#Antibiotic-resistant Microbes

[microbes-in-hats]

Staphylococcus aureus

Staphylococcus aureus is a type of bacteria with many known strains that have become resistant to antibiotics. Methicillin resistance (MRSA), vancomycin intermediate resistance (VISA), and vancomycin resistance (VRSA) are some examples of strains that are partially or fully resistant to antibiotics, making them major concerns in hospitals. It's estimated that only 2% of S. aureus strains are sensitive to penicillin antibiotics.

[auressea]

https://www.canada.ca/en/public-health/services/publications/drugs-health-products/canadian-antimicrobial-resistance-surveillance-system-report-2021.html

watching a tiktok and someone just described the black/blue gold/yellow dress meme as “one of the first things to ever go viral”

[reasonsforhope]

"An international research team has found almost a million potential sources of antibiotics in the natural world.

Research published in the journal Cell by a team including Queensland University of Technology (QUT) computational biologist Associate Professor Luis Pedro Coelho has used machine learning to identify 863,498 promising antimicrobial peptides -- small molecules that can kill or inhibit the growth of infectious microbes.

The findings of the study come with a renewed global focus on combatting antimicrobial resistance (AMR) as humanity contends with the growing number of superbugs resistant to current drugs.

"There is an urgent need for new methods for antibiotic discovery," Professor Coelho, a researcher at the QUT Centre for Microbiome Research, said. The centre studies the structure and function of microbial communities from around the globe.

"It is one of the top public health threats, killing 1.27 million people each year." ...

"Using artificial intelligence to understand and harness the power of the global microbiome will hopefully drive innovative research for better public health outcomes," he said.

The team verified the machine predictions by testing 100 laboratory-made peptides against clinically significant pathogens. They found 79 disrupted bacterial membranes and 63 specifically targeted antibiotic-resistant bacteria such as Staphylococcus aureus and Escherichia coli.

"Moreover, some peptides helped to eliminate infections in mice; two in particular reduced bacteria by up to four orders of magnitude," Professor Coelho said.

In a preclinical model, tested on infected mice, treatment with these peptides produced results similar to the effects of polymyxin B -- a commercially available antibiotic which is used to treat meningitis, pneumonia, sepsis and urinary tract infections.

More than 60,000 metagenomes (a collection of genomes within a specific environment), which together contained the genetic makeup of over one million organisms, were analysed to get these results. They came from sources across the globe including marine and soil environments, and human and animal guts.

The resulting AMPSphere -- a comprehensive database comprising these novel peptides -- has been published as a publicly available, open-access resource for new antibiotic discovery.

[Note: !!! Love it. Open access research databases my beloved.]"

-via Science Daily, June 5, 2024

[mindblowingscience]

Researchers have developed a new antibiotic that reduced or eliminated drug-resistant bacterial infections in mouse models of acute pneumonia and sepsis while sparing healthy microbes in the mouse gut. The drug, called lolamicin, also warded off secondary infections with Clostridioides difficile, a common and dangerous hospital-associated bacterial infection, and was effective against more than 130 multidrug-resistant bacterial strains in cell culture. The findings are detailed in the journal Nature. "People are starting to realize that the antibiotics we've all been taking—that are fighting infection and, in some instances, saving our lives—also are having these deleterious effects on us," said University of Illinois Urbana-Champaign chemistry professor Paul Hergenrother, who led the study with former doctoral student Kristen Muñoz.

Continue Reading.

[derinthescarletpescatarian]

My money is on fungus. E. coli doesn't survive heat very well but many fungal spores do.

