Toxin linked to motor neuron disease found in Australian algal blooms



File 20180503 153873 1srnuq3.jpg?ixlib=rb 1.1
Cyanobacterial blooms and algae are common in water bodies around the world. However, Australia is yet to monitor the growth of neurotoxins in our algae.
from http://www.shutterstock.com

Brendan Main, University of Technology Sydney

Algal blooms in major Australian rivers are releasing a toxic chemical that may contribute to the development of motor neuron disease (MND).

My colleagues and I tested algae from waterways in New South Wales, and found that a neurotoxin called BMAA was present in 70% of samples, including those from crucial water sources such as the Darling and Murrumbidgee rivers.

This compound is well known overseas, and has been found in waterways in the United States, Europe, Asia, and the Middle East. But this is the first time it has been detected in Australia. Although its presence has been suspected, it was never specifically tested until now.

Two samples containing BMAA were collected from the Murrumbidgee River, which runs through the NSW Riverina, a hotspot for MND in Australia. Positive samples were also collected in Centennial Park and Botany wetlands in central Sydney, as well as Manly Dam on Sydney’s Northern Beaches.




Read more:
What we know, don’t know and suspect about what causes motor neuron disease


In the past 30 years, Australian rivers have had the dubious honour of hosting some of the largest algal blooms in history. In 1991 a bloom stretched along more than 1,200km of the Darling River, prompting the New South Wales government to declare a state of emergency. The army was mobilised to provide aid to towns.

Since then, southeast Australia has had four large blooms, most recently in 2016. The future isn’t promising either. Rising water temperatures mean blooms are likely to increase in frequency and duration in the future.

Multiple state agencies monitor populations of types of bacteria in Australia, regularly testing water quality and issuing alerts when blooms are present. This testing is necessary because of the impressive number of toxins that cyanobacteria can produce, ranging from skin irritants to liver and neurological toxins. Most of these compounds are relatively fast-acting, meaning that their effects take hold rapidly after exposure.

The neurotoxic compound BMAA, however, is not currently part of regular testing, despite links between long-term exposure to algal blooms and the development of diseases such as MND. BMAA is known to be produced by a type of freshwater and marine bacteria, as well as some species of algae.




Read more:
Watch out, Australia: a red-hot summer means blue-green algae


How BMAA affects our health

Research in America found that regular participation in water-based recreational activity resulted in a threefold increase in the risk of developing MND. Satellite mapping also revealed that lakes prone to algal blooms were often surrounded by clusters of MND patients.

Southwestern NSW has become a focus for MND researchers since 2014, due to the presence of a hotspot for MND cases around the Riverina. The town of Griffith has reported a prevalence of this disease that is nearly seven times higher than the national average of 8.7 cases per 100,000 people. Hotspots like these can help researchers identify environmental factors that contribute to diseases.

This is particularly important in MND, in which only 5-10% of patients have a family history. The other 90-95% of cases are sporadic, occurring without warning. It is possible that BMAA exposure, in association with genetic, or other environmental risk factors, contributes to the high incidence of MND in the Riverina.




Read more:
Exposure to algae toxin increases the risk of Alzheimer’s-like illnesses


BMAA also has a similar structure to the amino acids that make up the proteins in our body. We hypothesise that this contributes to its toxicity and ability to build up in animal tissue and in plants that are exposed to contaminated water.

Similar to mercury, BMAA can accumulate in the food chain, which means that people could be consuming relatively large amounts of it through their diet. A US animal study found that dietary exposure to BMAA resulted in the formation of plaques and protein tangles in the brain, which are hallmark features of neurodegeneration.

Research now needs to focus on tracking and monitoring algal blooms to detect the presence of BMAA, and determining how long it remains in the ecosystem after these blooms occur.

The ConversationThis can potentially help to reduce human exposure to BMAA. Although the factors that cause MND are many and varied, we hope this understanding could ultimately help to reduce the number of people who develop the disease.

Brendan Main, PhD Candidate, University of Technology Sydney

This article was originally published on The Conversation. Read the original article.

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New research suggests common herbicides are linked to antibiotic resistance



File 20171117 7557 hxmg6.jpg?ixlib=rb 1.1
New Zealand researchers have found that the active ingredients in commonly-used weed killers like Round-up and Kamba can cause bacteria to become less susceptible to antibiotics.
from http://www.shutterstock.com, CC BY-ND

Jack Heinemann

Antibiotics are losing their ability to kill bacteria.

One of the main reasons for the rise in antibiotic resistance is the improper use of antibiotics, but our latest research shows that the ingredients in commonly-used weed killers like Round-up and Kamba can also cause bacteria to become less susceptible to antibiotics.

Herbicides induce gene activity

Already, about 700,000 deaths are attributable each year to infections by drug-resistant bacteria. A recent report projected that by 2050, 10 million people a year will die from previously treatable bacterial infections, with a cumulative cost to the world economy of $US100 trillion.

