Transcribed from the video above:
https://abc7.com/cats-covid-coronavirus-cure/6253361/
Coronavirus: Black market cure for cats with feline infectious peritonitis is illegal, but is saving thousands of lives
"I didn't even know about FIP and 24 hours later, I've got these meds in my hands," said one cat owner.
Cats are facing a pandemic of their own: a coronavirus strain that's estimated to kill tens of thousands of cats worldwide every year.
Feline infectious coronavirus, also known as FIP, is not a new virus and it is a different strain than the virus that causes COVID-19 in humans. Until now, it's been a death sentence for cats who develop the most severe forms of the infection.
Most cats develop the feline coronavirus at some point in their lives, but show little to no symptoms. In some cats, however, the virus mutates -- causing the deadly FIP.
"I didn't even know about FIP and 24 hours later, I've got these meds in my hands," Amy Shafer tells Eyewitness News.
Her 13-year old cat, Mr. Charlie Bear, was at death's door in late March of this year, in the grip of FIP.
"Vomiting, lethargy, decreased appetite and fever," Amy says. "He stopped playing with toys, eating not so much."
Amy's veterinarian told her there was no hope, that she "may want to bring him back in a day or two to have him put down."
Desperate to save the cat she says helped her through a difficult divorce, Amy and her boyfriend Christophe Liglet were tipped off to the Facebook group "FIP Warriors."
FDA says people can infect their pets with COVID-19
"So, they're just like a secret group, you have to be told about it," says Amy.
Later that same night, Amy and Christophe drove to Torrance to meet a couple they met through FIP Warriors who had a few vials to spare of a black-market drug for FIP-infected cats. Amy handed over $441 in cash for the illicit, possibly life-saving drug.
"It felt like a drug deal," recalls Christophe with a laugh. "I was like, I'm going to call the cops in five minutes if she's not out."
Amy says the results were almost immediate. His fever broke, he started gaining weight back and is now playing with toys and climbing his cat tree. Charlie Bear is about halfway through the 84-day treatment protocol which Amy estimates will cost between eight and ten-thousand dollars.
"I'm sure my family thinks I'm insane, but they would do the same," says Amy. "Charlie Bear is the best, he's just like a little person."
Dr. Niels Pedersen, a professor emeritus at UC Davis, devoted his 50-year career to studying FIP and searching for a cure.
"One percent of all cats die of FIP," Dr. Pedersen tells Eyewitness News. "This is a pandemic for cats."
Pedersen and his team at UC Davis found a cure in a drug known as GS-441524, or GS for short. It blocks the virus's ability to replicate.
"We did a field trial with 31 cats and were able to cure 25 of them," says Pedersen.
"It's miraculous," says Dr. Brian Murphy, who has since taken over the UC Davis feline coronavirus program. "I mean miraculous for me and super cool because we found this drug, a needle in a haystack."
The problem? GS-441524 is almost identical to remdesivir, the much talked about drug for COVID-19 in humans, manufactured by California-based Gilead. Early on, Gilead hoped remdesivir would prove to be successful in treating humans in Ebola.
Gilead invented and owns the patents for both GS-441524 and GS-5734 (remdesivir), and its scientists co-authored the UC Davis studies that demonstrate the drug's effectiveness in treating FIP. So far, however, Gilead has refused to license GS-441524 for use in cats.
Gilead did not respond to repeated requests for comment on this story, but told the Veterinary Information Network last year that the company is holding off on licensing GS-441524 to other parties for commercial development until remdesivir has FDA approval.
"It's very frustrating because we were faced with having this huge discovery, a great discovery," says Pedersen. "We had a drug that could safely and effectively cure most cats with FIP. This was a dream of 50 years."
UC Davis is now moving forward with testing a similar drug, GC376, in cats with FIP. That drug has been licensed by another company, California-based Anivive. Anivive is pursuing FDA approval to use the drug in cats and hopes to begin clinical trials at UC Davis later this year.
Murphy at UC Davis says his team gets emails weekly from cat owners desperate to get their cats into a clinical trial.
"We're sympathetic, empathetic toward their plight," says Murphy. "By the time we get around to doing our trial, that cat is going to be dead."
With no legal means of getting the drug, thousands of cat owners have turned to the black market. The drugs are knock-offs of GS-441524 and manufactured by various companies in China.
"The need is so intense and so great that people are going to find a way around it and that's what's happened," says Pedersen. "I warned Gilead about this."