I've had an ongoing science project for a few years now that I'd like to share. I've been leaving raw chicken breasts—real cheap, unregulated shit from the local mom-and-pop grocery store—out on my counter long enough for E. coli bacteria to develop. Then I microwave the chicken breasts and try to produce genetic mutations in the bacteria of each batch through microwave radiation, just in short bursts of 45 seconds per "rep" and maybe 3 "reps" per "set". The bacteria that do survive get fresh, raw chicken mixed into their feed and left to rest at room temperature for a few more days to grow. Then I just rinse and repeat until I see weird shit under the microscope. Sometimes I don't even need a microscope! Pic related, the fuzzy red mound is the modified E. coli (more obvious under a microscope). It's one of my most successful batches, a relative newcomer at only ten generations. I don't really microwave it any more because I'm pretty happy with it. This batch actually still has chicken inside, it's just completely covered in the bacteria "fur". Each bacterium is about a quarter the length and width of an eyelash. They aren't as quick at eating the chicken breasts as some of my other batches. I'm not sure how it happens, but between the actual chicken and the bacteria layer is some nasty chicken glob, like they slowly dissolve it or something. But this batch is definitely my "ambassador species" since it's pretty flashy with its beautiful maroon color and marimo-like appeal, and it doesn't make me sick too much. Anyone else doing something similar?

[brostateexam]

Ella Balasa was 26 when she realized the routine medical treatments that sustained her were no longer working. The slender lab assistant had lived since childhood with the side effects of cystic fibrosis, an inherited disease that turns mucus in the lungs and other organs into a thick, sticky goo that gives pathogens a place to grow. To keep infections under control, she followed a regimen of swallowing and inhaling antibiotics—but by the beginning of 2019, an antibiotic-resistant bacterium lodged in her lungs was making her sicker than she had ever been. 

Balasa’s lung function was down to 18 percent. She was feverish and too feeble to lift her arms over her head. Even weeks of intravenous colistin, a brutal last-resort antibiotic, made no dent. With nothing to lose, she asked a lab at Yale University whether she could volunteer to receive the organisms they were researching: viruses that attack bacteria, known as bacteriophages.

That January, Balasa trundled to New Haven from her home in Virginia, burdened with both an oxygen concentrator and doubts over whether the treatment might work. Every day for a week, she breathed in a mist of viruses that biologist Benjamin Chan, scientific director at Yale’s Center for Phage Biology and Therapy, had isolated for their ability to attack Pseudomonas aeruginosa, the multi-drug-resistant bug clogging Balasa’s lungs.

[magz]

New antibiotic kills pathogenic bacteria, spares healthy gut microbes

Article Date: May 29, 2024

Article Blurb: 

Researchers have developed a new antibiotic that reduced or eliminated drug-resistant bacterial infections in mouse models of acute pneumonia and sepsis while sparing healthy microbes in the mouse gut. The drug, called lolamicin, also warded off secondary infections with Clostridioides difficile, a common and dangerous hospital-associated bacterial infection, and was effective against more than 130 multidrug-resistant bacterial strains in cell culture.

[...]

Numerous studies have found that antibiotic-related disturbances to the gut microbiome increase vulnerability to further infections and are associated with gastrointestinal, kidney, liver and other problems.

[...] In a series of experiments, Muñoz designed structural variations of the Lol inhibitors and evaluated their potential to fight gram-negative and gram-positive bacteria in cell culture. One of the new compounds, lolamicin, selectively targeted some “laboratory strains of gram-negative pathogens including Escherichia coli, Klebsiella pneumoniae and Enterobacter cloacae,” the researchers found. Lolamicin had no detectable effect on gram-positive bacteria in cell culture. At higher doses, lolamicin killed up to 90% of multidrug-resistant E. coli, K. pneumoniae and E. cloacae clinical isolates. 

When given orally to mice with drug-resistant septicemia or pneumonia, lolamicin rescued 100% of the mice with septicemia and 70% of the mice with pneumonia, the team reported.  

Extensive work was done to determine the effect of lolamicin on the gut microbiome. 

“The mouse microbiome is a good tool for modeling human infections because human and mouse gut microbiomes are very similar,” Muñoz said. “Studies have shown that antibiotics that cause gut dysbiosis in mice have a similar effect in humans.”

Treatment with standard antibiotics amoxicillin and clindamycin caused dramatic shifts in the overall structure of bacterial populations in the mouse gut, diminishing the abundance several beneficial microbial groups, the team found.

“In contrast, lolamicin did not cause any drastic changes in taxonomic composition over the course of the three-day treatment or the following 28-day recovery,” the researchers wrote. 

