Phyllis Margaret Rountree | |
|---|---|
 young researcher | |
| Born | 13 January 1911 Hamilton, Victoria, Australia |
| Died | 27 July 1994 (aged 83) Darlinghurst, New South Wales, Australia |
| Nationality | Australian |
| Education | University of Melbourne |
| Occupation(s) | microbiologist and bacteriologist |
| Employer | Royal Prince Alfred Hospital |
Phyllis Margaret Rountree (13 January 1911 – 27 July 1994) was an Australian microbiologist and bacteriologist. She was an expert in staphylococcal infections.
Rountree was born in 1911 in Hamilton, Victoria. Her mother's brother, William Roy Hodgson was a noted diplomat, but she was inspired by her learned aunts. She went to school locally at Alexandra Ladies’ College before boarding in Hawthorn at the Tintern Church of England Girls’ Grammar School. [1] She studied zoology and bacteriology at the University of Melbourne. She had hoped to study medicine like her aunt but her father, a pharmacist, said she was "too young". [1] It was a chance visit to her home town by Harold Addison Woodruff that inspired Rountree and persuaded her father that she should take a master's degree and become a bacteriologist. [2]
She completed three years of a Council of Scientific & Industrial Research fellowship in 1934 by presenting her work to Professor James A. Prescott at the Waite Agricultural Research Institute in Adelaide. He made no additions or changes but she was not offered a permanent position and she put this down to systemic gender bias. She had enjoyed the relaxed attitude there but male colleagues had not spoken to her during her work breaks and she was sure that a man successfully completing three years of research would have been retained. [2] “‘Well now, it was very nice having you here dear, but we don't employ women permanently’” is how Rountree recalled her fellowship. She reflected on not being offered a continuing position at the institute, noting later in her life that “‘if I'd been a man, they probably would have found me something’”. [3] [4]
In 1936 she went to London where she studied for a post-graduate Diploma in Bacteriology at the School of Hygiene. She supported herself by working at the British Public Health Laboratory and she returned to Australia the following year. [5]
After a year of food testing during the war, [5] she started at the Royal Prince Alfred Hospital in 1944 [5] where she was suspected of recruiting communists. The commonwealth authorities decided she was not interested in this in the 1950s. At this time she was a recognised expert on staphylococcal infections [1] and she had noticed a growth in the number of surgical infections. There was a concern that this might have meant a return to pre-penicillin type infections. [7] This was not the case and she become the chief bacteriologist in 1961.
In 1954, a profoundly virulent strain of staphylococcus called “80/81” surfaced in Australia and soon after in Canada. The strain appeared initially during a study of infections in the nursery at Royal North Shore Hospital in Sydney, Australia. In the nursery, five infants were found to have staphylococcal lesions that were unresponsive to penicillin. The chief researchers who found this infection called on Rountree, who had been using the emerging technique of phage typing, to identify the strain of staphylococcus infecting the babies using phage typing. Rountree found that the strain could only be typed using chemically modified bacteriophages, leading the researchers to believe that it was a novel strain. Rountree was responsible for the study of all staphylococcal infections at RNS Hospital, and uncovered that almost 50% of strains present were of the new type before it vanished and was replaced by a new strain in June 1953 that was similarly untypable. Rountree worked with members of the Staphylococcal Reference Laboratory in London, England, particularly Dr. Robert E. O. Williams, who confirmed that the RNS strain she sent could not be typed by any of the bacteriophages in Williams’ laboratory. The phage was termed “80”; studies from March 1953 to March 1954 uncovered a new staphylococcus strain was detected in Canada at an Ottawa hospital that demonstrated an inability to be typed, named by its investigators “81”. Rountree’s 80 strain was ultimately found to be identical to the Canadian 81 strain found by Dr. E. T. Bynoe, Dr. R. H. Elder, and Dr. R. D. Comtois. In 1955, Rountree reported that staphylococcus strain 80/81 was the culprit of 19 of every 23 cases of staphylococcus infection in Australian neonates and that the strain was carried by babies into the general community, countering an initial finding that the strain was restricted to hospital-contracted infections. Strain 80/81 eventually came to be found in Australia, New Zealand, Canada, Great Britain, and across the United States. The infectious strain devastated hospitals and confounded providers and bacteriologists with symptoms that included severe skin lesions in infants, abscesses in mothers’ breasts, and nurses with severe boils. The 1950 epidemics in nurseries gave bacteriologists like Rountree and others an opportunity to revitalize infection control procedures in the absence of an effective antibiotic to treat the 80/81 strain. [8] [9] In 1956, Rountree and other medical and scientific professionals co-authored the first manual pertaining to the management of hospital nursery staphylococcal infection. [10] While the 80/81 strain’s prevalence faded in the 1960s, Rountree referenced this work she engaged in as the most important work of her career. [11] [1] In 1971 she was appointed Honorary Research Associate in Medical Microbiology at the University of New South Wales. [5]
