Investigation of Intestinal Parasites in Living Nursing Home

Objective: Intestinal infections are common in the elderly, presented with atypical symptoms and may be the cause of mortality with a more severe clinical manifestation. The weakening of cellular and humoral immunity by aging affects the intestinal flora and increases the risk of infection in the presence of chronic diseases. The aim of this study was to investigate the presence of possible parasitic agents in the intestinal system of ≥65-year-old nursing home residents through fecal examination, and to determine the demographic features (age and gender) of this elderly group. Methods: A total of 82 stool samples were examined (100x, 40x) with saline and iodine preparations, formol-ethyl acetate concentration process, trichrome and modified Erlich Ziehl Neelsen stained preparations. Results: One or more parasitological agents were detected in 17 (20.7%) of the 82 stool samples examined. The most common agent was Blastocystis spp. (13.4%), followed by Cryptosporidium spp. (2.4%) and Dientamoeba fragilis (2.4%). Conclusion: In this study, it was determined that attention should be given to elderly population with regard to intestinal parasitic infections. Because of changes in the immune system, more opportunistic factors could be detected. More frequent screening in public areas such as nursing homes is important for preventing infections.

Parasitic infections of the gut in children.

Parasitic infections of the gut have major implications for child health, but many questions remain unanswered. Protozoal parasites, especially cryptosporidiosis and giardiasis, cause diarrhoea and contribute to impaired growth, neurocognitive development and mortality. Entamoeba histolytica causes dysentery and may have more subtle effects on child growth. Helminth infections are mostly asymptomatic, and untargeted mass deworming has not been shown to be beneficial. However, children with heavy infections certainly benefit from antihelminthic treatment. Hepatosplenic schistosomiasis is a neglected problem on a massive scale, which causes portal hypertension and lifelong morbidity in individuals who get infected in childhood. Neurocysticercosis causes epilepsy and is a significant consequence of taeniasis solium, another neglected disease which is entirely preventable. Parasitic infections of the gut contribute to child health problems on a large scale. Fresh approaches are needed to prevention and treatment.

Host-Parasite Interactions Promote Disease Tolerance to Intestinal Helminth Infection.

Parasitic helminths are among the most pervasive pathogens of the animal kingdom. To complete their life cycle, these intestinal worms migrate through host tissues causing significant damage in their wake. As a result, infection can lead to malnutrition, anemia and increased susceptibility to co-infection. Despite repeated deworming treatment, individuals living in endemic regions remain highly susceptible to re-infection by helminths, but rarely succumb to excessive tissue damage. The chronicity of infection and inability to resist numerous species of parasitic helminths that have co-evolved with their hosts over millenia suggests that mammals have developed mechanisms to tolerate this infectious disease. Distinct from resistance where the goal is to destroy and eliminate the pathogen, disease tolerance is an active process whereby immune and structural cells restrict tissue damage to maintain host fitness without directly affecting pathogen burden. Although disease tolerance is evolutionary conserved and has been well-described in plant systems, only recently has this mode of host defense, in its strictest sense, begun to be explored in mammals. In this review, we will examine the inter- and intracellular networks that support disease tolerance during enteric stages of parasitic helminth infection and why this alternative host defense strategy may have evolved to endure the presence of non-replicating pathogens and maintain the essential functions of the intestine.

Subcutaneous injection of exosomes reduces symptom severity and mortality induced by Echinostoma caproni infection in BALB/c mice.

Recent studies have shown the importance of exosomes in the host-parasite relationship. These vesicles are an important part of the excretory/secretory pathway for proteins with the potential to alter immune responses. Therefore, in the present study, we examined the immunomodulatory role of exosomes in BALB/c mice using Echinostoma caproni as an experimental model of intestinal helminth infection. For this purpose, BALB/c mice were injected twice s.c. with purified exosomes of E. caproni, followed by experimental infection. We report a delay in the development of the parasite in mice immunised with exosomes, a concomitant reduced symptom severity and increased survival upon infection. Immunisations with exosomes evoked systemic antibody responses with high levels of IgM and IgG. IgG1, IgG2b and IgG3 are the subtypes responsible for the IgG increase. These antibodies showed specific recognition of exosomal proteins, indicating that these vesicles carry specific antigens that are involved in the humoral response. The administration of exosomes induced an increase of IFN-γ, IL-4 and TGF-ß levels in the spleen of mice prior to infection. The subsequent infection with E. caproni resulted in a further increase of IL-4 and TGF-ß, together with an abrupt overproduction of IL-10, suggesting the development of a Th2/Treg immune response. Our results show that the administration of exosomes primes the immune response in the host, which in turn can contribute to tolerance of the invader, reducing the severity of clinical signs in E. caproni infection.