Many more years of research are needed to extend the findings, Hergenrother said. 

[More in Article]

Note: The main scientific journal itself is paywalled (and not yet available in unpaywall nor sci-hub), Nature Journal Link

[henrysglock]

The blood thing is confusing, so they aren't related cause blood transfusions don't make the receptor and donor related but it's presented on the play as a bloodline/family tree thing? And do you still think el and Henry can be related outside of the blood transfusions?

It's presented very ambiguously!

Brenner says that Henry's as much a father to the children as he is in relation to the blood transfusions. I know in earlier showings they specified that Henry met the woman who was pregnant with 002, and that the mothers had been receiving transfusions. However, in the showings I saw, Brenner only says that 10 children had survived the transfusions. He never mentions mothers (the mentions of pregnant women only show up in one newspaper scrolling past at like. light-speed).

Which...You truly are preaching to the science choir here, Nonnie (and I say that lovingly). The blood thing has been fucking with me for a hot minute because, well...it straight up doesn't work like that, unless you start majorly stretching biology.

Brenner says Henry has a totally unique blood type, the same blood type Brenner Sr. had after his time in Dimension X in 1943. It caused Brenner Sr. to reject all blood types for transfusions. Which...this could make Henry a universal donor, I won't write that off entirely, but it's unlikely, imo, given that Brenner mentions survival rate. This means some of the babies rejected the blood transfusions and died (whether they received it via their mother or otherwise).

So it becomes more likely that they'd be looking for kids who have a predisposition to surviving the transfusions of the unique blood.

And that, my dearest Nonnie, is genetic.

So while there may be some wild-caught kids like Kali, it's likely there are also direct descendants.

On that note:

I feel like there's definitely still some confusion about the purpose of the transfusions, specifically in the way of correlation vs causation irt powers...so I thought I'd toss my 2¢ in.

Based on TFS canon so far, Brenner is intent on exploring Dimension X to further his father's work. But in order to do that, he needs subjects that can survive it. Imo, he's looking for what made Henry able to survive whatever happened to him. From what I've gathered, the transfusions seem to be less about giving children psionic powers and more about either collecting children who are predisposed to survival in Dimension X (akin to antibiotic resistance in microbes), or predisposing them to it (like a particularly harsh vaccine that only a select few survive, which is still a genetic/selective trait...just with an extra step: do they survive the vaccination?).

The fact that these children survived the blood transfusions and have psionic powers, many of which are shared abilities, makes me think there's some specific trait in these children's biological makeup that makes them predisposed to both characteristics. The children that survived the blood also have powers, in what seems to be all cases. Children who present these powers are more likely to tolerate transfusions, and vice versa. Correlation, not causation.

Thus, I firmly don't believe the blood transfusions gave the children abilities. I think it acts as a screening process, and the psionic abilities are a correlative marker of that ability to survive Henry's blood.

We do the same thing in microbiology all the time. Selective media. Grow the culture on a medium that's deadly to anything that doesn't have the desired trait, and whatever grows is the desired microbe (see: mannitol salt agar for pathogenic staphylococci). The medium didn't cause the microbe to change in order to survive, the microbe was just predisposed to surviving exposure to the selective agent. Correlation, not causation.

tl;dr: I think the transfusions are a selection technique, a screening process, to ensure Brenner gets the most important trait: Survival in Dimension X.

The children are all genetically similar in that trait, which leads to "you're a father to them irt your blood". It's a shared genetic trait between Henry and the children, whether it came from him via sex cells or if it evolved wild-caught. They all have his blood...blood like his. And what's the most efficient way to select for a genetic trait? A breeding program. So yes, I do still think some version of Henry and El are related.

(This isn't even getting into the music choices, with Henry singing TYBTM to baby El, which is the same song his blood-parent mother sang to him as a child, or the casting choices irt: Jamie and Millie. There's the blood stuff, and then there's the Everything Else about Henry and El.)