Much of Rountree’s work throughout her career was devoted to the study of Staphylococcus aureus, also known as 'golden staph', in addition to investigating its impact on the sterility of the hospital environment. [12] The early works of her career involved researching hospital blankets as infection sources, specifically wound cross-infection with the use of oiled blankets. Studying staphylococcus infections in the hospital would become a prominent theme throughout Rountree’s career, culminating in an extensive portfolio of research examining staphylococcus and staphylococcus bacteriophages. Rountree’s research spans into a variety of domains involving Staphylococcus with a central focus on Staphylococcus aureus. A few areas of Rountree’s focus include the study of staphylococcus resistance to penicillin, [13] methicillin, streptomycin, and neomycin, [14] lysogenicity in staphylococci, [15] nasal carriage of staphylococcus aureus in the general population, [16] and changes in the phage-typing patterns of staphylococci. [17] While the majority of Rountree’s work was published while she worked at Royal Prince Alfred Hospital, after her promotion to chief bacteriologist she published further notable works. One such piece includes “Observations on the distribution of Staphylococcus aureus in the atmosphere of a surgical ward”, [18] which was published in 1962 in volume 60 of The Journal of Hygiene. In the study, Rountree and Mary A. Beard studied the bacteria that accumulated in two surgical wards over the span of one year while simultaneously examining patient nasal swabs and the bacteriological portfolio of patients with sepsis. Their work demonstrated that there was one predominant strain in the hospital, found in the air, wounds, nasal cavities, and bedding. The results uncovered a potential link between the transmission of staphylococcus bacteria from patient to patient via bedding. Rountree’s work and recommendations led to measures that contributed to reducing the spread of infection through the adoption of cotton blankets that could be laundered at higher temperatures and more frequently than woolen blankets. Rountree’s research ultimately led to many contemporary practices of infection control, a greater understanding of staphylococcus bacteria in the scientific community, and further uncovering of the relationship between the hospital environment and infection.
Rountree won few awards and this may have been due to her reticence or that she didn't publish all her findings. [2]
Staphylococcus aureus is a Gram-positive spherically shaped bacterium, a member of the Bacillota, and is a usual member of the microbiota of the body, frequently found in the upper respiratory tract and on the skin. It is often positive for catalase and nitrate reduction and is a facultative anaerobe that can grow without the need for oxygen. Although S. aureus usually acts as a commensal of the human microbiota, it can also become an opportunistic pathogen, being a common cause of skin infections including abscesses, respiratory infections such as sinusitis, and food poisoning. Pathogenic strains often promote infections by producing virulence factors such as potent protein toxins, and the expression of a cell-surface protein that binds and inactivates antibodies. S. aureus is one of the leading pathogens for deaths associated with antimicrobial resistance and the emergence of antibiotic-resistant strains, such as methicillin-resistant S. aureus (MRSA), is a worldwide problem in clinical medicine. Despite much research and development, no vaccine for S. aureus has been approved.
Methicillin-resistant Staphylococcus aureus (MRSA) is a group of gram-positive bacteria that are genetically distinct from other strains of Staphylococcus aureus. MRSA is responsible for several difficult-to-treat infections in humans. It caused more than 100,000 deaths attributable to antimicrobial resistance in 2019.
Staphylococcus xylosus is a species of bacteria belonging to the genus Staphylococcus. It is a Gram-positive bacterium that forms clusters of cells. Like most staphylococcal species, it is coagulase-negative and exists as a commensal on the skin of humans and animals and in the environment.
Dicloxacillin is a narrow-spectrum β-lactam antibiotic of the penicillin class. It is used to treat infections caused by susceptible (non-resistant) Gram-positive bacteria. It is active against beta-lactamase-producing organisms such as Staphylococcus aureus, which would otherwise be resistant to most penicillins. Dicloxacillin is available under a variety of trade names including Diclocil (BMS).
Panton–Valentine leukocidin (PVL) is a cytotoxin—one of the β-pore-forming toxins. The presence of PVL is associated with increased virulence of certain strains (isolates) of Staphylococcus aureus. It is present in the majority of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates studied and is the cause of necrotic lesions involving the skin or mucosa, including necrotic hemorrhagic pneumonia. PVL creates pores in the membranes of infected cells. PVL is produced from the genetic material of a bacteriophage that infects Staphylococcus aureus, making it more virulent.
Lysostaphin is a Staphylococcus simulans metalloendopeptidase. It can function as a bacteriocin (antimicrobial) against Staphylococcus aureus.
Ceftobiprole (Zevtera/Mabelio) is a fifth-generation cephalosporin for the treatment of hospital-acquired pneumonia and community-acquired pneumonia. It is marketed by Basilea Pharmaceutica in the United Kingdom, Germany, Switzerland and Austria under the trade name Zevtera, in France and Italy under the trade name Mabelio. Like other cephalosporins, ceftobiprole exerts its antibacterial activity by binding to important penicillin-binding proteins and inhibiting their transpeptidase activity which is essential for the synthesis of bacterial cell walls. Ceftobiprole has high affinity for penicillin-binding protein 2a of methicillin-resistant Staphylococcus aureus strains and retains its activity against strains that express divergent mecA gene homologues. Ceftobiprole also binds to penicillin-binding protein 2b in Streptococcus pneumoniae (penicillin-intermediate), to penicillin-binding protein 2x in Streptococcus pneumoniae (penicillin-resistant), and to penicillin-binding protein 5 in Enterococcus faecalis.
