Transmission of two Australian strains of murine cytomegalovirus (MCMV) in enclosure populations of house mice (Mus domesticus).

To control plagues of free-living mice (Mus domesticus) in Australia, a recombinant murine cytomegalovirus (MCMV) expressing fertility proteins is being developed as an immunocontraceptive agent. Real-time quantitative PCR was used to monitor the transmission of two genetically variable field strains of MCMV through mouse populations after 25% of founding mice were infected with the N1 strain, followed by the G4 strain 6 weeks later. Pathogen-free wild-derived mice were released into outdoor enclosures located in northwestern Victoria (Australia). Of those mice not originally inoculated with virus, N1 DNA was detected in more than 80% of founder mice and a third of their offspring and similarly, G4 DNA was detected in 13% of founder mice and in 3% of their offspring. Thus, prior immunity to N1 did not prevent transmission of G4. This result is promising for successful transmission of an immunocontraceptive vaccine through Australian mouse populations where MCMV infection is endemic.

Ecological basis for fertility control in the house mouse (Mus domesticus) using immunocontraceptive vaccines.

Laboratory studies confirm the potential for fertility control in the house mouse Mus domesticus using mouse cytomegalovirus (MCMV) as a vector for an immunocontraceptive vaccine. This article presents an overview of key results from research in Australia on enclosed and field populations of mice and the associated epidemiology of MCMV. The virus is geographically widespread in Australia. It also persists in low population densities of mice, although if population densities are low for at least a year, transmission of the virus is sporadic until a population threshold of approximately 40 mice ha(-1) is reached. The serological prevalence of MCMV was high early in the breeding season of four field populations. Enclosure studies confirm that MCMV has minimal impact on the survival and breeding performance of mice and that it can be transmitted to most adults within 10-12 weeks. Other enclosure studies indicate that about two-thirds of females would need to be sterilized to provide effective control of the rate of growth of mouse populations. If this level is not maintained for 20-25 weeks after the commencement of breeding, the mouse population can compensate through increased recruitment per breeding female. The findings from this series of descriptive and manipulative population studies of mice support the contention that MCMV would be a good carrier for an immunocontraceptive vaccine required to sustain female sterility levels at or above 65%.

The prevalence of viral antibodies during a large population fluctuation of house mice in Australia.

We studied the seroprevalence of three viruses (mouse cytomegalovirus (MCMV), minute virus of mice (MVM), and mouse parvovirus (MPV)) in house mice (Mus domesticus) in 1995 7. In the first year average mouse density was less than 1 mouse/ha. From November 1995 to May 1996 the population increased at an average rate of 7% per week, a doubling time of about 10 weeks. From August 1996 to May 1997 the population increased at an average rate of 10% per week, a doubling time of about 7.5 weeks. From a peak around 250 mice/ha in May 1997, the mouse population fell 19% per week to 5 mice/ha in October 1997. The seroprevalence for all three viruses varied dramatically over time. MCMV had the highest seroprevalence (61.7%), followed by MVM (8.5%) and MPV (18.4%). Time series data indicated that MCMV spread rapidly through the population of mice once trap success was greater than 14% (40-100 mice/ha). By contrast MVM and MPV seroprevalence occurred with a 2-3 month and 3-4 month time lag, respectively. The current study supports the contention that MCMV would be a good carrier for an immunocontraceptive vaccine for controlling field populations of mice.

A manipulative field experiment to examine the effect of Capillaria hepatica (Nematoda) on wild mouse populations in southern Australia.

A 12-month manipulative field study of the effect of a liver parasite, Capillaria hepatica, on mouse populations (Mus domesticus) was conducted in the Mallee wheatlands of northwestern Victoria. There were 2 untreated and 4 treated sites each consisting of a 16 km2 sampling zone. The parasite was released in September (spring) 1993 into an increasing mouse population which had a medium density (100-250 mice per ha). A third untreated site was monitored from January 1994. A simple but effective baiting method was developed and with the assistance of local farmers about 40,000 mice were dosed on the 4 sites; an estimated 5-7% of the population. During a second release, a month later, a further 20,000 mice were infected, boosting the level of infection to around 10%. Two months after the release approximately 30% of the population was infected. Thereafter, although there was effective transmission of the parasite, this was associated with a significant reduction in prevalence with time. The parasite reduced host survival by 5-10%, although this difference was not statistically significant, and had a minimal effect on the breeding and the rate of growth of mouse populations. Densities of 500-800 mice per ha were attained at each site in autumn 1994. Thus a spring release of the parasite into a rapidly increasing mouse population in the Victorian Mallee wheatlands did not prevent the population from increasing. The occurrence of very dry conditions following its release and the low but sustained transmission of the parasite indicate that we need to know more about factors that influence the survival and transmission of the parasite under field conditions.

Polyarthritis in wild mice (Mus musculus) caused by Streptobacillus moniliformis.

