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Increased platelet factor 3 activity in Plasmodium falciparum malaria.

Platelet count and platelet factor 3 (pf 3) availability were determined in twenty five febrile subjects with no parasitologic Plasmodium falciparum malaria and in thirty eight febrile subjects with parasitologic malaria. Eighteen age and sex matched afebrile subjects without parasitologic malaria served as controls. Platelet counts were significantly lower in the malaria patients (p < 0.01) and in the non-parasitologic but febrile subjects (p < 0.01) than the control group. Platelet factor 3 activity was significantly higher in the febrile group (p < 0.01) than in the control subjects. Parasite density did not correlate either with platelet count or with platelet factor 3 clotting time.

Adolescent↗

Immunization of rainbow trout Oncorhynchus mykiss against Discocotyle sagiffata (Monogenea).

Rainbow trout Oncorhynchus mykiss were injected intraperitoneally with 2 different Discocotyle sagittata extracts dissolved in PBS and subsequently exposed to controlled infection. Immunization resulted in significantly reduced (p < 0.0001) worm intensities in > 50% of vaccinated fish (response arbitrarily defined as parasite burdens < mean control intensity - 1 SD), irrespective of the immunization regime (different parasite extracts, dosing and application schedules) employed. The protective effect of worm extract applied in Freund's complete adjuvant (FCA) did not differ significantly from extract given in PBS. Vaccination with embryonated parasite eggs extract and with FCA alone did not result in partial immunity, suggesting the observed protective effect is specific. Immunized fish had significantly higher specific antibody titres at the time of dissection (as determined by ELISA) than both naive and control fish. Overall, a significant negative correlation was found between antibody titres and worm burdens, suggesting immunoglobulins are implicated in mediating partial immunity. Western blot tests indicated the 2 different worm extracts used to immunize fish share antigens, but each one primarily induced recognition of a distinct band (30 and 38 kDa). Immunization seems to promote a shift between 2 equilibria, rather than progressively increasing protection. This would explain why boosting did not increase immunity, and why 2 different extracts primarily inducing recognition of 2 distinct antigens provide similar degrees of protection. Although several other non-specific and cellular factors are likely to be involved in controlling parasite numbers, it cannot be excluded that antibodies could be involved in mediating the observed partial immunity.

Animals↗

[Control of gastrointestinal strongylids in first year calves: use of Paratect Flex bolus at late pasture turnout].

The efficacy of the Paratect Flex-Bolus for the control of parasitic gastroenteritis in calves was evaluated in a field experiment in the Swiss midland region. The bolus was administered to 9 first year grazing calves at 4 to 5 months of age before turnout on June 26 while 9 calves remained as untreated controls. Both groups were rotated between 8 paddocks that had been pregrazed by older cattle in spring. For a period of 12 weeks the faecal egg output of the treated calves was reduced significantly (p < 0.05) compared to the controls, whereas no significant differences were observed in the mean serum pepsinogen values of both groups. At the end of the experiment (November 14) the bolus-treated calves showed a 4 kg weight gain advantage over the controls which was not significant. The mild infection levels in both groups were probably due to the low pasture contamination with infective larvae throughout the season which most likely resulted from the late turnout of the calves. An outbreak of dictyocaulosis was observed in both groups in October and confirmed that the Paratect Flex-Bolus provides insufficient protection against this infection.

Animals↗

Biological control potential of the obligate parasite Pasteuria penetransagainst the root-knot nematode, Meloidogyne incognita infestation in Brinjal.