On the FIP Warriors Facebook page, cat owners share before and after photos, guidance and support on how to get and use the drug. The group has swelled to more than 24-thousand members since its inception.
The FDA tells Eyewitness News that any unapproved drug is considered illegal, but cat owners are unlikely to be targeted by the FDA.
"In general, the FDA typically focuses its enforcement activities on the manufacturer and/or seller of the unapproved product, as opposed to the end user," says an FDA spokesperson.
"Anytime you use unapproved drugs, it's buyer beware," says Pedersen, who notes that no cure is 100% guaranteed and some cats do relapse after treatment.
Saving the lives of beloved pets with an illegal drug puts veterinarians who want to help in a legal and ethical bind.
"I do not purchase the product, I can't prescribe it," says an anonymous L.A. area veterinarian who agreed to speak anonymously with Eyewitness News. "It's a black market."
The veterinarian estimates she's treated 18 cats with the drug so far, and all but two survived.
"They're bright, happy with no signs of disease," she says. "They're happy at home with their owners or their rescue. And that was the amazing part to me because I had never seen that before. Prior to that, FIP was always a death sentence."
She realizes that administering the drug could potentially put her veterinary license in jeopardy.
"It is a risk," she says. "And if these pets did not do well and their lives were not improved or the quality of their life and longevity of their life was not improved, I would not do it."
Koi is a one-year old rescue cat who came down with FIP in mid-April. Her owner, a musician who goes by the stage name "Tillie," calls Koi her "little punk girl."
"It's scary because it's a lot of money," says Tillie. "You don't really have any guarantee."
Tillie says she couldn't bear the thought of losing Koi, after losing another beloved cat to cancer last fall.
"Within two days, I would say, we could tell it was working," Tillie says of the black-market drug. "She's a completely different cat, she runs around, she wants to get into everything."
Tillie knows it's a risk to flout the law, but says that potentially saving Koi's life is worth it.
"It would be really cruel to go after people just trying to save their animals," Tille says. "It's kind of the position that we've been put in, and it's either letting your animal die or do whatever you can to fight for them and that's what I'm going to do."
Got a tip? Email ABC7 Investigative Producer Lisa.Bartley@abc.com
My jaw dropped when I heard this doctor mention HIV, Hepatitis C, Ebola and Influenza, because in my research, I'd learned that those were all enveloped viruses... which is what a coronavirus is. So you can see this for yourself, I'm pasting some info from Google below...
People also ask
by JV Esplugues · 1996 · Cited by 65 · Related articles Oct 9, 1996 — Moderate somatic stress inhibits gastric acid secretion. ... described an emotionally related gastric hyposecretion in cats facing a barking dog.Some of the most common causes for low stomach acid include:
What Is Hypochlorhydria?Hypochlorhydria is a deficiency of hydrochloric acid in the stomach. Stomach secretions are made up of hydrochloric acid, several enzymes, and a mucus coating that protects the lining of your stomach. Hydrochloric acid helps your body to break down, digest, and absorb nutrients such as protein. It also eliminates bacteria and viruses in the stomach, protecting your body from infection. Low levels of hydrochloric acid can have a profound impact on the body’s ability to properly digest and absorb nutrients. Left untreated, hypochlorhydria can cause damage to the gastrointestinal (GI) system, infections, and a number of chronic health issues. Symptoms of low stomach acid are related to impaired digestion, increased susceptibility to infection, and reduced absorption of nutrients from food. Please note, I appreciate this article but there is a lot of conflicting information about the real cause of acid reflux. Many doctors believe it is because of too much acid in the stomach, whereas more and more doctors are starting to see that it's the opposite.... what happens is, if there's not enough stomach acid, then teh esophageal sphincter can't close properly, so acid leaks and gets into the esophagus, where it is NOT supposed to be. This causes the acid reflux. If the cat had enough stomach acid, the esophageal sphincter would have closed properly, and you wouldn't have that acid "spillage." Can Cats Have Acid Reflux?https://www.innovetpet.com/blogs/cats/cats-acid-reflux Can Cats Get Acid Reflux?Yes, cats can have acid reflux. In fact, it's pretty common. It can happen to any cat, but it is more likely to occur in young and senior cats. Unfortunately, because they can't talk to us, in human anyway, it's hard for them to tell us they're having heartburn or that their coughing or puking is from acid. What is acid reflux in cats?
