Pennsylvania Studies Blotchy Bass

The Express, Study analyzes blotchy bass syndrome in Commonwealth, and its cause

During a public meeting with the Pennsylvania Fish and Boat Commission on Tuesday, Jan. 7, the prevalence of blotchy bass syndrome within smallmouth bass in the Susquehanna and Juniata rivers was brought up.

Blotchy bass syndrome is hyper-pigmented melanistic skin lesions, which was first documented in the 1980s in the Hudson River in New York, and was first seen in Pennsylvania in 1986.

While it has been observed since 1986 in the Commonwealth, committee member Geoff Smith who gave the presentation regarding the syndrome noted that it was not something that came up locally until the 2010s.

 

“It really came to prominence locally in 2012 and it kind of set off the media attention with young-of-year smallmouth bass mortality,” Smith said. “We added it to our study of fish heal analyses we did in the field and (are) keeping track of it to better understand what was going on.”

At that time, contaminants to various issues was blamed for the cause, but a wide range of environmental and fish health analyses was already in place. According to pathology, aggregation of melanocytes in the upper two layers of the skin was to blame. It was non-cancerous and didn’t appear harmful, but it was unknown as to why. “When we requested funding, it didn’t allow us to look specifically at this, so we linked it into other studies and used existing funding,” Smith said.

 

Water quality and temperature were issues that were brought up to a cause, and an experiment was conducted alongside Lock Haven University to take wild fish and move them to a hatchery setting. It removed the water quality element. It helped to see whether that would make the blotches go away or not. “We had fish that lost color and some that gained color. It was our first suggestion that the condition itself was transmissible. It was a disease, which was something we did not expect,” Smith said.

USGS started looking at affected and unaffected tissues, affected tissues had viral particles. Further analysis saw they were from a class known as adomaviruses, something that was relatively new in North America according to Smith during his presentation.

There was a slightly different virus in largemouth bass.

This is the first I've heard of it. If I caught a bass like that, Smallmouth, Largemouth, or Striped, I would just assume it was it was a genetic or developmental fluke.

The Wombat has Rule 5 Sunday: Snow Bunny up and garnering clicks at The Other McCain.

Another Damn Virus to Worry About

Or two. First ‘Rare but dangerous’ tickborne virus spreading around Pa.: What you can do

Another illness transmitted by ticks is spreading around Pennsylvania, state officials announced. It’s called Deer Tick Virus and is a type of Powassan virus. DTV is considered “rare but dangerous,” officials said in a news release Tuesday that indicated the illness had been found in 15 Pennsylvania counties. By week’s end, that count was up to 16, including one contiguous to the Lehigh Valley.

As with Lyme disease, another tickborne illness, there is no vaccine to prevent the transmission of DTV in humans. Nor is there a medicine to treat it. (Lyme disease can be treated early through antibiotics.) That leaves caution and prevention as the best steps to avoid falling victim.  “Lyme disease has been present in all 67 counties for some time, and unfortunately, the prevalence of the very serious Deer Tick Virus appears to be increasing in some tick populations,” Pennsylvania Department of Environmental Protection Secretary Patrick McDonnell said in the release.

Powassan virus can be transmitted from tick to human in as little as 15 minutes after a bite occurs, while Lyme takes much longer to cause infection — often 24 hours or more after the tick attaches to the host. 

Initial symptoms of a DTV infection may include fever, headache, vomiting and weakness. Some people who are infected experience no symptoms, and an infection may go undetected. However, 91% of patients treated for DTV infections develop severe neuroinvasive disease, meaning it’s capable of infecting the nervous system.

Those who exhibit severe disease from Deer Tick Virus may experience encephalitis or meningitis and require hospitalization, with symptoms including confusion, loss of coordination, difficulty speaking, or seizures. About 12% of people with severe disease have died, and approximately half of survivors of severe disease have suffered long-term health impacts.

