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1979). Oral inoculation is required for anamnestic eosinophilia in S. vulgaris infections (Monahan et al. 1994).
Peripheral blood eosinophilia does not predict the severity of helminth infection. Peripheral blood eosinophilias may be higher in infected than na€ıve horses, as occurs with S. vulgaris, but among affected animals, no correlation is found between PBEs and lesion severity, number of larvae or adult worms (Bailey et al. 1984). Neither do PBEs correlate with the adult worm burden in horses with mixed strongyle infections (Round 1968). Isolated eosinophil counts therefore are unreliable indicators of clinically significant parasitism (Round 1973).
100 µm
Fig 1: Eosinophilic granulomas surround the degenerate remnants of Habronema larvae in a lesion on the sheath of an affected horse. Image courtesy of Dr Jason Struthers.
infection, life cycles, prior exposure and sampling times, but general observations are summarised as follows.
Peripheral blood eosinophilia is an attribute of helminth infection but is variable in character. Increases in peripheral blood eosinophils (PBEs) may be sustained, transient or biphasic, dose-dependent and with considerable individual variation. Eosinophils peak rapidly at about 2 weeks post- infection following P. equorum administration (Clayton and Duncan 1977), and at about 4 to 5 weeks following S. edentatus (McCraw and Slocombe 1974; Slocombe and McCraw 1975) and S. vulgaris (Duncan and Pirie 1975) infections, respectively. Eosinophil peaks occur at up to 8 weeks when both large and small strongyles are present (Thamsborg et al. 1998). Peripheral blood eosinophilia is variable in cases of lungworm infection in horses (MacKay and Urquhart 1979; Urch and Allen 1980), but a more predictable pattern is observed in donkeys (Urch and Allen 1980). A significant increase in PBEs is seen in horses naturally infected with small strongyles (Steinbach et al. 2006), but this is not a feature of horses suffering from larval cyathostomiasis (Giles et al. 1985). Peaks may recur at about 3 weeks in P. equorum infections (Clayton and Duncan 1977) and up to 18 weeks in S. vulgaris (Duncan and Pirie 1975) infections (McCraw and Slocombe 1974, 1978; Duncan and Pirie 1975; Slocombe and McCraw, 1975; Clayton and Duncan 1977; Thamsborg et al. 1998). Increases in PBEs may persist up to 12 weeks in mixed infections (Thamsborg et al. 1998).
Peripheral blood eosinophilia may show an anamnestic pattern. This is a function of the host’s integrated response to parasites, of which one component is immunologic memory. Peripheral blood eosinophilia peaks in secondary helminth infections occur earlier than in primary infections in S. vulgaris and small strongyle-infected horses, reflecting Th2-mediated anamnesis (Smith 1976; Bailey et al. 1989). A temporal relationship exists between lymphocyte transformation, complement-fixing antibodies and eosinophilia in S. vulgaris infections. Antibody and PBE peaks are biphasic, with antibodies preceding eosinophilia (Bailey et al. 1989). B cells, total lymphocytes and blood viscosity secondary to immunoglobulin production correlate with PBEs (Dixon et al.
Tissue eosinophilia occurs in response to larval migration, with many factors influencing the composition of the infiltrate. Eosinophils first appear at day 2 to 4 post-infection for many parasites including S. edentatus, S. vulgaris and P. equorum (McCraw and Slocombe 1974; Duncan and Pirie 1975; Clayton and Duncan 1979b). Infiltrates variably include neutrophils, mononuclear cells, plasma cells and macrophages. Mast cells range from absent in studies of A. perfoliata to prominent in studies of A. perfoliata and small strongyles, and correlation with eosinophils is inconsistent (Williamson et al. 1997; Collobert-Laugier et al. 2002; Pittaway et al. 2014). Higher densities of eosinophils may be associated with S4 larvae in S. vulgaris infections, and with L4 and degenerative larvae in small strongyle infections (Duncan and Pirie 1975; Steuer et al. 2018). Patterns also can be diffuse and irregular as in P. equorum infections, likely from persistent antigen (Clayton and Duncan 1979b). Eosinophilic granulomas are found within organs of the thoracic and abdominal cavities up to 72 weeks post-infection in large strongyle infections (McCraw and Slocombe 1974, 1978; Petty et al. 1992). Infiltrate composition is a function of parasite species and stage, and the age of the host (Clayton and Duncan 1979a; Petty et al. 1992; Collobert-Laugier et al. 2002). Horses over the age of 2 years show greater tissue eosinophilia than those under 2 years in naturally acquired small strongyle infections (Collobert-Laugier et al. 2002). Eosinophilic granulomas appear less severe in older animals with large strongyle infections, whereas with P. equorum infection, eosinophilic granulomas associated with larval remnants predominate in the older animals (Clayton and Duncan 1979b; Petty et al. 1992). Studies of A. perfoliata showed a correlation between tissue eosinophilia and worm count (Pearson et al. 1993; Fogarty et al. 1994), while other studies of S. vulgaris did not, suggesting that eosinophil distribution in the gastrointestinal tract may be independent of parasite exposure in some cases (Rotting et al. 2008). Evidence exists for both resident cell activation and cell recruitment in the defence against S. vulgaris (Dennis et al. 1988, 1993), but their relative importance is unclear. Oral, whole-organism inoculation is required for eosinophil influx into S. vulgaris-induced lesions (Monahan et al. 1994).
Eosinophils are a major effector in parasite killing but may have additional roles. Eosinophils are the primary cell type to adhere to, and the only type to inactivate, equine helminth larvae. This ability is acquired in vivo, as eosinophils from na€ıve ponies cannot inactivate S. vulgaris larvae in the presence of immune serum (Klei et al. 1992). In laboratory species, the absence of eosinophils does not compromise
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