Feline acid reflux is very similar to acid reflux in humans. Like us, cats are supposed to have a high amount of stomach acid, but there is such a thing as too much. With acid reflux, the cat produces more stomach acid than normal and it weakens their esophageal sphincter muscle, or this muscle becomes weakened for another reason. Either way, stomach acid starts coming up into the cat's esophagus and the esophagus is not equipped to handle stomach acid, burning and damaging the tissue. It's called acid for a reason. Acid reflux is often also called GERD or gastroesophageal reflux disease, a more descriptive and specific term. When it becomes severe enough to damage the esophagus, it becomes esophagitis. AgeYounger cats are more likely to develop acid reflux than adult cats because their esophageal sphincter muscle is not fully developed. Senior cats may have an increased risk because they are more likely to need surgeries, treatments, and medications that may cause temporary acid reflux or esophageal sphincter damage. StressLike humans, the cat body just doesn't work right when they're stressed. One of the ways this presents itself is that they can produce more stomach acid than their bodies can really handle. Too much stomach acid and gas can put excess pressure on the esophageal muscle and cause acid reflux. Treating acid reflux in catsAcid reflux isn't a disease that strikes a cat and can be eradicated like a cancer, it is a situation that arises from certain factors and can result again any time those factors are present. It can be chronic. To protect your cat, you have to diligently prevent those factors from rearing their head. This requires a long-term management plan and for you to be on the lookout for symptoms that the problem is recurring. Antacid for catsAs far as medicine goes, your vet will probably prescribe a low dose antacid for cats to manage the acid levels in their stomach. The word "antacid" may make you think of your medicine cabinet or the digestive aid aisle in the grocery store. But don't get too excited. Human antacids have spotty records for helping with feline acid reflux. PepcidIt is possible for you to give your cat Pepcid, but you should only do so with the guidance of a vet because you have to be mindful of creating a situation where the cat doesn't have enough stomach acid. This can cause serious issues that are as dangerous or even more so than the acid reflux. Long term or excessive Pepcid use can also damage the cat's kidneys. Pepto-BismolDo not give Pepto-Bismol to cats as the Bismuth subsalicylate that makes it work is dangerous to them. KaopectateKaopectate contains the same harmful substance as Pepto-Bismol as well as aspirin. Do not give this to your cat either. With any human medication or treatment, it is best to ask your vet before trying it out. Many will say it is fine to give your cat Pepcid, and go ahead, but with the vet's guidance. DietA wise acid reflux treatment in cats will include diet management. They should be eating higher-quality cat foods and less human food. Avoid giving them high fat foods as fat weakens the esophageal sphincter muscle. Lower protein food may also be advisable as protein does increase stomach acid. Soft food like more wet foods or dry food moistened with water or a wet food may help as they are easier to digest. Changing the amount of food and frequency of the food may be helpful as well. It is easier to digest food, and therefore less stomach acid is needed, to eat less food at a time. You might try feeding your cat less food more frequently so they get what they need without getting too full. This will require filling their bowl with less food to leave out or feeding them only on a schedule. When you start reading the ingredients and nutritional lists of popular commercial cat foods, you may think it'd be easier to make your own cat food. It may be a good idea to go the homemade cat food route, if you can, provided you make the cat food to your vet's specifications. It is common for people to think they're creating a healthy cat food for their cat and really be messing up their nutritional balance. There's a lot of complex planning in making a decent cat food that requires special knowledge of what cats at different ages need. Food restrictionSome vets will tell you not to feed your cat for a period of time after the visit to give the cat time to empty the food that is already in their digestive system before adding more. They will probably tell you what foods to begin feeding your cat when it is time for eating to resume. Esophageal sphincter muscle repairWith mild to moderate forms of acid reflux, the esophageal sphincter is usually able to strengthen itself when there is less acid to irritate it. Some medications to strengthen the muscle can facilitate matters. Severe GERD - esophagitis in catsThe most severe forms of