The efficacy of the obligate bacterial parasite, Pasteuria penetrans against the rootknot nematode, Meloidogyne incognita infestation was assessed in brinjal. The seedling pans with sterilized soil were inoculated with nematodes and root powder of P. penetrans were applied at different dosages viz., 0 x 10(6), 0.5 x 10(6) spores and 1 x 10(6) spores/pan. Seeds of brinjal cv Co2 were sown in the pans and seedlings were allowed to grow. The seedlings were transplanted to microplots containing sterilized soil. Observations on nematode infestation and plant growth were recorded at seedling, flowering, and fruiting stages. Nematode infestation was significantly reduced by P. penetrans treatment. There was 22, 75 and 86% reduction in nematode population of soil over control at seedling, flowering and fruiting stages, respectively, at higher spore density (1 x 10(6)). Egg mass production was decreased by 63, 78 and 89% over control at 35 (seedling), 100 (flowering) and 160 (fruiting) days after sowing respectively, at 1 x 10(6) spores treated soil. The parasitizing ability of P. penetrans increased with the age of the crop. At higher spore density the percentage of parasitization was increased from 52.0 (35 days after sowing) to 90.0 (160 days after sowing) %. At these stages of the crop, the spore load per juvenile also increased at the higher dose. The P. penetrans application enhanced the plant growth. The weight of the shoot was increased by 17.6% whereas root weight by 41.0% over the control at fruiting stage. The experimental results revealed the potential use of P. penetrans as biological control agent of M. incognita. Application of P. penetrans spores in the nursery is a good strategy since the mass multiplication is quite difficult.

Animals↗

Regulation and trafficking of three distinct 18 S ribosomal RNAs during development of the malaria parasite.

The human malaria parasite Plasmodium vivax has been shown to regulate the transcription of two distinct 18 RNAs during development. Here we show a third and distinctive type of ribosome that is present shortly after zygote formation, a transcriptional pattern of ribosome types that relates closely to the developmental state of the parasite and a phenomenon that separates ribosomal types at a critical phase of maturation. The A-type ribosome is predominantly found in infected erythrocytes of the vertebrate and the mosquito blood meal. Transcripts from the A gene are replaced by transcripts from another locus, the O gene, shortly after fertilization and increase in number as the parasite develops on the mosquito midgut. Transcripts from another locus, the S gene, begins as the oocyst form of the parasite matures. RNA transcripts from the S gene are preferentially included in sporozoites that bud off from the oocyst and migrate to the salivary gland while the O gene transcripts are left within the oocyst. Although all three genes are typically eukaryotic in structure, the O gene transcript, described here, varies from the other two in core regions of the rRNA that are involved in mRNA decoding and translational termination. We now can correlate developmental progression of the parasite with changes in regions of rRNA sequence that are broadly conserved, where sequence alterations have been related to function in other systems and whose effects can be studied outside of Plasmodium. This should allow assessment of the role of translational control in parasite development.

Animals↗

Efficacy of strips coated with Metarhizium anisopliae for control of Varroa destructor (Acari: Varroidae) in honey bee colonies in Texas and Florida.

Strips coated with conidia of Metarhizium anisopliae (Metschinkoff; Deuteromycetes: Hyphomycetes) to control the parasitic mite, Varroa destructor (Anderson and Trueman) in colonies of honey bees, Apis mellifera (Hymenoptera: Apidae) were compared against the miticide, tau-fluvalinate (Apistan) in field trials in Texas and Florida (USA). Apistan and the fungal treatments resulted in successful control of mite populations in both locations. At the end of the 42-day period of the experiment in Texas, the number of mites per bee was reduced by 69-fold in bee hives treated with Apistan and 25-fold in hives treated with the fungus; however mite infestations increased by 1.3-fold in the control bee hives. Similarly, the number of mites in sealed brood was 13-fold and 3.6-fold higher in the control bee hives than in those treated with Apistan and with the fungus, respectively. Like the miticide Apistan, the fungal treatments provided a significant reduction of mite populations at the end of the experimental period. The data from the broodless colonies treated with the fungus indicated that optimum mite control could be achieved when no brood is being produced, or when brood production is low, such as in the early spring or late fall. In established colonies in Florida, honey bee colony development did not increase under either Apistan or fungal treatments at the end of the experimental period, suggesting that other factors (queen health, food source, food availability) play some major role in the growth of bee colonies. Overall, microbial control of Varroa mites with fungal pathogens could be a useful component of an integrated pest management program for the honey bee industry.

