Reproductive rodent control is a novel approach that aims to reduce the number of new-borne rodents recruited into the local population. Traditional control methods, such as rodenticides, focus on reducing local rodent numbers solely by increasing the mortality rate. This can reduce numbers in the short term but does nothing to prevent rodents being recruited via reproduction and migration. Long-term bait use, which is often needed to suppress numbers, can also lead to undesirable outcomes, e.g., more selection pressure for resistance, and chemical residue contamination of feed and the farm environment. Reproductive control causes a delayed response, where mortality, either naturally or via other strategies, leads to a long-lasting reduction in the rodent population (Barlow et al., 1997).
Rodents can be controlled reproductively several ways, including surgery, disease, hormones and chemicals. Surgery (e.g. castration, ovariectomy, vasectomy and tubal ligation) is useful because its effects are permanent, but impractical for high-density field populations. Capillaria hepatica, a species of threadworm that is a natural rodent parasite, has potential to disrupt rodent reproduction (Spratt and Singleton, 1986). Field tests found it to be ineffective, particularly in low populations, because widespread parasite transmission could not be achieved (Singleton and Spratt, 1986). Risks that the parasite could be transmitted to rodent predators and, potentially to humans, make it unsuitable for rodent control.
ContraPest is a liquid contraceptive product designed as a bait additive to reduce the reproductive capacity of black (R. rattus) and brown rats (R. norvegicus). When ingested, the active compounds, Vinylcyclohexene dioxide and triptolide, inhibit sperm production (Hikim et al., 2000; Huynh et al., 2000) and cause the breakdown of ovarian follicles (Mayer et al., 2002, 2004; Xu and Zhao, 2010). ContraPest functions as a contraceptive – not a sterilant – therefore ongoing consumption is required for long-term effect. Trials on laboratory rat strains and wild-caught brown rats in the USA have demonstrated that the product is effective in suppressing reproductive capability. However, the duration of effects in wild rats in the field is also not known and there are no definitive studies demonstrating long-term effects using well-designed and replicated field trials (Brown and Henry, 2018). Despite this, ContraPest was registered and approved for commercial use in the USA by the Environmental Protection Agency (EPA) in August 2016. Although it is not APVMA-registered in Australia, this product has the potential to be applied in poultry operations.
Levonorgestrel and quinestrol are contraceptive hormones that are potential candidates for reproductive rodent control. They have been shown to impair rodent reproductive performance by reducing the size and function of male reproductive organs, disrupting sperm production, concentration and motility, and reducing female reproductive rate and litter size by inducing uterine oedema (Zhang, 2015). These hormones have been trialled in a 2:1 formula, known as EP-1, in attempts to control Mongolian gerbil (Meriones unguiculatus) populations in northern China. EP-1 was found to delay normal reproductive patterns, suppress birth rates, reduce the density and alter the age structure of the gerbil population (Fu et al., 2013). Laboratory trials have also shown levonorgestrel and quinestrol cause long-term antifertility effects in several rodent species (Brandt’s vole, Mongolian gerbils, and plateau pikas) (Zhang, 2015; Massawe et al., 2018). There are concerns about potential environmental contamination; however, both have relatively short half-lives (5–16 days) under field conditions, minimising the risk of non-target effects (Massawe et al., 2018). Levonorgestrel and quinestrol are promising candidates for reproductive rodent control, but more field testing is needed, specifically of Australian rodent species.
Other chemicals act as either agonists (facilitators) or antagonists (blockers) of gonadotrophin-releasing hormone (GnRH), which can cause male and female rodents to be infertile (Becker and Katz, 1997). Critically, hormonal effects are not permanent and may reach only a small proportion of the target population. Synthetic steroids, anti-steroids and anti-steroid receptors (e.g. diethylstilbestrol, RU486) can inhibit reproduction in rodents. Prolactin inhibitors can be used to disrupt lactation and gestation (e.g. bromocriptine, cabergoline) (Jochle, 1997). These chemicals are cost effective, widely available and can be delivered orally via baits or incorporated into implants. However, they must be regularly administered to ensure effectiveness and they can potentially affect non-target species.
The greatest barrier to controlling rodent fertility in the field is the widespread delivery of reproductive inhibitors to local and migrant populations (Chambers et al., 1999). Without this, there is no way to prevent fertile rodents from migrating onto farms and undermining successful reduction in local rodent population growth. More research is needed to develop species-specific mechanisms to effectively deliver anti-reproductive agents (Brown and Henry, 2018). Reproductive rodent control is a potentially useful strategy in poultry operations.