IL-22 mediates host defense against an intestinal intracellular parasite in the absence of IFN-γ at the cost of Th17-driven immunopathology.

The roles of Th1 and Th17 responses as mediators of host protection and pathology in the intestine are the subjects of intense research. In this study, we investigated a model of intestinal inflammation driven by the intracellular apicomplexan parasite Eimeria falciformis. Although IFN-γ was the predominant cytokine during E. falciformis infection in wild-type mice, it was found to be dispensable for host defense and the development of intestinal inflammation. E. falciformis-infected IFN-γR(-/-) and IFN-γ(-/-) mice developed dramatically exacerbated body weight loss and intestinal pathology, but they surprisingly harbored fewer parasites. This was associated with a striking increase in parasite-specific IL-17A and IL-22 production in the mesenteric lymph nodes and intestine. CD4(+) T cells were found to be the source of IL-17A and IL-22, which drove the recruitment of neutrophils and increased tissue expression of anti-microbial peptides (RegIIIß, RegIIIγ) and matrix metalloproteinase 9. Concurrent neutralization of IL-17A and IL-22 in E. falciformis-infected IFN-γR(-/-) mice resulted in a reduction in infection-induced body weight loss and inflammation and significantly increased parasite shedding. In contrast, neutralization of IL-22 alone was sufficient to increase parasite burden, but it had no effect on body weight loss. Treatment of an E. falciformis-infected intestinal epithelial cell line with IFN-γ, IL-17A, or IL-22 significantly reduced parasite development in vitro. Taken together, to our knowledge these data demonstrate for the first time an antiparasite effect of IL-22 during an intestinal infection, and they suggest that IL-17A and IL-22 have redundant roles in driving intestinal pathology in the absence of IFN-γ signaling.

Enteroparasitosis prevalence and parasitism influence in clinical outcomes of tuberculosis patients with or without HIV co-infection in a reference hospital in Rio de Janeiro (2000-2006)

Tuberculosis and intestinal parasites affect primarily low social and economic level populations, living clustered in precarious habitational settings. One of the interesting aspects of this interaction is the parasitism influence in cellular response to tuberculosis. In the present study, we evaluated the prevalence of enteroparasitosis in tuberculosis patients, HIV-infected and non HIV infected, and we observed the influence of helminth presence in the response to tuberculin skin test (TST) and tuberculosis clinical outcomes. From 607 clinical records reviewed, 327 individuals met the study inclusion criteria and did not present any exclusion criteria. The prevalence of enteroparasites observed was 19.6 percent. There was no significant association among TST result and the variables related to the presence of: helminthes, protozoa, and stool test for parasites result (p>0.5). Considering the survival of this cohort, we may observe that there is no significant difference (p>0.05) between the survival curves of parasited and non parasited individuals. Solely the variable "eosinophils" presents a statistically significant association (p<0.001) with helminthes, all other associations are considered not significant. Our findings neither show an association between helminthic infection and a favorable tuberculosis outcome, nor between parasitism and TST response, unlike other in vitro studies. Apparently, experimental data do not correspond to the clinical findings.

Gastrointestinal nematode infection exacerbates malaria-induced liver pathology.

Mixed parasite infections are common in many parts of the world, but little is known of the effects of concomitant parasite infections on the immune response or severity of clinical disease. We have used the nonlethal malaria infection model of Plasmodium chabaudi AS in combination with the gastrointestinal nematode Heligmosomoides bakeri polygyrus to investigate the impact of nematode infections on malarial morbidity and antimalarial immunity. The data demonstrate that wild-type C57BL/6 mice coinfected with both parasites simultaneously exhibit a striking increase in mortality, while mice deficient in IFN-gamma or IL-23 survive coinfection. The increase in mortality in wild-type mice was associated with severe liver pathology characterized by extensive coagulative necrosis and an increase in hepatic IFN-gamma, IL-17, and IL-22 mRNA expression. This is the first demonstration of increased malaria-associated pathology associated with a switch toward a proinflammatory environment, involving not only IFN-gamma but also the IL-17/IL-23 axis, as a result of coinfection with a gastrointestinal helminth.