Animals↗

Infection with Strongyloides venezuelensis induces transient airway eosinophilic inflammation, an increase in immunoglobulin E, and hyperresponsiveness in rats.

Infection by nematode parasites with a pulmonary migration in their life cycle and allergic asthma are two highly prevalent diseases in humans; therefore, one may expect both may occur concomitantly. There is a predominant and essential role of Th2 lymphocytes in the mechanisms underlying the control of parasite elimination as well as in the pathology observed in the asthmatic lung. The consequences of such situations have been explored, with controversial results, justifying the development of experimental models in which the relationship between allergic airway inflammation and helminth infection might be evaluated. The present work describes the inflammatory, humoral, and functional changes that occur in the lung of rats after single (subcutaneous inoculation of 1,500 L3 larvae) or multiple (five weekly subcutaneous inoculations of 1,500 L3 larvae) Strongyloides venezuelensis infections. The results show that the migration of S. venezuelensis larvae through the lungs of infected rats induces a local eosinophilic inflammation process which is mostly focal and parenchymal for rats infected a single time and which is peribronchial after multiple infections. The inflammatory process is accompanied by mucus hypersecretion, thickening of bronchial epithelial and muscle layers, and local increase in immunoglobulin E concentrations that peak after 5 to 7 days and are resolved after 12 days of single or multiple infections. The peak of lung immunopathologic changes observed in infected rats coincides with lung airway hyperresponsiveness (AHR), a key functional alteration in asthma. We propose that this experimental model is ideal to carry out further studies on immunoprotection against nematode infection versus immunopathology of allergic airway inflammation.

Animals↗

In vitro effect of recombinant interferon gamma in combination with LPS on amoebicidal activity of murine Kupffer cells.

The present study examines the role of liver macrophages (Kupffer cells), of C57BL/6 mice, as effector cells responsible for the killing of Entamoeba histolytica trophozoites in vitro. It was shown that unstimulated Kupffer cells were inefficient in the killing of E. histolytica trophozoites in vitro. Interferon gamma (IFN-gamma) alone was not able to activate Kupffer cells to amoebicidal state. However, Interferon gamma and lipopolysaccharide (LPS) acted synergistically in this phenomenon. It seems that the acquisition of amoebicidal activity is associated with the involvement of hydrogen peroxide, because the addition of catalase partially decreases the killing of this parasite by Kupffer cells. In addition, it appears that the amoebicidal activity of IFN-gamma-treated Kupffer cells is contact-dependent. Our results indicate that the immunologic production of IFN-gamma is important in the activation of Kupffer cells for controlling this parasite and that Kupffer cells are strong effector cells against the amoebae.

Animals↗

[Parasitic zoonoses in Japan, with special reference to the current topics].

The present situation of parasitic zoonoses in Japan is reviewed. A total of 51 species, i.e., 6 species of protozoan parasites, 14 species of trematode parasites, 11 species of cestode parasites, 18 species of nematode parasites and 2 species of acanthocephalan parasites are potential zoonotic parasites. Most (11 species) of the zoonotic nematodes provoke larva migrans. Habitats of zoonotic parasites vary greatly depending upon individual species. Some parasites cause heterotopic parasitism (e.g., Paragonimus westermani) and metastasis (Entamoeba histolytica). In larva migrans, parasites migrate through various parts of body tissues, affecting multiple organs (gnathostomiasis and sparganosis mansoni). The majority of parasitic zoonoses are food-borne infections. Some of them are an arthropod-borne (or -mediated) infection (dirofilariasis, thelaziasis and moniliformiasis), or acquired by percutaneous infection with cercariae (schistosome cercarial dermatitis) or 3rd-stage infective larvae (hookworm diseases). The diagnosis of parasitic zoonoses, especially larva migrans, is difficult; although some unique clinical symptoms and the presence of eosinophilia and/or increased level of serum IgE antibody are frequently seen in larva migrans, the application of various immunodiagnostic methods is usually required. For the prevention and control of parasitic zoonoses, the ingestion of not only strange food (e.g., snakes, frogs, slugs, etc.) but also raw fish and cuttlefish (sashimi) must be prohibited. Fishes and the meat of wild animals (e.g., bear and wild boar) should be frozen or thoroughly cooked before eating. Pets and domestic animals play an important role as a direct or indirect source of infection with various parasitic zoonoses. The treatment of those animals and/or the eradication of intermediate hosts (or vectors) of the parasites are thus required.