Through routine testing in the Pennsylvania DEP’s five-year pilot tick surveillance program started in 2018, “unusually high infection rates” of Deer Tick Virus have been found in adult tick samples taken from three sites: Fisherman’s Paradise public fishing area on Spring Creek in Centre County; Iroquois Trail near Tunkhannock in Wyoming County; and Lawrence Township Recreational Park in Clearfield County. At each of these three locations, the infection rate exceeded 80% of ticks sampled.

I can't imagine what would keep it from getting to Maryland. Deer don't move too far in their lifetime, but some wander, and a few ticks are going to ride across borders. 

Also,  First Case Of Avian Influenza Detected On Kent County, Delaware farm

Federal laboratory testing has confirmed a highly pathogenic H5N1 avian influenza (HPAI) case in a commercial broiler farm in Kent County, Delaware. Following an investigation by the Delaware Department of Agriculture and the U.S. Department of Agriculture’s (USDA) National Veterinary Services Laboratory confirmed poultry from this farm tested positive for highly pathogenic H5N1 avian influenza (HPAI).

This avian influenza detection follows previously announced cases on farms in New Castle County, Delaware, and Cecil and Queen Anne’s Counties, Maryland. Following these cases, federal and state partners have greatly expanded their surveillance sampling and testing regimen to better protect the poultry industry on the Delmarva Peninsula.

State officials have quarantined all affected premises, and the birds have been depopulated to prevent the spread of the disease. Birds from affected flocks will not enter the food system.

There is currently minimal risk to public health as there have been no human cases of HPAI in the United States. Avian influenza does not affect poultry meat or egg products, which remain safe to eat.

Avian influenza is a highly contagious airborne respiratory virus that spreads quickly among birds through nasal and eye secretions and manure. The virus can be spread in various ways from flock to flock, including by wild birds, through contact with infected poultry, by equipment, and on the clothing and shoes of caretakers. This virus affects poultry, like chickens, ducks, turkeys, and wild bird species such as ducks, geese, shorebirds, and raptors.

So, if the birds in your neighborhood start dropping dead at abnormal rates, this may be the cause. It would be worth reporting to authorities. 

There's Something Happening Here (Still)

You might have seen a few days ago when I floated an idea (in science we give them a Greek name hypothesis), that some substantial fraction of humanity is not susceptible to the Chinese Lung AIDS due to previous exposure to other coronaviruses. Not being in that field, or working at all, I just threw it out for consideration. But now, Rud Istvan, a scientist who occasionally posts (but more often comments) at Watts Up With That and actually has some real world knowledge of virology, has fleshed out that theory in Wuhan #Coronavirus and Covid-19 Rumination #5

We know from two inadvertent extreme ‘lack of social distancing’ “experiments”, Diamond Princess (DP) and CVN71 (Theodore Roosevelt, TR), that only about 15% (TR) to 19% (DP, with several more weeks of exposure) ever test positive for the virus. That means that something like 80-85% of people have an immune system that seems to handle the virus effortlessly even in highly infectious, high viral titer circumstances–so that not even a positive viral shedding test develops. This could just be a very good innate immune system; it could also be a primed active immune system (i.e. the population was NOT naïve). A very plausible explanation hypothesis is developed below with important ramifications for opening countries from extreme lockdown measures.

We know from those same two ‘experiments’ that between 45% (DP) and 55% (TR) test positive but are asymptomatic. Now, some of that is just the now known incubation period with a mean ~5 days from infection and 97.5% displaying symptoms within 11.5 days. But we know also from South Korea that of the ~10600 now tested positive but asymptomatic and quarantined 14 days, that ~20% NEVER developed even mild symptoms. This is likely also explained by the naiveté hypothesis developed below.

In what follows, the primary technical sources are the Journal of Virology on coronaviruses, ncbi.nlm.NIH.gov for science publications, www.CDC.gov, and for clinical morbidity a very new ‘anecdotal’ survey article at Sciencemag.org.