Mice trapped on farms in south-eastern Queensland had chronic abscessating osteoarthritides mainly involving the carpi and tarsi. Pleomorphic bacteria were shown by silver staining to be plentiful within lesions. Streptobacillus moniliformis was isolated from the joints, and streptobacillary polyarthritis was diagnosed. Other lesions observed included subcutaneous and hepatic abscesses.

Population declines in the snowshoe hare and the role of stress.

Every 10 years snowshoe hare populations across the boreal forest of North America go through a population cycle, culminating in a decline lasting 4 or more years. We tested the hypothesis that snowshoe hares during the decline are in poor condition and less able to respond to challenges in their environment by examining the stress response of male hares. Three groups from February and May, 1991 (the second year of the hare decline in the Yukon), were compared: baseline hares were collected to obtain resting hormone levels; control hares were wild animals caught at randomly placed sites; and fed hares were wild animals caught on supplementary fed areas. The latter two groups were sequentially bled to examine their response to dexamethasone (DEX) followed by adrenocorticotropic hormone (ACTH). Trapping and handling were stressful to the experimental hares as the initial blood levels of total and free cortisol levels were higher (especially in controls), testosterone levels were lower, and glucose levels were higher in experimental hares than in baseline hares. Control and fed hares showed similar total and free cortisol responses, falling to low levels after the DEX injection and increasing rapidly in response to the ACTH injection. However, control hares were in worse condition than fed hares as indicated by the higher free cortisol levels and lower maximum corticosteroid-binding capacity (MCBC) in control hares. In addition, though testosterone levels fell in both groups in response to DEX, only the fed hares showed a large, transitory increase 30 min after the ACTH injection. An unexpected finding was a dramatic increase in MCBC levels 30 min after the ACTH injection in both experimental groups, but it was more pronounced in the fed group. We conclude that the pituitary-adrenocortical feedback system in hares from declining populations is operating normally and that they should be able to cope with acute, short-term stressors, but that they are in poor condition and are exposed to higher levels of free cortisol than fed hares in good condition.

Prevalence of viral antibodies and helminths in field populations of house mice (Mus domesticus) in southeastern Australia.

A 13-month study of wild mice (Mus domesticus) in wheatlands in southeastern Australia contrasted changes in the seroprevalence of antibody to 13 viruses and the occurrence of helminths with changes in their population dynamics. Mice were seropositive for mouse hepatitis virus (MHV), rotavirus, minute virus of mice (MVM), mouse adenovirus (MAdV), reovirus (reo 3), and murine cytomegalovirus (MCMV). The seroprevalences of all but rotavirus varied significantly with time and increased with host density. Near the end of the study, host density declined rapidly and the seroprevalence of MVM and reo 3 increased significantly. These two viruses had low seroprevalence when host survival was high and high seroprevalence when host survival was low, indicating they may play a role in regulating mouse populations. In the case of MVM, there was evidence of a viral epizootic during the decline in mouse abundance. The prevalence of four helminths (Taenia taeniaeformis, Syphacia obvelata, and Vampirolepis spp.) differed significantly with time but showed no apparent association with host density. These findings highlight the need for further study on the effect of viruses on the population dynamics of mice.

A serologic survey for viruses and Mycoplasma pulmonis among wild house mice (Mus domesticus) in southeastern Australia.

Plasma samples from 267 wild house mice (Mus domesticus) trapped at 14 sites in southeastern Australia were screened for antibody to 14 viruses normally associated with laboratory-reared rodents and to Mycoplasma pulmonis. Serologic prevalence was high for murine cytomegalovirus (99%, n = 94), murine coronavirus (95%), and murine rotavirus (74%). Samples from mice collected at all sites contained antibody to these viruses. The serologic prevalence was lower for mouse adenovirus, strain K87 (37%), parvovirus (33%), and reovirus type 3 (28%), with substantial site-to-site variation. Plasma from mice collected at 12 sites contained mouse adenovirus or reovirus antibody, and samples from mice at eight sites contained parvovirus antibody. Parvovirus-antibody positive mice were typically from high density populations or from low density populations that had recently declined from high density. Antibody to lymphocytic choriomeningitis virus (LCMV) and Sendai virus occurred at only three sites, and the serologic prevalence was very low (9.6% and 1.8%, respectively). All of the LCMV-positive mice were from northeastern New South Wales. The presence of this zoonotic virus in a mouse plague-prone region raises questions about human health risks resulting from cohabitation with large numbers of mice. It appeared that mouse populations at high density or declining from high density had higher prevalence of viral antibody than populations that had been at low or moderate density for some time. Thus, viral epizootics may occur among high-density populations and may be responsible for or precipitate declines in mouse density. These data raise the possibility of rodent viruses having potential as biological control agents.

Molecular and biological characterization of new strains of murine cytomegalovirus isolated from wild mice.

