Diphyllobothriasis associated with eating raw pacific salmon.

The incidence of human infection with the broad tapeworm Diphyllobothrium nihonkaiense has been increasing in urban areas of Japan and in European countries. D. nihonkaiense is morphologically similar to but genetically distinct from D. latum and exploits anadromous wild Pacific salmon as its second intermediate host. Clinical signs in humans include diarrhea and discharge of the strobila, which can be as long as 12 m. The natural life history and the geographic range of the tapeworm remain to be elucidated, but recent studies have indicated that the brown bear in the northern territories of the Pacific coast region is its natural final host. A recent surge of clinical cases highlights a change in the epidemiologic trend of this tapeworm disease from one of rural populations to a disease of urban populations worldwide who eat seafood as part of a healthy diet.

Difilobotríase: estudo clínico / Diphyllobotriasis: clinical study

A difilobotríase é uma parasitose intestinal cuasada por cestódeos do gênero Diphyllobothrium, adquirida pela ingestão de cistos presentes nos tecidos de peixes. As manifestações clínicas são diversas, variando desde quadros assintomáticos até situações matizadas por intensa anemia macrocítica, decorrente da carência de vitamina B12. O diagnóstico é simples, sendo estabelecido a partir da identificação de problotes expelidos e(ou) do encontro de ovos nas fezes, sem necessitar de métodos especiais para o exame. O tratamento pode ser feito com praziquantel ou niclosamida. Pode se evitar esta parasitose através de medidas sanitárias e através do consumo cuidadoso de peixes.

Diphyllobotriasis is an intestinal parasitosis caused by Diphyllobotrium cestodes acquired through the ingestion of cysts found in the tissue of fishes. Clinical signs are diverse, from non-symptomatic presentations to severe macrocytic anemia, caused by lack of B12 vitamin. Diagnosis is simple to establish with the identification of proglottids passed out and(or) the presence of Diphyllobotrium eggs for parasitological tests. Treatment is conducted with praziquantel or niclosamide. This parasitoris can be easily avoided by keeping sanitary conditions and a careful preparation of fish.

Diphyllobothrium nihonkaiense (Yamane et al., 1986) in Switzerland: first molecular evidence and case reports.

We report the first cases of locally-acquired Diphyllobothrium nihonkaiense (Yamane, Kamo, Bylund and Wikgren, 1986) in Switzerland, confirmed by genetic analysis (18S rRNA, COI and ITS1-5.8S rRNA-ITS2 genes). Diphyllobothriasis in this country is attributed to the tapeworm D. latum (Linnaeus, 1758) but the increasing popularity of raw fish culinary specialities (sushi, carpaccio, tartare) brings out a new diagnostic problem, so that people can get infected by exotic species of tapeworms.

Diphyllobothriosis--experimental study.

For the first time the agent of diphyllobothriosis Lake Baikal is the cestoda D. dendriticum establishted by T.P. Chizhova and P.G. Gofman-Kadoshnikov (1962). D. dendriticum reaches maturity in human intestine, but it is considered, that the relationships between the parasite and human are facultative property (Klebonovski 1985). The results of the investigation of the diet of sea-gull nestlings (control-uninfected and experimental-infected birds with cestoda groups) and stress influence (starvation) on the mass loss in experimentally and naturally infected ones with different duration conditions adaptation of experiments are discussed in this article.

[The functional status of the small intestine and lipid metabolism in diphyllobothriasis patients]. / Funktsional'noe sostoianie tonkoi kishki i lipidnogo obmena u bol'nykh difillobotriozom.

198 diphyllobothriasis patients have been examined before and 1-2, 4-6, 10-12 months after dehelminthization. The absorption of fats and carbohydrates by the small intestine was studied; total lipids, total phospholipids and their range in the serum were determined. Fucose content in the intestinal juice and the overnight portion of urine was determined for functional evaluation of the mucosal protective barrier. The studies revealed alterations in lipid and carbohydrate absorptions by the small intestine as well as that of the mucosal protective barrier in the gastroduodenal zone, and changes in lipid metabolic values.

[Clinical observation periods for diphyllobothriasis patients depending on the invasion period]. / Sroki dispanserizatsii bol'nykh difillobotriozom v zavisimosti ot dlitel'nosti invazii.

Discrepancy between the terms of clinical observation and normalization of gastric functions was established on the basis of a time-course study of gastric secretory function in 189 diphylobothriasis patients examined before the treatment and 1-2, 5-6, 10-12 months after it. Recovery of the secretory function took less than 5-6 months in people recovered from short-term invasion (less than a year), while in patients recovered from long-term invasion (lasting more than a year) it took 10-12 months, and reduced secretory activity in the latter group was still observed in many cases 10-12 months after treatment. Results of the study may be used in optimization of terms and forms of clinical observation.

Effect of infection with Spirometra erinacei plerocercoid on thyroid hormone in mice.

Young, male ICR mice were given tap water or distilled water containing 200 mg/l propylthiouracil (PTU) and were then infected with 10 plerocercoids of Spirometra erinacei to investigate the effect of plerocercoid infection on thyroid hormone in their hosts. Plerocercoid infection stimulated growth in PTU-induced hypothyroid mice as if they had never received PTU treatment: there were increases in weight in the liver, skeletal muscle, and spleen, as well as enhancement of the head and body length, in spite of a greater decrease in serum T4 levels than was observed in PTU-treated controls. Furthermore, the intact mice infected with plerocercoids showed a decrease in serum T4 levels as well as in the concentration of T4-binding globulin. These observations suggest that the growth stimulation and the decrease in concentrations of serum T4 and T4-binding globulin associated with plerocercoid infection in mice probably resulted from secretion of a growth hormone-like substance produced by plerocercoids of S. erinacei.