[Diarrhea from the infectologist's point of view]. / Hasmenések az infektológus szemszögébôl.

Gastroenteritis is a nonspecific term for various pathologic states of the gastrointestinal tract. Gastroenteritis causing pathogens are the second leading cause of morbidity and mortality worldwide. In the developed countries diarrhea is the most common reason for missing work, while in the developing world, it is a leading cause of death. Internationally, the mortality rate is 5-10 million deaths each year. "Traveller's diarrhea" is a polyetiologic common health problem of international travellers which affects travellers generally for days, but it can result in chronic postinfectious irritable bowel syndrome as well. Infectious agents usually cause acute gastroenteritis either by adherence of the intestinal mucosa, or by mucosal invasion, enterotoxin production, and/or cytotoxin production. The incubation period can often suggest the cause of etiology. When symptoms occur within 6 hours of eating, ingestion of preformed toxin of S. aureus or Bacillus cereus should be suspected. The incidence of hypervirulent C. difficile associated colitis is an emerging problem as a healthcare system associated infection. While infectious agents do not commonly cause chronic diarrhea, those that do include C. difficile, Giardia lamblia, Entamoeba histolytica, Cryptosporidium, Aeromonas and Yersinia . Amoebiasis is the second to malaria as a protozoal cause of death. Infection with HIV is also a common cause of diarrhea.

Enteroparasitosis prevalence and parasitism influence in clinical outcomes of tuberculosis patients with or without HIV co-infection in a reference hospital in Rio de Janeiro (2000-2006).

Tuberculosis and intestinal parasites affect primarily low social and economic level populations, living clustered in precarious habitational settings. One of the interesting aspects of this interaction is the parasitism influence in cellular response to tuberculosis. In the present study, we evaluated the prevalence of enteroparasitosis in tuberculosis patients, HIV-infected and non HIV infected, and we observed the influence of helminth presence in the response to tuberculin skin test (TST) and tuberculosis clinical outcomes. From 607 clinical records reviewed, 327 individuals met the study inclusion criteria and did not present any exclusion criteria. The prevalence of enteroparasites observed was 19.6%. There was no significant association among TST result and the variables related to the presence of: helminthes, protozoa, and stool test for parasites result (p>0.5). Considering the survival of this cohort, we may observe that there is no significant difference (p>0.05) between the survival curves of parasited and non parasited individuals. Solely the variable "eosinophils" presents a statistically significant association (p<0.001) with helminthes, all other associations are considered not significant. Our findings neither show an association between helminthic infection and a favorable tuberculosis outcome, nor between parasitism and TST response, unlike other in vitro studies. Apparently, experimental data do not correspond to the clinical findings.

Fatal gastrointestinal parasitism in goats: 31 cases (2001-2006).

OBJECTIVE: To evaluate signalment, history, clinical and pathologic findings, and seasonal weather patterns in association with fatal gastrointestinal parasitism in goats. DESIGN: Retrospective case series. ANIMALS: 152 goats that were > 1 day of age. PROCEDURES: Characteristics including age and counts of coccidia oocysts and trichostrongyle ova (eggs) per gram of feces (EPG) in goats that died because of gastrointestinal parasitism and goats that died because of other causes were compared. Weather data and annual incidence of caprine fatal gastrointestinal parasitism were investigated. RESULTS: Death was attributed to gastrointestinal parasitism in 31 of 152 (20%) goats (median age, 5 months; range, 1 month to 7 years); deaths were attributed to coccidiosis (n = 7 goats; median age, 4 months; median EPG, 2,225), trichostrongylosis (6 goats; median age, 1.25 years; median EPG, 3,700), or dual infection (18 goats; median age, 6.7 months; median EPG, 8,088 coccidia and 5,475 trichostrongyles). Sudden onset of weakness or death was a common historical finding; diarrhea was evident in 15 goats. Common postmortem findings in these goats included cachexia, tissue pallor, poorly formed feces, and mesenteric lymphadenomegaly. Wet weather in spring and summer was associated with increased annual incidence of fatal gastrointestinal parasitism in goats. CONCLUSIONS AND CLINICAL RELEVANCE: Gastrointestinal parasitism is an important cause of death in goats. Clinical signs may not develop until just prior to death, and diagnosis is achieved via parasitologic evaluation of feces and necropsy. Seasonal weather patterns should be considered on an annual basis when designing parasite control programs for goats.