Animals↗

IFN-gamma-dependent nitric oxide production is not linked to resistance in experimental African trypanosomiasis.

Resistance to African trypanosomes is dependent on B cell and Th1 cell responses to the variant surface glycoprotein (VSG). While B cell responses to VSG control levels of parasitemia, the cytokine responses of Th1 cells to VSG appear to be linked to the control of parasites in extravascular tissues. We have recently shown that IFN-gamma knockout (IFN-gamma KO) mice are highly susceptible to infection and have reduced levels of macrophage activation compared to the wild-type C57BL/6 (WT) parent strain, even though parasitemias were controlled by VSG-specific antibody responses in both strains. In the present work, we examine the role of IFN-gamma in the induction of nitric oxide (NO) production and host resistance and in the development of suppressor macrophage activity in mice infected with Trypanosoma brucei rhodesiense. In contrast to WT mice, susceptible IFN-gamma KO mice did not produce NO during infection and did not develop suppressor macrophage activity, suggesting that NO might be linked to resistance but that suppressor cell activity was not associated with resistance or susceptibility to trypanosome infection. To further examine the consequence of inducible NO production in infection, we monitored survival, parasitemia, and Th cell cytokine production in iNOS KO mice. While survival times and parasitemia of iNOS KO mice did not differ significantly from WT mice, VSG-specific Th1 cells from iNOS KO mice produced higher levels of IFN-gamma and IL-2 than cells from WT mice. Together, these results show for the first time that inducible NO production is not the central defect associated with susceptibility of IFN-gamma KO mice to African trypanosomes, that IFNgamma-induced factors other than iNOS may be important for resistance to the trypanosomes, and that suppressor macrophage activity is not linked to either the resistance or the susceptibility phenotypes.

Animals↗

Delayed hypersensitivity to Toxoplasma and unrelated antigens in Toxoplasma-infected mice: induction and elicitation of delayed-type hypersensitivity by antigen-pulsed macrophages.

Delayed-type hypersensitivity (DTH) to Toxoplasma and unrelated antigens in Toxoplasma-infected BALB/c mice was investigated by the radioisotopic uptake method of Vadas et al. (Int. Arch. Allergy Appl. Immunol. 49: 670-692, 1975). DTH became positive on day 30 of infection and remained positive during chronic infection. The expression of DTH in mice infected with the relatively avirulent C37 strain of the parasite paralleled the Toxoplasma antibody response as detected by the Sabin-Feldman dye test. Mice sensitized with Toxoplasma, keyhole limpet hemocyanin, or sheep erythrocytes during the acute or chronic phase of Toxoplasma infection showed a DTH reaction similar to that of uninfected sensitized controls. No parasite antigens could be detected by immunofluorescence techniques on the surface of Toxoplasma-infected cells. When killed organisms were added to the cell cultures, specks of fluorescence appeared on cells containing intracellular parasites as well as on cells without intracellular organisms. That the antigens may be present in or on macrophages in a form readily recognizable by T cells is suggested by experiments in which we demonstrated that injection of uninfected normal macrophages pulsed with Toxoplasma-soluble antigens into the ears of chronically infected mice elicited a DTH reaction comparable to that observed when 10(6) Formalin-fixed tachyzoites were used as the test antigen. When macrophages pulsed with Toxoplasma antigen were used in attempts to induce DTH in naive uninfected mice, the intensity of the reaction was similar to that observed in infected mice.

Animals↗

[Human African trypanosomiasis].

