scholarly journals The fall and rise of group B Streptococcus in dairy cattle: suspected reintroduction from a human reservoir

2020 ◽  
Vol 2 (7A) ◽  
Author(s):  
Chiara Crestani ◽  
Taya Forde ◽  
Samantha Lycett ◽  
Mark Holmes ◽  
Karin Persson-Waller ◽  
...  

Streptococcus agalactiae, also known as group B Streptococcus (GBS), is a pathogen of humans and cattle, in which it is responsible for carriage or invasive disease and subclinical mastitis, respectively. From the 1950s to 1970s, thanks to successful mastitis control programs, the prevalence of GBS fell in the Swedish cattle population, but it re-emerged in the late 1990s. GBS was thought to consist of host-specific subpopulations but recent studies have shown that human and cattle subpopulations overlap, with different accessory genome elements providing survival advantages in each host species. We hypothesized that cattle-adapted GBS was eradicated and replaced by new GBS strains of human origin. Our aim was to explore the differences in GBS cattle population over six decades (pre-post non-detection), with a focus on the possible role of MGE in the evolution of these strains. Historical (n = 44, 1953 to 1978) and contemporary (n = 76, 1997 to 2012) GBS isolates from bovine milk samples were sequenced and analysed for WGS-MLST. Phylogenetic network analysis revealed the presence of six major clades: two of these were detected only up to 1970, two were only detected after 2004, and two were detected in both periods. Historical isolates were all tetracycline sensitive, whereas 51% of recent isolates harboured tet(M), which is considered a marker of human adaptation. Our data support the elimination of a bovine specific clade (CC61/67) and the emergence of new clades (CC1, CC103/314) that are likely of human of origin.

2021 ◽  
Author(s):  
Chiara Crestani ◽  
Taya L Forde ◽  
Samantha J Lycett ◽  
Mark A Holmes ◽  
Charlotta Fasth ◽  
...  

Group B Streptococcus (GBS; Streptococcus agalactiae) is a major neonatal and opportunistic bacterial pathogen of humans and an important cause of mastitis in dairy cattle with significant impacts on food security. Following the introduction of mastitis control programs in the 1950s, GBS was nearly eradicated from the dairy industry in northern Europe, followed by re-emergence in the 21st century. Here, we sought to explain this re-emergence based on short and long read sequencing of historical (1953-1978; n = 44) and contemporary (1997-2012; n = 76) bovine GBS isolates. Our data show that a globally distributed bovine-associated lineage of GBS was commonly detected among historical isolates but never among contemporary isolates. By contrast, tetracycline resistance, which is present in all major GBS clones adapted to humans, was commonly and uniquely detected in contemporary bovine isolates. These observations provide evidence for strain replacement and suggest a human origin of newly emerged strains. Three novel GBS plasmids were identified, including two showing >98% homology with plasmids from Streptococcus pyogenes and Streptococcus dysgalactiae subsp. equisimilis, which co-exist with GBS in the human oropharynx. Our findings support introduction of GBS into the dairy population due to human-to-cattle jumps on multiple occasions and demonstrate that reverse zoonotic transmission can erase successes of animal disease control campaigns.


PEDIATRICS ◽  
1978 ◽  
Vol 62 (4) ◽  
pp. 620-621
Author(s):  
Gerald W. Fischer ◽  
James W. Bass ◽  
George H. Lowell ◽  
Martin H. Crumrine

The article by Bortolussi et al. on pneumococcal septicemia and meningitis in the neonat (Pediatrics 60:352, September 1977) was of great interest to us, since we have been analyzing the effect of antibody directed against Streptococcus pneumoniae on group B Streptococcus type III. We have recently shown (unpublished data) that antibody directed against S. pneumoniae type 14 precipitates the hot hydrochloric acid-extracted polysaccharide antigen of group B Streptococcus type III. Further studies have shown that this antibody is opsonic for group B Streptococcus type III in an in vitro bactericidal assay and protective in a suckling rat model of group B Streptococcus type III sepsis.1


