Chordodes formosanus is a horsehair worm that has the praying mantis as its definitive host. Horsehair worms are obligate parasites that pass through different hosts at various stages. These worms can grow up to 90 cm long and can be extremely dangerous for their host, especially the praying mantis.[1][2]
The definitive host range of horsehair worms is limited to one or few species. Because nematomorphs are sometimes found after they have emerged from their host, definitive information on hosts is unknown in some species.
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High-intensity hookworm infections occur among both school-age children and adults, unlike the soil-transmitted helminths Ascaris and whipworm. High-intensity infections with these worms are less common among adults. The most serious effects of hookworm infection are the development of anemia and protein deficiency caused by blood loss at the site of the intestinal attachment of the adult worms. When children are continuously infected by many worms, the loss of iron and protein can retard growth and mental development.
While deficiencies in essential micronutrients like iron are thought to modulate the risk of infection caused by a variety of pathogens, to date little is known about the role host iron status might play in disease caused by hookworms (10, 11). Previous studies have shown that Syrian hamsters infected by oral gavage with infective A. ceylanicum hookworm larvae in the third stage (L3) experience growth delay and anemia, beginning approximately 14 days postinfection (5-7, 16, 17). Interestingly, despite resolution of anemia and reduction in intestinal worm burden, animals do not reach the weights of uninfected, age-matched controls as far out as 100 days postinfection (5), similar to growth kinetics observed in children who acquire hookworm infection in areas of endemicity (8, 30, 31). Thus, the hamster model of A. ceylanicum is an appropriate system for characterizing the pathogenesis of hookworm infection and is particularly well suited for probing host-parasite interactions in vivo.
In order to characterize the impact of host nutritional status on hookworm pathogenesis, experiments were designed to test the hypothesis that dietary iron impacts susceptibility to hookworm-associated anemia and growth delay. We report here evidence to support a bidirectional role for host iron in mediating hookworm pathogenesis, influencing both parasite development and host susceptibility to severe disease. Ultimately, these studies may provide new insights into the evolutionary mechanisms through which host and parasite compete for specific micronutrients.
Dietary iron restriction reduces clinical sequelae of hookworm infection. The effects of primary infection with A. ceylanicum on weight (A), blood hemoglobin (B), and serum iron levels (C) were determined in groups of hamsters maintained on a standard-iron (200 ppm) (left panels) or restricted-iron (10 ppm) (right panels) diet. * indicates statistical significance (P < 0.05). See Results for numerical values.
Dietary iron restriction reduces intestinal hookworm burden. Individual worm burdens are indicated by filled circles and means of each group by horizontal bars. Arrows indicate statistically significant reductions. PI, postinfection.
Intermediate dietary iron restriction increases the pathogenicity of primary hookworm infection. Animals were equilibrated on diets containing intermediate levels of iron (10, 40, 100, or 200 ppm) prior to infection with A. ceylanicum. Shown are data from measurements of percentages of the change in weight relative to weight on day 0 (A), blood hemoglobin concentration (B), and serum iron concentration (C) taken on day 22 postinfection. P values for statistically significant differences are shown above brackets.
Intermediate dietary iron restriction is associated with increased fecal egg excretion. Feces from infected animals was collected on day 23 postinfection, and hookworm eggs were quantified as described in Materials and Methods. Bars represent the mean numbers of eggs/gram counted in three separate samples of feces. Brackets indicate statistically significant differences between groups.
Intermediate dietary iron restriction is associated with increased mortality following hookworm infection. A survival curve is shown for animals maintained on intermediate (10-, 40-, 100-, 200-ppm) iron diets. Statistical significance of survival differences was analyzed using a log-rank test, with an overall significance level of 0.008. Pairwise comparisons also revealed significant differences between both groups B (40 ppm) and C (100 ppm) and group A (10 ppm), as well as between groups B and C and group D (200 ppm).