Human African trypanosomiasis (HAT) is caused by infestation with a flagellate protozoan, the trypanosome which is inoculated by the bite of the tsetse fly Glossina. The particular ecological conditions of parasites and vectors are such that the disease is only found in the intertropical regions of Africa. Although there are many species of trypanosomes, only two, belonging to the brucei group are likely to lead to HAT. These two species are quite similar morphologically but have different pathogenicity. Trypanosoma brucei gambiense found in West and Central Africa leads to a chronic form of the disease or sleeping sickness. T. b. rhodesiense leads to a more virulent and acute condition, although for each species of trypanosome there are strains of different virulence, which account, at least in part, for the interindividual variability in the clinical course. Immediately after penetration into the human organism, the trypanosome multiplies at the point of inoculation, producing a local inflammatory reaction. It then invades the whole organism, and the central nervous system (CNS). The involvement of the CNS leads to an irreversible demyelinating process ending by death without treatment. Apart from the initial stages, it is not easy to determine the phase of the disease that the patient is presenting. The parasite can escape the host immune response by varying the surface glycoprotein coat. Variable surface glycoproteins (VSG) are strongly antigenic and lead to great antibody response with immune lysis. But, some heterologous antigenic variants can survive to repopulate blood and other tissues. This mechanism of antigenic variation is under parasite genetic control. The trypanosome can release numerous pathogenic substances which cause alterations in cytokine/prostaglandin network. A 41-46 kDa molecule termed trypanosome-released lymphocyte trigerring factor may selectively activate CD8+ T cells to produce interferon-gamma which then activates macrophages but also promotes parasite growth. Activated macrophages release tumor necrosis factor alpha and nitric oxide (NO) which are trypanostatic static and other cytokines and prostanglandins. These macrophage relased substances enhance the immunosuppression and alter the blood brain barrier (BBB). So, trypanosomes and inflammatory cells can invade the CNS leading to a progressive meningoencephalitis with typical perivascular cuffings which explain neurological disorders and neuroendocrine alterations. The inflammatory cells (lymphocytes, astrocytes, glial cells) produce cytokines, NO and other mediators and enhance the CNS immunopathological process. The peri-ventricular regions, the tuberoinfundibula and thalamic-hypothalamic regions, are particulary involved. These disturbances lead to a progressively complete disruption of the normal sleep-waking cycle. Antibodies anti-CNS components (galactocerebrosides, neurofilaments, tryptophane) are also described in sera and cerebrospinal fluid (CSF) of HAT patients. Their presence may be due to cross reactions with comon epitopes between host and trypanosomes which can lead to a self-propagating autoimmune reaction, which accounts for the marked demyelination found in the late stage of the disease. The diagnosis of CNS involvement in not easy to establish in the early neurological phase in the absence of neurological signs and in absence of great chnages in CSF. This is an important problem because it is the basis to apply existing available drugs. pentamidine and suramin are effective only in early stages of the disease when CNS is not invaded. Melarsoprol is effective in all-stages: this is the drug of choice when CNS is involved. Unfortunaley, melarsoprol is toxic and, in 5% of treated patients, this drug can lead to arsenical encephalopathy which is often fatal. In the continuing search for new antitrypanosonal drugs, biochemical peculiarities of the trypanosome are used as drug garget, especially glycolysis, trypanothione, sensibil

Animals↗

THE MALARIA PARASITE RATE AND INTERRUPTION OF TRANSMISSION.

Present methods for assessment of the attack phase of malaria eradication are inadequate, particularly lacking any objective parasitological criteria of success. On the basis of previous observations and development of theory, the authors first postulate that the effects of complete interruption of transmission should, ideally, include a regular progressive decrease of falciparum parasite rates in the ratios of 1: 0.4 in 6 months, 1: 0.16 in 12 months and 1: 0.026 in 24 months. Analysis of a series of programmes in which complete interruption of transmission is known to have been achieved shows that this postulate is valid, and that it is not materially upset by strain differences of parasites or by differences in the ages of the subjects examined. Vivax rates appear to fall at approximately the same rate; the rarity of data for vivax malaria makes firm conclusions unsure, but the postulate can be extended to rates which are predominantly due to falciparum infection but include some admixture of other species. A second, arbitrary, postulate is made that the slowest acceptable rate of fall in 12 months should be in a ratio not less than 1: 0.22, which would secure ultimate eradication in about one-third more time than the ideal fall; on this basis statistical standards are set up for assurance of confidence that the minimum rate is exceeded. Slower rates of fall are then related to reproduction rates causing them, the findings being illustrated graphically and by mathematical theory.

