Showing posts with label Plasids. Show all posts
Showing posts with label Plasids. Show all posts

Monday, July 21, 2014

WWTPs As `Mixing Vessels’ For Resistant Bacteria

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Photo Credit USGS – Wastewater: The Primary Treatment Process

1. Screening 2. Pumping 3. Aerating 4. Removing sludge 5. Removing Scum 6. killing bacteria

 

 

# 8853

 

While it is not a scientifically recognized law, as is Boyle’s or Torricelli’s, all too often the Law of Unintended Consequences (LUC) seems equally immutable and pervasive in the universe.  For every action, we often see an unanticipated, and usually negative, reaction (almost invariably referred to as `bad LUC)

 

And man’s expanding technology, quite naturally, serves to amplify the impact of these consequences. 

 

While futurists worry about nanotechnology, or artificial intelligence ultimately leading to our demise 50 years from now, the world is facing a more immediate threat.  And it is, as you’ve already guessed, one of our own making.

 

Antibiotic resistance is probably the greatest public health threat facing mankind,  and soon - many health experts fear - we may face a post-antibiotic future.  One where simple wounds could kill once more, and elective surgeries could become too dangerous to perform.

 

In early 2012 World Health Director-General Margaret Chan expressed a dire warning about our dwindling antibiotic arsenal (see Chan: World Faces A `Post-Antibiotic Era’) – a sentiment echoed a year later by CDC Director Thomas Frieden during the release of a major US report on the threat (see McKenna On CDC Antibiotic Resistance Report).

 

Last April,  WHO: Antibiotic Resistance – Serious, World-Wide Threat we looked at an in-depth report showing just how close we are to finally seeing this grim future realized, while last year, we looked at a report from the  UK CMO: Antimicrobial Resistance Poses `Catastrophic Threat’.

 

While usually ascribed to too many people not finishing their antibiotic prescriptions, or the over prescribing of antibiotics for non-bacterial infections, there are many other reasons behind  rise of antibiotic resistance.

 

One of the less obvious ones that we’ve discussed in the past concerns Waste Water Treatment Plants (WWTPs), where sewage is gathered, and processed.  Undeniably a crucial part of our modern infrastructure, these plants literally make it possible for people to live in large cities, but in recent years they have also been implicated in aiding and abetting the creation of antibiotic resistant bacteria.

 

 

Over the weekend another study – this time by the UK’s University of Warwick – has made headlines (see Drug-resistant bacteria: Sewage-treatment plants described as giant 'mixing vessels' after scientists discover mutated microbes in British river), for which you’ll find the link below.

 

A little crib sheet for those non-scientists with a desire to read the full report:

 

  • Beta-lactamases are enzymes that confer resistance to β-Lactam antibiotics (penicillins, cephamycins & Carbapenems)  with  blaCTX-M-15,  perhaps the most common around the globe.
  • Carbapenems are class of broad spectrum antibiotics that includes imipenem, meropenem, doripenem, and ertapenem, that are often the drug of last resort for treating difficult bacterial infections. 
  • Enterobacteriaceae comprise a large family of Gram-negative bacteria that range from harmless strains to pathogenic invaders, and includes such familiar names as Salmonella, Escherichia coli, Klebsiella and Shigella.

 

The entire 7-page PDF is available online, and I’ll have more when you return.

 

Waste water effluent contributes to the dissemination of CTX-M-15 in the natural environment

G. C. A. Amos ,P.M.Hawkey , W. H. Gaze and E. M. Wellington

ABSTRACT (EXCERPT)


Results: We report the first examples of blaCTX-M-15 in UK river sediment; the prevalence of blaCTX-M-15 was dramatically increased downstream of the WWTP. Ten novel genetic contexts for this gene were identified, carried in pathogens such as Escherichia coliST131 as well as indigenous aquatic bacteria such as Aeromonas media.The blaCTX-M-15 gene was readily transferable to other Gram-negative bacteria. We also report the first finding of an  imipenem-resistant E. coli in a UK river.


Conclusions: The high diversity and host range of novel genetic contexts proves that evolution of novel combinations of resistance genes is occurring at high frequency and has to date been significantly underestimated. We have identified a worrying reservoir of highly resistant enteric bacteria in the environment that poses a threat to human and animal health

(Continue . . . )

 

The inability of waste-water plants to kill all of the bacteria during their processing, combined with the pooling of resistant  & non-resistant bacteria together, provides an opportunity for new, resistant bacteria to form, and to then enter the environment.


The lead author of this report, Professor Elizabeth Wellington of the University of Warwick, is quoted in The Independent article saying:

 

“The problem is we use river water to irrigate crops, people swim or canoe in rivers, and both wildlife and food animals come into contact with river water. These bacteria also spread during flooding, and with more flooding and heavy rain this could get worse.


Stricter regulations and higher levels of sewage treatment, with an emphasis on preventing untreated sewage being discharged during a storm, are needed to halt the rise of antibiotic resistance in the environment, Professor Wellington said.


We’re on the brink of Armageddon and this is contributing to it. Antibiotics could just stop working”

 

Complicating matters, WWTPs  are also called upon to deal with drugs and chemicals either dumped into the system, or excreted from humans in their waste.  In recent years we’ve seen a number of reports on detectable levels of drugs in rivers and streams that passed relatively intact through treatment facilities, including antibiotics and antiviral meds.