The capacity of adult hookworms to cause significant losses of blood and iron during feeding has been well established using in vivo models (4, 5, 21). Hookworm infection has long been associated with iron deficiency anemia, and data from human studies generally confirm an inverse correlation between intensity of infection, as estimated by fecal egg counts, and blood hemoglobin levels (9, 22, 33-35). It has generally been presumed that individuals who are iron deficient are likely more susceptible to hookworm anemia, due to reduced total body iron stores in the face of iron loss from gastrointestinal hemorrhage. However, it has also been suggested that hookworm infection modulates iron metabolism in the host, resulting in enhanced reabsorption from the gut as a means of compensating for hookworm-associated blood loss (10, 11). Such a compensatory mechanism was originally put forth to explain the fact that death from overwhelming hookworm anemia is rare, despite calculations that show that iron losses from hookworm infection are likely to far exceed dietary intake in many communities of high endemicity (11, 24).
These observations on the role of host dietary iron on hookworm pathogenesis may ultimately have an impact on how control strategies in areas of endemicity are implemented and evaluated. In particular, the degree to which dietary iron supplementation may directly impact hookworm development on the one hand and host susceptibility on the other needs to be more carefully evaluated in laboratory- and field-based studies. Ultimately, by making severely iron-deficient individuals only marginally less so, iron supplementation may enhance the potential for hookworm larvae to successfully establish infection in the intestine. Conversely, supplementation may improve the iron status of some individuals so that they are no longer susceptible to the most severe form of the disease. In other words, the effect of iron supplementation should no longer be viewed solely from the perspective of the host, but also as a potential effector of hookworm development and/or virulence.
Researchers at Scripps Institution of Oceanography at the University of California San Diego have made a discovery with potential human health impact based on a study of parchment tubeworm, the marine invertebrate Chaetopterus sp., that resides in muddy coastal seafloors.
A new study published today in Biochemical Journal finds that the tubeworm, also known for its bioluminescence, has a ferritin with the fastest catalytic performance ever described, nearly eight times faster than that of human capabilities.
Ferritin, present in nearly all living organisms, is an important protein that manages iron metabolism in cells by storing and releasing it in a controlled manner. In humans, its function is critical to balance iron in the blood.
This discovery also has important human health implications for biomedical research, as ferritin is an essential protein for those with iron deficiency and overall iron metabolism issues. This discovery can be a new tool in future research of ferritin to use in patients, thanks to its biocompatibility and ability to carry, protect and deliver small molecules as medication to specific targets.
De Meulenaere describes ferritin as being shaped like a soccer ball, with openings that take up iron when available, store it and release it when needed. That specific structure allows for a wide range in applications, from medical to environmental. It could help target medication release, function as a safe contrast agent, while also being used for water treatment by selectively taking up and storing contaminants.
This study was funded by the Air Force Office of Scientific Research (grant no. FA9550-17-0189), which is interested in learning more about the unique bioluminescent properties of the worm, the outstanding performances of the worm ferritin, and the resilient properties of the tube encasement, within a larger framework studying biomimetic systems.
Introduction: Worm infestations are a common occurrence in low-income countries. Anemia due to iron deficiency can be brought on by human intestinal worms. The authors report a case of an 86-year-old frail older adult with upper gastrointestinal (GI) bleeding caused by a worm infestation most likely to be hookworm.
Case presentation: An 86-year-old male, presented to the Emergency Department with complaints of bilateral lower limb swelling and shortness of breath for 4 days associated with melena for 2 months. The authors made a provisional diagnosis of heart failure precipitated by anemia. Upper GI endoscopy revealed multiple whitish exudates, which are resistant to water jets. Multiple worms were noted in the second part of the duodenum. Based on clinical evaluation and endoscopy, the diagnosis of oesophagial candidiasis and iron deficiency anemia secondary to upper GI bleeding due to Hookworm infestation was made.
Clinical discussion: In low-income countries, especially those involving the tropical area, worm infestation should be considered as an important cause of obscure acute GI bleeding and severe anemia. Usually, malignancy is suspected in an older adult with severe anemia but hookworm infestation is a treatable disease with a good prognosis and complete recovery. The most commonly used drugs for treatment are mebendazole and albendazole. In a low-income country with a high burden of worm infestations, empirical treatment of iron deficiency anemia with single dose albendazole has been recommended. be457b7860
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