Intestinal Acanthocephaladiosis in Olrog's gulls (Larus atlanticus): Profilicollis chasmagnathi as possible cause of death.

In 2003 and 2005, mortality events were observed among hatch-year Olrog's gulls (Larus atlanticus) in a breeding colony in the Bahía Blanca estuary, Argentina. Freshly dead chicks were collected for parasitologic and parasite-associated pathologic studies. Profilicollis chasmagnathi was found at various intensities in all of the birds examined (n=28). On gross and histopathologic examinations, severe lesions ranging from intestinal obstruction to complete perforation were present in small and large intestines of the birds. Larval forms of P. chasmagnathi were being found in prey items of L. atlanticus in the study area, which suggests that diet may play a central role in the epidemiology of disease and mortality events in this species.

T-helper-1 and T-helper-2 immune responses in mice infected with the intestinal fluke Neodiplostomum seoulense: their possible roles in worm expulsion and host fatality.

Neodiplostomum seoulense is highly pathogenic and lethal to experimental mice; most worms are expelled within 2 mo of acquisition. In this study, T-helper (Th) cell immune responses were studied in N. seoulense-infected BALB/c mice. Spleen and mesenteric lymph node (MLN) cells of infected mice proliferated in response to parasite antigens; CD4+ T cells proliferated more than CD8+ T cells. Antigen-induced interferon (IFN)-gamma (a Th1 cytokine) secretion began to increase at day 7 postinfection (PI) in spleen and MLN cells, and this was maintained at day 28 PI, whereas interleukin (IL)-4 (a Th2 cytokine) secretion was somewhat lower. Similar results were observed for mRNA signals of IFN-gamma and IL-4. Antigen-specific serum total immunoglobulin (Ig)G, IgG1, IgM, and IgA levels (Th2-induced) were elevated from days 7 to 14 to day 28 PI, and IgG2a (Th1-induced) was elevated at days 21 to 28 PI. Interestingly, the numbers of macrophages (Th1- or Th2-induced), which were found to kill N. seoulense worms in vitro, increased remarkably during days 14-28 PI in spleens and small intestines of infected mice. This study shows that mixed Th1 and Th2 responses occur during the course of N. seoulense infection in BALB/c mice. Heavy infiltrations of macrophages in the small intestine may participate in host damage and worm expulsion.

Mortality in Laysan ducks (Anas laysanensis) by emaciation complicated by Echinuria uncinata on Laysan Island, Hawaii, 1993.

In November 1993, unusual mortality occurred among endangered Laysan ducks on Laysan Island, one of the remote refugia of the Northwestern Hawaiian Islands National Wildlife Refuge (USA). Ten live ducks were emaciated, and blood samples documented anemia, heterophilia, and eosinophilia. Pathology in 13 duck carcasses revealed emaciation, marked thickening of the proventricular wall, abundant mucus, and nodules in the gastrointestinal tract. Histology revealed granulomata associated with nematodes in the proventriculus, small intestines, and body walls of nine of 10 ducks examined on histology. We suspect that low rainfall and low food abundance that year contributed to enhanced pathogenicity of parasite infection, either through increased exposure or decreased host resistance. Because the Laysan duck is found only on Laysan island and is critically endangered, translocation of this species to other islands is being considered. Given that we have not seen pathology associated with Echinuria spp. in native waterfowl on other Hawaiian Islands and given the parasite's potential to cause significant lesions in Laysan ducks, it will be important to prevent the translocation of Echinuria spp.

Internal parasites of free-ranging guanacos from Patagonia.

In the winter of 2000, a greater than 80% reduction in the guanaco population located in Cabo Dos Bahi;as Wildlife Reserve, Chubut, Argentina, was evident due to massive mortality attributed to starvation. Twelve guanacos were necropsied and samples were analyzed at the Parasitology Laboratory of Facultad de Ciencias Veterinarias, Universidad Nacional del Litoral. Fecal analysis revealed developmental stages of Nematodirus sp., Marshallagia sp., Trichuris sp. and Eimeria spp. Histopathological analysis showed the presence of Sarcocystis sp. in muscle and fascia cysts. Other parasites recovered included Dictyocaulus filaria, Trichuris tenuis and Moniezia expansa. Of these, D. filaria and M. expansa possibly reflect interactions with domestic sheep. This is the first time that T. tenuis has been reported in guanacos.

Hyperinfective strongyloidiasis in the medical ward: review of 27 cases in 5 years.