Reduction of lactogenic receptors in female hamster liver due to the human growth hormone analog produced by plerocercoids of the tapeworm, Spirometra mansonoides.

The inductive effect of GH on hepatic lactogenic receptors is suspected of being due to a direct somatogenic action. Plerocercoid larvae of the tapeworm, Spriometra mansonoides, produce a factor that stimulates body growth, suppresses endogenous GH, and specifically displaces [125I]human (h) GH from hepatic receptors. Plerocercoid growth factor (PGF) mimics the growth-promoting actions of GH, but it has not been shown to duplicate all of the activities reported for GH. An important function of GH is its role in the maintenance of liver receptors for lactogenic hormones. This study was undertaken to determine if treatment of female hamsters with PGF would increase, decrease, or have no effect on liver receptors that bind hGH. Since hGH binds to somatogenic as well as lactogenic receptors, it was necessary to demonstrate the specificity of PGF's effects on [125I]hGH binding. PGF-treated (15 pleocercoids sc) hamsters had accelerated body growth, suppressed serum GH, and a marked reduction in [125I]hGH and [125I]ovine PRL binding to hepatic microsomes. Specific binding of [125I] bGH was unaltered by PGF treatment. The difference in [125I] hGH binding was due to a reduction in receptor number and not to receptor occupancy or reduced affinity. Serum GH was normalized after 10 days of estradiol benzoate (25 micrograms/day) injections, but the binding capacity for [125I]hGH of the PGF-treated group was less than half that of the control group. The fact that estrogen injections normalized serum GH, but not hGH binding, indicates that down-regulation of these receptors by PGF cannot be entirely explained on the basis of reduced levels of serum GH. The lack of any effect of PGF treatment on [125I]bGH binding suggests that the hepatic somatogenic receptors were not involved and that the reduction in receptors for [125I]hGH was associated with the lactogenic component of hGH.

Effects of Spirometra erinacei plerocercoids on the growth of Snell dwarf mice.

Snell normal and dwarf mice were infected with Spirometra erinacei plerocercoids collected in Japan, to investigate the relationship between the growth-promoting effects of plerocercoids and the growth hormone releasing factor and the somatostatin--growth hormone--somatomedin axis in the host. Infection with plerocercoids caused increases in body weight and weights of muscle, liver, spleen and heart in the normal male mice, and increases in the head--body length, body weight and weights of muscle, liver, spleen, kidney and heart in the normal female mice, but did not increase the weight of the fat pad. Infection with plerocercoids caused increases in body weights and weights of muscle, liver and spleen in the male dwarf mice, and increases in the head--body length, body weight and weights of muscle, liver, spleen and kidney in the female dwarf mice. These observations suggest that plerocercoids promote the growth of dwarf mice as well as normal mice. As the dwarfism of Snell mice is due to a defective anterior pituitary gland, it seems that plerocercoids do not stimulate secretion of growth hormone from the pituitary. Accordingly, it seems to be more probable that the larvae secrete a growth hormone-like substance.

Delay of puberty onset in males due to suppression of growth hormone.

Infection with Spirometra mansonoides at 22 days of age was associated with delayed sexual maturation in the male rat. Balanopreputial separation occurred at 46.7 +/- 0.8 days in controls and at 50.6 +/- 0.9 days in worm-treated rats (p less than 0.02). This was accompanied by a delay in the normal prepubertal testicular and seminal vesicle weight increases. LH remained normal but serum FSH was depressed as early as 25 days of age. The castration response in worm-treated rats was comparable to that of controls, when the FSH levels were normalized as percentages of resting level. The LH response to castration was diminished. The acute FSH and LH response to GnRH was normal and pituitary stores of gonadotrophin, as estimated by radioimmunoassayable concentrations of FSH and LH, were normal. It can be concluded that puberty onset in males is not linked to body weight gain pe se, and that the absence of endogenous GH secretion affects both sexual maturation and gonadotrophin secretion in the prepubertal period.

Biological effects of Spirometra erinacei plerocercoids in several species of rodents.

Observations were made of the biological effects on infection with plerocercoids of Spirometra erinacei on normal female Snell mice, male chinese hamsters, golden hamsters, normal and hypox rats. Plerocercoid infection caused the strongest growth-promoting effect on normal Snell mice. In mice, this effect appears to be independent of strain. Chinese hamsters infected with these larvae showed similar growth. The infected normal rats and golden hamsters, however, showed a weight increase in the skeletal muscle only, while the hypox rats exhibited no effect at all. The elevation in the concentration of serum triglyceride was observed in all the animals investigated except for rats. Golden hamsters, in particular, exhibited a marked increase in the concentration of serum free fatty acids and total cholesterol. There was close correlation between the concentrations of serum triglyceride and free fatty acids, and the regression coefficient of the resulting linear regression equation for the experimentals was higher than that for the controls. This suggests that serum triglyceride results from an increased concentration of serum free fatty acids derived from stimulated lipolysis. The total cholesterol concentration in the serum decreased in chinese hamsters infected with larvae. The serum glucose concentration increased in normal Snell mice but decreased in chinese and golden hamsters. No difference in glycerol and free fatty acid concentration was observed in infected animals except for golden hamsters.