[turtlesandfrogs]

In completely different topics, but still related to ecosystems and long-ingnored microbiomes, I was reading a paper recently

That basically said that the diversity of your microbiome was more dependant on the diversity of plants you eat than whether you ID as a vegan or omnivore (which makes sense to me because I know plenty of vegans who self-identify as junk food vegans), and that the people who ate 30 or more types of plants regularly had much more diverse microbiomes, which is good. Also those folks had fewer genes for antibiotic resistance in their microbes, which is good, and higher CLA abundance, which is also good.

It occurs to me now that a sensible starting point to act on this information would be to count up the different kinds of plants that I eat at least somewhat regularly, but instead I decided to expand my dietary horizons by foraging more regularly. So, behold, Dock (rumex) leaves/shoots that I cooked up with some red beans and rice because it turns out the complex carbs in beans & whole grains are good for your gut microbe pets:

Well, off to actually count the plants that I eat regularly up!

[acti-veg]

Hey Acti Have you heard the latest about H5N1 (bird flu) not only crossing from animals to humans, but also transmission in via handling/consuming of animals? https://twitter.com/Globalbiosec/status/1775709161738895706

It is worrying, but it is important to keep it in perspective. I have heard about the new human cases, but I think some of the coverage on it is a little bit misleading. I’ve seen lots of people using it as a way to conclude that eating chicken/eggs means you’re risking catching bird flu; but this is hyperbolic and the evidence that it carries a significant risk of contamination is just not there.

The World Health Organisation found that all the human cases were linked to close contact with infected animals or contaminated environments. The new case in the US is significant because it’s linked to handling cattle rather than chicken, but risk to the public is still very low - much lower than the likes of E. coli, Campylobacter, or Salmonella which chicken already carries a risk of.

The virus is not well adapted to infect humans, and even less so to transfer between humans. It is workers and non-human animals who we should be most concerned about when it comes to bird flu, rather than the wider public. No human or animal should have to endure being exploited in filthy, overcrowded, demoralising conditions where the risk of disease is so high.

Bird flu represents a major pandemic risk and it would be truly disastrous if transmission between humans and other animals become common. The conditions in factory farms and the overuse of antibiotics in animal agriculture has created the perfect environment for an antibiotic resistant microbe to emerge. However, as troubling as all such cases are, we are not there yet.

[scotianostra]

On 6th August 1881 Sir Alexander Fleming was born in Lochfield, near Darvel.

Well before Fleming accidentally discovered penicillin he tried to convince doctors in the field hospitals of World War One that treating wounds with antiseptic, not only cleaned the wounds but also lowered the soldier’s natural resistance to infection because they were killing white blood cells. His mentor Almroth Wright believed that a saline solution – salt water – should be used to clean deep wounds, because this did not interfere with the body’s own defenses and in fact attracted white cells. Fleming proved this result in the field.

Wright and Fleming published their results, but most army doctors refused to change their ways, resulting in many preventable deaths.

After the war Fleming discovered an enzyme called Lysozyme, an important role in the prevention of bacterial infections, while this was an important breakthrough in preventing infections in the first place it had little or no effect on many other microbes that infect humans. Lysozyme is present in the body, for instance it is i in tears, saliva, sweat, and other body fluids, It destroys bacteria that attempts to enter our body through these passageways. In the case of tears, they protect our eyes from bacterial invaders.

Fleming had left a jar of mould unattended during a holiday. On returning to work he noticed that a jar of Staphylococcus bacteria – a green yellow mould – had covered the dish except one area which was clear of the bacteria – rather like a halo effect.

This was Fleming’s great Eureka moment – the moment he correctly deduced that some antibacterial agent had crept in and successfully stopped the bacteria. He later identified this antibacterial agent as a rare form of Penicillium notatum which had drifted in from a mycology lab nearby. He later talked about the importance of chance in this discovery.

"I have been trying to point out that in our lives chance may have an astonishing influence and, if I may offer advice to the young laboratory worker, it would be this—never neglect an extraordinary appearance or happening. It may be—usually is, in fact—a false alarm that leads to nothing, but may on the other hand be the clue provided by fate to lead you to some important advance."