BACKGROUND: Hyperinfective strongyloidiasis is rare, but the mortality rate is very high. It occurs most commonly in immunocompromised patients. We reviewed the clinical presentation and mortality rate of cases managed in our facility. METHOD: Twenty-seven patients with hyperinfective strongyloidiasis admitted to our medical ward over a 5-year period were prospectively studied. RESULTS: In our study, there were 18 males and 9 females (mean age, 58 years). Weight loss, gastrointestinal symptoms, hypoproteinemia, and anemia were the main clinical presentations. Mortality rate was 26%; human T-lymphotropic virus (HTLV-1) infection, chronic alcoholism, eosinopenia, sepsis, and prerenal azotemia on admission were poor prognostic factors. HTLV-1 infection was the main underlying disease in 71% of patients, and 44% of patients had a history of chronic alcoholism. CONCLUSION: Early diagnosis and treatment with thiabendazole may reduce mortality in hyperinfective strongyloidiasis. Hyperinfective strongyloidiasis may also be a clinical marker of HTLV-1 infection in areas where both entities are endemic or in immigrants from such areas.

Updating the DALYs for diarrhoeal disease.

Estimates of global disease burden remain high on the international research and policy agenda as a forum for ranking health priorities. Within this, the quality of life or years lived with varying degrees of disability has been recognized as an important outcome that should be considered alongside estimates of mortality. Recent studies into the long-term consequences of diarrhoeal diseases on physical and mental development suggest that the disability adjusted life year calculations for these conditions could require updating.

Expression of interleukin-9 leads to Th2 cytokine-dominated responses and fatal enteropathy in mice with chronic Schistosoma mansoni infections.

Mice infected with Schistosoma mansoni develop Th2 cytokine-mediated granulomatous pathology that is focused on the liver and intestines. In this study, transgenic mice constitutively expressing IL-9 were infected with S. mansoni and the outcome of infection was determined. Eight weeks after infection, transgenic mice with acute infections had a moderate increase in Th2 cytokine production but were overtly normal with respect to parasite infection and pathological responses. Transgenic mice with chronic infections died 10 weeks after infection, with 86% of transgenic mice dead by week 12 of infection, compared to 7% mortality in infected wild-type mice. Stimulation of mesenteric lymph node cells from infected transgenic mice with parasite antigen elicited elevated interleukin-4 (IL-4) and IL-5 production and reduced gamma interferon and tumor necrosis factor alpha production compared to the responses in wild-type mice. Morbid transgenic mice had substantial enlargement of the ileum, which was associated with muscular hypertrophy, mastocytosis, eosinophilia, goblet cell hyperplasia, and increased mucin expression. We also observed that uninfected transgenic mice exhibited alterations in their intestines. Although there was hepatic mastocytosis and eosinophilia in infected transgenic mice, there was no hepatocyte damage. Death of transgenic mice expressing IL-9 during schistosome infection was primarily associated with enteropathy. This study highlights the pleiotropic in vivo activity of IL-9 and demonstrates that an elevated Th2 cytokine phenotype leads to death during murine schistosome infection.

Morbilidad y mortalidad por enfermedades infecciosas intestinales *001/009: Cuba, 1980/1999 / Morbidity and mortality from intestinal infectious diseases *001/009: Cuba 1980/1999

En los últimos 20 años la mortalidad por enfermedades infecciosas intestinales en menores de 5 años en el mundo se ha reducido de manera significativa; sin embargo, en 1998 se registraron en el nivel mundial 2,2 millones de defunciones en los menores de 5 años. En la actualidad todavía la mortalidad seconsidera un problema de salud muy serio, sobre todo en los países subdesarrollados. En Cuba, la mortalidad por estas enfermedades en los menores de 5 años se ha reducido de manera notable, aunque la morbilidad constituye un problema importante de salud en ciertos meses del año por las alzas estacionales de la enfermedad. Este artículo muestra los resultados del trabajo desplegado a partir de 1980 en el cual se puso en ejecución el Programa Mundial de Control de las Enfermedades Diarreicas por la Organización Mundial de la Salud, que en Cuba es una continuación del Programa Nacional de Lucha contra la Gastroenteritis que se inició en 1962. Los datos de morbilidad se ofrecen desde 1985 según diferentes grupos de edades. Las reducciones en la morbilidad han sido discretas; en los menores de 1 año fue del 30,8 porciento; en el grupo de 1 a 4 años, 8,0 porciento; en los menores de 5 años del 20,1 porciento; en los de 5 a 14 años del 3,5 porciento y en los menores de 15 años del 15,8 porciento. Las tasas de mortalidad disminuyeron en el período de 1980 a 1999 en el 91,0 porciento en los menores de un año; el 50,0 porciento en los niños de 1 a 4 años; 85,7 porciento en menores de 5 años; en 66,7 porciento en el grupo de 5 a 14 años, y en 81,1 porciento en los menores de 15 años. Los elementos fundamentales que han contribuido a esta disminución en la mortalidad por enfermedades diarreas han sido, en primer lugar el uso de las sales de rehidratación oral, en la prevención y tratamiento de la deshidratación, el uso racional de antimicrobianos, el incremento de la lactancia materna exclusiva, la capacitación de los recursos humanos, el tratamiento intensivo por parte de nuestros profesionales de la salud frente al paciente crítico y el manejo correcto de la diarrea en la atención primaria de salud