acid reflux, where the esophagus has been badly damaged, occurs when it turns into esophagitis. This is when very serious conditions develop. Carafate can line an ulcerated esophagus to protect it from further damage and promote healing. Antibiotics may be given to prevent infections in damaged tissues of the esophagus, and pain medications may be given if the damage has progressed to a point where the cat's discomfort and pain cannot be alleviated by simply reducing the acid content in their stomach. Please note, this study mentions proton pump inhibititors, which I am not a big fan of. I also believe they can do more harm than good in a person with COVID-19,, simply because I know they tend to cause inflammation in humans, and they also lower the production of stomach acid that is necessary to kill viruses. https://www.vin.com/apputil/content/defaultadv1.aspx?pId=11181&id=3852215 An Overview of Gastric Mucosal Injury and Healing World Small Animal Veterinary Association World Congress Proceedings, 2004 Colin F. Burrows, BVetMed, PhD, MRCVS, DACVIM University of Florida, College of Veterinary Medicine Gainesville, FL, USA The canine and feline stomach suffers from a wide spectrum of primary and secondary disease. Most, if not all of these can cause vomiting and abdominal pain and are associated with some degree of damage to the gastric mucosa. The purpose of this paper is to review the mechanisms that facilitate or impair gastric mucosal protection in order to permit better understanding and treatment of gastric disease. Why doesn't the stomach digest itself? Physicians, physiologists and many others have been puzzled by this question since René Antonoine Ferchault de Réamur, the 18th century man of many sciences, showed that juice secreted by the stomach could digest meat. One answer of course is that it sometimes does. Under some circumstances gastric juice can produce ulcers and even destroy most of the stomach lining. Normally, however, the stomach wall staunchly resists attack; as Claude Bernard observed, it behaves as if it was made of porcelain. Gastric juice contains hydrochloric acid, one of the most corrosive acids known. At the concentration secreted by the gastric mucosa this acid is capable of dissolving zinc and is deadly to cells. Yet in the stomach it ordinarily acts only to perform the useful actions of killing ingested bacteria, softening fibrous foods and promoting pepsin formation. In the normal stomach this corrosive juice is prevented from contacting and damaging the stomach wall by a complex and interrelated series of physical and chemical processes that are only now beginning to be fully understood. Collectively these processes are called the gastric mucosal barrier and comprise the structural and functional protection of the stomach against its own secreted acid and pepsin as well as against the ravages of refluxed bile and pancreatic enzymes and ingested abrasive or toxic materials. There are five interrelated components: 1) the gastricepithelial cells; 2) gastric mucosal blood flow and local acid base balance; 3) gastric mucus; 4) mucosal prostaglandins and associated cytoprotection; and 5) the epithelial cell basement membrane. The Gastric Epithelial Cells The epithelial cells of the gastric mucosa form a formidable barrier against penetration by luminal contents, including hydrogen ions. The cells have very tight junctions, a lipid-rich, hydrophobic, acid-repelling mucosal surface, and secrete bicarbonate and mucus. The gastric mucosa is routinely exposed to trauma, indeed, focal destruction of the mucosal barrier is a normal physiologic event, occurring for example, during intragastric digestion of a meal, after thermal, mechanical or osmolar damage and after ingestion of several different types of drug. Normally, however, the mucosa can repair or minimize this damage almost as soon as it occurs by a process of epithelial cell migration called restitution. This is a physiological event in which the epithelial cells at the mouth of the gastric glands adjacent to a damaged area flatten themselves and project finger like processes called lamellipodia. These extend over the underlying basal membrane and eventually fuse to form a new intact epithelial barrier. Gastric Mucosal Blood Flow The gastric mucosal blood supply has been called the mainstay of the gastric mucosal defense mechanisms that sustain a healthy gastric mucosa. Mucosal blood flow is achieved in a variety of ways, foremost of which is a unique vascular supply that maximizes mucosal oxygenation, bicarbonate delivery and buffering. Bicarbonate, a byproduct of acid production, is carried up to the mucosal surface by capillaries that surround each gastric gland. This bicarbonate escapes from the capillaries into the submucosa underneath the mucosa from where it is taken up by the epithelial cells and secreted into