Fleming named this fungus penicillin and tried to grow it in his lab. He published his discovery in the “Journal of Experimental Pathology” in 1929 but did not receive much attention at the time as most of his clinical trials had been inconclusive and penicillin could not be produced in large enough quantities to be useful. Fleming was convinced that the fungus had limited usefulness but his research was taken up by two researchers from Oxford University named Ernst Chain and Howard Florey. These two were successful in producing purified penicillin which became indispensable during World War II, and helped to save thousands of lives through its use in antibiotics. In 1945, as a result of their combined efforts and discoveries, Fleming, Chain and Florey were jointly awarded the Nobel Prize in Medicine.

So the untidiness of a Scottish scientist ultimately led to countless many lives being saved, Fleming himself predicted that one day the antibiotics might be less effective, as is the case nowadays, we wait in hope of another "accident"

[charlotte-of-wales]

PRINCE WILLIAM BECOMES PATRON OF THE APPEAL TO CREATE THE FLEMING CENTRE

Prince William has become Patron of a new appeal, launching today, to create The Fleming Centre which will drive a global movement to tackle antimicrobial resistance.

The Centre will be based at St. Mary's Hospital in Paddington, London, where Sir Alexander Fleming discovered penicillin, the first antibiotic, in 1928 and changed the course of medicine forever. This important programme of work is being led by Imperial College London and Imperial College Healthcare NHS Trust, which includes St Mary's Hospital.

Antimicrobial resistance occurs when the microbes that cause infections develop resistance to treatments such as antibiotics and antifungals and already kills over one million people around the world each year. It has been caused by the widespread misuse and overuse of antibiotics and other antimicrobials which has led to the global spread of drug-resistant microbes. If the problem is not resolved, it is estimated that by 2050, drug-resistant microbes will lead to around ten million deaths per year.

In order to effectively tackle antimicrobial resistance, global awareness and behaviour change is needed alongside scientific advances. The aim of The Fleming Initiative - the driving force behind the construction of an initial Centre in London - is to put society at the heart of solving this problem.

The Fleming Centre will deliver exhibitions and engagement activities to educate, inspire and catalyse action, convening diverse global voices and building consensus for change. At the Centre, scientists will work alongside patients, members of the public and policy makers to scope, test and scale solutions, so that antibiotics can continue to keep us all safe. It is hoped that this transformative approach at the London Centre will act as a blueprint which can be shared and adapted to local contexts around the globe.

In becoming Patron of the appeal to build the Centre, Prince William will support efforts over the next five years to make these ambitious plans to overcome global anti-microbial resistance a reality.

via Kensington Palace

[stanfave3-72217]

River microbes near wastewater treatment plants express high levels of antibiotic resistance genes, study shows

[mariacallous]

Chinese Hospitals Are Housing Another Deadly Outbreak

In Beijing and other megacities in China, hospitals are overflowing with children suffering pneumonia or similar severe ailments. However, the Chinese government claims that no new pathogen has been found and that the surge in chest infections is due simply to the usual winter coughs and colds, aggravated by the lifting of stringent COVID-19 restrictions in December 2022. The World Health Organization (WHO) has dutifully repeated this reassurance, as if it learned nothing from Beijing’s disastrous cover-up of the COVID-19 outbreak.

There is an element of truth in Beijing’s assertion, but it is only part of the story. The general acceptance that China is not covering up a novel pathogen this time appears reassuring. In fact, however, China could be incubating an even greater threat: the cultivation of antibiotic-resistant strains of a common, and potentially deadly, bacteria.

Fears of another novel respiratory pathogen emerging from China are understandable after the SARS and COVID-19 pandemics, both of which Beijing covered up. Concerns are amplified by Beijing’s ongoing obstruction of any independent investigation into the origins of SARS-CoV-2, the virus that causes COVID-19—whether it accidentally leaked from the Wuhan lab performing dangerous gain-of-function research or derived from the illegal trade in racoon dogs and other wildlife at the now-infamous Wuhan wet-market.