IL-10 is required for prevention of necrosis in the small intestine and mortality in both genetically resistant BALB/c and susceptible C57BL/6 mice following peroral infection with Toxoplasma gondii.

The role for IL-10 in the immunopathogenesis of acute toxoplasmosis following peroral infection was examined in both genetically susceptible C57BL/6 and resistant BALB/c mice. C57BL/6-background IL-10-targeted mutant (IL-10-/-) mice all died in 2 wk after infection with 20 cysts of the ME49 strain, whereas only 20% of control mice succumbed. Histological studies revealed necrosis in the small and large intestines and livers of infected IL-10-/- mice. The necrosis in the small intestine was the most severe pathologic response and was not observed in control mice. Treatment of infected IL-10-/- mice with either anti-CD4 or anti-IFN-gamma mAb prevented intestinal pathology and significantly prolonged time to death. Treatment of these animals with anti-IL-12 mAb also prevented the pathology. Significantly greater amounts of IFN-gamma mRNA were detected in the lamina propria lymphocytes obtained from the small intestine of infected IL-10-/- mice than those from infected control mice. In common with C57BL/6-background IL-10-/- mice, BALB/c-background IL-10-/- mice all died developing intestinal pathology after infection. Control BALB/c mice all survived even after infection with 100 cysts and did not develop the intestinal lesions. Treatment with anti-IFN-gamma mAb prevented the pathology and prolonged time to death of the infected IL-10-/- mice. These results strongly suggest that IL-10 plays a critical role in down-regulating IFN-gamma production in the small intestine following sublethal peroral infection with Toxoplasma gondii and that this down-regulatory effect of IL-10 is required for prevention of development of IFN-gamma-mediated intestinal pathology and mortality in both genetically resistant BALB/c and susceptible C57BL/6 mice.

The cost effectiveness of strategies for the treatment of intestinal parasites in immigrants.

BACKGROUND: Currently, more than 600,000 immigrants enter the United States each year from countries where intestinal parasites are endemic. At entry persons with parasitic infections may be asymptomatic, and stool examinations are not a sensitive method of screening for parasitosis. Albendazole is a new, broad-spectrum antiparasitic drug, which was approved recently by the Food and Drug Administration. International trials have shown albendazole to be safe and effective in eradicating many parasites. In the United States there is now disagreement about whether to screen all immigrants for parasites, treat all immigrants presumptively, or do nothing unless they have symptoms. METHODS: We compared the costs and benefits of no preventive intervention (watchful waiting) with those of universal screening or presumptive treatment with 400 mg of albendazole per day for five days. Those at risk were defined as immigrants to the United States from Asia, the Middle East, sub-Saharan Africa, Eastern Europe, and Latin America and the Caribbean. Cost effectiveness was expressed both in terms of the cost of treatment per disability-adjusted life-year (DALY) averted (one DALY is defined as the loss of one year of healthy life to disease) and in terms of the cost per hospitalization averted. RESULTS: As compared with watchful waiting, presumptive treatment of all immigrants at risk for parasitosis would avert at least 870 DALYs, prevent at least 33 deaths and 374 hospitalizations, and save at least $4.2 million per year. As compared with watchful waiting, screening would cost $159,236 per DALY averted. CONCLUSIONS: Presumptive administration of albendazole to all immigrants at risk for parasitosis would save lives and money. Universal screening, with treatment of persons with positive stool examinations, would save lives but is less cost effective than presumptive treatment.