the surface mucus layer. The bicarbonate is trapped here and neutralizes any hydrogen ions that may diffuse into the mucus layer. As a result, the surface of the mucosa is maintained at a pH of about 7.2 while the pH of the lumen may be as low as 1.5. The bicarbonate-rich mucosal blood flow also maintains intramucosal acid base neutrality such that any hydrogen ions that may leak into the submucosa through a damaged epithelium are quickly neutralised. A decrease in mucosal blood flow however, will result in an increase in mucosal hydrogen ion concentration with subsequent tissue damage. Mucus Secretion Mucus neck cells produce the bulk of gastric mucus. This forms a viscid unstirred protective layer of varying thickness over the surface mucosa that traps secreted bicarbonate and lubricates the lining of the stomach. When damaged the epithelial cells themselves rupture and release copious quantities of protective mucus that forms a bicarbonate-rich protective mucus cap over the denuded area. Surrounding epithelial cells can migrate over the basal membrane and under this protective mucus cap. Prostaglandin Secretion and Cytoprotection Cytoprotection refers to the ability of certain substances to maintain tissue or cellular integrity in the face of mucosal damage. The term was originally coined to describe the ability of prostaglandins to reduce or eliminate hemorrhagic damage in mucosa exposed to injury. The term has been extended however, to describe a similar protective ability for a large number of endogenous and exogenously administered substances with anti-ulcerogenic effects. Cytoprotection is based upon the ability of these substances to inhibit acid secretion, stimulate mucus and bicarbonate secretion, and increase mucosal cell turnover and blood flow. Prostaglandins PGE2 and PGF2aare perhaps the best known examples of cytoprotectants. However, IL-1 and TNF released during inflammation increase mucosal blood flow and cytoprotection, as do exogenously administered sulfhydryl compounds such as acetylcysteine, glutathione and penicillamine. Epidermal growth factor which is found in saliva as well as in the gastric mucosa plays an important role in maintaining and stimulating mucosal cell turnover. The Basal Membrane This, the last defensive barrier is important for the process of restitution. The basal membrane is permeable to fluid and electrolytes and when disrupted allows an inrush of hydrogen ions and proteases from the gastric lumen. These invoke an inflammatory response and mark the changeover from physiologic to pathologic (i.e., inflammatory) repair of the mucosa. BARRIER DISRUPTION Pathologic and inflammatory barrier disruption occurs in virtually every type of gastric disease as well as in a variety of less well appreciated circumstances such as stress, brain and spinal cord injury, hypotension, hypoadrenocorticism, sepsis, uremia, liver disease, hypoproteinemia and protein-calorie malnutrition (Table 1). Most instances of barrier disruption associated with this diverse group of disorders can be attributed to a decrease in gastric mucosal blood flow, except for the hypoproteinemic or cachectic patient in which decreased cell turnover also plays a role. Table 1. Disorders associated with a disrupted mucosal barrier
In humans and some other species, infection with the Gram negative gastric bacteria Helicobacter is associated with gastric and duodenal injury. Mucosal damage from infection with H. pylori in humans is associated with the cytotoxic effects of a number of bacterial metabolites including ammonia, endotoxin, and a variety of inflammatory peptides. The organism also inhibits somatostatin secretion allowing an increase in acid secretion. Strangely, these properties do not appear to be present in the Helicobacter species (e.g., H. felis, H. bizzozeroni) that infect the dog and cat. Gastric structure and function for example, are no different between infected and uninfected dogs. The exact role of Helicobacter infection, if any, in the genesis of gastric lesions in the dog and cat therefore remains to be elucidated. Virtually every critically ill patient has some degree of gastric mucosal damage that is evidenced by gastric erosions or ulceration with associated hemorrhage. This sometimes "hidden" injury very often prolongs patient morbidity, and if unappreciated or untreated may progress to a serious or life-threatening condition. An appreciation of the processes of barrier disruption and repair, together with an understanding of current methods for facilitating or enhancing the repair process are therefore important for most clinicians. THE RESPONSE TO INJURY A break in the gastric mucosal barrier allows hydrogen ions and pepsin to diffuse into the mucosa from the lumen and sodium ions to diffuse in the opposite direction. Back-diffusion of acid and pepsin into the tissues stimulates