Mitigation

The CDC says that there are four common cold coronavirus serotypes causing something between 15 and 35% of all common colds, (about 5% more are DNA adenoviruses that do not mutate much so immunity to them is long lasting), with the remainder caused by about 100 different rhinovirus serotypes.

For all three common cold virus types, the route of transmission is known to be cough, touching (handshake after cough), or hand face contact (cough droplets to a surface, touch surface, then touch mouth, nose, eyes.) This is why common colds are only weakly seasonal while flu is strongly seasonal. That is why for COVID-19, social distancing, frequent hand washing, and consciously NOT face touching ‘work’. From a transmission perspective, Wuhan is ‘just’ another coronavirus.

An aside argued in rumination #4 and in other previous comments to others. Observational fact: flu is strongly seasonal, common colds are not. The reason lies in route of transmission. Inhaling infected aspirate principally spreads flu (aspirate particles are less than 5 microns). These aspirate particles dry out rapidly in dry indoor winter air (high surface to volume ratio) and remain circulating for many hours. In summer humidity, they don’t dry out and sink ‘rapidly’ to where they cannot be inhaled. Winter contact route of flu transmission exists but is distinctly secondary according to my personal communications with Dr. Fauci summer of 2009. Anything less than an N95 respirator will not prevent you from catching flu. Quarantine is ineffective. Annual flu shot is advised.

Now, there are two Covid-19 possibilities. Dr. Fauci might be right that it could be seasonal like flu, implying primary infection route would be inhaled aspirate. In which case, all the public mask nonsense is pointless. Or, it is ‘just’ another corona virus, the three recommended mitigation measures work, and public masks are still nonsense–unless you have active mild symptoms: dry cough plus fever >100.4F. In which case you should quarantine yourself and not be in public even with a mask.

Lack of transmission under extreme circumstances in 80-85% of cases

The four common cold coronaviruses are: 229E and NL63 in the ‘alpha’ serotype group, and OC43 and HKU1 in the ‘beta’ serotype group. Wuhan is also in the beta serotype group. All four common cold coronavirus spike proteins have two binding sites. In all four, the S1-CTD site binds the ACE2 receptor on epithelial cells such as line the nose, mouth, throat, and lungs. So their spike proteins, just like Wuhan, ‘key’ to that cellular receptor lock as well (as after being fully humanized) to another that varies. S1-CTD is a natural target for antibodies.

My naiveté hypothesis is that those exposed but not ‘infected’ on DP and TR may actually have been, but had a coronavirus common cold in the sufficiently recent past that their active immune system is NOT naïve thanks to S1-CDT. The antibodies simply clear the Wuhan virus before it can sufficiently replicate to even be detected. A lesser degree of immunity (older exposure) might allow the virus to sufficiently replicate to be detected, but not ever sufficiently to cause symptoms before the active immune system spools up to finally clear it.

If this naiveté hypothesis is correct, then the country should be opened immediately using the steps outlined by President Trump on Thursday. THAT is a HUGE deal economically. My hypothesis came about as I thought more about my vicious coronavirus cold referenced in guest post #1—without fever, so not Wuhan, but at 9 day duration plus more cough and less runny nose, also not Rhino. Hence a personal recent experience motivation for rumination #5.

What, having a previous disease might make you immune, or at least resistant to new disease? What a novel thought!

Well, not exactly. In fact the original vaccine against Smallpox was developed based on Edward Jenner's observation that milk maids, who commonly caught Cowpox (which turned out to be a virus related to Smallpox) did not commonly catch Smallpox during epidemics. In fact, the very word "vaccinate" come from Vacinnae, which was the medical term for Cowpox, as compared to  Variola for Smallpox.

If true, this would also point to research lines for a vaccine for multiple coronaviruses.

Don't bet your life on this because I said so.

Hope in the Time of the Plague

Willis Eschenbach, an occasional writer at Watts UP With That, who seems to have a great statistical talent, as well as a way of making sense of data has evaluated the data from the Diamond Princess, the first cruise ship quarantined, and has what seems like good news: Diamond Princess Mysteries

First, despite ample opportunity, 83% of the passengers and crew never got the disease. Age didn't make much difference. So, whether it was the isolation after the problem was discovered or a wide spread natural immunity to the virus, most people were spared. Either is good news for us, and dramatically cuts down the severity of our expectations.