1984 ◽  
Vol 5 (10) ◽  
pp. 305-315
Author(s):  
Sarah S. Long

The summary in Table 1 could be used as a mental checklist for the pediatrician who examines a child with fever. Whether the pediatrician opts to "keep the rules" or appropriately decides to "break the rules," knowledge of the guidelines will help him to focus his approach and to adopt attitudes of caution in certain circumstances. The body of knowledge of infectious agents chemotherapeutic agents has burgeoned over the past 40 years; the rules have changed very little. Thus, the rules might also serve as standards against which "new discoveries" that dictate departure from an established mode of clinical practice would have to be weighed. The adage, "Name the bug before you choose a drug," is especially germaine to pediatrics. Potential pathogens or "bugs" continually change as the patient's age, exposure, and immunity change. The serious diseases they cause mandate that initial treatment be given with the best "drugs." The age-related causes of bacterial meningitis presented in Table 2 could serve as a primer for age-related causes of other invasive disease as well. For bone, joint, and soft tissue infection as well as for septicemia without a focus the age line for group B Streptococcus and H influenzae would be extended upward and S aureus would be added for all ages. Although the relative importance of each pathogen for each clinical entity might vary, therapeutic considerations would be appropriately served by a schema such as this. Unfortunately, the susceptibility of pathogens to antimicrobial agents will continue to change. Fortunately, new and potentially better therapeutic agents will continue to be discovered or invented. When new problems of antibiotic resistance emerge or when superior therapeutic modalities are proved, the pediatrician must be knowledgeable of such events and be prepared for change.


2020 ◽  
Vol 5 (1) ◽  
pp. 30 ◽  
Author(s):  
Sudipta Roy Chowdhury ◽  
Srabani Bharadwaj ◽  
Suresh Chandran

Early-onset neonatal sepsis (EOS) is a major cause of neonatal death and long-term neurodevelopmental disabilities among survivors. The common pathogens causing EOS are group B streptococcus (GBS) and Escherichia coli. Haemophilus influenzae (H. influenzae) is a Gram-negative coccobacillus that can cause severe invasive disease and can be divided into either typeable or non-typeable strains. H. influenzae serotype b (Hib) is the most virulent and the major cause of bacterial meningitis in young children prior to routine immunization against Hib. Hib infection rates have dramatically reduced since then. However, a number of studies have reported an increasing incidence of non-typeable H. influenzae (NTHi) sepsis in neonates worldwide and concluded that pregnant women may have an increased risk to invasive NTHi disease with poor pregnancy outcomes. We present a case of fulminant neonatal sepsis caused by NTHi in an extremely preterm infant and discuss potential preventative measures to reduce its re-emergence.


1997 ◽  
Vol 177 (4) ◽  
pp. 780-785 ◽  
Author(s):  
Mary E. Hannah ◽  
Arne Ohlsson ◽  
Elaine E.L. Wang ◽  
Anne Matlow ◽  
Gary A. Foster ◽  
...  

Author(s):  
Kirsty Le Doare ◽  
Christine E. Jones ◽  
Paul T. Heath

Group B Streptococcus (GBS) is a leading cause of early neonatal infection and neonatal mortality, with long-term adverse neurodevelopmental outcomes in up to 50% of survivors of GBS meningitis. GBS has a likely underappreciated role in causing preterm birth and stillbirth. GBS colonizes the vagina and gastrointestinal tract of the pregnant woman, and transmission to the infant occurs during or just before delivery. Although the majority of these infants do not develop invasive disease, maternal colonization is a prerequisite for early onset disease (0–6 days of life, most commonly associated with sepsis and respiratory distress) and a significant risk factor for late onset disease (7–89 days of life, most commonly associated with sepsis and meningitis). The introduction of intrapartum antibiotic prophylaxis has resulted in significant declines in the incidence of early onset disease but provides no protection against late onset disease.