further acid and pepsin secretion, decreases mucosal blood flow and decreases gastric motility. The acid also damages connective tissue and submucosal capillaries to cause focal mucosal hemorrhage and microulceration. If sufficiently severe and prolonged overt gastric ulceration may occur. Mucosal integrity, however, is rapidly reestablished if the inciting cause is removed or if appropriate and prompt treatment is given. Of concern to the clinician are factors that may delay or impair epithelial cell restitution and the repair process, such as hypoxia, sepsis or concomitant drug therapy. Corticosteroids for example, decrease gastric epithelial cell renewal and while relatively harmless in the healthy animal may delay repair or exacerbate mucosal injury in the sick one. It should be noted however that methyl prednisolone sodium succinate at a dose of 30mg/kg/day for two days induced gastric hemorrhage in 100% of healthy normal dogs and that the synthetic prostaglandin misoprostol did not prevent the hemorrhage. Nonsteroidal anti-inflammatory drugs (NSAIDs) are another group of compounds that exacerbate underlying disease and delay repair, primarily through their inhibition of cyclooxygenase and a decrease in mucosal prostaglandin concentration. Recent attention has focused on the fact that there are two types of cyclooxygenase (cyclooxygenase 1 and 2 or COX-1 and COX-2). COX-1 is constitutively expressed in most cells and tissues, notably platelets, endothelial cells, stomach and kidney. COX-1 plays a key role in the synthesis of prostaglandins responsible for mucosal cytoprotection. COX-2 on the other hand is typically undetectable in normal tissue but is induced in inflammatory conditions by cytokines or lipopolysaccharides. NSAIDs exert their antiinflammatory effect through the inhibition of COX-2 whereas many of their adverse effects are due primarily to the inhibition of COX-1. Several COX-2 specific antiinflammatory drugs have recently been introduced and purportedly reduce inflammation while sparing the gastric mucosa. Aspirin inhibits both cyclooxygenases but in addition, when the intragastric pH is less than 4.0, it undergoes a change in lipid permeability and is absorbed directly into the gastric epithelial cell where it disrupts cellular function. The drug is also purported to facilitate bile reflux in the dog. The canine stomach is particularly sensitive to NSAIDs and none of these drugs should be considered "safe" in this species. FACILITATION OF MUCOSAL REPAIR The most important concept in dealing with the disrupted mucosal barrier is to recognize that disruption is widespread and that it can occur in such a wide variety of diseases (Table 1). Barrier disruption occurs routinely for example in hypoadrenocorticism, peritonitis, pyometra, pneumonia, liver disease, hypoproteinemia, severe trauma, uremia and in most if not all primary gastric diseases. The most important remedy in all these disorders is to treat the underlying disease. All other actions are of secondary, but nevertheless still considerable importance. Drug therapy, however, remains the mainstay of treatment. These fall into two main groups 1) antisecretory drugs and 2) cytoprotectants that are usually combined to achieve an optimum effect (Table 2). Table 2. Drugs that augment the mucosal barrier
Antisecretory Drugs A variety of compounds have been used to reduce acid secretion but most widely used are the H2 receptor antagonists such as cimetidine, ranitidine and famotidine. Cimetidine interferes with the cytochrome p450 system in the liver and can influence the action of some drugs (e.g., ketoconazole, theophylline, propranolol, quinidine and metronidazole) and the absorption or effect of others (e.g., metoclopramide and sucralfate). Cimetidine, however, is ineffective against aspirin-induced mucosal injury in dogs. Ranitidine binds much more strongly to the H2 receptor on the parietal cell and therefore requires a lower frequency of administration as well as indirectly increasing gastric motility. Cimetidine also has additional protective effects on the mucosal barrier (increased cell turnover, mucus production, mucosal blood flow, bicarbonate secretion and cellular integrity). Famotidine inhibits stress-induced decreases in gastric mucosal blood flow and has the benefit of once daily dosage which makes it attractive to many clients. The prophylactic use of H2 receptor antagonists should therefore be routine in critically ill patients. Omeprazole, is another very effective antisecretory drug. Cimetidine, famotidine and ranitidine block only histamine-induced acid secretion but omeprazole blocks all acid secretion by inhibiting H+K+ATP'ase at the luminal surface of the parietal cell. While a major portion of the therapeutic efficacy of omeprazole involves inhibition of gastric acid secretion, some of its cytoprotective