Of those who got the disease 48% had no symptoms. Very young were largely spared symptoms. Starting at 20, many more showed symptoms, but it declined as they got older. Even older people had about a 50% of asymptomatic disease. This is bad news for spreading the virus, but good for having it.

Finally, some historical perspective:

Science Validates "Man-Flu"

It's all about the children: Viruses may have evolved to hit men hard but go easy on women

Many infections cause more severe illness in men than women. Men infected with tuberculosis are 1.5 times more likely to die than women; men infected with human papillomavirus are five times more likely to develop cancer than women; and men infected with Epstein-Barr virus are at least twice as likely to develop Hodgkin’s lymphoma as women.

Many think this pattern is because of differences between the sexes’ immune systems. But another explanation is that women are more valuable hosts. Women can pass infections to their children during pregnancy, birth and breastfeeding, so there’s an evolutionary pressure on viruses to be less harmful to them, say Francisco Úbeda and Vincent Jansen at Royal Holloway University of London.

In order for a virus to infect others, it needs to produce more copies of itself in the body. Making their host ill is an unavoidable consequence of this. “That’s not something a pathogen particularly sets out to do because it’s shooting itself in the foot, should it have one,” says Jansen.

The researchers used mathematical modelling to show that, for pathogens that affect both sexes, natural selection in theory should favour those that cause less illness in women – as long as they can be transmitted from mother to child.

This evolutionary pressure, they argue, could explain a longstanding puzzle: why human T-cell lymphotropic virus type 1 (HTLV-1) progresses to leukaemia much more commonly in Japanese men than Japanese women, but affects both sexes equally in the Caribbean. They argue that this discrepancy is because women breastfeed their babies more commonly and for longer in Japan – giving the virus more opportunity to enter another host.

For this to be the case, though, the virus would have to be able to detect whether it’s inside a man or a woman. We don’t yet know how it would do this, but it’s not impossible, says Jansen. “There are all sorts of hormonal and other pathways that are slightly different between men and women,” he says.

If we were to identify a mechanism, that would open the possibility of manipulating it. “We could try to make the virus think it’s in a female body rather than a male body and therefore take a different course of action,” says Jansen.

In theory, a virus should generally evolve to spare it's host (although, other evolutionary pressures, say towards an increase in infectiousness might run counter to that), while the host should also evolve to resist the virus. Maybe it's women who are evolving faster to reduce the effects of viruses, because they have more at stake.

Wombat-socho has "Rule 5 Sunday: The Week Before Christmas" ready for your viewing pleasure at The Other McCain.

Could Fish Medicine Save Your Life?

This forgotten WWI antiseptic could be the key to fighting antibiotic resistance

An antiseptic used in WWI hospitals has been revived after seven decades, and is showing great promise in preventing the common cold, and could be the key to fighting antibiotic resistance - one of the biggest ever threats to global health.

The simple antiseptic, made from coal tar, was replaced by penicillin after the war, and fights both viral and bacterial infections in an entirely different way - one that could prevent pathogens from mutating to outsmart our medications.
. . .
Called Acriflavine, the antiseptic is derived from coal tar, and comes in the form of a reddish brown or orange powder.

It was first used in the early 1900s as a topical treatment to prevent flesh wounds from getting infected, and was widely used in hospitals and homes to treat everything from urinary tract infections and gonorrhoea until the 1940s, when penicillin came to the fore.

It’s now been more than 70 years since penicillin became the most important tool we have to fight bacterial infections, and its days appear to be numbered.

Many of the deadliest pathogens in the world have managed to mutate into forms that our penicillin-based drugs can’t recognise or destroy, and now antibiotic-resistant bacteria kill roughly 700,000 people each year around the world.