Studies of the prevalence of antibody to murine cytomegalovirus (MCMV) in free-living wild mice (Mus domesticus) trapped in diverse regions of Australia and on a sub-Antarctic island indicated that 90% of 468 mice had serum antibody to MCMV. Twenty-six field isolates of MCMV were plaque-purified from salivary gland extracts of representative seropositive mice. These isolates varied considerably in their ability to replicate in the salivary glands of weanling BALB/c mice with 9 of 15 failing to reach significant titres in this organ and the titres of the remaining 6 strains varying by at least 100-fold. The high frequency of restriction fragment length polymorphisms observed suggests widespread genetic heterogeneity exists among the strains. This observation was mirrored at the polypeptide level by Western blot analyses with polyclonal antisera to MCMV. The isolation in this study of four genetically distinct strains of MCMV from a single wild mouse and several strains from other individual mice demonstrates that multiple infections with MCMV may be commonplace in wild mice.

The geographic distribution and host range of Capillaria hepatica (Bancroft) (Nematoda) in Australia.

The geographic distribution, host range and prevalence of Capillaria hepatica were recorded in 4629 house mice, Mus domesticus, 263 black rats, Rattus rattus, and 58 Norway rats, R. norvegicus. The parasite was found at five localities, all in or near large towns along the coast. The two Rattus species appeared to be the primary hosts of C. hepatica in Australia. Published and unpublished data on helminth infections of Australian native mammals from 1162 murids (26 species), 3018 marsupials (67 species) and 99 monotremes (two species) were compiled. Only seven animals from three murid species were infected with C. hepatica; all were from the same rainforest in northern Queensland. C. hepatica was distributed widely, occurring in the house mouse, black rat and Norway rat on a 10,850 ha farm but there was no infection in cattle, sheep or goats (abattoir records). Also, 52 rabbits, four cats and one fox (shot samples) and 27 marsupial mice, Sminthopsis crassicaudata (museum specimens), had no sign of C. hepatica infection. Overall, the results indicate that transmission of C. hepatica to native, domestic and feral mammals is rare, presumably because of ecological constraints on egg embryonation and survival. In the light of these findings, the potential use of C. hepatica as a biological agent to control mouse plagues in Australia is discussed.

Can the nematode Capillaria hepatica regulate abundance in wild house mice? Results of enclosure experiments in southeastern Australia.

The hypothesis that a liver-inhabiting nematode, Capillaria hepatica, can regulate abundance of the house mouse (Mus domesticus) was tested in enclosures, in southeastern Australia. Changes in mouse abundance, and the relationship between mortality and host abundance were compared in three treatment and three control populations. Any effect of C. hepatica on mouse abundance was masked by an unknown regulating factor(s). This factor(s) caused density-dependent mortality in the control and treatment populations and, together with strong seasonal trends in parasite transmission, confounded our test of the ability of C. hepatica to regulate the abundance of house mice. The seasonal trends in transmission have important implications for the potential of this parasite as a biological control agent and for models of the interaction of C. hepatica and mouse populations. Transmission of C. hepatica apparently occurred throughout the 18 month study, further supporting its potential as a biological agent in the control of mouse plagues in this region.

The potential of Capillaria hepatica to control mouse plagues.

The potential of helminths as bio-control agents of mammalian pests has been largely ignored. However, the nematode Capillaria hepatica is currently being examined for its potential to control population outbreaks of house mice in Australia. Grant Singleton and Hamish McCallum discuss laboratory and ecological studies of the parasite and host, and describe the results of two models that explore the interaction between C. hepatica and mouse populations.

Models to assess the potential of Capillaria hepatica to control population outbreaks of house mice.

Population outbreaks of house mice (Mus domesticus) occur periodically in the wheatlands of southeastern Australia. This paper uses mathematical models to assist in the evaluation of the potential of a nematode, Capillaria hepatica, as a biological control agent to reduce the severity of these 'plagues'. C. hepatica is unique amongst helminths of mammals in that its eggs are released only upon the death of an infected host. The major goal of the modelling in this paper is to determine the impact of this feature on the population dynamics of the host-parasite interaction. Simple differential equation models are used to examine the general properties of the system and determine which population parameters are most crucial to the outcome of the interaction. These models are supplemented by age-structured models which investigate the initial behaviour of the system after introduction of the parasite. The necessity of host death for transmission is a strongly destabilizing factor, suggesting that C. hepatica cannot regulate most populations stably in the absence of strong resource limitation, although it has the potential to depress mouse populations below infection-free levels. Although C. hepatica influences mouse fecundity at lower burdens than it affects mortality, the age-structured models show that parasite-induced host death cannot be neglected. Because transmission requires host death, the parasite life-cycle operates on a time-scale similar to that of the hosts, and introduction of the parasite as early as possible in the development period of an outbreak will therefore be necessary to achieve substantial reductions in plague intensity.