White-footed mouse

Adults are 90–100 mm (3.5–3.9 in) in length, not counting the tail, which can add another 63–97 mm (2.5–3.8 in). A young adult weighs 20–30 g (0.7–1.1 oz). While their maximum lifespan is 96 months, the mean life expectancy for the species is 45.5 months for females and 47.5 for males. In northern climates, the average life expectancy is 12–24 months.^[3] The species is similar to Peromyscus maniculatus.^[4]

•  
  In Quetico Provincial Park, Ontario
•  
  Female on a staghorn sumac

White-footed mice are omnivorous, and eat seeds and insects. They are particularly voracious predators of the pupal stage of the invasive spongy moth (formerly termed the gypsy moth).^[5] They are timid and generally avoid humans, but they occasionally take up residence in ground-floor walls of homes and apartments, where they build nests and store food.^[6] White-footed mice spend substantial time in trees and bushes, sometimes taking unoccupied old bird nests and building roofs on them.^[7]

 

Like the North American deer mouse, this species may carry hantaviruses, which can cause severe illness in humans. It has also been found to be a competent reservoir for the Lyme disease–causing spirochete, Borrelia burgdorferi.^[8] The white-footed mouse is the favored host for the parasitic botfly Cuterebra fontinella.^[9]

The white-footed mouse is one of the most common mouse species used as laboratory mice after the house mouse, and their domesticated version is called Peromyscus leucopus linville.^[10] Such domesticated mice are also kept as pets^[11][12] and have been bred to have many different colors.^[13]

Native populations of P. leucopus in New York city are isolated by dense human infrastructure and are largely confined to small urban forest islands such as Prospect Park and Central Park.^[14] The limited gene flow caused by human activities and coupled with a bottleneck event in urban populations has been powerful enough to lead to evolutionary divergence of urban white-footed mice.^[14][15]

New York City mice exhibit local adaptations to diet-mediated selective pressures of urban habitats. Being opportunistic feeders, urban P. leucopus populations subsist on food discarded by humans as a readily available source of nutriment, thereby consuming a lot more fat and carbohydrates than rural populations.^[16] Results of a landscape genomics study showed evidence of positive selection in mitochondrial genes of urban mice that are responsible for lipid and carbohydrate breakdown and digestion.^[16] Isolated P. leucopus populations inhabiting NYC parks show signs of molecular-level adaptation to urban food resources.^[16] The differential evolution of metabolic processes in urban P. leucopus populations is thought to contribute to their success and survival in NYC urban forests.^[16] Furthermore, the morphology of urban white-footed mice may be changing to adapt to alternative food sources. For instance, the teeth of white-footed mice in New York City are shorter than the teeth of rural mice.^[16] This change in physical traits could be explained by the availability of higher-quality food sources in urban forests, which negates the need for long, powerful teeth.^[16]

Urban populations of P. leucopus may be under unique selective pressures due to increased routine exposure to pollutants and toxins. A comparative transcriptome study found evidence of positive selection acting on the genes of urban mice that play major roles in detoxification and xenobiotic metabolism.^[17] The genes under positive selection pressure include CYP1A1 and Hsp90, which are known to be involved in the metabolism of foreign substances and drugs.^[18] High concentrations of heavy metals such as lead and mercury in NYC park soils pose a unique selective pressure that likely led urban populations of P. leucopus to develop metabolic adaptations to the toxicity of urban forest environments.^[17] Furthermore, exposure of pollutants is known to induce hypermethylation of DNA.^[18] A study showed that in urban white-footed mice, a gene coding for a demethylase enzyme is under positive selection.^[18] This means that urban populations of white-footed mice that live in highly polluted environments uniquely benefit from an active demethylase enzyme that removes methyl groups from DNA.^[18]

City-dwelling white-footed mouse populations are densely concentrated in isolated urban parks, which makes sperm competition a particularly powerful source of selection in urban environments.^[19] Genetic studies have identified signs of molecular-level evolution of reproductive processes in urban white-footed mouse populations. Genes associated with spermatogenesis, sperm locomotion, and sperm-egg interactions in urban mice show a divergent pattern of regulation compared to their rural counterparts.^[19] Therefore, the intensified sperm competition of dense mouse populations in urban forests has driven them to develop faster, more efficient sperm than that of rural mice.

Urban environments are saturated with large numbers of novel and familiar pathogens that are introduced by transportation, traffic, and trade.^[20] The elevated occurrence of pathogens is a driver of directional selection in which genetic variants that more efficiently resist infection are favored. The outcome of this selection can be seen in genetic divergence between urban and rural P. leucopus populations at loci that regulate the innate immune response and inflammation.^[21] Furthermore, a study has found evidence of positive selection acting on genes that modulate pathogen recognition in urban mice.^[21] Immunoregulatory proteins that are found on T lymphocytes are overexpressed in urban mice when compared to rural populations.^[21] These findings suggest that the immune systems of NYC white-footed mice may be evolving to recognize and respond to pathogens more efficiently. The divergence between rural and urban white-footed mice is especially prominent due to impeded gene flow between these populations, which is caused by landscape barriers including roads, highways, and pedestrian sidewalks.^[22] Monitoring the strength of immune defenses in P. leucopus is of special importance because they are commonly infected with dangerous pathogens such as hantaviruses and Borrelia burgdorferi.^[22]