properties are probably associated with its action on the mucosal vasculature. Oral omeprazole for example, maintains mucosal blood flow in the face of mucosal damage and decreases mucosal production of the vasoconstrictor phospholipid platelet activating factor (PAF). Cytoprotective Drugs These include synthetic prostaglandins, sucralfate, antacids containing aluminum, and the bismuth sub-salts. Sucralfate is a complex polymer of sucrose with multiple substitutions of sulfate and aluminum salts. At a pH <4.0 it undergoes a change in chemical configuration, developing a positive charge which binds electrochemically with the negative charge in serum protein to form a protective layer over ulcerated areas which protects the mucosa against further injury by acid, pepsin and bile salts. The drug also stimulates the synthesis and release of prostaglandins, epidermal growth factor and nitric oxide as well as augmenting other aspects of the mucosal barrier such as gastric mucosal blood flow, bicarbonate secretion and mucus production. Sucralfate also stimulates angiogenesis in injured gastric mucosa. The bismuth subsalts and aluminum containing antacids at doses less than those required to neutralize acid also exert beneficial effects on the mucosal barrier through augmented prostaglandin synthesis. CONCLUSION Gastric mucosal damage and repair are ongoing processes in the normal stomach with repair, primarily through epithelial cell restitution, rapidly restoring the ravages of normal wear and tear. The repair process however, may be impaired in gastric disease as well as in a variety of other diseases that weaken gastric defenses. If unrecognized and untreated this will increase patient morbidity with the likelihood of overt ulceration. Treatment with H2 receptor antagonists and cytoprotective drugs is critical to patient well being. Speaker Information (click the speaker's name to view other papers and abstracts submitted by this speaker) Colin F. Burrows, BVetMed, PhD, MRCVS, DACVIM I was surprised to read, tonight, that dogs don't appear to be susceptible to SARS-COV2, whereas cats are (see highlights from the study further down the page). Then I thought, wait a minute... that makes sense, because I've worked with a lot of animal rescue groups, and have seen many cats die from FIP (Feline Infectious Peritonitis), which is a coronavirus... but for whatever reason, you never hear about dogs getting any type of Infectious Peritonitis. I had to wonder: Why does COVID-19 affect Cats, but not dogs? Here's an excerpt from the article I read: https://www.nature.com/articles/s41579-020-00459-7 Besides wildlife, researchers investigated the susceptibility of domesticated and laboratory animals to SARS-CoV-2 infection. The study demonstrated experimentally that SARS-CoV-2 replicates efficiently in cats and in the upper respiratory tract of ferrets, whereas dogs, pigs, chickens and ducks were not susceptible to SARS-CoV-2 (ref.43). The susceptibility of minks was documented by a report from the Netherlands on an outbreak of SARS-CoV-2 infection in farmed minks. Although the symptoms in most infected minks were mild, some developed severe respiratory distress and died of interstitial pneumonia44. Both virological and serological testing found evidence for natural SARS-CoV-2 infection in two dogs from households with human cases of COVID-19 in Hong Kong, but the dogs appeared asymptomatic45. Another serological study detected SARS-CoV-2 neutralizing antibodies in cat serum samples collected in Wuhan after the COVID-19 outbreak, providing evidence for SARS-CoV-2 infection in cat populations in Wuhan, although the potential of SARS-CoV-2 transmission from cats to humans is currently uncertain46. That got me trying to find a connection between cats and humans, that we don't share with dogs, so tonight I did some research on Feline Infection Peritonitis. I've done a good amount of research on FIP in the past, because I was trying to figure out a treatment for it myself! FIP is like a death sentence, and no vet could seem to figure out how to treat it. I, too, had a cat that passed away, over 10 years ago, from FIP, and it was horrible. They go downhill very quickly when the virus takes hold. Well, last year, not even 6 moths before the COVID pandemic, I was talking to someone who works with the Nine Lives Foundation (a nonprofit that has helped me get a lot of rescue cats spayed and neutered). She told me that 9 Lives has just discovered a veterinarian who discovered a cure for FIP, and they're sending their FIP-positive cats there. Naturally, I've been wondering if that cure is related somehow to changing the cat's pH, to make them more alkaline. I've wanted to meet this doctor in person and ask him questions about the treatment, but it's on a very long list of things I need to do, and I just hadn't gotten around to it yet.