Animals↗

Host resistance and immune deviation in pigeon cytochrome c T-cell receptor transgenic mice infected with Toxoplasma gondii.

Resistance to Toxoplasma gondii has been shown to be mediated by gamma interferon (IFN-gamma) produced by NK, CD4(+), and CD8(+) T cells. While studies of SCID mice have implicated NK cells as the source of the cytokine in acute infection, several lines of evidence suggest that IFN-gamma production by CD4(+) T lymphocytes also plays an important role in controlling early parasite growth. To evaluate whether this function is due to nonspecific as opposed to T-cell receptor (TCR)-dependent stimulation by the parasite, we have examined the resistance to T. gondii infection of pigeon cytochrome c transgenic (PCC-Tg) Rag-2(-/-) mice in which all CD4(+) T lymphocytes are unreactive with the protozoan. When inoculated with the ME49 strain, PCC-Tg animals exhibited only temporary control of acute infection and succumbed by day 17. Intracellular cytokine staining by flow cytometry revealed that, in contrast to infected nontransgenic controls, infected PCC-Tg animals failed to develop IFN-gamma-producing CD4(+) T cells. Moreover, the CD4(+) lymphocytes from these mice showed no evidence of activation as judged by lack of upregulated expression of CD44 or CD69. Nevertheless, when acutely infected transgenic mice were primed by PCC injection, the lymphokine responses measured after in vitro antigen restimulation displayed a strong Th1 bias which was shown to be dependent on endogenous interleukin 12 (IL-12). The above findings argue that, while T. gondii-induced IL-12 cannot trigger IFN-gamma production by CD4(+) T cells in the absence of TCR ligation, the pathogen is able to nonspecifically promote Th1 responses against nonparasite antigens, an effect that may explain the immunostimulatory properties of T. gondii infection.

Acute Disease↗

The role of IL-12 in experimental Trypanosoma cruzi infection.

Host resistance to Trypanosoma cruzi infection is dependent on both natural and acquired immune responses. During the early acute phase of infection in mice, natural killer (NK) cell-derived IFN-gamma is involved in controlling intracellular parasite replication, mainly through the induction of nitric oxide biosynthesis by activated macrophages. We have shown that IL-12, a powerful inducer of IFN-gamma production by NK cells, is synthesized soon after trypomastigote-macrophage interaction. The role of IL-12 in the control of T. cruzi infection in vivo was determined by treating infected mice with anti-IL-12 monoclonal antibody (mAb) and analyzing both parasitemia and mortality during the acute phase of infection. The anti-IL-12 mAb-treated mice had higher levels of parasitemia and mortality compared to control mice. Also, treatment of infected mice with mAb specific for IFN-gamma or TNF-alpha inhibited the protective effect of exogenous IL-12. On the other hand, TGF-beta and IL-10 produced by infected macrophages inhibited the induction and effects of IL-12. Therefore, while IL-12, TNF-alpha and IFN-gamma correlate with resistance to T. cruzi infection, TGF-beta and IL-10 promote susceptibility. These results provide support for a role of innate immunity in the control of T. cruzi infection. In addition to its protective role, IL-12 may also be involved in the modulation of T. cruzi-induced myocarditis, since treatment of infected mice with IL-12 or anti-IL-12 mAb leads to an enhanced or decreased inflammatory infiltrate in the heart, respectively. Understanding the role of the cytokines produced during the acute phase of T. cruzi infection and their involvement in protection and pathogenesis would be essential to devise new vaccines or therapies.

Animals↗

Efficiency of Duddingtonia flagrans against Trichostrongyle infections of sheep on mountain pastures.