1995 ◽  
Vol 78 (2) ◽  
pp. 491-498 ◽  
Author(s):  
T. D. Murphy ◽  
R. L. Gibson ◽  
T. A. Standaert ◽  
D. E. Woodrum

Group B Streptococcus (GBS) causes an impairment of diaphragmatic pressure generation (Pdi) in 2-wk-old piglets, whereas 4-wk-old piglets are unaffected. In this study, we examined the effect on 4-wk-old piglets of a higher dose of GBS than previously utilized. We sought to determine whether an eicosanoid product of arachidonic acid metabolism accounted for the decrease in Pdi during GBS infusion and whether thromboxane A2 (TxA2) is the putative eicosanoid mediator of decreased Pdi during GBS infusion. Measuring Pdi during phrenic nerve stimulation, we studied four groups of anesthetized spontaneously breathing 4-wk-old piglets. Group 1 (GBS) was infused with live GBS, which caused a decrease in Pdi by 1 h at 20-, 30-, 50-, and 100-Hz stimulation frequencies. Group 2 [GBS + indomethacin (Indo)] was pretreated with Indo before GBS infusion. In the GBS + Indo group, Pdi did not decrease throughout 4 h of GBS infusion. Because Indo proved to be protective of Pdi during GBS infusion, we examined the role of TxA2, the only eicosanoid present at 1 h in the serum of GBS-infused piglets. Group 3 was infused with the TxA2 analogue U-46619 only for 1 h. Group 4 was treated with the TxA2-receptor antagonist SQ-29548 before and concomitant with GBS infusion for 1 h; the SQ-29548 was then discontinued, and GBS was continued for 1 h more. In the U-46619-infused group, Pdi decreased at 1 h, and in the SQ-29548-treated group, Pdi did not decrease during GBS infusion.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 46 (1) ◽  
Author(s):  
Alberto Berardi ◽  
◽  
Tiziana Cassetti ◽  
Roberta Creti ◽  
Caterina Vocale ◽  
...  

Abstract Background Group B streptococcus (GBS) is a leading cause of sepsis, pneumonia and meningitis in infants, with long term neurodevelopmental sequelae. GBS may be associated with poor pregnancy outcomes, including spontaneous abortion, stillbirth and preterm birth. Intrapartum antibiotic prophylaxis (IAP) is currently the only way to prevent early-onset disease (presenting at 0 to 6 days of life), although it has no impact on the disease presenting over 6 days of life and its implementation is challenging in resource poor countries. A maternal vaccine against GBS could reduce all GBS manifestations as well as improve pregnancy outcomes, even in low-income countries. Main body The term “PREPARE” designates an international project aimed at developing a maternal vaccination platform to test vaccines against neonatal GBS infections by maternal immunization. It is a non-profit, multi-center, interventional and experimental study (promoted by the St George University of London. [UK]) with the aim of developing a maternal vaccination platform, determining pregnancy outcomes, and defining the extent of GBS infections in children and mothers in Africa. PREPARE also aims to estimate the protective serocorrelates against the main GBS serotypes that cause diseases in Europe and Africa and to conduct two trials on candidate GBS vaccines. PREPARE consists of 6 work packages. In four European countries (Italy, UK, Netherlands, France) the recruitment of cases and controls will start in 2020 and will end in 2022. The Italian PREPARE network includes 41 centers. The Italian network aims to collect: GBS isolates from infants with invasive disease, maternal and neonatal sera (cases); cord sera and GBS strains from colonized mothers whose infants do not develop GBS infection (controls). Short conclusion PREPARE will contribute information on protective serocorrelates against the main GBS serotypes that cause diseases in Europe and Africa. The vaccine that will be tested by the PREPARE study could be an effective strategy to prevent GBS disease.


Sign in / Sign up

Export Citation Format

Share Document