooling was raised by the hookworm intervention." Bleakley 2007, Pg 97.
"Following World Health Organization recommendations (WHO (1992)), schools with geohelminth prevalence over 50 percent were mass treated with albendazole every six months, and schools with schistosomiasis prevalence over 30 percent were mass treated with praziquantel annually. All treatment schools met the geohelminth cut-off in both 1998 and 1999. Six of twenty-ﬁve treatment schools met the schistosomiasis cut-off in 1998 and sixteen of ﬁfty treatment schools met the cut-off in 1999." Miguel and Kremer 2004, Pg 168-169.
"The 75 schools involved in this program were experimentally divided into three groups (Groups 1, 2, and 3) of 25 schools each: the schools were first stratified by administrative sub-unit (zone), listed alphabetically by zone, and were then listed in order of enrollment within each zone, and every third school was assigned to a given program group; supplementary appendix A contains a detailed description of the experimental design. The groups are well-balanced along baseline demographic and educational characteristics, both in terms of mean differences and distributions, where we assess the latter with the Kolmogorov-Smirnov test of the equality of distributions (Table 1). The same balance is also evident among the subsample of respondents currently working for wages (see Supplementary Appendix Table A1)." Baird et al. 2011, Pg 6-7.
"The question of whether – and how much – child health gains improve adult living standards is of major intellectual interest and public policy importance. We exploit a prospective study of deworming in Kenya that began in 1998, and utilize a new dataset with an effective tracking rate of 83% over a decade, at which point most subjects were 19 to 26 years old. Treatment individuals received two to three more years of deworming than the comparison group. Among those with wage employment, earnings are 21 to 29% higher in the treatment group, hours worked increase by 12%, and work days lost to illness fall by a third. A large share of the earnings gains are explained by sectoral shifts, for instance, through a doubling of manufacturing employment and a drop in casual labor. Small business performance also improves significantly among the self-employed. Total years enrolled in school, test scores and self-reported health improve significantly, suggesting that both education and health gains are plausible channels." Baird et al. 2011, abstract.
"Deworming treatment individuals consume 0.096 more meals (s.e. 0.028, significant at 99% confidence, Panel C) than the control group, and the externality impact is also large and positive (0.080, s.e. 0.023, 99% confidence). This suggests that deworming led to living standard gains in the full sample." Baird et al. 2011, Pg 17. See Pg 41 for full set of related results, including overall household consumption.
"We examine school enrollment and attendance using two different data sources in Table 9. In Panel A, the dependent variable is school enrollment as reported by the respondent in the KLPS-2 survey, which equals one if the individual was enrolled for at least part of a given year. These show consistently positive effects from 1999 to 2007 both on the deworming treatment indicator and the externalities term, and the total increase in school enrollment in treatment relative to control schools over the period is 0.279 years (s.e. 0.147, significant at 90% confidence). Note that there is no treatment effect estimate for 1998 since all students were enrolled at some point in 1998, as a criterion for inclusion in the KLPS sample. The treatment effect estimates are largest during 1999- 2003 before tailing off during 2004-07, as predicted in the optimal educational investment framework above since the current opportunity cost of time is rising relative to the later benefits of schooling as individuals age.
The data in Panel B is school participation, namely, being found present in school by survey enumerators on the day of an unannounced school attendance check. This is our most objective measure of actual time spent at school, and was a main outcome measure in Miguel and Kremer (2004). The enrollment measure in Panel A misses much of the attendance variation captured in this measure. However, two important limitations of the school participation data are that it was only collected during 1998-2001, and only at primary schools in the study area; the falling sample size between 1998 to 2001 is mainly driven by students graduating from primary school. School participation rates also rise significantly in the deworming treatment group, by 0.074 (s.e. 0.023) and 0.068 (s.e. 0.023) in 1998 and 1999, respectively, before dropping off somewhat in later years (particularly in 2000). Total school participation gains are 0.129 of a year of schooling (s.e. 0.064, significant at 95% confidence). Given that the school enrollment data misses out on attendance impacts, which are sizeable, a plausible lower bound on the total increase in time spent in school induced by the deworming intervention is the 0.129 gain in school participation from 1998-2001 plus the school enrollment gains from 2002-2007, which works out to 0.304 years of schooling." Baird et al. 2011, Pg 21-22.