The bacteria we study are potential human pathogens. Seventy years ago pathogens were uniformly susceptible to antibiotics used in medicine and agriculture. That has changed. Now some are resistant to all but one or two remaining antibiotics. Some strains are resistant to all.


Read more: Drug resistance: how we keep track of whether antibiotics are being used responsibly


When bacteria were exposed to commercial herbicide formulations based
on 2,4-D, dicamba or glyphosate, the lethal concentration of various antibiotics
changed. Often it took more antibiotic to kill them, but sometimes it took less.
We showed that one effect of the herbicides was to induce certain genes that they all carry, but don’t always use.

These genes are part of the so-called “adaptive response”. The main elements of this response are proteins that “pump” toxins out of the cell, keeping intracellular concentrations sublethal. We knew this because the addition of a chemical inhibitor of the pumps eliminated the protective effect of the herbicide.

In our latest work, we tested this by using gene “knockout” bacteria, which had been engineered to lose just one pump gene. We found that most of the effect of the herbicide was explained by these pumps.

Reduced antibiotic use may not fix the problem

For decades we have put our faith in inventing new antibiotics above the wisdom
of preserving the effectiveness of existing ones. We have applied the same invention incentives to the commercialisation of antibiotics as those used with mobile phones. Those incentives maximise the rate of product sales. They have saturated the market with phones, and they saturate the earth with antibiotic resistant bacteria.

Improper use of antibiotics is a powerful driver of the widespread resistance.
Knowing this naturally leads to the hypothesis that proper and lower use will make the world right again. Unfortunately, the science is not fully on the side of that hypothesis.

Studies following rates of resistance do generally find a decrease in resistance to specific drugs when their use is banned or decreased. However, the effect is not a restoration of a pre-antibiotic susceptibility, characterised by multi-year effectiveness of the antibiotic. Instead, resistance returns rapidly when the drug is used again.

This tells us that once resistance has stablised in populations of bacteria, suspended use may change the ratio of resistant to susceptible but it does not eliminate resistant types. Very small numbers of resistant bacteria can undermine the antibiotic when it is used again.

Herbicides and other pollutants mimic antibiotics

What keeps these resistant minorities around? Recall that bacteria are very
small, but there are lots of them; you carry 100 trillion of them. They are also found deep underground to high up in the atmosphere.

Because antibiotics are so powerful, they eliminate bacteria that are susceptible and leave the few resistant ones to repopulate. Having done so, we now have lots of bacteria, and lots of resistance genes, to get rid of, and that takes a lot of time.

As our work suggests, the story is even more complicated. We are inclined to think of antibiotics as medicine and agrichemicals, hand soaps, bug sprays and preservatives as different. Bacteria don’t do this. To them, they are all toxic.

Some are really toxic (antibiotics) and some not so much (herbicides). Bacteria are among the longest lived organisms on earth. Nearly four billion years of survival has taught them how to deal with toxins.

Pesticides as antibiotic vaccines

Our hypothesis is that herbicides immunise the bacteria from more toxic
toxins like antibiotics. Since all bacteria have these protections, the use of widely used products to which they are exposed is particularly problematic. So these products, among others, might keep bacteria ready for antibiotics whether or not we are using them.

We found that both the purified active ingredients and potential inert ingredients in weed killers caused a change in antibiotic response. Those inert ingredients are also found in processed foods and common household products. Resistance was caused below legally allowed food concentrations.

What does this all mean? Well for starters we may have to think more carefully about how to regulate chemical commerce. With approximately eight million manufactured chemicals in commerce, 140,000 new since 1950, and limited knowledge of their combination effects and breakdown products, this won’t be easy.

The ConversationBut neither is it easy to watch someone die from an infection we lost the power to cure.

Jack Heinemann, Professor of Molecular Biology and Genetics

This article was originally published on The Conversation. Read the original article.

Cameroon: Elephant Poachers Captured


The link below is to an article on the arrest of a number of poachers linked to the slaughter of elephants in Cameroon. We have been following news on the crisis in Cameroon and though the reported arrest of poachers is good news, the damage has already been done.

For more visit:
http://www.earthweek.com/2012/ew120330/ew120330c.html

Koalas: Trees the Key to Growing Populations


A recent report on Koala populations has concluded that more trees are the key to growing populations and spreading habitats. Hardly sounds surprising does it – the article is linked to below.

For more visit:
http://sydney.edu.au/news/84.html?newsstoryid=6826

 

Declining Penguin Numbers Linked to Whales?


The following link is to an article that looks into the decline of Krill and the impact on Penguins. The rising number of Whales is also having an impact on Penguin numbers because of competition for declining Krill.

For more visit:
http://news.nationalgeographic.com/news/2011/04/110411-penguins-antarctica-decline-krill-whales-warming-environment-animals/