Abstract
ABSTRACTStreptococcus agalactiae, or group B Streptococcus (GBS), infects diverse hosts including humans and economically important species such as cattle and fishes. In the context of human health, GBS is a major cause of neonatal infections and an emerging cause of invasive disease in adults and of foodborne disease in Southeast Asia. Here we show that GBS is able to establish a systemic infection in Galleria mellonella larvae that is associated with extensive bacterial replication and dose-dependent larval survival. This infection model is suitable for use with GBS isolates from both homeothermic and poikilothermic hosts. Hypervirulent sequence types (ST) associated with invasive human disease in neonates (ST17) or adults (ST283) show increased virulence in this model, indicating it may be useful in studying GBS virulence determinants, albeit with limitations for some host-specific virulence factors. In addition, we demonstrate that larval survival can be afforded by antibiotic treatment and so the model may also be useful in the development of novel anti-GBS strategies. The use of G. mellonella in GBS research has the potential to provide a low-cost infection model that could reduce the number of vertebrates used in the study of GBS infection.
Highlights
Streptococcus agalactiae, or group B Streptococcus (GBS) is a Gram-positive multi-host pathogen and a major cause of human neonatal infections and mortality
To begin to assess the suitability of G. mellonella larvae as an infection model for GBS isolated from its major hosts, we tested the susceptibility of larvae to dosedependent killing by GBS from human, bovine and piscine origin
The use of Galleria mellonella larvae as bacterial infection model has been developed as an alternative to murine or other vertebrate models of infection to contribute to the 3Rs of animal use in scientific research
Summary
Streptococcus agalactiae, or group B Streptococcus (GBS) is a Gram-positive multi-host pathogen and a major cause of human neonatal infections and mortality. GBS was initially described in 1887 as an animal pathogen responsible for mastitis in ruminants and largely eradicated in some countries with a highly developed dairy industry, remains a major cause of bovine mastitis in many countries [1]. In the 1970s GBS was described as the leading cause of human neonatal infectious morbidity and mortality with two distinct GBS-associated syndromes: early-onset disease occurring 0–6 days after birth and late-onset disease occurring 7 days–3 months after birth [7,8]. Adult GBS infections are often associated with underlying co-morbidities, but a recent foodborne outbreak of invasive ST283 GBS disease in Singapore was linked to the consumption of raw fish and occurred in previously healthy adults [16,17]. Despite some level of host adaptation, e.g. association of ST17 with human neonatal infectious disease [10], ST67 with cattle [18] and association of ST7, ST283 and clonal complex (CC) 552 with poikilothermic animals [19], host-association
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