"Test score performance is another natural way to assess deworming impacts on human capital and skills. While the impact of deworming on primary school academic test score performance in 1999 is positive but not statistically significant (Table 10, Panel B), there is suggestive evidence that the passing rate did improve on the key primary school graduation exam, the Kenya Certificate of Primary Education (point estimate 0.046, s.e. 0.031). There is also some evidence that English vocabulary knowledge (collected during the 2007-09 survey) is somewhat higher in the deworming treatment group (impact of 0.076 standard deviations in a normalized distribution, s.e., 0.055). The mean effect size of the 1999 test score, the indicator for passing the primary school leaving exam, and the English vocabulary score in 2007-09 taken together does yield a normalized point estimate of 0.112 that is statistically significant at 90% confidence (s.e. 0.067), providing suggestive evidence of moderate human capital gains in the treatment group. As expected, there is no effect on the Raven’s Matrices cognitive exam, which is designed to capture general intelligence rather than acquired skills (Panel B). While many would argue that nutritional gains in the first few years of life could in fact generate improved cognitive functioning as captured in a Raven’s exam – as Ozier (2010) indeed does find among younger siblings of the deworming beneficiaries – it was apparently already 'too late' for such gains among the primary school age children in our study." Baird et al. 2011, Pg 22.
"There is evidence that adult health also improved as a result of deworming. Respondent self-reported health (on a normalized 0 to 1 scale) improved by 0.041 (s.e. 0.018, significant at 95% confidence, Table 11, panel A). Many studies have found that self-reported health reliably predicts actual morbidity and mortality even when other known health risk factors are accounted for (Idler and Benyamini 1997, Haddock et al. 2006, Brook et al. 1984). Note that it is somewhat difficult to interpret this impact causally since it may partially reflect health gains driven by the higher adult earnings detailed above, in addition to the direct health benefits of earlier deworming. Yet the fact that there were similar positive and statistically significant impacts on self-reported health in earlier periods, namely, in surveys administered in 1999 before most in sample individuals were working (see Table 11, panel C and Miguel and Kremer 2004), suggests that at least part of the effect is directly due to deworming. In terms of other health outcomes, there is no evidence that deworming improved self- reported happiness or wellbeing or reduced major health shocks. Total health expenditures by the respondent in the last month are significantly higher in the treatment group (91.1 Shillings, s.e. 30.0), suggesting that they may have greater ability or willingness to make health investments, but interpretation is again complicated by the fact that such spending also reflects health needs. Despite the finding that the number of meals consumed is larger for deworming treatment individuals (in Table 8), deworming did not lead to higher body mass index (Table 11, Panel B). Nor are there detectable height gains, and these non-impacts hold even when we restrict attention to younger individuals (those in grades 2-4 in 1998, regression not shown)." Baird et al. 2011, Pg 22-23. See Pg 44 for full related results, including height, weight-for-height (body mass index) and health spending.
"The most important factor in the econometric identification strategy is the randomized assignment of pupils to deworming treatment through the deworming program. Group 1 schools received free deworming treatment starting in 1998; Group 2 schools began in 1999, while Group 3 schools began receiving treatment in 2001. All school re- ceived treatment from 2001-2003. Thus in 1998, Group 1 schools were treatment schools, while Group 2 and 3 were comparison schools. In 1999, Group 1 and Group 2 schools were treatment schools and Group 3 schools were control schools. Table 4.1 shows the PSDP treatment schedule. Our sample consists of pupils that were in grades 2-7 in 1998 (primary school goes through grade 8). This variation in group, as well as variation in initial grade, provides us with between zero and six years of treatment for each individ- ual. For example, a Group 1 pupil in grade 2 in 1998 would be assigned six years of treatment, while a Group 3 pupil in grade 6 in 1998 would be assigned only one." Baird 2007, Pg 106-107.
Baird 2007, Table 4.8, Pg 138.