Four years ago, during the early weeks of the COVID-19 outbreak, Beijing failed to report the new virus and then denied airborne spread. At pains to maintain their fiction, Chinese authorities punished doctors who raised concerns and prohibited doctors from speaking even to Chinese colleagues, let alone international counterparts. Chinese medical statistics remain deeply unreliable; the country still claims that total COVID-19 deaths sit at just over 120,000, whereas independent estimates suggest the number may have been over 2 million in just the initial outbreak alone. Now, Chinese doctors are once again being silenced and not communicating with their counterparts abroad, which suggests another potentially dangerous cover-up may be underway.

We don’t know exactly what is happening, but we can offer some informed guesses.

The microbe causing the surge in hospitalization of children is Mycoplasma pneumoniae, which causes M. pneumoniae pneumonia, or MPP. First discovered in 1938, the microbe was believed for decades to be a virus because of its lack of a cell membrane and tiny size, although in fact it is an atypical bacterium. These unusual characteristics makes it invulnerable to most antibiotics (which typically work by destroying the cell membrane). The few attempts to make a vaccine in the 1970s failed, and low mortality has provided little incentive for renewed efforts. Although MPP surges are seen every few years around the world, the combination of low mortality and difficult diagnostics has meant there is no routine surveillance.

Although MPP is the most common cause of community-acquired pneumonia in school children and teenagers, pediatricians such as myself refer to it as “walking pneumonia” because symptoms are relatively mild. Respiratory Syncytial Virus (RSV), influenza, adenoviruses, and rhinoviruses (also known as the common cold) all cause severe inflammation of the lungs and are far more common causes of emergency-room visits, hospitalization, and death in infants and young children. Why should MPP be acting differently now?

One contributing factor to the severity of this outbreak may be “immunity debt.” Around the globe, COVID-19 lockdowns and other non-pharmaceutical measures meant that children were less exposed to the usual range of pathogens, including MPP, for several years. Many countries have since seen rebound surges in RSV. Several experts agree with Beijing’s explanation that the combination of winter’s arrival, the end of COVID-19 restrictions, and a lack of prior immunity in children are likely behind the surging infections. Some even speculate that that substantial lockdown may have particularly compromised young children’s immunity, because exposure to germs in infancy is essential for immune systems to develop.

In China, MPP infections began in early summer and accelerated. By mid-October, the National Health Commission had taken the unusual step of adding MPP to its surveillance system. That was just after Golden Week, the biggest tourism week in China.

Infection by two diseases at the same time can make things worse. The usual candidates for coinfection in children—RSV and flu—have not previously caused comparable surges in pneumonia. One difference this time is COVID-19. It is possible that the combination of COVID-19 and MPP is particularly dangerous. Although adults are less susceptible to MPP due to years of exposure, adults hospitalized for COVID-19 who were simultaneously or recently coinfected by MPP had a significantly higher mortality rate, according to a 2020 study.

Infants and toddlers are immunologically naive to MPP, and unlike COVID-19, RSV, and influenza, there is no vaccine against MPP. It seems implausible that no child (or adult) has died from MPP, yet China has not released any data on mortality, or on extrapulmonary complications such as meningitis.

Most disturbing, and a fact being downplayed by Beijing, is that M. pneumoniae in China has mutated to a strain resistant to macrolides, the only class of antibiotics that are safe for children less than eight years of age. Beyond discouraging parents to start ad hoc treatment with azithromycin, the most common macrolide and the usual first-line antibiotic for MPP, Beijing has barely mentioned this fact. Even more worrying is that WHO has assessed the risk of the current outbreak as low on the basis that MPP is readily treated with antibiotics. Broader azithromycin resistance in MPP is common across the world, and China’s resistant strain rates in particular are exceptionally high. Beijing’s Centers for Disease Control and Prevention reported macrolide resistance rates for MPP in the Beijing population between 90 and 98.4 percent from 2009 to 2012. This means there is no treatment for MPP in children under age eight.

Fears over a novel pathogen are already abating. After all, MPP is rarely lethal. But antimicrobial resistance (AMR) is. Responsible for 1.3 million deaths a year, AMR kills more people than COVID-19. No country is immune to this growing threat. Since China, where antibiotics are regularly available over the counter, leads the world in AMR, it is inconceivable that this issue hasn’t yet come up, particularly during WHO’s World AMR Awareness week, from Nov. 18 to Nov. 24.