Last year, I met a couple who was distraught because their kitten whom they had adopted from 9 Lives, had FIP, and they were told he was going to die and there was no cure. I tried to help this couple, giving them antioxidant alkaline water. I also gave them some hypochlorous acid (HOCl), since that stuff seemed to work like a miracle for my 2 cats that got extremely sick a few years ago (it seems to do a really good job of killing worms). I was hoping there was a chance maybe it could kill the virus, since I've never seen any virus it did not kill. But sadly, it just wasn't enough to save the kitty, and she still passed away. I was really heartbroken that she didn't live, and kept wondering what could have been done differently. If I could do it all over again, I would skip the HOCl altogether, now that I know coronaviruses seem to thrive in an acidic environment. Because I now know that a coronavirus has a fatty lipid bilayer that appears to break down when exposed to a surfactant or emulsifier, I would have given that couple just the 11.5 pH water our machine makes, and skipped the 2.5. When I did my own experiments to see how quickly I could dissolve a layer of fat with this 11.5 pH liquid, I have to say it was one of the things that worked well (Note: as a distributor of these machines, I am not able to tell any person they should drink this water - the company is very adamant about the fact that the only waters they recommend for drinking are the ones in the 7.0 to 9.5 range). I'm just bringing this up because I know of other people who have the machines, who consumed very small amounts of the other "strong" types of water, but they drank it entirely at their own risk, knowing the company does NOT recommended those waters for human consumption. I can report that when I gave my cats the 2.5 pH water (aka hypochlorous acid), I was shocked to see how much it helped them. I don't remember exactly what city she said he was in, but I remember it was somewhere up north, about an hours' drive from 9 Lives. I remember this because I was thinking, wow, that's about an hour-long drive, to take all the cats there. Also, I had thought to myself, I want to meet this guy and buy him lunch and ask him about his methods! And I remember thinking it would take me about an hour of driving (with no traffic) to get to where he was. I had been meaning to get in touch with the gal I spoke with at Nine Lives, to ask her for the name of the doctor who found a cure for FIP, but... it's on a VERY long to-do list and I just hadn't had the time to make the calls, yet. Then, tonight, I was doing some research on FIP in cats, after learning SARS-2 seems to affect cats, but not Dogs (I highlighted what I read, below). In trying to figure out what the connection is between humans and cats (but not humans and dogs), I did some FIP research on YouTube (knowing cats are susceptible to FIP), and stumbled upon this video below. This has got to be the same guy 9 Lives is sending their FIP+ cats to (I need to double check with 9 Lives, but I'd bet money on it).
UC Davis professor who created cure for coronavirus in cats says drug should 'receive more attention' Sadly, it doesn't come as a surprise that this drug isn't getting much attention, despite the fact that it's really incredible that anyone could have come up with a treatment for FIP, given how long a cure has eluded veterinarians. Sadly, it really does seem as if the things that work REALLY WELL just never seem to come to light if it's not a big money maker. For anyone who thinks this sounds like some kind of conspiracy theory, you may want to do some research on Fenbendazole. Fenbendazole is a cheap dog-deworming drug that has been used by many people to reduce or even eliminate their cancer. Last year, I saw a news story about a guy named Joe Tippens who had Stage 4 cancer in his lungs, liver, pancreas, neck and bones. His insurance company spent over a million dollars treating him with modern methods, which were unsuccessful. He was basically sent home to die. But then one day, a veterinarian told him about a cheap dog de-worming medication that cost 5 bucks, that had been helping a lot of people with cancer. Figuring he had nothing to lose, Joe Tippens took the medication, and guess what? ONE HUNDRED PERCENT of his cancer went away. I realize that, for anyone who's never read about this before, that is going to sound way too good to be true. Well, the guy sure sounds like he's telling the truth, and he has the proof that not only did he have several types of stage 4 cancer, and he also has proof that he was declared cancer free. You can read about his story by clicking HERE, and decide for yourself. This is a bittersweet story for me, because I lost a close family friend to Cancer, and I only learned about this treatment about 6 months after she passed away. I sure wish one of the doctors at her hospital could have told us about this treatment, but... nope! Fenbendazole and Mebendazole discovered to be effective at killing cancer cells over ten years ago. In fact, John Hopkins University even mentioned it in their newsletter! So...how come we never heard about it? I don't have a definite answer for that one, and I really do not want to believe that this lack of publicity could have anything to do with the fact that there are a lot of people out there who would lose a lot of money, if it was discovered that cancer was something that was dirt cheap, and people could buy it right off Amazon. But I can't rule that out, either. Not surprisingly, the price of Fenbendazole has gone up somewhat (and Joe Tippens said the manufacturer tried to raise the price WAY up, but you can still get it fairly cheap - maybe because it's a common drug that's manufactured all over the world). The cost is nowhere close to the cost of chemotherapy. It's profitable for humans to be sick - but not livestock Years ago, I listened to this audiobook by Joel Wallach, called "Dead Doctors Don't Lie," and Dr. Wallach noticed that animals were being given a lot more nutrition than most humans were. Why? Because it meant the farmers would get more profits. It is far more profitable for livestock animals to be healthy, than it is for humans, because livestock animals are a commodity that can be sold. A sick cow cannot (or should I say should not) be sold. A sick human being becomes a commodity in the U.S.. when they get sick. I highly recommend listening to this presentation by Dr. Wallach: Dead Doctors Don't Lie (Original Audio) https://www.catvirus.com/treatment.htm
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