Since Wastewater Treatment Plants depend upon microbial activity in order to breakdown or `digest’ sewage, large quantities of antibiotics in the sewage could inhibit microbial activity, resulting in the failure of WWTPs and the discharge of under-treated wastewater into the environment

 

In 2007, I looked at the issue of what might happen if millions of people simultaneously began taking Tamiflu ® during a pandemic and releasing it into our environment, prompted by a study conducted at the Centre for Ecology and Hydrology in Oxford, England. 

 

More recently, investigators looking at the levels chemicals in rivers downstream from a pharmaceutical manufacturing hub in India, found staggering amounts of antibiotics along with signs of resistant bacteria in 2011.

 

That story was  well covered by Maryn McKenna on her Superbug Blog (see Drug residues and drug resistance in water: Not good).

 

While I’m sure most of us would like to simply `flush and forget it’, the truth is wastewater infrastructures around the world are continually called upon to deal with new, and sometimes difficult challenges, and in many places the technology simply isn’t currently up to the task. 

 

All of which makes me wonder if when Nietzsche’s said `That which does not kill me, makes me stronger’, he wasn’t really talking about bacteria and viruses.

Tuesday, April 12, 2011

Study: Adaptation Of Plasmids To New Bacterial Species



# 5487

 

 

The subject of Plasmids – tiny snippets of DNA that can be easily transferred between different types of bacteria – has been of particular interest since that is one of the modes by which bacteria can acquire antibiotic resistance.

 

The NDM-1 (New Delhi metallo-ß-lactamase-1) enzyme – which has received considerable attention these past few months -  is one of the types of resistance that can be carried on plasmids, raising concerns that it could spread to other types of bacteria.  

 

It may help if you think of plasmids as vehicles that can travel between different types of bacteria, and the resistance genes (like NDM-1) as one of its passengers.

 

Since it requires physical contact between two different types of bacteria for plasmids to transfer, man-made environments where many types of bacteria are thrown together -  such as sewage treatment plants and contaminated water supplies -  are of great interest to microbiologists studying plasmids.

 

 

Last week, we learned via a Lancet Study, that resistant bacteria were found in 4 per cent of samples tested from New Delhi’s water supplies and 30 per cent of tested sewage sites (see Lancet Study: NDM-1 In New Delhi Water Supply).

 

The researchers identified 11 new species of bacteria carrying the NDM-1 gene, including strains which cause cholera and dysentery.

 

 

While not looking specifically at NDM-1 plasmid transfer, we’ve a new study published in Nature Communications on evolutionary changes in one common family of Plasmids; IncP-1.

 

The IncP-1 Plasmid was first identified in 1969 at a Birmingham (U.K.) hospital riding on Pseudomonas aeruginosa and Klebsiella aerogenes bacterial strains, and contained genetic coding that allowed their hosts to survive contact with multiple antibiotics  (cite Spread and survival of promiscuous IncP-1 plasmids).

 

Since that time IncP-1 has been the subject of interest among microbiologists, but evolutionary information on how it adapts to new bacterial hosts has been sparse.

 

Today’s open access study seeks to fill in some of those gaps.

 

The IncP-1 plasmid backbone adapts to different host bacterial species and evolves through homologous recombination

Peter Norberg, Maria Bergström, Vinay Jethava, Devdatt Dubhashi & Malte Hermansson

Nature Communications Volume: 2, Article number: 268 DOI: doi:10.1038/ncomms1267

ABSTRACT

Plasmids are important members of the bacterial mobile gene pool, and are among the most important contributors to horizontal gene transfer between bacteria. They typically harbour a wide spectrum of host beneficial traits, such as antibiotic resistance, inserted into their backbones.

 

Although these inserted elements have drawn considerable interest, evolutionary information about the plasmid backbones, which encode plasmid related traits, is sparse.

 

Here we analyse 25 complete backbone genomes from the broad-host-range IncP-1 plasmid family. Phylogenetic analysis reveals seven clades, in which two plasmids that we isolated from a marine biofilm represent a novel clade.

 

We also found that homologous recombination is a prominent feature of the plasmid backbone evolution. Analysis of genomic signatures indicates that the plasmids have adapted to different host bacterial species. Globally circulating IncP-1 plasmids hence contain mosaic structures of segments derived from several parental plasmids that have evolved in, and adapted to, different, phylogenetically very distant host bacterial species.

(Continue . . . )

 

 

 

If all of this seems a bit technical (and it is), we have a press release from the University of Gothenburg that helps clear some of it up.

 

The `money quote’ is:

 

The research team's findings show that IncP-1 plasmids can move, and have moved, between widely differing bacterial species and in addition have interacted directly with one another, which can increase the potential for gene spreading.

 

But follow the link below to read the release in its entirety.

 

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Antibiotic resistance spreads rapidly between bacteria

The part of bacterial DNA that often carries antibiotic resistance is a master at moving between different types of bacteria and adapting to widely differing bacterial species, shows a study made by a research team at the University of Gothenburg in cooperation with Chalmers University of Technology. The results are published in an article in the scientific journal Nature Communications.

 

More and more bacteria are becoming resistant to our common antibiotics, and to make matters worse, more and more are becoming resistant to all known antibiotics. The problem is known as multi-resistance, and is generally described as one of the most significant future threats to public health Antibiotic resistance can arise in bacteria in our environment and in our bodies. Antibiotic resistance can then be transferred to the bacteria that cause human diseases, even if the bacteria are not related to each other.

 

(Continue . . . )