Any infectious disease physician would want to know: Did WHO asked China the obvious question—what is the level of azithromycin resistance of M. pneumonia in the current outbreak—and include the answer in its risk assessment? Or did it ask about resistance to doxycycline and quinolones, antibiotics that can be used to treat MPP in adults? Even if WHO did ask, China isn’t telling, and WHO isn’t talking.

China’s silence isn’t surprising. Its antibiotic consumption per person is ten times that of the United States, and policies for AMR stewardship are predominantly cosmetic. While surveillance is China’s strong point, reporting is not.

Despite Spring Festival, the Chinese celebration of the Lunar New Year and another peak travel period, approaching in February 2024, WHO hasn’t advised any travel restrictions. It should have learned the danger of accepting Beijing’s statements at face value. Four years ago, Beijing’s delay enabled more than 200 million people to travel from and through Wuhan for Spring Festival. That helped COVID-19 go global. Since China’s AMR rates are already so high, importing AMR from other countries isn’t a major concern for China. Export is the issue, and China’s track record in protecting other countries is abysmal.

Rather than repeating the self-serving whitewashing coming from Beijing, WHO should be publicly pressing China about the threat of mutant microbes. Halting AMR is essential. Before antisepsis and antibiotics, surgery was a treatment of last resort. Without antibiotics, we lose 150 years of clinical and surgical advances. Within ten years, we are at risk of few antibiotics being effective. It may not be the novel virus that people were expecting, but the next pandemic is already here.

[flyonthewallmedstudent]

Finegoldia magna

Cold open with a case report:

60M with a past history of previous wrist fracture presents with worsening pain and swelling, erythema and reduced range of motion, after suffering an abrasion from changing a tire.

the previous injury resulted from an MVA 9 yrs prior with a closed rist fracture

there was also a history of ETOH use and possible malnutrition, which can result in immunosuppression

Xray showed extensive changes in the wrist bones compared to past years with near loss of several, suggestive of pyogenic arthritis

Aspiration of the wrist joint grew Finegoldia magna

What is it

not actually uncommon

but is more commonly associated with post op infections or prosthetic joint infections (so case reports are harder to find in this category)

previously known as peptostreptococcus (sounds like peptobismol) but was renamed following 16S rna sequence availability, so in older texts/articles you'll still see it's old name

it's a commensal, so normal part of our microflora, but is opportunistic like so many other pathogens we usually live with and covers our body

It is a Gram Positive Anaerobe, of the same flavour of clostridium. Remember there's fewer gram positive anaerobes than there are aerobes. So consider it in cultures if there's only growth in the anaerobe bottle and it's gram positive (purple). Usually it likes mucosal surfaces, such as the GI or GU tracts, but it doesn't mind skin either. It's considered a "gram positive anaerobic cocci" (GPAC) and has increasing prevalence and antibiotic resistance in the group.

Image source

Increased risk and when to think of it

chronic ulcers, diabetic ulcers

associated with biofilms (always bad, requires prolonged duration of antibiotics)

prosthetic joints

prosthetic valves

as it is opportunistic, also consider it in the immunocompromised

In the case above, the patient had septic arthritis, for which anaerobes account for 20% of cases. And Finegoldia is often the culprit in the case of post op and prosthetic joint infections. Rarely affects normal joints or healed joints from previous closed trauma years prior.

In chronic wounds it can impair healing via Protein L, which bindings to antibodies, causing immunomodulatory effect.

Bit of history

named for Sydney Finegold, an American physician who was a founding member of IDSA (infectious diseases society of American) and one of its early former presidents

but the name did make me think of 'fine gold'

Treatment

luckily susceptible to penicillin - but there is growing resistance, hence relevance of always chasing susceptibility

alternatives: metronidazole (typical class that covers anaerobes), tazocin and carbapenems

also has increasing resistance to clindamycin (a consideration in penicillin allergy or during empirical therapy for wounds)

Resources:

case report

wikipaedia

microbe canvas