Baylisascaris laevis (Leidy, 1856) Sprent, 1968

Sapp, Sarah G. H., Gupta, Pooja, Martin, Melissa K., Murray, Maureen H., Niedringhaus, Kevin D., Pfaff, Madeleine A. & Yabsley, Michael J., 2017, Beyond the raccoon roundworm: The natural history of non-raccoon Baylisascaris species in the New World, International Journal for Parasitology: Parasites and Wildlife 6 (2), pp. 85-99 : 93-94

2.3. Baylisascaris laevis

Baylisascaris laevis uses rodents instead of carnivores as definitive hosts that makes it unique among the other Baylisascaris spp. in the New World ( Berry, 1985). The parasite was first described in 1856 by Leidy as Ascaris laevis from naturally infected groundhogs ( Marmota monax ). Later it was reassigned to the genus Baylisascaris ( Sprent, 1968) .

Among the New World Baylisascaris species, B. laevis is generally smaller and wider than other species of Baylisascaris ( Table 1). This species also has the smallest spicules and largest dorsal lip compared to other Baylisascaris spp. ( Babero, 1960a; Sprent, 1968). Other differences involve the posterior end of the male and female worms with the female B. laevis tail abruptly tapered to a sharp point and the male tail narrowed mid-tail and appears swollen at the end ( Tiner, 1951; Berry, 1985). Other diagnostic features included indistinct knobby protrusions near the cloacal opening of males ( Tiner, 1951). The external genitalia of female B. laevis more anterior compared to B. columaris and B. procyonis ( Berry, 1985) .

2.3.1. Host range

The most commonly reported definitive host of B. laevis is the groundhog, a member of the Sciuridae family. Infections in other Scuridae hosts have been reported in the Alaska marmot ( M. broweri ), hoary marmot ( M. caligata ), yellow-bellied marmot (M. fl aviventris), Olympic marmot ( M. olympus , California ground squirrel ( Otospermophilus beecheyi ), Barrow ground squirrel ( Spermophilus parryi barrowensis ), Richardson's ground squirrel ( U. richardsonii ), and long-tailed ground squirrel ( Urocitellus undulatus ) ( Berry, 1985).

2.3.2. Differences in life cycle compared to other Baylisascaris spp.

B. laevis is the only member of the genus that has a strictly monoxenous life cycle with the apparent loss of a paratenic host during evolution. Development from L2 to adult occurs entirely in the sciurid definitive host ( Berry, 1985). Unlike other Baylisascaris spp. , larvae which migrate throughout the body of paratenic hosts, B. laevis only migrate within the liver and lungs of their hosts ( Babero, 1960b).

When larvated eggs are ingested, L2 hatch and migrate to the liver by 10‾12 DPI and develop into L3. These larvae migrate to the lungs where they molt into L4 that are coughed up and swallowed. Once in the small intestine they continue to develop into adults within the wall of the small intestine ( Babero, 1960b). Adults enter the intestinal lumen, mate, and produce eggs that are then shed in feces. Reinfection likely occurs when embryonated eggs adhering to fur are ingested during grooming ( Berry, 1985). B. laevis can produce liver lesions in its sciurid host ( Tiner, 1953b).

2.3.3. Ecology and epidemiology

Although the distribution of known B. laevis sciurid hosts extends throughout North America, the parasite has only been reported in New York, Pennsylvania, California, and Alaska. Outside the United States it has been reported in southern Ontario and Saskatchewan, Canada ( Berry, 1985). Further surveillance is needed to characterize the distribution of B. laevis in North America.

A few studies have been conducted on the seasonality of B. laevis infectious. During a 2 year study in southern Ontario, Canada, B. laevis prevalence peaked in September, with intensity showing similar seasonal variation ( Berry, 1985). Prevalence was lowest during winter months and increased during the spring, similar to the annual cycles observed in B. columnaris and B. procyonis ( Berry, 1985) . This seasonality of B. laevis seems to be primarily driven by feeding habits; groundhogs and ground squirrels continually feed throughout the spring and summer, and then in the fall begin to consume less in preparation for hibernation. In the winter, absence of ( Young and Sims, 1979) and physiological changes accompanying hibernation, such as lowered temperature, heart and metabolic rate of hosts, likely prevents B. laevis from developing if acquired late in the year ( Babero, 1960b). Despite lower rates of shedding in the winter, eggs can persist in the environment because they are resistant to sub-zero temperatures. Most (94%) non-embryonated eggs survived –10 C temperatures after exposure for 10 days, while> 70% of embryonated L 3 eggs survived –10 C temperatures for 16 days ( Berry, 1985). Also, eggs deposited in the environment are often protected from extreme temperatures because they are covered by leaf litter and snow or in subterranean burrows ( Berry, 1985).

2.3.4. Experimental infections

A variety of species have been assessed as experimental hosts for B. laevis using experimental infections. Babero (1959) conducted oral infection trials to assess susceptibility and pathology of B. laevis infection in eleven species including laboratory mice, laboratory rats (Rattus norvegicus), cotton rats ( Sigmodon hispidus ), hamsters, guinea pigs ( Cavia porcellus ), thirteen-lined ground squirrel ( Ictidomys tridecemlineatus ) and Franklin ground squirrels ( Poliocitellus franklinii ), opossums ( Didelphis virginiana ), groundhogs, domestic cats, and raccoons. Many of these experimental hosts were examined for infection via necropsy, although details on the duration of infection and stages recovered are not given so interpretation is difficult.

Some inoculated hosts developed disease, including a groundhog with signs of pneumonia due to larva migration. Two guinea pigs, who died ~40 days post infection, exhibited dyspnea, bloody stools, ataxia and emaciation. Granulomatous liver lesions were frequently observed, sometimes containing L2 larval sheaths, as well as foci of pulmonary hemorrhage ( Babero, 1959). In separate experimental infections of laboratory mice, larvae apparently did not become completely encapsulated in the liver, but lesions due to migration of the larvae through the liver were present ( Tiner, 1953a). Other experimental infections on multiple hosts (groundhogs, ground squirrels, cats, mice, guinea pigs, and hamsters) showed that larvae become encapsulated in the liver. When larvae migrated to the lungs, very few were retained, and even fewer were found in the small intestine after migration was completed ( Babero, 1960b).