• Monongahela virus

• Anderson JF, Johnson RC, Magnarelli LA (1987). "Seasonal prevalence of Borrelia burgdorferi in natural populations of white-footed mice, Peromyscus leucopus". Journal of Clinical Microbiology. 25 (8): 1564–1566. doi:10.1128/JCM.25.8.1564-1566.1987. PMC 269274. PMID 3624451.
• Rogic A, Tessier N, Legendre P, Lapointe FJ, Millien V (2013). "Genetic structure of the white-footed mouse in the context of the emergence of Lyme disease in southern Québec". Ecology and Evolution. 3 (7): 2075–2088. Bibcode:2013EcoEv...3.2075R. doi:10.1002/ece3.620. PMC 3728948. PMID 23919153.
• Barthold SW, Persing DH, Armstrong AL, Peeples RA (1991). "Kinetics of Borrelia burgdorferi dissemination and evolution of disease after intradermal inoculation of mice". The American Journal of Pathology. 139 (2): 263–273. PMC 1886084. PMID 1867318.
• Bunikis J, Tsao J, Luke CJ, Luna MG, et al. (2004). "Borrelia burgdorferi infection in a natural population of Peromyscus leucopus mice: a longitudinal study in an area where Lyme borreliosis is highly endemic". The Journal of Infectious Diseases. 189 (8): 1515–1523. doi:10.1086/382594. PMID 15073690.
• Brunner JL, LoGiudice K, Ostfeld RS (2008). "Estimating reservoir competence of Borrelia burgdorferi hosts: prevalence and infectivity, sensitivity, and specificity". Journal of Medical Entomology. 45 (1): 139–147. doi:10.1603/0022-2585(2008)45[139:ercobb]2.0.co;2. PMID 18283955. S2CID 10702776.
• Burgess EC, French JB Jr, Gendron-Fitzpatrick A (1990). "Systemic disease in Peromyscus leucopus associated with Borrelia burgdorferi infection". The American Journal of Tropical Medicine and Hygiene. 42 (3): 254–259. doi:10.4269/ajtmh.1990.42.254. PMID 2316794.
• Goodwin BJ, Ostfeld RS, Schauber EM (2001). "Spatiotemporal variation in a Lyme disease host and vector: black-legged ticks on white-footed mice". Vector-Borne and Zoonotic Diseases. 1 (2): 129–138. doi:10.1089/153036601316977732. PMID 12653143.
• Hofmeister EK, Ellis BA, Glass GE, Childs JE (1999). "Longitudinal study of infection with Borrelia burgdorferi in a population of Peromyscus leucopus at a Lyme disease-enzootic site in Maryland". The American Journal of Tropical Medicine and Hygiene. 60 (4): 598–609. doi:10.4269/ajtmh.1999.60.598. PMID 10348235.
• Horka H, Cerna-kyckovaa K, Kallova A, Kopecky J (2009). "Tick saliva affects both proliferation and distribution of Borrelia burgdoferi spirochetes in mouse organs an increases transmission of spirochetes by ticks". International Journal of Medical Microbiology. 299 (5): 373–380. doi:10.1016/j.ijmm.2008.10.009. PMID 19147403.
• Martin LB, Weil ZM, Kuhlman JR, Nelson RJ (2006). "Trade-offs within the immune systems of female white-footed mice, Peromyscus leucopus". Functional Ecology. 20 (4): 630–636. Bibcode:2006FuEco..20..630M. doi:10.1111/j.1365-2435.2006.01138.x.
• Martin LB, Weil ZM, Nelson RJ (2007). "Immune defense and reproductive pace of life in Peromyscus mice". Ecology. 88 (10): 2516–2528. Bibcode:2007Ecol...88.2516M. doi:10.1890/07-0060.1. PMC 7204533. PMID 18027755.
• Ostfeld RS, Miller MC & Hazler KR (1996) Causes and consequences of tick (Ixodes scapularis) burdens on white-footed mice (Peromyscus leucopus). J Mammal ; 77:266–273.
• Ostfeld RS, Schauber EM, Canham CD, Keesing F & al. (2001) Effects of acorn production and mouse abundance on abundance and Borrelia burgdorferi infection prevalence of nymphal Ixodes scapularis ticks. Vector Borne Zoonot Dis ; 1:55–63
• Pederson AB, Grieves TJ (2008) 'he interaction of parasites and resource cause crashes in wild mouse population. J Anim Ecol ; 77:370–377
• Schwan, TG, Burgdorfer, W, Schrumpf, ME, Karstens, RH. (1988) The urinary bladder, a consistent source of Borrelia burgdorferi in experimentally infected white-footed mice (Peromyscus leucopus). J Clin Microbiol ; 26:893–895
• Schwan TG, Kime KK, Schrumpf ME, Coe JE, et al. (1989). "Antibody response in white-footed mice (Peromyscus leucopus) experimental infected with the Lyme disease spirochete (Borrelia burgdorferi)". Infection and Immunity. 57 (11): 3445–3451. doi:10.1128/IAI.57.11.3445-3451.1989. PMC 259851. PMID 2807530.
• Schwanz LE, Voordouw MJ, Brisson D, Ostfeld RS (2011). "Borrelia burgdorferi has minimal impact on the Lyme disease reservoir host Peromyscus leucopus" (PDF). Vector-Borne and Zoonotic Diseases. 11 (2): 117–124. doi:10.1089/vbz.2009.0215. PMID 20569016. Archived from the original (PDF) on 2016-09-21. Retrieved 2014-04-24.

• White-footed Mouse, State University of New York, College of Environmental Science and Forestry
• White-footed Mouse, CanadianFauna.com
• White-footed Mouse, Canadian Biodiversity Website
• "Deer-mouse" . Encyclopedia Americana. 1920.