AMIDOSTOMUM ANSERIS (GIZZARD WORM)

CAUSATIVE AGENT (CLASSIFICATION, morphology) Gizzard worms comprise sev­eral nematode species ofthe Superfamily Tricho- strongyloidea, Family Amidostomatidae (App. 1: Table 1) (McDonald 1974); two important genera are Amidostomum and Epomidiosto- mum (Tuggle and Friend 1999, Fedynich and Thomas 2008).

host range and distribution Amidosto- mum anseris is a nematode infecting the gizzards of wild and domestic geese (Anderson 1992); it also has been reported from ducks, swans, ardeids, and grebes (MacNeill 1970, Wehr 1971, Gylstorff and Grimm 1987). This common parasite has been reported from North America, Eurasia, and Africa (McDonald 1974, Tuggle and Crites 1984, Gylstorff and Grimm 1987, Gicik and Arslan 2003, Borgsteede et al. 2006).

life cycles and variations Amidostomum anseris lives in the gizzard lining of its avian hosts and has a direct life cycle. The eggs are inhibited by the high body temperature of the host from developing beyond an early set of cleavage cells until shed into the external environment (Geller 1962). After developing to the first (L₁) stage, the larvae undergo two more molts and become infec­tive L₃ larvae. There is some conflict in the litera ture on the extent to which larval development occurs in the egg, with references both to eggs hatching L1 larvae that immediately shed their cuticle (Cowan 1955, Tuggle and Friend 1999), and to eggs containing infective L3 stages (Enigk and Dey-Hazra 1970, Stradowski 1971). In the lat­ter case, eggs are reported to reach the infective stage in 23 days at 20 C (Enigk and Dey-Hazra 1970). The pre-patent period (time from infection by L₃ larvae to shedding of eggs by gravid females) in goslings is 14 to 31 days (Stradowski 1977).

Larvae can swim and even rise to the surface of a water column, but both eggs and larvae are very susceptible to desiccation (Enigk and Dey- Hazra 1970). In freezing temperatures, eggs can survive but most exposed L₃ larvae are killed.

RESERVOIRS AND TRANSMISSION Wild and domestic geese are considered the primary reser­voirs for A. anseris. Most infections of susceptible hosts follow ingestion of L₃ larvae. When goslings were given eggs and L₃ larvae of known age, few fully developed L3 larvae still in eggs matured into adult worms, but most L₃ larvae given at least one hour after hatching from eggs became estab­lished in the gizzard (Stradowski 1971).

Infective larvae occasionally can penetrate intact skin; the prepatent period of worms in such cases was 15 to 18 days, similar to birds infected orally (Enigk and Dey-Hazra 1968). It appeared that after invading the skin, the larvae migrated to the lungs and appeared in the mucus of the trachea 16 to 32 hours later. It is not clear whether these worms ever were able to mature and complete the life cycle in the gizzard, and to shed fertile eggs.

Among ducks, those up to 6 months of age are susceptible to infective larvae (Stradowski 1972). However, few infective larvae mature and the prepatent period is much longer; thus ducks are not as suitable as geese to host A. anseris (Stradowski 1972).

CLINICAL EFFECTS AND IDENTIFICATION Adult nematodes live in the linings of the giz­zard and proventriculus. Heavily infected birds experience severe necrosis of the gizzard lining and subsequent weight loss—often weighing only half as much as healthy birds; they also typically are infected with large numbers of other parasites (Herman 1969).

Diagnosis usually requires identifying the adult parasite in the gizzard of a carcass (Wehr 1971). Laboratory diagnosis can be through the diagnosis of eggs in the feces, but usually requires an expert to identify them.

population effects This parasite can be a serious problem among wild geese (Herman and Wehr 1954, Tuggle and Friend 1999), and often is associated with high goose densities. While A. anseris is the best-known pathogen among water­fowl (Tuggle and Friend 1999), A. acutum also is associated with severe mortality, in combination with food shortage, among adult eiders (Somate- ria mollissima) in Europe (Borgsteede 2001).

special problems Transmission potential is greatest in crowded, continuously used habitats. Canada geese from Pea Island National Wildlife Refuge on the coast of North Carolina have expe­rienced considerable mortality from the effects of Amidostomum anseris infections (Herman and Wehr 1954, Herman et al. 1955). Severe impacts were associated with inclement weather forc­ing the birds away from the offshore breeding grounds and being crowded onto the island, with food that was lower in protein and in inadequate supply (Herman 1969). In similar circumstances, mortality occurred among Aleutian cackling geese (Branta hutchinsii Ieucopareia) in coastal California, at a time when this subspecies was listed as endangered (R. Botzler, personal records).

control With domestic animals, fenbadazol and carbon tetrachloride have been used (Gylstorff and Grimm 1987), as has flubenda- zole (Vanparijs 1984). No control efforts have been reported among wild birds.