"Along with health outcomes we also look at the impact of years of deworming on a number of education and labor market outcomes. Given that we see benefits to health from deworming, we might expect that these gains would translate into educational gains. The education results are shown in Table 4.12. We do see some evidence that deworming treatment decreases your likelihood of dropping out for the overall sample, which is driven by benefits for males and those in low infection areas. Increasing treatment from zero to six years decreases your likelihood of dropping out by 6 percent and is significant at the 10% level. These results are similar to those found by Johnson and Schoeni (2007) for the US, who find that low birth weight (their measure of health status) does not influence results for highest grade attended, but does affect dropout rates. It is interesting that our significant education results are for different sub-groups than our health results. This observation suggests that our education gains are not necessarily being driven by health gains. Overall, we see very little in terms of educational or labor market gains when looking at our overall sample or our sub-samples. The coefficients are generally positive, but insignificant. With our sample still in a very transitional stage with many still in school, and others still moving between school and the labor force, it is hard to draw conclusive results from this evidence. We will have clearer results (or absence ofresults) for the impact of deworming on education and labor force participation once we collect the third round of data." Baird 2007, Pg 122.
"We do find consistent negative impacts of deworming on cognitive performance,
although for the most part these results are insignificant and small. Looking at the mean effect result for the entire sample, one finds that increasing treatment by one year decreases, albeit insignificantly, the average cognitive score by 0.005 standard deviations. These negative coefficients may result from the fact that treatment leads more vulnerable pupils to stay in school, pupils who are likely to have lower test scores to begin with." Baird 2007, Pg 122.
See the "How well would the studies generalize to other settings?" section of our 2012 blog post on the studies.
Deworming substantially improved health and school participation among untreated children in both treatment schools and neighboring schools, and these externalities are large enough to justify fully subsidizing treatment." Miguel and Kremer 2004, abstract.
Ozier 2011, Pg 9.
"A concern about the feasibility of sustainable control with BZAs is the possible emergence of drug resistance among human STHs. BZA resistance occurs because of the spread of point mutations in nematode-tubulin alleles. This phenomenon has already resulted in widespread BZA drug resistance among STHs of ruminant livestock. There is still no direct evidence for BZA resistance among human STHs, although such resistance could account for an observed failure of mebendazole for human hookworm in southern Mali, as well as a diminished efficacy against hookworm in Zanzibar following frequent and periodic use of mebendazole (Albonico and others 2003). PZQ resistance must also be considered, especially as it begins to be widely used in Sub-Saharan Africa (Hagan and others 2004). Should PZQ resistance develop, there will be new demands for antischistosomal drugs. Recently, the artemisins have shown activity against schistosomulae and were successful in protecting against S. japonicum in China (Hagan and others 2004)." Jamison et al. 2006, Pg 479.
World Health Organization 2006, Pg 41.
World Health Organization 2006, Pg 41.
World Health Organization 2006, Pg 41.
“The age-dependent patterns of infection prevalence are gen- erally similar among the major helminth species, exhibiting a rise in childhood to a relatively stable asymptote in adulthood (figure 24.1). Maximum prevalence of A. lumbricoides and T. trichiura is usually attained before five years of age, and the maximum prevalence of hookworm and schistosome infec- tions is usually attained in adolescence or in early adulthood. The nonlinear relationship between prevalence and intensity has the consequence that the observed age-prevalence profiles provide little indication of the underlying profiles of age inten- sity (age in relation to worm burden). Because intensity is linked to morbidity, the age-intensity profiles provide a clearer understanding of which populations are vulnerable to the different helminths (figure 24.1). For A. lumbricoides and T. trichiura infections, the age-intensity profiles are typically convex in form, with the highest intensities in children 5 to 15 years of age (Bundy 1995). For schistosomiasis, a convex pattern is also observed, with a similar peak but with a plateau in adolescents and young adults 15 to 29 years of age (Kabatereine and others 1999). In contrast, the age-intensity profile for hookworm exhibits considerable variation, although intensity typically increases with age until adulthood and then plateaus (Brooker, Bethony, and Hotez 2004). In East Asia it is also common to find the highest intensities among the elderly. However, more generally, children and young adults are at higher risk of both harboring higher levels of infection (thus greater levels of morbidity) and becoming reinfected more quickly. Both may occur at vital stages in a child’s intellectual and physical development.” Hotez et al. 2006, Pgs 469-470.