In addition to common hospital superbug, methicillin-resistant Staphylococcus aureus (MRSA), experts are now concerned that gonorrhoea is about to become resistant to all remaining drugs, and there are already resistant strains of tuberculosis, pneumonia, and E. coli being circulated.
. . .
So what makes Acriflavine a better fit than penicillin for our very serious superbug problem?

Gantier and his team revisited the drug that showed so much success in the early 20th century, because until now, no one had investigated how it actually works.

"Early scientific literature notes its antibacterial qualities in test tubes, but its very effective action on the skin has never been fully defined," Gantier told Bill Condie at Cosmos.

The team investigated its behaviour in human cell cultures, and figured out that it binds to the DNA of the patient to kick the immune system into action when a viral infection was taking place.

At the same time, the antiseptic also binds to viral DNA in the body, slowing the spread of viruses as the immune system prepares itself.

If you Google acriflavine, you will soon see that one of  it's major uses these days is as a fish medicine. Back in my teen years, when I worked in a tropical fish store, we used to make an all purpose "fish tonic", which consisted largely of methylene blue and acriflavine. The blue and the yellow acriflavine made it a lovely green color.  We had a huge (OK, maybe 500 g) bottle of powdered acriflavine, and the medicine was made up by adding a teaspoon or so of each (no measurements actually involved), plus a little salt and some other secret (but probably ineffective) ingredients into a gallon jar, mixing it, and bottling it. A few teaspoons would turn a tank green for a couple of days, until the dyes were degraded or absorbed. It was remarkably effective for a large number of fish diseases.

Once when I had a smashed finger nail that was starting to go bad, I drilled a hole in the nail to let out the pus and flushed it with the TNT special tonic (TNT aquarium was the name of the fish store). It stopped the infection in its tracks, at the cost of a green finger tip for a few days.

I'm surprised a DNA intercaliting agent is being considered for internal use, though. They are general presumed to be carcinogenic based on the possibility of DNA damage.

Can Science Kill the Common Cold?

Scientists crack virus code

Researchers at the Universities of Leeds and York have identified a previously unknown code contained within the strands of genetic material in rhinoviruses, the most frequent cause of the common cold.

Using a computer-based model, the researchers worked out not only how to read the messages hidden within the sequence of a virus's ribonucleic acid (RNA), but also how to "jam" the messages and stop the virus from deploying.

Dr Roman Tuma, from the University of Leeds, told the Daily Telegraph: "We have understood for decades that the RNA carries the genetic messages that create viral proteins, but we didn't know that, hidden within the stream of letters we use to denote the genetic information, is a second code governing virus assembly.

"It is like finding a secret message within an ordinary news report and then being able to crack the whole coding system behind it."

I'd like a little better explanation than that, but I wouldn't trust the average reporter to convey the information

 But don't expect a general "cold vaccine" to appear at the pharmacy any time soon.

The discovery – published in the Proceedings of the National Academy of Sciences Early Edition – is still at a theoretical stage, with trials on animal viruses required before scientists are able to develop a drug for humans.

Given that the cold is such a mild disease, more an annoyance than a threat to anyone but the sickest and oldest of us, a vaccine will have to be virtually flawless, with no or minimal side effects to be acceptable for the public.

But I sure hope to see it in my lifetime. I hate colds, it seems like they linger for weeks. Georgia came down with one a couple of days ago, and is suffering through a runny nose and cough. It seems inevitable that I'll get it, although we're trying hard to avoid it.

Giant Virus Found Frozen in Tundra

Giant virus revived from deep freeze in Siberian tundra

A 30,000-year-old giant virus has been revived from the frozen Siberian tundra, sparking concern that increased mining and oil drilling in rapidly warming northern latitudes could disturb dormant microbial life that could one day prove harmful to man.

The latest find, described online Monday in the Proceedings of the National Academy of Sciences, appears to belong to a new family of mega-viruses that infect only amoeba. But its revival in a laboratory stands as “a proof of principle that we could eventually resurrect active infectious viruses from different periods,” said the study’s lead author, microbiologist Jean-Michel Claverie of Aix-Marseille University in France.