A staphylococcal infection or staph infection is an infection caused by members of the Staphylococcus genus of bacteria.
mecA is a gene found in bacterial cells which allows them to be resistant to antibiotics such as methicillin, penicillin and other penicillin-like antibiotics.
Staphylococcus capitis is a coagulase-negative species (CoNS) of Staphylococcus. It is part of the normal flora of the skin of the human scalp, face, neck, scrotum, and ears and has been associated with prosthetic valve endocarditis, but is rarely associated with native valve infection.
Staphylococcus is a genus of Gram-positive bacteria in the family Staphylococcaceae from the order Bacillales. Under the microscope, they appear spherical (cocci), and form in grape-like clusters. Staphylococcus species are facultative anaerobic organisms.
SaPIs are a family of ~15 kb mobile genetic elements resident in the genomes of the vast majority of S. aureus strains. Much like bacteriophages, SaPIs can be transferred to uninfected cells and integrate into the host chromosome. Unlike the bacterial viruses, however, integrated SaPIs are mobilized by host infection with "helper" bacteriophages. SaPIs are used by the host bacteria to co-opt the phage reproduction cycle for their own genetic transduction and also inhibit phage reproduction in the process.
Staphylococcus hyicus is a Gram-positive, facultatively anaerobic bacterium in the genus Staphylococcus. It consists of clustered cocci and forms white circular colonies when grown on blood agar. S. hyicus is a known animal pathogen. It causes disease in poultry, cattle, horses, and pigs. Most notably, it is the agent that causes porcine exudative epidermitis, also known as greasy pig disease, in piglets. S. hyicus is generally considered to not be zoonotic, however it has been shown to be able to cause bacteremia and sepsis in humans.
Enzybiotics are an experimental antibacterial therapy first described by Nelson, Loomis, and Fischetti. The term is derived from a combination of the words “enzyme” and “antibiotics.” Enzymes have been extensively utilized for their antibacterial and antimicrobial properties. Proteolytic enzymes called endolysins have demonstrated particular effectiveness in combating a range of bacteria and are the basis for enzybiotic research. Endolysins are derived from bacteriophages and are highly efficient at lysing bacterial cells. Enzybiotics are being researched largely to address the issue of antibiotic resistance, which has allowed for the proliferation of drug-resistant pathogens posing great risk to animal and human health across the globe.
Mary Barber was a British pathologist and bacteriologist who studied antibiotic resistance in bacteria. She was one of the pioneers in this field, documenting the phenomenon of penicillin resistance early on.
Staphylococcus schleiferi is a Gram-positive, cocci-shaped bacterium of the family Staphylococcaceae. It is facultatively anaerobic, coagulase-variable, and can be readily cultured on blood agar where the bacterium tends to form opaque, non-pigmented colonies and beta (β) hemolysis. There exists two subspecies under the species S. schleiferi: Staphylococcus schleiferi subsp. schleiferi and Staphylococcus schleiferi subsp. coagulans.
Staphylococcus pseudintermedius is a gram positive coccus bacteria of the genus Staphylococcus found worldwide. It is primarily a pathogen for domestic animals, but has been known to affect humans as well. S. pseudintermedius is an opportunistic pathogen that secretes immune modulating virulence factors, has many adhesion factors, and the potential to create biofilms, all of which help to determine the pathogenicity of the bacterium. Diagnoses of Staphylococcus pseudintermedius have traditionally been made using cytology, plating, and biochemical tests. More recently, molecular technologies like MALDI-TOF, DNA hybridization and PCR have become preferred over biochemical tests for their more rapid and accurate identifications. This includes the identification and diagnosis of antibiotic resistant strains.
Karen M. Frank is an American clinical pathologist and microbiologist researching the pathogenesis of Staphylococcus aureus pneumonia and resistant gram-negative bacteria. She is a senior clinician, principal investigator, and chief of laboratory medicine at the National Institutes of Health Clinical Center.
Vincent A. Fischetti is a world renowned American microbiologist and immunologist. He is Professor of and Head of the Laboratory of Bacterial Pathogenesis and Immunology at Rockefeller University in New York City. His Laboratory is the oldest continuous laboratory at Rockefeller that started in 1926 and headed by 4 leading scientists over its near 100 year history: Homer Swift, Maclyn McCarty, Emil Gotschlich and now Vincent Fischetti. Keeping with the historical theme of infectious diseases, Fischetti's primary areas of research are bacterial pathogenesis, bacterial genomics, immunology, virology, microbiology, and therapeutics. He was the first scientist to clone and sequence a surface protein on gram-positive bacteria, the M protein from S. pyogenes, and determine its unique coiled-coil structure. He also was the first use phage lysins as a therapeutic and an effective alternative to conventional antibiotics.
John Edward Blair was an American bacteriologist and serologist. He was the president of the American Society for Microbiology in 1962.
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