The control of sheep nematode parasites in extensive mountain/transhumant management systems using the nematophagous fungus Duddingtonia flagrans was assessed in this study. Two groups of Churra Tensina ewes were allowed to graze for 8 weeks in autumn on two separate paddocks of infected pasture near their winter sheds in the valley. At lambing, ewes and their twin lambs were turned out into the same paddocks for the following 12 weeks. One group of ewes received a daily dose of 5 x 10(5) chlamydospores of Duddingtonia flagrans/kg live weight per day both in autumn and in spring, while the other group was used as a non-treated control. Daily dosing of grazing ewes with the fungus D. flagrans had a clear effect on reducing autumn pasture contamination. This had a subsequent effect on the over-wintering larvae population that was confirmed by a 20% lower worm burden of tracer lambs kept in early spring on the paddock previously grazed by fungus treated ewes. In spring, pasture contamination was also significantly reduced in the paddock grazed by fungi-treated ewes and their lambs showed a 61% lower worm burden and a better performance than the control lambs. Results herein show that fungal spores fed to sheep at critical times with regard to the epidemiology of parasite infection, can have a significant effect on the infective larvae present on pasture, which could further improve lambs performance. This novel approach to parasite control would be of interest amongst both organic and conventional sheep farmers operating in mountain regions.

Animals↗

Controlled tests of activity of ivermectin against natural infections of migratory large strongyles and other internal parasites of equids.

Four controlled tests (experiments A, B, C, and D) were conducted in naturally infected yearling equids to evaluate activity of ivermectin (0.2 mg/kg IM) against migrating Strongylus vulgaris and S edentatus in mesenteric arteries and ventral abdominal wall, respectively. Data were also obtained on activity against other internal parasites of the gastrointestinal tract and eyeworms. The type and number of equids in the experiments were as follows: experiment A-3 ponies, 2 treated and 1 non-treated; experiment B-4 mixed-bred horses, 2 treated and 2 nontreated; experiment C-5 mixed-bred horses, 3 treated and 2 nontreated; experiment D-4 mixed-bred horses, 2 treated and 2 nontreated. Intervals between treatment and necropsy were 35 days in experiment A, 52 to 53 days in experiment B, 38 to 41 days in experiment C, and 45 days in experiment D. Efficacious killing of retroperitoneal forms of S edentatus in the ventral abdominal wall was obtained in the 4 experiments. Only dead worms or fragments were recovered from treated animals, while living 4th-stage and/or 5th-stage S edentatus was present in nontreated equids in each test. A similar killing effect on S vulgaris in cranial mesenteric arteries was recorded in 2 experiments (B and D); only 1 dead 5th-stage worm was found in 1 of the treated yearlings in experiment B, whereas living 4th- and 5th-stages of S vulgaris were found in the nontreated controls in both experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Developing and establishing bee species as crop pollinators: the example of Osmia spp. (Hymenoptera: Megachilidae) and fruit trees.

The development of a bee species as a new crop pollinator starts with the identification of a pollination-limited crop production deficit and the selection of one or more candidate pollinator species. The process continues with a series of studies on the developmental biology, pollinating efficacy, nesting behaviour, preference for different nesting substrates, and population dynamics of the candidate pollinator. Parallel studies investigate the biology of parasites, predators and pathogens. The information gained in these studies is combined with information on the reproductive biology of the crop to design a management system. Complete management systems should provide guidelines on rearing and releasing methods, bee densities required for adequate pollination, nesting materials, and control against parasites, predators and pathogens. Management systems should also provide methods to ensure a reliable pollinator supply. Pilot tests on a commercial scale are then conducted to test and eventually refine the management system. The process culminates with the delivery of a viable system to manage and sustain the new pollinator on a commercial scale. The process is illustrated by the development of three mason bees, Osmia cornifrons (Radoszkowski), O. lignaria Say and O. cornuta (Latreille) as orchard pollinators in Japan, the USA and Europe, respectively.

Animals↗