“We know that those non-dangerous viruses are alive there, which probably is telling us that the dangerous kind that may infect humans and animals -- that we think were eradicated from the surface of Earth -- are actually still present and eventually viable, in the ground,” Claverie said.

I'm relatively confident that the only reason they managed to identify this virus a being revived from the tundra is because it's such an unusual virus; I'm sure the frozen tundra from 30K year ago was chock full of the ordinary viruses that we encountered daily and don't bother us at all, viruses that infect bacteria, viruses that infect plants, viruses that infect all the soil microorganisms, and invertebrates. Viruses have to be fairly specialized to infect organisms; they need to be adapted to proteins in the host cell to infect; the further an organism is from the "normal host" the less likely a virus is to find a foothold.  I suppose it's possible that a given piece of Siberian tundra was shit on by a sick Neandertal, Denisovan or early modern human 30,000 years ago; but if true, it's probable that if it was a serious illness, mankind has already evolved immunity to it.

Now we get to the fund raising part of the story:

With climate change making northern reaches more accessible, the chance of disturbing dormant human pathogens increases, the researchers concluded. Average surface temperatures in the area that contained the virus have increased more steeply than in more temperate latitudes, the researchers noted.

“People will go there; they will settle there, and they will start mining and drilling,” Claverie said. “Human activities are going to perturb layers that have been dormant for 3 million years and may contain viruses.”

People have been mining and drilling in all kinds of environments for a long time, exposing old sediments possibly carrying viable viruses.  It hasn't caused a problem yet.

I would hasten to add that the fact that there is frozen tundra there at all proves that during the peak of the previous interglacial, it was already warmer there than it is now.

Giant Virus Found in Sea

Just like something out of Pacific Rim... which I just may see someday.

Scientists have found a new virus thought to be the biggest ever seen on Earth.

The virus, dubbed Pandoravirus, is one micrometre big - up to ten times the size of other viruses - and only six per cent of its genes resemble anything seen on Earth before.

This has led French researchers to believe the virus may have come from an ancient time or even another planet, such as Mars.The giant virus is only found underwater and is not thought to pose a serious risk to humans.

I find it highly improbable that these viruses originated on Mars.  If they had originated and evolved entirely separately, it would be virtually impossible for a virus to capture and co-opt the cellular machinery of an terrestrial organism, like other viruses do.  Speaking of which, how do these viruses get by?

They took the samples to their laboratory and put them in a solution packed with antibiotics in an attempt to kill any bacteria present.


These bacteria-free samples were then exposed to amoebas knowing that if they died, there must be something else in the samples killing them. This proved to be successful and large amounts of Pandoravirus were spawned.

They infect amoebas.  I don't see why that would make them be especially big, but there may be a good reason.  My guess is that these represent a fairly old and primitive branch of viruses, something half way between a bacterium and a virus.  It's difficult to see how viruses evolved, and three hypothesis have been advanced:

Regressive hypothesis

Viruses may have once been small cells that parasitized larger cells. Over time, genes not required by their parasitism were lost. The bacteria rickettsia and chlamydia are living cells that, like viruses, can reproduce only inside host cells.

Cellular origin hypothesis

Some viruses may have evolved from bits of DNA or RNA that "escaped" from the genes of a larger organism. The escaped DNA could have come from plasmids (pieces of naked DNA that can move between cells) or transposons (molecules of DNA that replicate and move around to different positions within the genes of the cell)

Coevolution hypothesis

This is also called the virus-first hypothesis and proposes that viruses may have evolved from complex molecules of protein and nucleic acid at the same time as cells first appeared on Earth and would have been dependent on cellular life for billions of years. 

I can imagine the large viruses originating from infections cells, and not having lost so much as to become like the smaller, more simple viruses.  Perhaps it has to do with the nature of the environment they "live" in, or the type of organisms they infect.

Anyway, it's a neat finding.